[
    {
        "Introduction to Shock": "hello and welcome to chapter 13 shock of the emergency care and transportation of the sick and injured 12th edition you complete this chapter and the related coursework you will have an understanding of the different types of shock the process of perfusion the signs and symptoms associated with shock application of the assessment process with the shock patient and the general and specific emergency care provided to patients experiencing shock okay so let's get started",
        "Definition of Shock": "shock when you think of shock also think of hypoperfusion you're going to hear those terms interchangeably often okay so it's defined as an inadequate cellular perfusion and any compromise in perfusion can lead to cellular injury or death okay and so in the early stages the body is going to attempt to maintain homeostasis",
        "Pathophysiology of Perfusion": "diffusion is the passive process in which molecules move from an area with a higher traction of molecules to a lower area concentration so this is how oxygen and carbon dioxide move across the alveoli the majority of oxygen is carried to the tissues attached to hemoglobin now carbon dioxide can be transported in the blood from tissues back to the lungs in three ways so carbon dioxide could be dissolved in plasma it could be combined with water in the form of bicarbonate and also attached to the hemoglobin okay so carbon dioxide is that waste product that's released from the cells and can combined with water in the bloodstream to form bicarbonate right so just a little bit more on that and once it reaches the lungs the bicarbonate breaks back down into carbon dioxide and water and the carbon dioxide is then exhaled in cases of poor perfusion remember this is called shock the transportation of the carbon dioxide out of the tissues will become impaired and this results in dangerous buildup of waste products and it can cause cellular damage so shock refers to a state of collapse and failure of the cardiovascular system that leads to inadequate circulation okay to protect vital organs the body directs blood flow from organs that are more tolerant of low flow such as let's say the skin and the intestines to organs that cannot tolerate low blood flow and these are organs such as the heart brains and lungs okay so early recognition of the signs and symptoms of shock can save lives and shock is a life-threatening and requires immediate recognition and treatment the cardiovascular system consists of three parts so it consists of the pump the container and the contents and so this is the heart the blood vessels or all the tubes in the body that blood goes through and the blood okay so this is a great slide you've seen it probably already in the um body systems chapter but this is a great slide like i said that illustrates the cardiovascular system and it shows those three parts so it's showing you the heart on the vessels and the blood so the perfusion triangle so these three parts can be refused referred to as the perfusion triangle the heart blood vessels in the blood and when a patient is in shock one or more of these three parts is not working properly okay so blood pressure is the pressure of blood within the vessels at any moment we know that and the systolic pressure is the peak arterial pressure and that means it's the pressure generated every time the heart contracts and then the diastolic pressure is the pressure maintained within the arteries while the heart rests between heartbeats pulse pressure is the difference between the systolic and the diastolic so the systolic minus the diastolic is the pulse pressure so let's say that somebody has a a 140 heart or 140 systolic over 80 so the pulse pressure is going to be 140 minus 80 is going to be 60. and it signifies the amount of force the heart can generate with each contraction so a pulse pressure less than 85 millimeters of mercury may be seen in patients with shock so for example this might be somebody who has a blood pressure of a hundred and ten over ninety now that pressure difference is only twenty so that can signify patients um who may be in shock all right so blood flow through the capillary buds is regulated by the capillary sphincters and this is uh circular muscle walls that constrict and dilate these sphincters are under a control of the autonomic nervous system which regulates involuntary functions such as swelling and digestion and these sphincters are also in other areas such as and they respond to stimuli such as heat cold or the need for oxygen or the need for waste removals and the regulation of blood flow is determined by cellular needs so perfusion also requires adequate oxygen from the lungs nutrient in the form of glucose and waste removal which is primarily through the lungs okay so mechanisms are in place to help support the respiratory and cardiovascular system when the need for perfusion of vital organs is increased and this includes the autonomic nervous system and hormones okay so the sympathetic side of the autonomic nervous system which is responsible for the fight or flight will assume more control of the body's function during a state of shock okay so remember we have the sympathetic and the parasympathetic and the sympathetic takes over um when the body is in the state of shock okay so this response by the autonomic nervous system causes release of hormones such as epi and norepi these hormones increase the heart rate and the strength of the cardiac contractions as well as vasoconstricting non-essential areas okay so primarily in the skin and gastrointestinal tract and this response causes all of the signs and symptoms of shock in a patient",
        "Causes of Shock": "so let's talk about causes of shock now there's three of them and remember that perfusion triangle we could go all the way back to that because if there is a problem it's one of those basic three things that are failing so either you have a pump failure you have a poor blood vessel function or you have low fluid volume okay so we when we look at it we look at this illustration on the slide and it shows those three basic causes of shock okay super simple it's either a pump problem a fluid problem or the vessels the tube problem and this table on the slide shows those signs of shock resulting from those three basic problems and so that's what we're going to talk about today so you have cardiogenic and obstructive and obstructive it it's further broken down into tension cardiac tamponade and pulmonary emboli and then in poor vessel function you have distributive shock inside of distributive shock you have septic neurogenic anaphylactic and the psychogenic shock and then low fluid of course you have hypovolemic shock inside of hypovolemic it's the hemorrhagic and the non-hemorrhagic is how it's going to be broken down and we're just going to go through those different types of shock next",
        "Cardiogenic Shock": "okay so cardiogenic shock remember cardiogenic shock is the first one and it is a pump failure problem cardiogenic and obstructive are a pump failure problem okay and it's caused by an adequate function of the heart or pump failure and a major effect is the backup of blood into those pulmonary vessels and the resulting buildup of pulmonary fluid is called pulmonary edema and so a lot of times cardiogenic shock is caused simply by some type of heart failure right so we have some type of heart attack perhaps the muscle of the heart is failing okay and it develops when a heart cannot maintain that output to meet the demands of the body so cardiac output of course is the volume of blood that the heart can pump per minute and it's dependent on a bunch of factors so the heart must be it must have adequate strength remember so if the heart is uh weakened from different heart attacks um then it does not uh have that ability to contract and that's called the myocardial contractibility the heart must also receive adequate blood to pump and that's the preload it has to have the blood ready to go into those chambers and then the resistance to the flow in the peripheral circulation must be appropriate okay so the afterload must be okay all right so we're still talking about different types of pump failure problems remember i'll go back to the slide one more time and the next pump failure problem we're going to have is the obstructive shock and this means that the pump is not able to work because of some type of obstruction okay so some type of obstruction is going on",
        "Obstructive Shock": "and this is called by a mechanical obstruction meaning the heart is not able to beat but it's still the heart problem okay so it's not a muscle it's not too weak it's actually literally obstruction obstructed and so this is um it prevents adequate flow of blood from the heart chambers okay so there's three of them and it's cardiac tamponade tension pneumo and pulmonary emboli and we're going to talk about that more okay so um cardiac tamponade so this is a collection of fluid between the pericardial sac and the myocardium and that is called a pericardial infusion so you have that sack that that surrounds the heart and there's fluid in it and so the literally the heart cannot um cannot beat cannot contract if the fusion becomes large enough it can prevent the ventricles from filling and that's a position that's a condition called cardiac tamponade it's caught it can be caused by a blunt or penetrating trauma that causes the hemorrhage around that heart inside the sac the signs and symptoms of cardiac tamponade are referred to beck's triad so when you think about cardiac tamponade you really need to think about bex triad so there's three things hence the triad the first one is the presence of the jugular vein distension and obviously the blood can't get can't return from that superior vena cava so it's backing up into those jugular veins you're also going to hear muffled heart tones because there's fluid in that sac so it's going to make a muffled and then of course the narrowing pulse pressures where the systolic and dystolic begin to um to merge okay so that's called narrowing pulse pressures so first thing of the obstructive shock is we have cardiac tampon",
        "Obstructive Shock Continued": "the next one is the pneumo so this is caused by air that has damaged the lung tissue and the air normally is held within the lung escapes into the chest cavity and so the lung collapses if the pneumo is left untreated air will accumulate in that chest chest cavity and apply pressure to the organs and this is including the heart and the vessels and so when that air has um put enough pressure on the heart the heart is going to be not going to be able to be just like in the cardiac tamponade and um and so you have that obstructive shock from the tension okay then there's the third one third obstructive type shock and that is the pulmonary emboli so this is basically just a blood clot when you see the embolism you think clots and it occurs in the pulmonary circulation that blocks the flow of blood through the pulmonary vessels okay so when a massive pulmonary emboli occurs it can prevent blood from being pumped from the right side of the heart into the left resulting in a complete backup of blood in the right ventricle and leading to catastrophic obstructive shock and complete pump failure all right so that was the um cardiogenic shock and now we're going to move into distributive shock okay so here we are distributive shock this is because of the poor vessel function so now we're into the the vessels this is actually the tubes of the cardiovascular system is what we're",
        "Distributive Shock": "talking about okay distributive shock this results in when there's some type of widespread dilation of those small arterioles small venules or maybe both and the circulation of blood pulls into the expanded vascular beds and the tissue perfusion decreases okay so distributive shock remember there's different types of distributive shock and we'll go back up to the slide there's septic neuro anaphylactic and psychogenic okay so we're going to talk about the four of those next septic shock and um it occurs as a result of a severe infection usually bacteria in which toxins are generated by bacteria or by infected body tissues okay so what you have is widespread dilation of those vessels combined with plasma loss through the injured vessel walls and because of the the decrease in that fluid you're gonna it result in shock",
        "Distributive Shock Continued": "okay and that's the same same thing that the last slide just shows all right so neurogenic shock is the next type of distributive shock remember there's four of them and this is usually a result of some type of spinal cord injury basically the muscles of the in the walls of the blood vessels are cut off from that nervous system and nerve impulses that cause them to contract and so what's going to happen is all the vessels below that level of the spinal cord injury are going to dilate widely increasing the size and capacity of the vascular system and of course then blood is going to pull you're going to lose lose the the good container right so you're going to lose that next we have anaphylactic shock this is that third type of shock it occurs when a person reacts violently to a substance to which he or she has been sensitized so sensitization means becoming sensitive to that substance that they did not initially cause a reaction and then each each time they are exposed to that sensitization it tends to produce produce a more severe reaction okay so this table on the slide lists the signs and symptoms of the anaphylactic shock okay and then the fourth and final type of distributive shock of the vessel problem is going to be the psychogenic shock and this is when a patient is in um when they're in psychogenic shock they've had some type of sudden reaction of the nervous system that produces a temporarily and a generalized vascular dilation and usually they'll have a sinkable episode okay usually life-threatening causes include some type of irregular heartbeat or some type of brain injurism but you also have non-lethal left life-threatening events which include maybe hearing some bad noise or bad new news or experiencing fear or unpleasant sights such as some type of blood okay now we move into the fluid issue right so now we have the fluid problems and um so that the the one that we're going to talk about is hypovolemic shock and of course there's two there's hemorrhagic and non-hemorrhagic and we'll get into those next but um the result is obviously an inadequate amount of fluid or volume in that circulatory system so this is the blood part um the third third thing right so you have the the pump problem vessel problem and now the blood problem okay so this occurs with usually some thermal burns you could have thermal burns and we'll talk about the different types",
        "The Progression of Shock": "okay all right so you have stages of shock so the different stages of shock okay so you have the compensated where the body is able to compensate then you have the decompensate and then once shock has progressed too far it becomes irreversible so no way to assess when the patient has reached this point just you that's why we need to recognize and treat shock very early um well before the patient transforms into this decompensated state okay the table on the slide lists the signs and symptoms of compensated versus decompensated shock so very good to get to know those different signs okay all right so blood pressure will be the last measurable factor to change with shock and so when the blood pressure is evident um shock has well developed okay when a drop in blood pressure when you see that so this is particularly true in infants and children who can maintain their pressure until they have blood loss that is more than half their blood volume okay so by the time pressure drops in infants and children who are in shock they're pretty close to death okay so expect shock in many emergency medical situations also expect shock if a patient has one of the following conditions so say that they have multiple fractures or some type of abdominal or chest injury spinal injury severe infection a heart attack or anaphylaxis okay",
        "Scene Size-up": "all right so now we're just gonna go through um how you treat the patient so we're gonna start off with the scene size up of course and make sure that the scene's safe and then try and determine that mechanism of injury or nature of illness",
        "Primary Assessment": "then do that primary assessment and when you suspect some type of shock",
        "Rapid Exam and Treatment": "you should probably do a rapid exam all right so we're going to do a real rapid exam and we want to determine the loc level of consciousness and identify and treat any of those life-threatening concerns first okay so determine the priority of the patient transport it's if there's a massive hemorrhage you may be required to put on that tourniquet remember direct pressure dressings when tourniquets are not feasible or available so before the airway is opened you should stop that bleeding so if the patient has life-threatening external hemorrhage it should be addressed first like i said even before the airway then the abcs must be assessed and treated and and treatments for shock provided okay so provide high flow to to assist with profusion of damaged tissues if the patient has signs of hypoperfusion you need to treat aggressively and provide rapid transport so request an advanced life support as necessary to assist with more aggressive shock management",
        "General Impression and Circulation": "all right and then of course our general depression we're going to determine the need for spinal immobilization and we're going to do airway and breathing so we need to assess the airway to ensure that it's patent and it quickly assess the breathing and then of course there's a circulation and we're going to assess the patient's circulatory status to see if there's any clues regarding the presence of shock okay we're going to check for the distal pulse if there is none check for the central remember the carotid and determine if the pulse is fast slow weak strong or altogether absent a rapid pulse suggests compensated shock so in shock or compensate shock the skin may be cool clammy or ashen and if the patient has no pulse and is not breathing of course we're going to begin cpr and assess for and identify any life threats bleeding and trauma patients and we're going to treat it immediately of course so quickly assess skin color temp condition and check for cap refill okay our determination of our transport so we're going to determine whether the the patient should be treated as high priority whether advanced life support is needed and which facility to transport to",
        "History Taking": "all right so after that we're going to do history taking and after life threats have been managed determine the chief complaint of course and then obtain a sample history",
        "Secondary Assessment": "we're going to do the secondary assessments and this includes a physical exam so we're going to repeat the primary assessment followed by a focused assessment and the secondary 4 trauma is going to be a focus assessment okay and so we're going to perform it of the entire body and we're going to um to look uh very closely if if our trauma patient has any significant illness or injury okay and we're going to do this if the patient gives you a poor general impression or you find problems in the primary assessment or if your patient has a medical problem but it's not responsive or if your patient has problems that were not noted in the primary assessment these assessments should be performed quickly but thoroughly to ensure that you did not miss any significant or life-threatening problems or delay needed care so whether your examination is is of the entire body system or specific area if the life-threatening problem is found so treat it immediately okay and then you're going to do the vital signs and then we're going to reassess a patient so we're going to reassess the patient's vital signs interventions chief complaint abc's and mental status then we're going to determine what interventions are needed for the patient based on the assessment findings okay so we're going to focus on supporting the cardiovascular system we're going to treat for shock early and aggressively by providing oxygen and keeping the patient warm that's how we treat for shock remember",
        "Emergency Medical Care for Shock": "all right so emergency care for shock we're going to begin immediate treatment for shock as soon as we recognize the condition exists we're going to follow local precautions control all external bleeding obvious external bleeding make sure the patient has an open airway and then inline maintain inline stabilization if necessary we're going to comfort calm and reassure the patient while maintaining the patient in the supine position we're never going to allow the patients to eat or drink prior to being evaluated by a physician so no food or drink and of course if c-spine is indicated we're going to put the patient on the backboard okay and we need to remember that adequate ventilation may be a major factor in the development of shock so we have to provide oxygen assistance sometimes and use airway adjuncts when needed we have to prevent body loss by placing blankets under and in over the patient and we need to transport the patient and treat additional injuries and route and then consider rendezvous advanced life support if possible and consider a helicopter aero medical if needed accurately record the patient's vital signs appropriately every five minutes throughout treatment and transport",
        "Treating Cardiogenic Shock": "okay so specifically cardiogenic shock how are we going to treat these patients and this is a result of that it could be a result of a heart attack and because it cannot generate the necessary power to pump and so usually patients with cardiogenic shock they do not have an injury but they may have chest pain and patients with cardiogenic shock should not receive nitro um if they are hypotension tensive remember okay so signs and symptoms of that cardiogenic shock are going to be a lot of times low blood pressure or a weak irregular pulse cyanosis around the lips or under the fingernails anxiety and nausea so we want to place these guys in the position that eases the breathing and give them a high flow o2 and then initiate prompt transport and advanced life support if they're not already on scene we should consider rendezvousing with them in route",
        "Treating Obstructive Shock": "then how are we going to treat obstructive shock so for cardiac tamponade we're going to increa increasing cardiac output should be the priority so we want to try and give them high flow oxygen and they're going to need surgery that's the only definitive treatment okay and then for tension pneumo of course that the next obstructive shock we're going to give them high flow 2 and a non-rebreather to try and prevent that hypoxia chest decompression is required to relieve that pressure however that's an advanced life support skill and so you should try and get als there assistance early in the call if available because um they're going to need to get that like i said the chesty compression but do not delay transport to wait for them okay",
        "Treating Septic Shock": "okay so treating septic shock um this requires hospital management including antibiotics so we want to use standard precautions because of um any type of risk of infections and uh transport promptly so give them high flow of two and possibly support the ventilations with the bvm preserve the body heat and notify a specialized sepsis team if available to meet the patient in the emergency department room",
        "Treating Neurogenic Shock": "so emergency treatment we're gonna obtaining and maintaining of course proper airway c-spine may be and assisting inadequate breathing conserving body heat and ensure the most effective circulation possible okay so we're going to transport the patient promptly to the facility capable of managing oh neurogenic shock now we're on neurogenic shock okay",
        "Treating Anaphylactic Shock": "and then now we're moving into anaphylactic shock so the most effective treatment for a severe acute allergic reaction is to administer epi um by the way of an i am intramuscular so that's for anaphylaxis so a patient with anaphylaxis requires immediate transport high flow o2 possibly assistance with the bvm and try to find out what caused the reaction and how it was received okay so keep in mind that a mild reaction may worsen suddenly um so just because of the potential for airway compromise you might want to request an advanced life support backup as soon as possible",
        "Treating Psychogenic Shock": "and then the psychogenic shock so in any uncomplicated case of fainting once the patient collapses and becomes supine of course the circulation to the brain is restored and with that a normal state of functioning so psychogenic shock could worsen other types of shock but if it appears that the patient fell as a result of the psychogenic shock just checked for injuries especially in older patients so if the patient reserve reports not",
        "Treating Psychogenic Shock Continued": "being able to walk after the fall though it is related to psychogenic shock you should suspect another problem maybe like a head injury or a hip injury so transport promptly and all patients with loss of consciousness should be transported to the emergency department for an evaluation even if they appear normal once we arrive on scene",
        "Treating Hypovolemic Shock": "all right and then the last type of shock treating hypovolemic shock and so obvious you're going to stop that external bleeding that's the first thing you want to do and the best initial method of course is direct pressure and then if direct pressure does not work you're going to use a tourniquet okay so handle the patient gently and keep them warm and recognize internal bleeding and provide aggressive general support okay so secure and maintain an airway and provide respiratory support if needed including oxygen and of course ventilations so transport the patient as rapidly as you can to the emergency department",
        "Treating Shock in Older Patients": "treating shock in older patients so older patients generally have more serious complications than younger and so many older patients take numerous medications and this could either mask or mimic signs of shock so treating a patient pediatric or geriatric in shock is no difference of course no different than treating any other shock patient we need to provide inline spinal stabilization and um if it's not indicated maintain the patients in a position of comfort okay so control life-threatening hemorrhages immediately with direct pressure then suction as necessary and provide high flow oxygen as via non-rebreather mask we want to maintain body temp as with all of these patients and then rapid transport with all of the patients once again all right",
        "Review and Conclusion": "so that concludes the information portion of this slide or lecture and we're going to go ahead and start talking about the review questions okay see how much we've learned so the term shock is most accurately defined as what do we know what do we know it is hypoperfusion so when you hear shock think hypoperfusion and that's that state of collapse of the cardiovascular system okay anaphylactic shock is typically associated with all right i think it's probably year to carry a localized welts would be a mild severe headache they could but not usually yep you're dicarion that's hives and it's a allergic reactions all different types okay caused by those histamines signs of compensated shock include all of the following except okay i think it's the feeling of impending doom nope compensated shock is the body um basically they're able to maintain perfusion um so the only one would be weak or absent peripheral pulses and that is probably decompensated shock okay when treating a trauma patient who's in shock lowest priority should be given to so trauma patient i think it's splinting hot fractures right because we're going to do all the other thing yeah splinting fractures is a secondary uh secondary issue right potential causes of cardiogenic shock include all but the following okay so inadequate heart function yes disease of the muscle tissue yes impaired electrical system yes usually the bacteria infection is going to be a distributive right so that's a distributive issue okay 60 year old woman who presents of 80 over 60 okay so that's only a 20 point different a pulse rate of 110 and model skin and the temp of 103. okay so the temperature is the key thing here and when you see that temp you're going to think septic shock she's got some type of infection and she's in shock because we know because of the blood pressure okay so septic shock all right a patient with neurogenic shock would least likely present with to kidney so breathing fast yes hypotension yes tachycardia i'm gonna say no i'm gonna say no because usually the signal will not get to the heart perfect so it's um remember that sympathetic nervous system is compromised it's not going to be able to um to know that it needs that b or norepi right and so tachycardia is the correct answer with neurogenic shock all right 20 year old is kicked in the belly during an assault his abdomen is rigid and tender heart rate 120 and respirations of 30. how should we treat this patient okay so the what i'm going to say is let's see where in the belly doesn't say i'm thinking a liver or spleen and it's because they're bleeding so both it could be both there you go and so we could just go with the hypovolemic so the liver laceration and the ruptured spleen could both cause hypovolemic shock so that's the answer 33 year old woman who has a rash facial swelling and hypotension 10 minutes after being stung there you go she is in anaphylactic shock we've given her high to flow too she needs epi epi's going to do the exact opposite of what um of what that just did so it's epi is going to reverse all of those bad things okay although the following of potential causes of impaired tissue perfusion accept so right away increased number of red blood cells is not going to do it we know it's a pump volume or vessel problem so a is the correct answer okay so this concludes chapter 13 shock lecture so if you like this um this lecture go ahead and subscribe to the channel we're going to put out all of the chapters in this book within the next couple weeks alright have a great day"
    },
    {
        "Introduction": "and welcome to chapter 17 cardiovascular emergencies of the emergency care and transportation of the sick and injured 12th edition after you complete this chapter and the related coursework you will understand the significance and characteristics of the anatomy and physiology of the cardiovascular system cardiovascular emergencies the pathophysiology of respiration and perfusion signs and symptoms of the most common cardiac conditions the indications contraindications and the use of an aed and the general care of a patient experiencing a cardiac emergency we'll be able to apply this fundamental knowledge to patient assessment and management during in-classroom scenarios okay so cardiovascular disease has been\nthe leading killer of americans since the 1900s and it accounts for about one of every three deaths ems can help reduce deaths by providing the following services so we can encourage people to follow a healthy lifestyle access medical care early provide more cpr training of lay people increased use of evolving technology in dispatching cardiac arrest response public access to defibrillation devices and recognition of the need for advanced life support care and also the use of cardiac specialty centers when they are available",
        "Anatomy and Physiology": "so let's talk about some anatomy and physiology of the cardiovascular system so the jobs the heart job is to pump blood to supply oxygen and rich red blood cells to the tissues of the body remember the heart is divided down the middle into the left and right sides each with an upper chamber which is the atrium to receive incoming blood and the lower change of chambers which is the ventricles to pump outgoing blood this figures figure shows an illustration of the four chambers of the heart so blood leaves each of the four chambers of the heart through one-way valves which keep the blood flowing in the circulatory system in the proper direction the aorta that's the body's main artery it receives blood ejected from the left ventricle and delivers it to all the other arteries that supply the body's tissues and this figure on the slide illustrates the hearts the blood supply so the right side of the heart receives oxygen poor blood from the venous circulation and the left side receives oxygen rich blood through the pulmonary arteries okay so the heart's electrical system controls the heart rate and coordinates the work of the atria and ventricles the heart generates its own electrical impulse starting at the sinus node the impulse passes through the atria to the ventricles automaticity allows spontaneous circulation without a stimulus from a nerve source as long as the impulses come from the sa node and other myocardial cells will contract when the impulse reaches them if no impulse arrives however the other myocardial cells are capable of creating their own impulses and stimulating circulation okay so this figure on the side illustrates the conduction system of the heart so at the top you see in the green the sa node traveling down through those pathways to the av node into the bundle of his and then finally into the purkinje fibers the left bundle branch okay and so the autonomic nervous system controls involuntary activities of the body the autonomic nervous system has two parts which normally balance one another you have the sympathetic nervous system and then you have the parasympathetic nervous system the myocardium must have a continuous supply of oxygen and nutrients to pump blood so cardiac output is increased by increasing the heart rate or stroke volume in a normal heart the increased oxygen demand of the myocardium itself is accomplished by increasing the blood of the blood delivered to the myocardium by dilating the coronary arteries the coronary arteries are blood vessels that supply blood to the heart muscle so they start at the first part of the aorta just above the aortic valve the right coronary artery supplies blood to the right atrium and right ventricle and in most people the inferior wall of the left ventricle the left coronary artery supplies blood to the left atrium the left ventricle and divides into two major branches just a short distance from the aorta and so you could see on this figure on the slide it illustrates those arteries the different coronary arteries okay the arteries supply oxygenated blood to different parts of the body and so we have the right and left carotid arteries and they supply blood to the head and the brain the right and left subclavian arteries supply the upper extremities the brachial arteries supply the arms the radial and ulnar arteries supply the lower arms and hands the right and left iliac artery supply the groin pelvis and legs and the right and left femoral arteries supply the legs the anterior and posterior tibial arteries supply the lower legs and feet the arterioles and capillaries are smaller vessels that receive blood from the arteries capillaries are one cell thick and it exchanges nutrients and oxygens for waste at a cellular level connects our arterials to venules okay so the venules and veins receive blood from the capillaries the venules are the smallest branches of the veins the vena cava returns oxygen poor blood to the heart you have the superior vena cava that carries blood from the head and the arms back to the right atrium then the inferior vena cava it carries blood from the abdomen kidneys legs back to the right atrium so blood consists of types of cells and fluid you have the four types and that's the red blood cells and those carry oxygen and remove the carbon dioxide then you have white blood cells and those are the fighters they fight infections the platelets help blood to clot and plasma is the fluid that the cells float in so blood pressure is the force of the circulating blood against the artery walls so when you talk about the systolic blood pressure it's the maximum pressure generated in the arms and legs during the contraction of the left ventricle during the time period known as systole diastole is the blood pressure against the artery walls when the left ventricle is relaxing and then there's the pulse and that's felt when the blood passes through the artery during systole so peripheral pulses are felt in the extremities and central pulses are felt near the trunk of the body in this figure it shows the different areas to take the pulse and so you'll see the femoral the brachial the carotid radial posterior tibial and the dorsalis pedis okay so the cardiac output is defined as the volume of blood that passes through the heart in one minute and so you could calculate that by multiplying the heart rate by the volume of blood ejected with each contraction or also known as a stroke volume so but in the field stroke volume can be roughly determined by the heart rate and the strength of the patient's pulse perfusion describes a constant flow of oxygenated blood to the tissues we have to have good perfusion um in order to have good perfusion though we have to have a well-functioning heart we have to have adequate volume of fluid or blood and the blood vessels must be appropriately constricted to match the volume of blood valuable okay so if perfusion fails though we're going to have cellular death and eventually the patient's going to die all right so we've talked a little about the anatomy let's talk a little bit about the physi the pathophysiology okay so heart related chest pain usually stems from ischemia which is decreased blood flow to the heart or inefficient supply of oxygen nutrients ischemic heart disease involves a decrease in blood flow to one or more portions of the heart muscle and if the blood flow is not restored the tissue is going to die so here's atherosclerosis and it's a disorder in which calcium and cholesterol build up and form plaque inside the walls of the blood vessels it can cause complete occlusion or block of a coronary artery and other arteries of the body so fatty material accumulates as a person ages resulting in the narrowing of the luminum aluminum and so the inner wall of the artery becomes rough and brittle if a brittle plaque develops a crack or for unknown reasons the ragged edge of the crack activates blood clotting system so the results would be a blood clot that would partially or completely block the luminum of the artery and that is atherosclerosis",
        "Pathophysiology": "a thromboembolism is a blood clot that floats through a blood vessel if it reaches an area too narrow to pass it stops and blocks that flow so tissues downstream of the blood clot will suffer from hypoxia if too much time has passed before the blood flow is resumed the tissues will die this sequence of events is known as a myocardial infarct or a classic heart attack the death of heart muscle can severely diminish the heart's ability to pump in the united states coronary artery disease is the number one cause of death for men and women the peak incidence of heart disease is between about 45 and 64 years old so but it can strike in individuals reigning ranging from their teens to their 90s risk factors place a person at higher risk for an ami or acute myocardial infarction some of these risk factors we can control and controlling risk factors are cigarette smoking or high blood pressure elevated cholesterol diabetes lack of exercise and obesity but some risk factors we cannot control and the major uncontrollable risk factors are old age family history race ethnicity and the male being male sex acute coronary syndrome describes a group of symptoms caused by a myocardial ischemia so this includes temporary myocardial ischemia which results in angina pectoris or a more specific condition or more more serious condition an acute myocardial infarct angina pectoris occurs when the heart's need for oxygen exceeds the available supply usually during physical or emotional stress so it can result from a spasm of the artery but is most often a symptom of atherosclerotic coronary artery disease it may be triggered by large meal or sudden fear or when increased oxygen man goes away the pain typically goes away so angina pain is commonly described as crushing squeezing or somebody is standing on my chest it's usually felt in the mid portion of the chest or under the sternum it can radiate into the jaws or arms frequently the left arm mid back or epigastrum it usually lasts from three to eight minutes but rarely longer than 15 minutes it may be associated with shortness of breath nausea or sweating usually disappears promptly with rest supplemental oxygen or nitro although angina does not usually lead to death or permanent heart damage it is a warning sign that should be taken seriously unstable angina is characterized by pain or discomfort that occurs in the absence of a specific increase in the myocardial oxygen demand stable angina is characterized by pain in the left in the chest of coronary origin that occurs in response to exercise or some physical activity that increases the demand on the heart that is beyond the heart's capacity to increase its own blood flow patients experiencing chest pain or discomfort should always be treated as if they're having an acute myocardial infarct\nthe pain of an ami or acute myofa cardial infarct signals the actual death of cells in the area of the heart where the blood flow is obstructed once the cells are dead the cells cannot be revived they will turn to scar tissue and become a burden to the beating heart about 30 minutes after blood flow is cut off the heart muscle begins to die after about two hours as many as half of the cells in that area may be dead after about four to six hours more than 90 percent of the cells will be dead opening the coronary artery with either a clot busting which is a thrombolytic drug or angioplasty it's a way of clearing the artery can prevent permanent damage if it's done within the first few hours after the onset of symptoms so immediate transport is essential it is more likely to occur in the left ventricle and so signs and symptoms of an ami include the following sudden onset of weakness nausea and sweating chest pain discomfort or pressure that is often crushing or squeezing that does not change with each breath pain discomfort or pressure in the lower jaw arms back abdomen or neck an irregular heartbeat or sinkable episode shortness of breath nausea vomiting pink frothy sputum or sudden death\nthe pain of an acute myocardial infarct differs from pain of angina in three ways it may or may not be caused by exertion and can occur at any time sometimes the person is sitting quietly or even sleeping it does not resolve in a few minutes rather it can last between 30 minutes to several hours and it may or may not be relieved by rest or nitro not all patients who are having an ami experience pain or recognize when it occurs so when called to the scene where the chief complaint is chest pain complete a thorough assessment no matter what the patient says so some physical findings of an ami and cardiac compromise include appearance a general appearance of fear or nausea or some type of poor circulation the pulse could be faster irregular or bradycardic the blood pressure could be decreased normal or elevated respirations could be normal or rapid in labor mental status or fillings of impending doom sudden death cardiogenic shock or congestive heart failure okay so let's talk about dysrhythmias and so dysrhythmias describes an abnormality of the heart rhythm so first uh dysrhythmia we're going to talk about is a premature ventricular contractions and they are an extra beat in a damaged ventricle they're usually harmless and common among healthy as well as sick people then then you have tachycardia and so that's a fast rapid heartbeat and it could be 100 beats or more a minute then bradycardia that describes an unusually slow beating of the heart that's 60 beats per minute or less you could also have a rhythm called ventricular tachycardia and it describes a very rapid heart rate rhythm this is a 150 to 200 beats and it can deteriorate very fast into a rhythm called ventricular fibrillation so ventricular fibrillation describes the disorganized ineffective quivering of the ventricles and no blood is pumped through the body and the patient usually becomes unconscious within seconds defibrillation may convert this arrhythmia so think of ventricular fibrillation fibrillation we want to defibrillate it so defibrillation defibrillation is what we use to convert it or an aet defibrillation is the process of shocking the heart with a specialized electrical current to restore a normal cardiac rhythm it can save lives if the shock is delivered within the first few minutes of sudden death cpr must be initiated until the defibrillator is available then chances of survival diminish appropriately seven to ten percent each minute until a defibrillation is accomplished a systole is the next heart rhythm we're going to talk about it's a dysrhythmia and a systole is basically the absence of all electrical activity it usually reflects a long period of ischemia and nearly all patients with a sleep will die all right so let's talk about cardiogenic shock and so cardiogenic shock is going to occur when the body tissue doesn't get enough oxygen and this is because of the heart all right and so this will cause body organs to malfunction cardiogenic shock is often caused by a heart attack the heart lacks the power to force enough blood through the court the circulatory system and it is more common in an acute myocardial infarction affecting the inferior and posterior regions of that left ventricle it's important to recognize shock in the early stages so that leads us into congestive heart failure all right so congestive heart failure often occurs within the first few days after a myocardial infarct and so what it is is congestive heart failure develops when increased heart rate and an enlargement of that left ventricle no longer make up for the decreased heart okay so it's called congestive because the lungs become congested with fluid and that's pulmonary edema once the heart fails to pump effectively so it occurs suddenly or it could occur slowly over months in an acute onset of congestive heart failure severe pulmonary edema is accompanied usually by pink frothy sputum and severe dipsnia so with right-sided heart failure blood backs up in the vena cava this causes fluid to collect in other parts of the body so you could have what's called dependent edema so swollen ankles such as in the feet and legs right-sided heart failure can result in an inadequate supply of blood to the left ventricle so this results in a drop in the systemic blood pressure patients may result may present with signs of both left and right sided heart failure because the left side failure often leads to the right side failure hypertensive emergencies involve any systolic blood pressure greater than 100 millimeters per mercury or a rapid increase in the systolic pressure sudden severe headaches is a common size also some other symptoms are strong bounding pulse and ringing in the ears nausea and vomiting dizziness warm skin some nosebleeds altered mental status or sudden development of pulmonary edema untreated a hypertensive emergency can lead to a stroke or a dissecting aortic aneurysm so transport patients to the hospital as quickly and safely as possible consider advanced life support assistance depending on transport distance and time so an aortic aneurysm describes a weakness of the wall of the aorta the aorta dilates at that weakened area in which a it's susceptible to rupture and if it ruptures blood loss will cause the patient to die almost immediately uncontrolled hypertension is a primary cause of dissecting aortic aneurysm a dissecting aneurysm occurs when the inner liner of the aorta becomes separated allowing blood flow to allowing blood to flow at high pressure between those layers signs and symptoms include very sudden chest pain located in the anterior part of the chest or the back between the shoulder blades it may be difficult to differentiate the pain of a dissecting aortic aneurysm from an acute myocardial infarct so transport the patients to the hospital as quickly and safely as possible so on this table you're going to see the difference between the acute myocardial infarct and the dissecting aneurysm and what i like to note point out is that with the onset of pain with a heart attack or ami you have a gradual usually slow onset of pain and it has a tightness or pressure with that aneurysm it's abrupt without additional symptoms and usually you'll see it or hear it as sharp or tearing okay severity with a heart attack increases with time whereas the dissecting it is maximum on onset",
        "Scene Size-up": "okay so let's get into the patient assessment so in the patient assessment we're going to do that scene size up always and a cure ensures same safety and we're going to determine that it's a nature of illness we're going to use the dispatcher info clues and comments from family members and bystanders",
        "Primary Assessment": "our primary assessment when we form that general impression if the patient's unresponsive and not breathing we're going to start cpr right away and call for an aed we're going to assess the patient's airway and breathing if dizziness or fainting has occurred due to cardiac compromise we're going to consider the possibility of a spinal injury okay so assess breathing to determine whether their the ailing heart is receiving adequate oxygen so if they have shortness of breath or with no signs of respiratory distress if oxygen saturation is less than 95 administer oxygen at 4 liters if they do not improve quickly apply oxygen with a non-rebreather if not breathing or breathing inadequately we're going to apply 100 oxygen with the bag valve mask pulmonary edema if that's present we're going to do positive pressure ventilations with the bag valve mask or we could use cpap okay we're going to assess the patient's circulation pulse rate and quality skin color nature and temp capillary refill we're going to consider treatment for cardiogenic shock early to re reduce the workload of the heart we're going to position the patient in the comfortable position usually sitting up and while supported we're going to make a transport decision based on whether you were able to stabilize life threats during the primary assessment so the remainder of the assessment can be performed in route if time allows most patients with chest pain should be transported immediately we're going to follow our local protocol for determining what receiving facility is most appropriate we're going to determine whether to use lights or sirens for each patient based on an estimated transport time and as a general rule patients with cardiac problems should be transported in the most gentle stress relieving manner okay so the next part of our",
        "History Taking": "patient assessment is the history taking and we're going to investigate the chief complaint and because patients experience an acute myocardial infarct will have different signs and symptoms seriously consider all complaints of chest pain or discomfort shortness of breath and dizziness if a patient is experiencing dyspnea is it due to exertion or related to the patient's position and is it continuous or does it change with each breath if the patient has a cough is it does it produce sputum and does the patient have nausea and vomiting fatigue headache or palpations ask about recent post trauma um obtain sample history and of course this is from the responsive patient and this is the the history of the patient so we're gonna ask have you ever had a heart attack have you been told that you have heart problems do you have any risk factors for coronary artery disease in addition we're going to ask what allergies is the patient at taking medications and include those opq rst when obtaining the symptoms as part of the sample history so this slide displays the mnemonic for assessing pain and it'll show you the opqrst mnemonic and that's the onset provocation palpation quality region radiation severity and timing",
        "Secondary Assessment": "next part of the patient assessment is the secondary assessment and of course because it's a chest pain situation we're going to focus on the cardiac and respiratory systems circulation and respirations we're going to measure and record the patient's vital signs so the pulse respirations systolic and diastolic pressures in both arms and if available we're going to use a pulse ox if continuous blood pressure monitoring is available we're going to use that as well and we're going to repeat at appropriate intervals and note the time that each set of vital signs is taken and recorded if patients with chest pain it is very valuable to have a 12 lead tracing from as early as possible after the onset of chest pain",
        "Reassessment": "and then our reassessment so we're going to repeat the primary assessment by checking to see whether the patient's chief complaint and condition have improved or are deteriorating we're going to reassess vital signs at least every five minutes or anytime significant changes in the patient's condition occurs sudden cardiac arrest i is always a risk with patients experiencing cardiovascular emergency so if cardio cardiac arrest occurs have an aed immediately available and if not perform cpr immediately until the aed is available then reassess your interventions provide transport if not performed already communication and document so alert the emergency department about the patient's condition and estimated time of arrival and follow your instructions of the medical control and document your assessment and treatment of the patient",
        "Emergency Medical Care for Chest Pain or Discomfort": "emergency medical care for chest pain or discomfort okay so let's talk about this so we're going to ensure a proper position of comfort allow patients to sit up if most comfortable loosen tight clothing give oxygen if indicated so continually reassess oxygen saturation in in the patient's respiratory status you can use a nasal cannula for patients with mild dipsnia or a non-rebreather mask for patients with more serious respiratory difficulty if pulmonary edema is present cpap may be indicated assist unconscious patients with breathing as well with uh or with those an obvious respiratory distress and depending on your protocol prepare to administer low dose aspirin and assist with prescribed nitro so let's talk about aspirin aspirin prevents new clots from forming or new existing clots from getting bigger so recommended dose is between 120 or 162 to 324 we're going to lose use low dose aspirin which is 81 milligrams then nitro nitro is available in a small tablet spray or skin patch the mechanism of injury relaxes the muscles of the blood vessel walls dilates coronary arteries and increases blood flow and supply to the heart it decreases the workload of the heart side effects include decreased blood pressure severe headache contraindications are systolic blood pressure less than 100 milli meters of mercury head injury or the use of dis disrectile dysfunctional drugs within 24 to 48 hours maximum prescribed dose has already been taken which is three doses that's a contraindication and also cardiac monitoring okay so for an ecg to be reliable and useful the electrodes must be placed in consistent positions on each patient okay certain basic principles should be followed to achieve the best skin contact and minimize artifact in the signal guiding principles it may be okay it may occasionally be necessary to shave body hair from the electrode site rub the electrodes bristly with alcohol swab before application to remove oils and dead tissues from the surface of the skin attach the electrodes to the ekg cables before placement confirm that the appropriate electrode now attached to the cable is placed at the correct location on the patient's chest or limbs so this is going to show you cardiac monitoring limb placement sites okay so that there's the limb leads on the left side of the slide and then the 12 lead once all electrodes are in place switch on the monitor print a sample rhythm strip the strip shows any artifact verified that the electrodes are firmly applied to the skin and the monitor cable is plugged correctly we're going to follow the skill drill in 17-2",
        "Heart Surgeries and Cardiac Assistive Devices": "okay so heart surgeries and cardiac assistant devices so over the last 40 years hundreds of thousands of open heart surgeries have been performed to bypass damaged segments of coronary arteries in the heart in a coronary artery bypass graft a blood vessel from the chest or leg is sewn directly from the aorta to the coronary artery beyond the point of obstruction percutaneous transluminal coronary angioplasty dilates the affected artery rather than bypassing it and involves the following steps so a tiny balloon is attached to the end of each to attach the end of a long thin tube and introduced into the large artery the tube is threaded into the narrow coronary artery and inflated the balloon is then deflated and the tube and the balloon are removed sometimes a stent is placed inside the artery patients who have had bypass procedures may or may not have a long scar on their chest treat chest pain in a patient who has had any of these procedures in the same way you would treat chest pain in patients who have not had the heart surgeries some people have cardiac pacemakers to maintain a regular cardiac rhythm and rate\nthey are inserted when the electrical system of the heart is so damaged that it cannot function properly these battery-powered devices deliver an electrical impulse through the wires that are in direct contact with the myocardium the generating unit typically resolves resembles a silver dollar and is usually placed under the heavy muscle or fold of the skin in the upper left upper portion of the chest so emts normally do not need to be concerned about problems with pacemakers when they do not function properly pacemakers can cause the patient to experience syncope dizziness or weakness due to an excessively slow heart rate the pulse will year ordinarily be less than 60 beats per minute and a patient with a malfunctioning pacemaker should be promptly transported to the emergency department when the aed is used the patches should be should not be placed directly over the pacemaker okay so automatic implantable cardiac defibrillators are sometimes used in patients who have survived cardiac arrest due to ventricular fibrillation these devices continuously monitor the heart rhythm and deliver shocks as needed treat these patients like you would any other acute myocardial infarction including performing cpr and using an aed if the patient goes into cardiac arrest the electricity from the aed that is implanted is so low that it will have no effect on rescuers so then there's an external defibrillator vest and this is a vest with a built-in monitoring electrodes and defibrillation pads which is worn by the patient under under his or her clothing the vest is attached to a monitor worn on the belt or hung from a shoulder strap the device uses high energy shocks similar to an aed so you should avoid contact with the patient if the device warns you that it's about to deliver a shock the vest should remain in place while cpr is being performed unless it interferes with the compressions if it is necessary to remove the device or the vest simply remove the battery from the monitor and then remove the device then you have lvads lvads are left ventricular assist devices and this is used to enhance the pumping of that left ventricle in patients with severe heart failure or in patients who need a temporary boost due to mi the most common ones have an internal pump unit and have an external battery pack the pumps are almost all continuous so most patients will not have a palpable pulse unless the device malfunctions you should not have to deal with it contact medical control if there is any doubt in what to do and you need to transport all lvad supplies and battery packs with the patient then there's cardiac arrest so cardiac arrest is the complete cessation of cardiac activity electrical mechanical or both if it is indicated in the field by the presence of absence of carotid pulse cardiac arrest was almost always terminal until the in the advent of cpr and external defibrillation in the 1960s with good cpr early defibrillation and access to advanced care it's possible for some patients to survive cardiac arrest without neurological damage",
        "Automated External Defibrillation": "okay so now we're going to talk about aeds and this is an automated external defibrillation and it involves the use of a small computer and that computer is an aed that analyzes electrical signals from the heart it identifies ventricular fibrillation and is extremely accurate it administers a shock to the heart when needed so\nuh come in different models and the models require some operator interaction so such as like applying pads or turning the machine on the operator must push a button to deliver an electrical shock and many use a computer device synthesizer to advise the emt which steps to take and most of the aeds are semi-automated or extremely accurate\nan advantages of aeds include quick delivery of electrical shock they're easy to operate you don't have to have advanced life support providers on scene remote adhesive defibrillator pads are safe to use and large pad area with manual paddles which means that transmission of electricity is more effective efficient other considerations when using the aeg includes so not all patients in cardiac arrest need an electrical shock so all patients in cardiac arrest should be analyzed with an aed though but some do not have shockable rhythms for example a systole which is that flat line indicates that there's no electrical activity so it will not need a shock and then a rhythm called pulseless electrical activity and this usually refers to a state of cardiac arrest that exists despite an organized electrical complex that will not need an electrical shock okay but early defibrillation is an essential intervention for patients experiencing cardiac arrest few patients who experience sudden cardiac arrest outside the hospital survive unless a rapid sequence of events take place and so these are called the chain of survival links and you need to have all of them linked or else there's not going to be survivability so we need to have recognition of early warning signs and we need to call ems immediately okay and then immediate cpr needs to be done with emphasis on high quality chest compressions rapid defibrillation needs to occur basic and advanced ems needs to take place and then advanced life support with post-arrest care and then finally recovery and here this figure illustrates the chain of survival cpr helps patients in cardiac arrest by prolonging the period during which defibrillation can be effective rapid defibrillation has successfully resuscitated many patients in cardiac arrest and defibrillation works best if takes place within two minutes of the onset of cardiac arrest non-traditional first responders are being trained to use aeds the fifth step in the chain of survival is advanced life support and post-arrest care this involves the continued ventilations at 10 to 12 breaths a minute maintain oxygen saturation between 99 or 94 to 99 ensure the blood pressure is above 90 millimeters of mercury use a targeted temperature management when the patient arrives at the hospital cardiopulmonary and neurologic support along with advanced assessment techniques and interventions when indicated then the final step in the chain is recovery so this is recovery can take a year or longer for many of the ten percent of victims of out of the hospital cardiac arrest who are fortunate enough to survive when integrating the aed and cpr into patient care keep the following in mind it is usually important to work the aed and cpr in sequence apply the aed only to pulseless unresponsive patients and do not touch the patient while the aed is analyzing the heart rhythm and delivering shocks and cpr must stop while the aed is delivering the shock aed maintenance is important so become familiar with the maintenance procedures required for the brand of aed that your service uses you want to read the operator's manual three most common errors in using an aed include failure of the machine to shock v-fib applying the aed to a patient who's moving squirming or being transported or turning the aed off before analysis or shock is complete then there's operator errors and the operators errors include failing to apply the aed pads to the patient not pushing the analyze or shock buttons when the machine advises you or pushing the button instead a power button instead of the shock button one hits advise so make sure the battery is properly maintained and check your equipment including your aed daily at the beginning of each shift also ask the manufacturer for checklist of items that should be checked daily weekly or less often report any aed failures that occurs while caring for the patient to the manufacturer and to the us food and drug administration be sure to follow the appropriate ems procedures for notifying these these organizations medical direction should approve the written protocol that you will follow in caring for patients in cardiac arrest the emt team and your services medical director or quality improvement officer should review each incident in which the aed is used quality improvement involves both the individuals using the aed and responsible ems system managers the review should focus on speed of defibrillation shocks should be delivered within one minute of the call and mandatory continuing education with skill competency review is generally required for ems providers",
        "Emergency Medical Care for Cardiac Arrest": "so emergency medical care for cardiac arrest so let's talk about this so when preparing to use the aed it's the emt's job to make sure that the electric electricity from the aed injures no one do not defibrillate patients in pooled water electricity will diffuse through the pooled water you can defibrillate a soaking patient but dry the patient's chest first and do not defibrillate patients who are touching metal that others are touching okay we're also going to carefully remove nitro patches from the patient's chest and we're going to wipe the area with a dry towel before we defibrillate to prevent ignition of the patch it's it is often helpful to shave a hairy patient's chest before the placement uh to increase conductivity we're going to determine the patient's nature of illness or mechanism of injury because we might need to perform spinal mobilization for trauma patients during the primary assessment we're going to call for advanced life support assistance in if in a tiered system with a patient in cardiac arrest and use a well-organized team approach so on the figure on this slide displays the aed algorithm and cpr indicates cardiopulmonary resuscitation if you witness a patient in cardiac arrest begin cpr starting the with chest compressions and attach the aed as soon as it is available so you can see the skill drill for the steps using the aed follow local protocols for patient care following aed use after the aed protocol is completed one of the following will likely occur so you'll have pulse which is regained and that's called rosk and brass stands for return of spontaneous circulation or rosc there's no pulse and the aed indicates no shock is advised or no pulse and the aed indicates that the shock is advised if advanced advanced life support is responding to the scene stay where you are and continue the sequence of shocks and cpr if advanced life support is not responding to the scene and protocols agree begin transporting with one of the following the patient regains a pulse six to nine shocks are delivered where the machine gives you three consistent messages separated by two minutes of cpr that no shock is advised okay if you have cardiac arrest during transport if you're traveling to the hospital and an unconscious patient with an unconscious patient and the patient becomes pulseless immediately stop the vehicle you want to begin cpr if the aed is not immediately ready then we're going to call for advanced life support and other available resources based on the circumstances we need to analyze a rhythm deliver the shock if indicated and immediately resume cpr continue resuscitation according to your local protocol if you're in route with a conscious patient who is having chest pain and becomes unconscious of course check the pulse stop the vehicle begin cpr analyze a rhythm deliver the shock begin chest compressions and continue resuscitation according to your local protocol including transporting to the hospital you want to coordinate with advanced life support personnel according to your local protocol so if you have an aed if it's available do not wait for paramedics to arrive notify advanced life support personnel as soon as possible after you recognize a cardiac arrest you do not want to delay defibrillation when paramedics arrive inform them of your actions to the point and then interact with them according to your local protocols",
        "Management of Return of Spontaneous Circulation": "okay so this is going to next we're going to talk about rosk and that's return of spontaneous circulation so when you achieve ross we're going to monitor spontaneous respirations we're going to provide oxygen via bag valve mask at 10 breaths a minute we're going to maintain oxygen sets between 95 and 99 assess the patient's blood pressure and see if the patient can follow simple commands if advanced life support is not on scene or in route immediately begin transport to the closest appropriate hospital depending on local protocols",
        "Review": "okay so that concludes chapter 17 cardiovascular emergencies next we're going to go through the review questions to see how much we've learned okay all of the following are common signs and symptoms of cardiac ischemia except all right so i'm pretty sure it's headache usually if you have cardiac ischemia it's the heart's demand for oxygen you could have shortness of breath or chest pain but a headache is not usually a common sign okay when palpating the radial pulse of a 56 year old man you note that the pulse rate is 86 beats per minute and irregular so what do you think this indicates i'm pretty sure it's going to say dysrhythmia because we know arrhythmias or arrhythmias are regular and dysrhythmia is irregular stands for irregular okay 56 year old man is having a acute myocardial infarc which of the falling blood vessels have become blocked and we know that the um uh the arteries are the the things that deliver blood to places oxygenated blood so it's going to be an artery and we know that the coronary arteries in general are the ones that uh give the blood to the myocardium okay so the coronary arteries major controllable risk factors of an acute myocardial infarction and so these are factors we could control we can't control our age or our history and we can't control the fact of if we're male or female and so it's going to be cigarette smoke okay a patient with cardiac arrest secondary um fib has the greatest chance of survival and we know v fib we need to defib and so um we're going to d fib it's provided within two minutes v fib always want to defib okay 59 year old woman presents with chest pressure she's conscious and alert but her skin's pale cool and clammy your first step in providing care should be all right so our first step when we see that color i think they're probably going to want us to do i think oxygen right yep oxygen so that right really far up in that uh is going to be oxygen in our assessment okay if a patient with an implanted pacemaker is in cardiac arrest you should we're just not going to put the pads on the pacemaker i'm pretty sure yeah and so the only modification we're going to do is we're just not going to put the pads on the implanted pacemaker the main advantage of an aed is all right we're going to get the shocks there it's it is easier than performing cpr and there's no need for advanced life support to be there so i think d all of the above after administering nitro tablet to patient you should so we should check the expiration prior to um we're going to reassess the blood pressure we're going to we're not going to choose a tablet because we're going to put it under the tongue and we should have checked that prescription before so i think it's going to be b yep every five minutes okay and finally nitro is contra indicated in patients well right there right in front of us it's going to be systolic pressure less than 100 millimeters of mercury okay thank you so much for joining me for chapter 17 chest pain lecture if you like this lecture go ahead and subscribe to the channel because we're going to be putting out all of the chapters in the care in emergency care and transportation of the sick and injured 12th edition okay thank you"
    },
    {
        "Introduction to Critical Patient Management": "hello and welcome to chapter 40 management and resuscitation of the critical patient expertise in critical thinking and decision making are essential tools when you are confronted with a critical patient the process involves conducting a rapid assessment performing life-saving treatment and developing a differential field diagnosis this chapter discusses the approach that you should take when you are confronted with a critical patient",
        "Essential Skills for Managing Critical Patients": "so expertise in critical thinking and decision making are essential when working with a critical patient as we said this involves conducting a rapid assessment providing life-saving treatment developing a differential field diagnosis and what that is is a short list of potential causes also working diagnosis when guides when you're guiding treatment so most likely a condition prompting the need for medical care from the list of potential diagnosis if the patient is critical you must be well trained to make the right decision time appropriately and provide the right care so a patient may need to be transported to appropriate care and it may also involve having the right equipment using the right resources crew management leadership skills prioritation and compliance at with protocols and working with public safety personnel and family members managing critical patients may involve being confronted with pre-morbid or perry arrest conditions",
        "Developing Critical Thinking and Decision-Making Abilities": "developing critical thinking and decision making abilities so excellent decision making comes with experience students must acquire entry-level knowledge and skills with guided experience so training is developed to prepare entry-level medics internships help pull this together didactic lab skills and clinical experiences so state and national certification registration and licensure follows",
        "Understanding Critical Patients": "when caring for critical patients you will be confronted with premorbid conditions major trauma and patients in perry arrest period so the peri-rest period is the period just before or just after cardiac arrest so care must be taken to prevent progression or regression into cardiac arrest examples of this includes unstable dysrhythmias shock syncope myocardial ischemia or heart failure promorbid conditions include conditions that precede the onset of disease now disease is the life-threatening trauma or medical condition that needs to be rapidly identified and managed these could be sorted into those occurring in presumed to be healthy adults or those occurring in unhealthy adults many patients have pre-existing conditions putting them in a critical patient category patients with trauma such as full thickness burn over 20 percent of the total body surface area or head chest and abdomen involved in hemorrhage leading to shock also acute coronary syndrome are acs heart failure renal failure uncontrolled hypertension uncontrolled diabetes obesity electrolyte imbalance electrocution drowning or submersion hypothermia drug toxicity stroke near fatal asthma anaphylaxis pulmonary embolism",
        "The EMS Approach to Diagnosis": "okay so let's talk about the ems approach to diagnosis critical patients often complain about altered mental status difficulty breathing severe pain and chest pain follow a standard approach to determine a field diagnosis consider and rule out different conditions this leads to a differential diagnosis to consider the differential diagnosis for a patient with an altered mental status you may use the mt ship acronym okay and so it's just so slightly different than the aeiou tips that some of you have heard of i'm sure but the m acronym mt ship acronym the m starts with medication overdose or non-compliance also the m could be metabolic causes the t is tumor trauma or toxins the s is seizure or stroke the h is hypoxia hyperthermia or hypothermia hyper or hypoglycemia hypertensive crisis hypovolemia or hypo or hyperkalemia also i is infection and uremia and the p is psychiatric or behavioral disorders to consider the differential diagnosis for a patient with chest pain we consider ischemia ischemic chest pain indicating a possible cardiac condition also gi causes such as heartburn esophageal spasm hiatal hernia gallbladder or pancreas problems musculoskeletal problems such as casteochondritis or sore muscles injured ribs or a pinched nerve also there are respiratory causes that could cause chest pain such as pulmonary emboli pleurisy pneumothorax or asthma then there's panic attacks shingles or cancer in the chest your experience will be your guide in determining serious problems",
        "The Role of Intuition in Critical Decision Making": "the rule of in intuition in critical decision making so intuition comes with experience and it's hard to teach described as a pattern of pattern of recognition and matching based on previous experience it can be used to up triage the patient rather than to down triage so if instinct tells you that the patient is more serious than he or she seems treat treated as such but if instinct tells you otherwise investigate the complaint pattern recognition in the field doesn't mean that you are equally as good as in other fields so don't misuse an analogies and make decisions based on intuition that draws on incorrect experiences decisions based on intuition can make communication difficult team members may have a hard time staying on board with the thought process so organizational scholar carl weck came up with a five-step process for communicating intuitive decisions so here they are you're going to ask here is what i think we are dealing with here is what i think we should do here is why and here is what we should keep our eyes on and then you say now talk to me are there any other concerns",
        "Bias to Decision Making": "so bias in decision making biases can lead to faulty decision making confirmation bias is a tendency to gather and relay on information that confirms your views and avoids or downplays information that does not conform to your pre-existing hypothesis there's also anchoring bias and this is allowing an initial reference point to distort your estimates brain allows you to begin at a reference point and adjust from there often seen in financial negotiations and price setting be mindful about making a misjudgment based on overconfidence search for information refuting the differential diagnosis look at all angles of the problem when treating a patient with classic presentations of a specific condition don't assume the patient has a condition before obtaining information some principle applies in patients who don't present with classic signs and symptoms don't prematurely jump to conclusions when assessing a critical patient",
        "A Snapshot of Critical Decision Making": "okay so a snapshot of critical decision making so here's a scenario you have been dispatched to a home of a 62 year old woman complaining of pressure in the center of her chest the scene appears safe but you pay special attention to the environment you are you are entering you introduce yourself to the patient and ask about her chief complaint the patient tells you her physician determined that her chest pain was caused by stress and acid reflux antacids have not alleviated crushing sensation beneath her breastbone pain is accompanied by nausea and tingling in her right arm your partner places her on oxygen using a non-rebreather and obtains her vital signs you give her four baby aspirin to chew once you determine that she has no cardiac history no allergies and is not taking in anticoagulant you go through the opqrst pneumonic to help elaborate on the chest pain it is determined that she is tachycardic and has slight hypertension you listen to her lung sounds and your partner obtains a 12 lead there is slight crackling in the bases of her lungs your partner transmits the results to the nearest hospital with a coronary catheterization lab the patient has st segment elevation in three continuous leads 2 3 and avl she fits the stem a protocol for an inferior wall myocardial infarct criteria for percutaneous coronary intervention is within a 90-minute window your partner starts an iv to start morphine sulfate and metaprolol you obtain or you determine that it is best to take her to the hospital two miles beyond the closest hospital because it has a coronary catheterization lab when the patient is lifted from the couch to sit in the stair chair she passes out the ekg changes from sinus tac to v-fib you and your partner move the patient to the floor you begin chest compressions while the defibrillator pads are placed on the patient an oropharyngeal airway is inserted and bag mass ventilations are started with supplemental oxygen with the pads in place compressions are stopped and the first shock at 200 joules is delivered cpr compressions resume you need to make sure personnel perform specific tasks at the right time which includes getting the mechanical cpr device ready to deploy with no interruption for more than 10 seconds ensuring bls ventilations are effective when and switching to an automatic transport ventilation ventilator with impendent threshold device starting an iv to administer one milligram of epi one milligram per milliliter every three minutes until the pulse returns also you need to ensure a fresh person will supply chest compressions for the second two minutes also draw up 300 milligrams of amiodarone because an antidis rhythmic will need to be administered you re analyze and shock the patient every two minute intervals after the third shock the patient has rhythm but no pulse cpr is continued anti-disrhythmics are administered the table shows the h's and t's these are the questions of cardiac arrest you take a minute to consider the causes you consider reversible causes so you look there are no signs of trauma or symptoms of gi bleeding the systolic pressure was slightly high but not likely hemorrhaging there's she's not a diabetic and initially was alert so low levels of glucose are unlikely no signs of respiratory distress and not cold to the touch so pulmonary emboli and hypothermia are not likely st elevation mi or stemi and vague present an older vague presentation in older females so it's likely a massive ami or coronary thrombosis after the first shock the patient wakes up you assure her all her needs are taken care of crew members are assigned to package and carry the patient one medic starts an amiodarone drop drip and prepares a mild sedative once in a row you contact the ed to update staff and another 12-lead ecg is transmitted you reassess vital signs document the incident and discuss the situation with the patient because the ecg was transmitted initially the patient is admitted directly to the cath lab",
        "Understanding Shock": "so let's talk about shock shock is the state of collapse and failure of the cardiovascular system where blood circulation shows slows and eventually ceases this leads to insufficient perfusion to the organs and tissues normal compensatory mechanisms to maintain systolic blood pressure and brain perfusion during distress so this can accompany a broad spectrum of events if not treated properly shock will injure the body's vital organs and lead to death",
        "Anatomy and Physiology of Perfusion": "so let's talk about the anatomy and physiology of perfusion perfusion is the circulation of blood within an organ or tissue adequate amounts to meet the cell's needs for oxygen nutrients and waste removal it requires having a working cardiovascular system it also requires adequate gas exchange in the lungs glucose in the blood and waste removal so the cardiovascular system requires three components to keep the blood moving you have to have the functioning heart adequate fluid volume and that's the body and the blood fluids intact system of tubing capable of reflex adjustments in response to changes in pump output and fluid volume the heart's contractility allows it to increase or decrease the volume of blood being pumped with each contraction and that's the stroke volume the heart can vary the speed at which it contracts by raising and lowering the pulse rate cardiac output you'll see it written as co is a volume of blood that the heart can pump per minute the heart must be or must have adequate strength and this is determined by the heart's ability or muscle to contract and this is called myocardial contractility the heart must also receive adequate blood to pump as soon as the blood increases pre-contraction pressure or preload builds up preload is the stretching of the cardiac muscles prior to contraction as preload increases the heart muscles stretch one muscles are stretched myocardial contractility increases and cardiac output increases the resistance of flow or to flow is called the afterload and it must also be present so the blood pressure is generated by the contraction of the heart and the dilation and constriction of the blood vessels it's carefully controlled by the body to ensure adequate circulation in various tissues and organs it's considered a rough measure of perfusion it varies directly with cardiac output systemic vascular resistance and blood volume systemic vascular resistance is the resistance of blood within all of the blood vessels except the pulmonary vessels the systemic pressure or the systolic pressure is the pressure generated every time the heart contracts and the diastolic pressure is the pressure maintained within the arteries while the heart rests between heartbeats perfusion depends on cardiac output systemic vascular resistance and transportation of oxygen so cardiac output is the heart rate times the stroke volume and the blood pressure is the cardiac output times the systemic vascular resistance the mean arterial pressure and that's written as map is the patient's blood pressure so the map takes into consideration the systolic blood pressure and the diastolic blood pressure so blood pressure required to sustain organ perfusion roughly it's roughly 60 millimeters per mercury in the average person if the map falls below normal for a certain period of time result will be ischemia of the organs from lack of perfusion and so map or the mean arterial pressure is equal to the diastolic blood pressure plus one-third and the one-third is the systolic blood pressure minus the diastolic blood pressure okay the table shows how to calculate a mean arterial pressure okay so the pulse pressure that's the difference between the systolic and the diastolic pressures the blood pressure is refused via the cardiac system or the cardiovascular system okay so this is controlled by the autonomic nervous system which is composed of competing systems the sympathetic nervous system prepares the body for physical activity during a stressful situation it does this by increasing pulse rate blood pressure and respiratory rate it dilates blood vessels which in areas needed for the physical activity and constricts blood vessels in areas involved in reproductive reproduction and restoration nerve signals travel between the brain and the body via nerves traveling through the spinal cord the nerves leave the spinal cord and spread out to the affected tissues in those areas epi and norepi is released from the adrenal glands into the bloodstream to activate a sympathetic response to those areas and then you have the parasympathetic nervous system and this is responsible for rest and regeneration it opposes every action of the sympathetic nervous system it does the exact opposite it decreases pulse rate lowers blood pressure and lowers respiratory rate it constricts blood vessels in muscular tissue and dilates blood vessels in the digestive system the figure on this slide shows the sympathetic and the parasympathetic nervous systems",
        "Respiration and Oxygenation": "okay so respiration and oxygenation we talk about this what it feels like in every chapter but it's important so when you breathe alveoli thin walled air sacs receive oxygen air felt oxygen-rich air oxygen is dissolved in the bloodstream and attaches to the blood's hemoglobin oxygen molecules from the oxygenated blood pass through the alveolar walls into pulmonary capillaries if blood is not properly circulated some cells and organs will not receive proper nutrients oxygen and carbon dioxide pass across thin tissue layers through diffusion diffusion is a passive process molecules from an area of higher concentration of molecules to an area of lower concentration there are more oxygen molecules in alveoli alveoli then in the blood so oxygen moves from the alveoli into the blood if there are more carbon dioxide molecules in the blood than in the inhaled air so carbon dioxide moves from the blood into the alveoli carbon dioxide is dissolved in plasma and attaches to the blood's hemoglobin carbon dioxide combines with water to create carbonic acid carbonic acid concentrations are high just as the blood is moving towards the lungs at the lungs the carbonic acid breaks down and carbon dioxide is exhaled",
        "Regulation of Blood Flow": "so regulation of blood flow let's talk about blood flow through the capillary beds is regulated by capillary sphincters sphincters constrict and dilate to increase or decrease blood flow under control of the autonomic nervous system it regulates involuntary functions like sweating and digestion response to other stimuli like heat cold and the need for oxygen and waste removal not all cells have the same needs at the same time so regulation of blood flow is determined by cellular need this is accomplished by vessel constriction or dilation with sphincter constriction or dilation perfusion is accomplished by heart blood vessels and all the blood working together",
        "Pathophysiology of Shock": "so let's look at the pathophysiology of shock now shock can result from inadequate cardiac output a decreased systemic vascular resistance or the inability of red blood cells or rbcs to deliver oxygen to tissues disturbances will create a buildup of dangerous waste products that could lead to death of an organ inadequate perfusion will cause damage to cells as well as the body if shock persists death will ultimately occur the body compensates by shunting blood from organs that are more tolerant of low flow such as the skin and intestines to vital organs that cannot tolerate hypoperfusion and those organs are the heart brain and lungs the cardiovascular system consists of the heart blood vessels and arteries and the fluid or the blood this is known as the perfusion triangle shock means one part is not working properly so the blood carries oxygen and nutrients through the vessels to the capillary beds to the tissue cells supplies are exchanged for waste products created during metabolism so blood contains red blood cells white blood cells platelets and plasma blood clots control blood loss so they form depending on one of the following if there is a retention of blood because of blockage in circulation or if there's changes in the vessel wall or the blood's ability to clot injury causes platelets to aggro aggregate at the injury site red blood cells become sticky and clump together fibrin refu reinforces red blood cells and clots are prone to rupture because blood is always moving due to pressure when the body senses that pressure in the system is falling um a hormonal mechanisms are are triggered so the sympathetic nervous system will assume control and that's the fight-or-flight response of the body's functions during shock the parasympathetic system controls involuntary functions by sending signals to the cardiac smooth and glandular muscles epi and norepi cause changes in the pulse rate strength of the cardiac contractions and vasoconstriction in non-essential areas so actions maintain pressure in the system and sustaining profusion to the vital organs occurs our body fluid shifts to maintain pressure so this response occurs within seconds and it causes signs and symptoms of shock",
        "Compensation for Decreased Perfusion": "and so this compensation for decreased perfusion mechanisms occur the body responds to any event that leads to decreased perfusion in order to preserve those vital organs baroreceptors located in the aortic arch and the carotid sinuses sense decreased blood flows they activate a vasomotor center in the medulla oblongata to begin constriction of the vessels this will increase blood blood pressure and chemoreceptors measure shifts in carbon dioxide in the arterial blood they will regulate respiratory rate and control an acid base balance in the body stimulation normally occurs when the systolic pressure is between 90 or 60 to 80 milligrams of mercury in adults or lower in children vasomotor center increases the arterial pressure by constricting blood vessels this will drop and pres this drop in pressure causes the artery walls to not stretch as much and baroreceptors stimulation is decreased normally baroreceptor stimulation prevents vasoconstriction from happening and leads to a vasodilation in the peripheral circulatory system it decreases pulse rate and contractility and causes the arterial pressure to decrease without drop with dropping pressure baroreceptors are not stimulated for vasodilation and vessels constrict to raise the blood pressure the sympathetic nervous system is stimulated as the body recognizes a potential catastrophic event adrenal glands release epi and norepi into the bloodstream this causes tachycardia and increases contractility of the heart this causes venous and anterior constriction and a decreasing blood flow to the skin muscles gi tract and kidneys so blood is then redistributed to the heart and the brain capillary hydrostatic pressure decreases in compensated phases of shock this will allow fluid from the interstitial compartments to flow into the vessels next a system in the kidneys is activated and antidiuretic hormone is released from the pituitary gland this triggers salt and water retention and peripheral vasoconstriction it increases blood pressure and cardiac output and fluids shift from interstitial tissues into the vascular compartment the spleen releases red blood cells to augment the blood's oxygen carrying capability the overall response of the initial compensatory mechanisms is to increase preload stroke volume and pulse rate this will allow the body to compensate for volume loss of up to 25 percent myocardial oxygen demand increases if perfusion persists eventually the compensatory mechanisms cannot keep up with the demand cardiac output and ejection fraction decreases and tissue perfusion decreases leading to impaired cell metabolism systolic blood pressure decreases fluid leaks from the vessels and this causes systemic and pulmonary edema fusion to the brain and cardiac or coronary arteries decrease and cells will shift from aerobic metabolism and aerobic means that they have the adequate oxygen supply to an anaerobic metabolism and that's when cellular processes occurring in the absence of oxygen the shifts oxygen hemoglobin dissociation curve to the right to increase tissue oxygen delivery decreases cardiac function making the heart susceptible to circulating catecholamines other signs of hypoperfusion include dusky skin color and imperimentation the release of epi or epinephrine improves cardiac output by increasing the pulse rate and strength alpha 1 responses include vasoconstriction increases in peripheral vascular resistance and increased afterload alpha 2 effects ensure regulated release of alpha one beta responses affect the heart and lungs bronchial dilation increases pulse rate contractility and conductivity norepi effects are mostly alpha 1 and alpha 2 in nature centers on vasoconstriction and increasing peripheral vascular resistance this allows the body to shunt blood from areas of lesser need to areas of greater need it maintains circulation to the brain and the body will shut blood away from the following tissues in this order first from the placenta then the skins then the muscle then the gut the kidneys liver heart then finally lungs skin and muscles can survive with minimal blood flow for longer periods than major organs if blood supply is inadequate to major organs for more than 60 minutes they will develop complications this is referred to as the golden period failure of compensatory mechanisms to preserve perfusion leads to decrease in preload and cardiac output myocardial blood supply and oxygen decrease reducing myocardial perfusion coronary artery perfusion decreases this leads to myocardial ischemia and then normal functions of the liver and pancreas are impacted and this inhibits the insulin release gastrointestinal motility is decreased this causes stress ulcers to develop and diminish kidney perfusion decreases urine output this leads to kidney failure if not perfused within reperfuse within 45 minutes to an hour normal urine output is between 30 to 40 milliliters an hour an output of less than 500 milliliters a day is considered allegoria and can lead to adequate kidney insufficiency",
        "Shock-Related Events at the Capillary and Microcirculatory Levels": "shock-related events at the capillary and micro-circulatory levels so a decreased perfusion leads to cellular ischemia this means minimal blood flow passes through capillaries and causes cells to switch from an aerobic metabolism to an anaerobic metabolism decreased circulation leads to blood basically just staging in the capillaries okay so the pre-capillary sphincter relaxes post-capillary sprinklers remain constricted and this causes capillaries to become engorged with fluid capillary sphincters regulate blood flow through the capillary beds under control of the atomic nervous system automatic autonomic nervous system blood flow is determined by capillary needs and blood flow is accomplished by basal constriction or dilation the body can tolerate anaerobic metabolism for only a short time this leads to system acidosis and depletion of the body's energy reserves incomplete glucose breakdown leads to accumulation of hyaluric acid and it's transformed to lactate and other acid byproducts so acidosis develops and hydrogen ions and lactic acid accumulate in the blood and body ischemia stimulates increased carbon dioxide by the tissues excess carbon dioxide combines with intracellular water to produce carbonic acid this reacts with other buffers to form more intracellular acidotic substances so acidosis serves as an indirect measure of tissue perfusion acid blood inhibits hemoglobin in the red blood cells from binding with other carrying oxygen this adds to cellular oxygen depth depth so sodium is inclined to diffuse into the cells sodium potassium pump normally sends sodium back out against the concentration gradient this involves active transport and an ample supply of atp reduce atp results in dysfunctional sodium potassium pump and then excessive sodium diffusions into the cells and this depletes the interstitial compartment intracellular enzymes that usually help digest and neutralize bacteria are bound with impermeable membranes so cellular flooding explodes the membrane and releases the enzymes they auto digest the cell and this leads to late phase of shock in its irreversible or terminal shock accumulating acids and waste products act as potential vasodilators this decreases venous return and diminishes blood flow to vital organs and tissues when the aortic pressure falls below a mean arterial pressure of or map of 60 millimeters of mercury coronary arteries no longer fill the heart is weakened and cardiac output falls myocardial depression factors release from ischemic pancreas and further decrease the pumping of pumping action of the heart reduced blood flow supply results in slowing or stopping of the sympathetic nervous system activity metabolic waste are released into the slow flowing blood this leads to plaque platelet aggregation and formation of microthrombi stretch capillary walls lose their ability to retain large molecules so they leak into surrounding interstitial spaces oxygen transport decreases and it increases cellular hypoxia the buildup of lactic acid and carbon dioxide act as a potent vasodilator this leads to relaxation of the post-capillary sphincters accumulation washes into the venous circulation increases metabolic acidosis and referred to as capillary washout ischemia and necrosis lead to multiple organ dysfunction syndrome white blood cells and blood clotting systems are impaired decreased resistance to infection and coagulation may occur so dic or disseminated intravascular coagulation what happens is proteins that control clotting become active under abnormal circumstances 97 of patients who die from hemorrhagic shock have evidence of coagulation defects frequent abnormalities are elevated prothrombin depressed platelet counts or elevated partial thromboplastin time this complicates septic shock",
        "Multiple-Organ Dysfunction Syndrome": "okay so we mentioned it on the last slide but let's talk about it again multiple organ dysfunction syndrome or mods okay so this is a progressive condition characterized by failure of two or more organ or organ systems that were initially unharmed by the acute disorder or injury so there are six organ systems and they're surveyed during this diagnosis okay so it could be respiratory hepatic renal hematologic neurologic or cardiovascular each system is assigned a score to determine the risk so example it's like a glascal coma score for the neurologic system each type of tissue has its own time that it can be deprived of oxygen before it will die we call this the warm ischemic time the effects of poor perfusion depend on how much time transpires prior to adequate reperfusion the brain and central nervous system tissue is four to six minutes skin and muscles that's up to two hours so when poor perfusion is not restored in the first hour blood is diverted in the order of the skin and muscles the gut the liver than the kidneys a single injury can have devastating impacts on multiple organs and organ systems patients have a mortality rate of about 60 to 90 percent this is the leading cause of death following septic traumatic and brain injuries and it's classified as primary or secondary so you have the primary which is the direct result of that insult then you have a secondary and this encompasses the organ dysfunction that occurs as an integral component of the patient's response so when it occur when an injury or infection triggers a massive systemic immune inflammatory or coagulation response the results is an increase in inflammat inflammatory mediators and activation of the following systems okay so first you have a complement system and this is overactive system that activates phagocytes it introduces further inflammation and damage to cells then you have the coagulation system so that has epithelial damage and coagulation becomes uncontrolled the results in microvascular thrombus formation and tissue ischemia then you have the calicrine kinin system and this release of bradykinin leads to tissue hypoperfusion overactivity results in a maldistribution of systemic and organ blood flow so the body attempts to compensate by alerting or accelerating tissue metabolism and this acceleration leads to tissue hypoxia tissue hypoperfusion exhaustion of the cell fuel supply or that's otherwise known as atp metabolic failure lysosome breakdown anaerobic metabolism and acidosis then you have impaired cellular function so the progression causes various organs to malfunction this is typically develops within hours or days after resuscitation so the signs and symptoms are hypotension insufficient tissue perfusion uncontrollable bleeding multi-system organ failure or possible low-grade fever from an inflammatory response such as tachycardia or dipsnia it's possible diff it's possible difficulty oxygenating patients due to lung injury and respiratory distress from 14 to 21 days renal and liver failure can develop the gi and immune systems may collapse and patients may undergo cardiovascular collapse death is typical within days two weeks of the insult this affects specific organs and organ systems the heart and it may result in dysrhythmias or muscle ischemia infarction or pump failure also peripheral pulses are weak or absent and extremities are cyanotic and cold next with the lungs you have failure as seen by the respiratory distress syndrome or a non-cardiogenic pulmonary edema pulmonary arterial pressures increase producing pulmonary hypertension and pulmonary capillary blood flow reduction results in impaired gas exchange reduced pea o2 level and increased pao2 level alveolar cells are ischemic interstitial or intra alveolar edema at low wage pressures occur so what happens is there is respiratory failure increase in carbon dioxide respiratory acidosis so central nervous system what happens when you have this the multi-organ dysfunction syndrome it decreases the cellular or cerebral perfusion pressure and blood flow result in confusion reduce responses to verbal and painful stimuli and unresponsiveness and then the kidneys so you have a reduced renal blood flow and it results in acute tubular necrosis which leads to a buildup output of urine output of greater than 20 millimeters of an hour and so retention of toxic waste in the blood and worsened metabolic acidosis when it comes to the liver you have the failure to filtrate bacteria which leads to a vulnerability and infection you have the inability to metabolize waste products and this leads to increased levels of toxins in the blood cell death increases enzyme levels also in the blood and then you have the gi tract and the ischemic gut syndrome occurs and the gut leaks and contributes to the progression of shock",
        "Causes of Shock": "so what are the causes of shock well shock results from many conditions and damage occurs because of insufficient perfusion of organ and tissues if shock is not promptly arrested and reversed the patient will die a high index of suspicion for shock in emergency medical situations are and you should expect shock to accompany a massive external or internal bleed multiple fractures abdominal or chest injury spinal injury severe infection a major heart attack or anaphylaxis and we mentioned this earlier and mention it throughout paramedic school because this is what we uh what we see right so there are three basic causes of shock and we it's a pump failure a low blood volume or poor vessel function the certain categories of patients are more at risk of course and we talked a little bit about that patients with trauma are bleeding massive mis pregnant women patients in septic shock and older adults",
        "The Progression of Shock": "so when you talk about the progression shock occurs in two successful phases it's compensated and decompensated these phases are also called the four grades of hemorrhage and four classes of shock classes one and two are compensated classes three and four are decompensated you need to be able to recognize the signs and symptoms early on and begin immediate treatment before the damage occurs be aware of subtle body changes that exhibit while the body is compensating anticipate potential for shock from the scene size up and evaluate the mechanism do not rely on one sign or symptom to determine the phase of shock you need to provide rapid assessment in immediate transportation",
        "Decompensated Shock": "when it comes to compensated shock this is the earliest stage of shock where the body is still able to compensate for the blood loss level of responsiveness is the best indication of tissue perfusion okay so release of chemical mediators causes blood arterial pressure to remain normal or elevated the rate and depth of the respiration will increase and the blood pressure is maintained when it comes to decompensated shock this is a result of the blood volume dropping more than 30 percent compensatory mechanisms are failing sometimes treatment will result in recovery though once the blood pressure drop is detected shock will begin to develop especially true in adults and children um so our children and infants blood pressure may be maintained until the loss of 35 35 to 45 percent of blood volume consider in an emergency and start transport in less than 10 minutes provide fluid resuscitation and route",
        "Irreversible (Terminal) Shock": "so there are causes of irreversible shock we call this terminal shock at a point which shock has progressed to a terminal phase and basically um it's aggressive you aggressive treatment does not always usually result in recovery you should provide aggressive treatment and route to the trauma center",
        "Scene Size-up": "okay so let's go through this we're going to do our assessment so a patient assessment of shock with the size up um you're going to do size up for seeing for hazards follow standard precautions determine the number of patients and the need for additional or specializes response quickly assess the moi or the nature of illness this can give you clues about the causes and the shock or the extent of the bleeding",
        "Primary Survey": "now we're in the primary survey so you want to form your general impression how does the patient look some do not pass the look test and will need to be fast tracked to the moi noi patients who do not greet you may be concentrating on breathing injuries or the pain assess the patient's mental status using afu and introduce yourself and ask the name location in the day of the week airway breathing if you suspect cardiac arrest use the cab so remember c-a-b-d-e that is circulation compressions airway breathing disability and exposure otherwise if they're if if they're breathing or if they're not in cardiac arrest you could do the abcs so abcs are airway breathing circulation patients with life-threatening airway problems cannot speak or will be fragmented which is one to two word sentences manage immediate threats to the patient's airway and breathing so you have to position the patient's airway clear the airway of secretions and administer oxygen if difficulty breathing is suspected examine the chest look for flail segments any impaled objects or holes that need to be sealed then assess for adequacy of the patient's ventilation in response to the volume and rate all right then there's circulation so take the cabd we talked about that approach and perform chest compressions if you suspect the patient does not have a pulse in patients with a pulse determine if it's adequate to sustain life in conscious patients assess the pulse at the radius unconscious of course we're going to do the carotid if you know the patient is hypotensive provide immediate transport the rapid exam is meant to detect injuries that are life-threatening and need immediate action also note the patient's skin color temp and condition your transport decision so if the patient needs to be prioritized and so these are the ones so if a patient has shock from a medical problem you need to fast track the assessment if the patient has shock from trauma let the mechanism guide your assessment of the major body cavities and regions",
        "History Taking": "when it comes to history taking you want to history taking secondary assessment reassessment can be done in route during that high priority patient so keep on seeing care two essential items that must be done before moving unless the patient is pinned and you suspect a delay of extrication delay establishing ioi b access until you are in route",
        "Secondary Assessment": "okay and then the secondary shock is considered hypovolemic or hemorrhagic until otherwise proven there are phases of shock in that relate of course we just talked about that so compensated in decomp a drop in systolic blood pressure or altered mental status indicates the blood or the body can no longer compensate other indicators indicators include end tidal carbon dioxide and lactic buildup all right and then your reassessment so reassess",
        "Reassessment": "the primary assessment vital signs chief complaint and any treatment performed by the patient determine what interventions you are or what are needed for the patient treat for shock focus on supporting this cardiovascular system patients in decompensated shock will need rapid intervention most shock interventions do not require a physician's order but some do",
        "Special Considerations for Assessing Shock": "so for healthy considerations for assessing shock healthy fit young adults are equipped to combat life-threatening body loss aerobic exercise results in the resilience resilient cardiovascular system okay a healthy weight along with diet of low salt low low fat and low cholesterol prepare the body to handle the effects of epi and norepi release during shock",
        "Emergency Medical Care of a Patient With Suspected Shock": "all right so airway and ventilatory support are the top priority when we treat shock we need to maintain an open airway in suction as needed administer high flow o2 and control external hemorrhages we need to look for signs of internal hemorrhages as well because we need to consider potential for loss in an area of hemorrhage iv therapy can be helpful for implementing initial therapies perform and route establish iv access with more with two 16 or 18 bore catheters administer iv volume expanders to replace blood loss and this could be an isotonic crystalloid it should be used maintain perfusion without increasing internal or uncontrollable external hemorrhages in the absence of traumatic brain injury consider 250 milliliter boluses with re-evaluation of blood pressure to a minimum of four doses in pre-hospital environment prior to obtaining online consultation radial pulses equate to a systolic pressure of about 80 to 90 milli millimeters of mercury if signs of tension pneuma perform a needle decompression and with suspected cardiac tamponide recognize the need for expedited expedite and for pericardial centesis in the emergency department and follow your local advanced life support protocols non-pharmacologic interventions include proper positioning of the patient prevention of hypothermia and rapid transport also apply the cardiac monitor consider the need for a regional trauma center air medical support may be the best option and provide that psychological support and morale when it comes to iv therapy",
        "IV Therapy": "iv lines are sorted inserted to provide a route for replacement of fluids potential replacement or administration of of medication okay so all patients in hypovolemic shock should need iv fluid replacement so an iv access should be obtained in patients who are likely to develop hypovolemic shock due to one of the more following conditions external bleeding internal bleeding vaginal bleeding fracture of the pelvis or femur severe or widespread burns heat exhaustion or irretractable vomiting and diarrhea also neurologic or neurogenic shock iv lines should be inserted to keep the vein open in case of a need for emergency administration of drugs so patients with poor cardiac output have blood shunted away from the skin and skeletal muscles so uh traditional use of d5w has been discontinued and replaced with normal saline",
        "Volume Expanders and Plasma Substitutes": "so volume expanders and plasma substitutes hypovolemic shocks should be treated with volume expanders to replace what is lost and that's a rate altering medication may be administered to enhance perfusion also indicated for obstructive shock and spinal shock a variety of solutions have properties similar to those of plasma and they're used to maintain circulatory volume but they can't replace red blood cells platelets or plasma proteins and do not carry the risk for hepatitis or hiv plasma substitutes and volume expanders include dectrin and that's a high molecule weight glucose palmar it stays in the vascular space due to its large size and it tends to coat red blood cells and may cause clotting problems in large quantities though plasma protein factor that's the next one and that contains serum globulin it's extensive it's reported to produce hypotension reactions in some patients though and then you have some other starch solutions and they do not interfere with clotting or blood typing",
        "Crystalloids": "crystalloids that's a solution that do not contain proteins or other large molecules they rapidly across capillary walls into tissues you must administer two to three times the volume of the blood loss fluids of choice when only salt and water have been lost the current debate about the role of crystalloids versus colloids in the treatment of shock so practical considerations favor using crystalloids in the field for initial fluid resuscitation but commonly used crystalloids are normal saline lactated ringers and crystalloids do not carry oxygen and they change the viscosity of the blood by thinning it and dissolve clotting factors so most advanced life support protocols limit the number of leaders you can administer to the patient okay so like we mentioned earlier",
        "Pathophysiology, Assessment, and Management of Specific Types of Shock": "the three primary classifications of shock they coincide with the conditions that cause them so cardiogenic distribution and hypovolemic and we talked about this so cardiac cardiogenic results in the weakening of the pump distribution is when you have broken down the chemical causes um so there's septic shock or neurogenic shock and then there are other causes of tissue perfusion um basically those are conditions that obstruct the flow of oxygen and that's the obstructive shock the initial management is the same for each type of shock all right so we always want to maintain the airway administer supplemental oxygen put the patient in the position of comfort obtain vital signs and obtain iv io access and then maintain the body heat when it comes to cardiogenic shock",
        "Cardiogenic Shock": "this occurs when the heart cannot circulate a significant or sufficient amount of blood that's adequate for the peripheral oxygen delivery many diseases can cause destruction or inflammation of the heart right so most commonly associated with the acute myocardial infarction and it's accommodated or accompanied by 40 dysfunction of the left ventricle and some experts consider ventricular fibrillation as the ultimate form of cardiogenic shock and manifest with poor contractility decreased cardiac output and impaired ventricular fill filling all right and there's populations at a greater risk and those are older adults patients with a history of diabetes and those with a history of an ami with an injection fraction of less than 35 percent diagnosis may be difficult in the field because once a diagnosis has been made newer treatment modalities have greatly improved long-term prognosis prolonged efforts to stabilize the condition of the patient in the field are not recommended you want to expedite the transport as soon as possible place a patient in the position of comfort and secure the airway all right consider bipap or cpap apply electrodes document the rhythm and obtain the 12 lead administer the crystallite solution via iv and auscultate the lungs some ems systems use dopamine at low doses in the beta range if the patient has a map of less than 60 all right so combination drug therapies is often needed in the hospitals while they're there so including cardiac catheterization hemodynamic monitoring and insertion of an atra aortic balloon pump all right so then let's talk about treatment and uh and what obstructive shock is causes are not directly associated with blood loss fluid pump failure or vasodilation they occur when blood flow to the heart or great vessels is blocked so common causes are tension pneumo cardiac tamponade a pulmonary emboli or carbon monoxide poisoning so tension pneumo is caused by damage of the lung tissues and what happens is a it allows air held within the lung to escape the chest cavity if untreated a significant amount of air will accumulate in the chest cavity and apply pressure to the structures of the mediastinum shifting of trapped air chest organs towards the uninjured side and this is that tracheal deviation life-threatening conditions due to the kinking of the vena cava that occurs in the mediastinum shifts only action that prevents death in the decomposition of an injured chest okay so a needle uh chest compression is uh the skill that many providers are allowed to perform and then cardiac tamponize that's caused by blunt trauma or penetrating trauma tumors or pericarditis it can progress quickly and it occurs when blood leaks into that tough fibrous membrane it's the pericardium the treatment for this is a pericardial centesis and what they do is they insert a needle attached to a syringe into the chest to penetrate the pericardium and withdraw the fluid the technique is risky and rarely performed anymore by paramedics so signs include muffled heart tones systolic blood pressure merging so narrowing of those pulse pressures all right and then distributive shock so this occurs when there's a widespread dilation of the resistance vessels and those are the small arterioles um and the um the small vessels so or both circulating blood volume pulls in the vascular beds and tissue perfusion decreases its most common types of distributive shock are septic neurogenic anaphylactic and psychogenic there's also septic shock the presence of sepsis syndrome and the systolic blood pressure of less than 90 or a decrease from the baseline blood pressure of more than 40 a subset of sepsis in which underlying circulatory cellular and metabolic abnormalities are associated with a greater risk of mortality than the sepsis alone so that's sepsis shock with sepsis shock it's a complex problem because there's insufficient volume of fluid in the container also fluid is leaking and collecting in the respiratory system and a larger than normal vascular bed must contain the volume smaller than normal volume of intravascular fluid this presents similar to hemorrhagic shock and treatment requires complex hospital management so transport as quickly as possible and give them high flow o2 and ventilatory support may be necessary okay so when it comes to this distributive shock give normal tensive patients dopamine to maintain blood pressure and renal profusion give norepi to a patient who remains in warm shock and give epi to patients who remain in cold shock we want to use blankets to conserve body heat and administer fluid boluses to maintain radial pulse when it comes to neurogenic shock usually this is from a spinal cord injury and muscles in the walls of the blood vessels are cut off from the nerve impulses that cause them to contract so you're going to have the all the vessels um at the level of that injury just dilate and so patients experience relative hypovolemia leading to hypotension then bradycardia occurs skin is pink warm and dry because of the cutaneous vasodilation so epi and norepi are not released spinal shock so that's a local neurologic condition that occurs after spinal injury and it produces motor and sensory losses what it will happen is it'll damage to damage the spinal cord can cause injury to the autonomic nervous system secondary cord injury develops over a few days and severe pain may be present about the level of the injury spinal shock is characterized by flaccid paralysis of flaccid sphincters and absent reflexes care is similar to general management approach for any patient with shock keep them warm immobilize them injury spinal cord injuries can distribute or disrupt thermoregulatory mechanisms so determine the necessity for iv fluids on hemodynamic status so with pure neuro neurogenic shock vagal blockers and vasopressor agents may be used but better advantage then they have a better advantage than over hydrating a patient and consider a steroid use per your protocol and then you have anaphylactic shock this occurs when a person reacts violently to a substance to which he or she has been sensitized sensitized and no there's no blood volume or no vascular damage only slight possibility of direct cardiac muscle injury patient will experience widespread vascular dilation and when the container is larger the blood volume is less of course and this is going to lead to poor oxygen and perfusion and it could be fatal and the following slide shows the effects of anaphylaxis all right and then the immune system chemicals are released when exposed to that allergen it causes bronchial constriction as well as uticaria widespread vasodilation and then angioedema that's a re-occurrent reconcurrent large areas of subcutaneous edema of sudden onset and usually disappear within 24 hours and mainly seen in young women management needs to occur quickly then you have the psychogenic shock and that's a sudden reaction of the nervous system that produces a temporary generalized vasodilation it results in syncope blood pulls in the dilated vessels and life-threatening causes can include an irregular heartbeat or a brain aneurysm there are other causes though and it could be a recede of bad news or fear of unpleasant signs so circulation of the blood is usually restored and its normal function continues if a patient falls though you need to check for injuries and assess the patient thoroughly for any other abnormality so record your initial observation of vital signs in the level of consciousness and obtain an ekg learn from the bystanders about how long the person was unresponsive and anything happening before the fainting all right and then we have hypovolemic shock this is just uh because of inadequate blood volume you could have it hemorrhagic or non-hemorrhagic so bleeding or not bleeding so non-hemorrhagic hypovolemia shock occurs when the blood or the fluid loss is contained in the body abnormal losses of fluids and electrolytes occur through gi losses or loss of fever losses because of fever increase or excessive sweating or internal losses and those internal losses could be basically pancreatitis some type of inflammation and plasma losses from burns drains or granulating wounds other causes of body fluid could be ascites diabetic acute renal failure or osmotic diuresis early signs of shock are restless and imagine anxiety long-term therapy aims to restore the body chemicals and then sometimes uh they're because of diet dehydration and that could be from loss of appetite nausea vomiting fainting our physical exam reveals poor skin turgor shrunken or furrowed tongue or sunken eyes maybe weak or rapid pulse so raising of more than 15 beats when the patient is raised from the recovery um to a sitting position so obtain those um hype orthostatic vital signs give a dehydrated patient iv fluids and keep the patient flat or in the trandelenburg position establish and maintain an open airway and on your way to the emergency department establish at least one ibor peripheral vein if protocol requires blood draws administer saline or lactated bringers consider administering 20 milliliters per kilogram in 250 ml boluses and then check the blood pressure okay consider the use of warmed fluids also if the patient vomits administer an anti-dynamic and anti-medic monitor the patient's rhythm mental status pulse rate blood pressure spo2 and end tidal and if you feel a pulse over the femoral artery but do not over the radial artery the sys the systolic pressure is between 70 and 80. right so medical control may order sodium bicarb to treat that acidosis or vasopressor to enhance vasoconstriction but don't wait for blood pressure to fall before suspecting shock and starting treatment the goal in treating shock is to save the lung brain and kidneys the best indication of brain perfusion is the mental status so kidney perfusion can be gauged by urine output in the fuel you can estimate the patient's peripheral perfusion by testing the cap refill but it's not most reliable indicator and relay on the patient's state of consciousness to tell you how well the vital organs are being perfused so the ability to breathe in adequate amounts of oxygen affects the ventilation process of respiration if insufficient amounts of oxygen in the blood are produced so some poisoning may affect the ability of the cells to metabolize or carry oxygen carbon monoxide binds to hemoglobin rather than allowing oxygen to bind so this results in an increased uh carbon dioxide in the body and cyanide impairs the in the ability of cells to metabolize so cellular asphyxia may occur an abnormally low amount of red blood cell causes anemia so what happens is it may result from chronic or acute bleeding or deficiency in vitamins or minerals tissues may become hypoxic so pulse ox may indicate adequate saturation but there could still be an increase in carbon dioxide when treating a patient in shock from poor perfusion you must seal a hole in the chest or stabilize impaled objects secure and maintain the airway clear the mouth and throat of obstructions assess the o2 and end title and vital signs and determine the need for ventilations determine the most appropriate transport destination so when preparing to transport a shock patient ask yourself when where and how limit the on scene time of 10 minutes or less and know how to assess aeromedical transport consider the priority of the patient in the ability of the trauma center local protocols may deal with these issues patients in shock may benefit from early surgical intervention and transport to a facility with appropriate capabilities if specific facility is not available medical control will help make that decision so this may involve transport to a local facility and then they may have to transport them to a tertiary care facility okay so that concludes chapter 40 management and resuscitation of the critical patient we hope that you enjoyed this lecture and go ahead and subscribe to the channel because more lectures are to come"
    },
    {
        "Introduction": "hello and welcome to chapter 17 cardiovascular emergencies and this is part three if you remember in part one we went over the anatomy and physiology in part two we covered a lot about the ecg components and so part three we're going to discuss dysrhythmias interpretation and um the different treatments of the dysrhythmias okay so let's get started okay so when you're talking about dysrhythmias there is an approach to interpreting them and there's a method and when you look at the ecg strips you're going to be on alert for specific things and you're going to go in a specific order and so first you're going to identify the waves so you want to look at the p q r s and t waves and they you want to measure the p r i interval i'm going to measure the q restoration determine the rhythm regularity measure the heart rate okay so we're going to notation of whether the p waves are upright and fall within normal parameters so let's start talking about",
        "Regular Rhythm": "this so when it comes to the red rhythm regularity you want to determine whether it's regular and it can be done by simply measuring the distance between those r waves so when the rhythm is regular it's if the distance between the r waves are exactly the same and so you can see that on the slide you have a regular rhythm okay but remember on the last slide i said you could have any regular rhythm but it goes even more in depth you can have an irregularly irregular rhythm and that is when no two r waves are equal and then you could also have a regularly irregular rhythm and that's if the r waves are irregular but they appear to follow a pattern and so in the first one you could see it's an irregularly irregular rhythm second one there is in there there is regular irregularity okay when you determine the heart rate use the six second method and so this strip that you're going to see on the screen that is a six second strip the fastest method for measuring a heart rate is from the ecg on a six second strip and so what you could do is this can be used on regular any regular rhythms you want to count the number of qrs complexes in a six second strip and then you're going to multiply it by 10 to obtain the heart rate and so if you look on this strip you see one two three four five and you could multiply that by 10 and so you have a heart rate of 50. okay so there's the sequence method it's reserved for regular rhythms and so what you could do is memorize the following numbers you can 300 150 100 75 60 and 50. you find the r wave on the heavy line and count off the above sequence for each large box you land on until you reach the next r wave so if the rnr interval spans fewer than three large boxes the rate is greater than 100 and that of course is tachycardia if it is more than five large boxes then the rate is less than 60 and of course that's bradycardia the 1500 method is the most accurate typically used for heart rate that exceeds 150 and can only be used on regular rhythms count the number of small boxes between the two qrs complexes and of course the two qrs complexes we're talking about the rnr interval and then divide it by 1500 okay so if you have 23 small boxes you then you divide that by 1500 you're gonna get 153 for the heart rhythm",
        "Cardiac Dysrhythmias": "great all right so specific cardiac dysrhythmias so cardiac dysrhythmias can be induced by many events the flow of electricity through damaged or oxygen deprived tissue is different than healthy tissue which may appear on ecg as irregularities many can be traced to ischemia especially the cardiac conduction system ischemia often causes spontaneous depolarization generating a premature complex that may interfere with multiple impulse conduction and induced dysrhythmias many dysrhythmias cause no serious symptoms so it's difficult to estimate the number of people affected dysrhythmias are the most common cause of a cardiac arrest and dysrhythmias are classified in numerous ways you have disturbances of the automaticity or disturbances of the conduction and rhythms that are too fast which are tachydysrhythmias or too slow which are brady dysrhythmias life-threatening or non-life-threatening and by the site from which they arise",
        "Sinus Bradycardia": "some rhythms originate in the sa node so of course we have the normal sinus rhythm and this arises in the sa node with an ischemic rate of 60 to 100 beats per minute with a regular rhythm and minimum variations between the rr intervals the p waves are upright and it precedes each qrs complex so the pri interval is point to 0.20 seconds and the qrs is 0.11 seconds or less you have sinus bradycardia and that's next the pacemaker is still in the sinus node but it's a rate of less than 60. and the upright p wave precedes every qrs still so the pr is still interval is 0.12 to 0.2 0 seconds and the qrs is 0.11 seconds so it's a very slow heart rate leading to an adequate co and precipitates heart electricity instability so etopic pacemakers in the av junction or ventricles may start to fire and produce escape beats when the sinus rate becomes too slow so in healthy adults and conditioned athletes sinus bradycardia may be asymptomatic but may occur during sleep and other adult sinus bradycardia may cause altered mental status ischemic chest discomfort acute heart failure and hypotension treatment is indicated when the signs and symptoms persist despite adequate oxygen and breathing",
        "Management of Symptomatic Bradycardia": "okay so management of symptomatic bradycardia so the goals for management of emergency care include adequate oxygenation ventilation and perfusion correct the rhythm disturbance and restore a stable perfusing rhythm so searching for the underlying cause which may be hypoxia hypothermia shock altered mental status av block toxin exposure and so also an electrolyte disorder or increased intracranial pressure or other factors um so we want to the emergency care that we want to administer is we want to maintain that open airway you're going to assist breathing as necessary and administer supplemental oxygen as needed to maintain an spo2 of 90 or higher apply the cardiac monitor blood pressure monitor and pulse ox and maintain or obtain a 12 lead but do not delay emergency care establish an iv infusion of normal saline obtain a finger stuck blood glucose level and treat hypoglycemia administer atropine iv bolus for symptomatic bradycardia or a condition block conduction block at the level of the av node and repeat atropine every three to five minutes until the desired heart rate is achieved usually 60 beats per minute or faster or until the dosage limit of three milligrams has been reached if atropine is ineffective and the patient's symptoms or hemodynamic instability persist then consider transcutaneous pacing or the administration of dopamine or epi infusion transport the patient for definitive care this figure shows the recommended treatment guidelines for adult bradycardia with a pulse algorithm",
        "Artificial Pacemakers": "okay so next we're going to talk about artificial pacemakers they deliver repetitive bursts of electrical impulses to the heart and artificial pacemakers current can depolarize the myocardial tissue and substitute for a blocked non-functional natural pacemaker transcutaneous pacemaker transcutaneous pacemakers depolarize the myocardium by delivering electrical energy through the skin of the chest a small electrical charge passes through the patient's skin between one external pacemaker pad and another the energy increases until the heart begins to react to the stimulus this response called capture is usually associated with ventricular depolarization it's characterized by a wide qrs complex on the ecg and should result in a corresponding pulse",
        "Artificial Pacemaker Failure": "okay so use of t cp in the following situation so a patient with bradycardic dysrhythmia that severely reduces co and does not respond to atropine a symptomatic patient with an artificial pacemaker failure so to properly initiate tcp refer to skill drill 17-2",
        "Sinus Tachycardia": "okay next rhythm we're going to talk about is the sinus stack and that is a rhythm that originates in the sa node as well the sa node is still the pacemaker but the rate is between 101 and 180 beats per minute it's a regular rhythm a bright p wave precedes every qrs complex and the pr in a pri interval is 0.12 to 0.20 seconds and the qrs complex is 0.11 seconds or less sinus attack may result from various cases including pain fever hypoxia hypovolemia exercise stimulation of the sympathetic nervous system certain drugs caffeine nicotine or alcohol hypoxia metabolic alkalosis hypokalemia and hypocalcemia can lead to electrical instability prompting the firing of cells that normally do not generate impulses treatment is related to the underlying cause",
        "Sinus Dysrhythmia": "now we're going to talk about sinus dysrhythmia this is a slight variation in the cycling of the sinus rhythm usually exceeding 0.12 seconds between the longest and shortest cycles associated with respiratory cycle fluctuations the rate increases during inspiration and decreases during expiration the sa node is still the pacemaker and an upright p wave precedes every qrs complex sinus dysrhythmia is often found in children and young adults and tends to diminish with age",
        "Sinus Arrests": "now we're going to talk about sinus arrests this is still a rhythm originating in the sa node the sa node fails to initiate an impulse which eliminates the p wave qrs complex and or the t wave from one cardiac cycle then resumes normal functioning the atrial and ventricular rates are usually within normal limits when regular rhythm except for the absence of the complexes there's an upright p wave and they precede every qrs possible causes include ischemia of the sa node increased vagal tone or carotid sinus massage occasional episodes are not significant unless the heart rate drops below 60 beats a minute treatment may include a temporary pacemaker in the field or a permanent pacemaker placed once in the hospital",
        "Sick Sinus Syndrome": "sick sinus syndrome and that's a syndrome and is a variety of rhythms involving a poorly functioning sa node common in older adults patients may exhibit syncope dizziness palpations or may have other symptoms it shows on the ekg as sinus bradycardia sinus arrest and sa block or alternating patterns of extreme bradycardia and tachycardia",
        "Atrial Rhythms": "okay so rhythms originating in the atria there are impulses from an area in the atria so upright p waves preceding each qrs and complex and some rhythms generated from the atria produce upright p waves preceding each qrs but they are not all as well rounded as those generated from the sa node premature atrial complexes so not technically a dysrhythmia but an atopic complex within another rhythm the premature atrial complex occurs earlier than the next expected complex which produces an abnormally r on r interval between it and in the previous complex causing an irregular rhythm an upright p wave precedes each qrs but its difference it differs from the p wave originating in the sa node",
        "Premature Atrial Complexes": "so pacs are not always conducted to the ventricles a non-conducted pac is the presence of a p wave that occurs early on the ecg and is not followed by qrs do not confuse it with an av block pacs occur infrequently and have no particular pattern the p wave will be shorter in the p and p intervals pac is very common and can be caused by stress stimulants or other conditions and when pacs are frequent treatment is focused on correcting the underlying cause",
        "Supraventricular Tachycardia": "so let's talk about supraventricular tachycardia or svt next svt is a rhythm originating from the site above the ventricles svt is a ventricular rate faster than 100 beats at rest in patients with normal ventricular functioning tachycardia with the rate of less than 150 beats rarely causes sewer signs and symptoms the ventricular filling time is greatly lowered when the ventricular rate exceeds 150 beads when the ventricular rate reaches 150 to 180 beats per minute the p waves if present with the svg tend to be completely obscured by the t wave of the preceding beat the most common type of svt is called av nodal reentrant tachycardia it's associated with re-entry which is the spread of then impulse through the tissue already stimulated by the same impulse another conditions like the presence of myocardial ischemia a premature impulse can trigger a series of rapid beats these impulses could get stuck in a repetitive pattern generating multiple atopic beats in a very rapid rhythm patients sometimes have a physical finding known as cannon a-waves created when a disassociation between the atrium and the ventricle occurs and can indicate deteriorating functionality of the right ventricle or increasing right ventricular and diastolic pressure treatment depends on the severity of the patient's symptoms and may include medication or electrical therapy to slow the heart rate down this figure shows the process of reentry the spread of the impulse through the tissue that's already been stimulated note the following for the management of tachycardia with the pulse tachycardia is more complicated situation than bradycardia so tachycardia can originate from it from a supraventricular pacemaker site narrow qrs complexes a ventricular origin with wide qrs complexes in most cases the rhythm is ventricular and should be treated accordingly goals for emergency medical care include maintain the oxygenation ventilation and perfusion correct the rhythm disturbance and restore a sinus rhythm and search for the underlying causes there are many possible variations of the signs this requires judgment before treatment is begun decide on the seriousness of the signs and symptoms and the paramedic must decide if signs and symptoms indicate tachycardia or another condition if the patient is stable and exhibiting related signs related to tachycardia therapy such as vagal maneuvers and medications are recommended if unstable signs and symptoms are determined to result from tachycardia use of electrical therapy with synchronized cardioversion is recommended follow the procedure for emergency care of an adult who has tachycardia with a pulse maintain the airway assist breathing if necessary and apply supplemental oxygen as needed to maintain an spo2 of 94 grader apply the cardiac monitor and monitor the blood pressure pulse ox and get a 12 lead and do not delay emergency care establish an iv infusion of normal saline obtain blood figure stick glucose and treat hypoglycemia if present if the qrs is narrow the patient is stable and there are no contraindications then perform vagal maneuvers if the following rhythm persists then administer adenosine intravenously followed by a dose with a 20 milliliter fluid bolus if the qrs is narrow and the patient is unstable then consider sedation before performing synchronized cardioversion transport the patient for definitive care and follow the recommended treatment guidelines for adult tachycardia with a pulse as shown in figure 17-42 also it's shown on this slide fagal maneuvers alone will terminate up to 25 of svt caused by re-entry attempt before starting medication therapy",
        "Cardiac Massage": "many types exist in the cardiac sinus massage and the valsalva maneuver okay cardiac massage also known as the carotid sinus pressure assess for brutes before performing this procedure so risk of high thromboembolism in some patients such as those with advanced age coronary disease or high cholesterol the vasava maneuver is more commonly used or the vagal maneuver in which the patient bears down as if attempting to do a bowel movement administer adenosine if the vagal maneuvers are infected and if the patients with the narrow qrs complex remain stable so administer administer at an iv cyclosis to the patient's heart and follow with a 20 ml fluid bolus of normal saline be prepared for a short run of a systole if the first dose of adenosine is unsuccessful then administer a double dose of adenosine and administer it again within one to two minutes if needed repeat the dose again in one to two minutes if a dentist does not convert the rhythm rapidly transport the patient to the medical facility",
        "Tachycardia Algorithm": "if at any time the condition of svt becomes unstable you should move the unstable arm of the tachycardia algorithm the tachycardia patient in an unstable condition requires electrical therapy with synchronized cardioversion okay so cardioversion is indicated for v-tac and svt associated with severely compromised co sedate the patient first if performing cardioversion on a responsive patient benzodiazepines such as valium and midazolam or versed are commonly administered for sedation follow your local protocol to properly perform cardioversion return refer to your skill dural 17-3",
        "Pre-excitation": "okay so pre-excitation is what we're going to talk about next and this refers to early depolarization of the ventricular tissue by means of an accessory pathway between the atrium ventricular ventricles the accessory pathway is an extra bundle of myocardial tissue that forms a connection between the atria and the ventricles outside the normal conduction system a v reentrant tachycardia is a reentry svt involving an av node and an accessory pathway the most common pre-excitation disorder is wolf parkinson-white syndrome and it's characterized by a short pian r p ri interval non-specific qt wave changes a wide qrs an appearance of a delta wave on the ecg you have lone ganglion levine syndrome and it also causes pre-excitation of the ventricular tissue it's characterized by a short pri interval a normal qrs duration so patients with this white wolf parkinson's white syndrome are suspected susceptible to tachydysrhythmias care of the patient with either of these syndromes include seeking the advice of a physician basing treatment on the gravity of the patient's instability qrx complex with and the ventricular rhythm regularity oh and atrial fibrillation we're going to talk about next it still is originating in the atria a afib is a rhythm in which the atria no longer contracts but instead fibrillates or quivers with no organized contraction the condition occurs when cells in the atria depolarize immediately or independently rather than in response to an sa node impulse a f or a fib results in just fibrillating of the atria",
        "Atrial Fibrillation": "a fib is characterized by no visible p wave on the ecg strip no pri to measure irregularity there it's irregularly irregular and afib is common rhythm for older adults afib increases the risk of stroke because blood within the fibrillating atria tends to clot stable but asymptomatic patients may may be prescribed an anticoagulant such as warfarin or coumadin beta blockers calcium channel blockers or digoxin unstable patients may need synchronized cardioversion and pre-hospital treatment for afib is uncommon in stable patients",
        "Atrial Flutter": "the next rhythm we're going to talk about is a flutter you may flutter is a rhythm in which the atrial impulse fires at a rate too fast for the ventricles to keep up atrial complexes are known as flutter waves or f waves rather than p waves with a distinct sawtooth shape resembling a picket fence one or more of the f waves gets blocked in the avim node resulting in several f waves before each qrs complex the rhythm is usually regular with consistent conduction or irregular with the qrs complex measuring 0.11 seconds or less a flutter can degenerate into afib and patients are often prescribed anticoagulants because these patients are thought to have some type of risk of thromboembolism as patients with a fib a beta blocker calcium channel blocker may be administered if the patient is stable but asymptomatic and synchronized cardioversion may be necessary if the patient is unstable pre-hospital treatment of afib is uncommon in stable patients",
        "Wandering Pacemaker": "all right another rhythm originating in the atria is the wandering pacemaker so the wandering pacemaker of the heart moves from the sa node to various locations within the atria or av junction the rate is usually 60 to 100 beats with a slightly irregular rhythm and r on our interval based on the pacemaker site an upright p wave precedes each qrs complex however the p wave shapes vary indicating multiple sites of origin so wondering pacemaker is characterized by a pri of 0.12 to 0.20 seconds and it varies based on the complex origin if seen in children older adults and athletes the treatment is indicated in the pre-hospital setting only if the dysrhythmia is associated with a slow rate and the patient is symptomatic so treatment would be the same for symptomatic sinus bradycardia",
        "Multifocal Atrial Tachycardia": "okay so multifocal atrial tachycardia and they this is otherwise known as matte multiple thetopic sites within the atria depolarize at different but rapid rates and it's characterized by a rate of more than 100 beats per minute in effect multifocal atrial tack is a tachycardic wandering pacemaker within a regular rhythm and pr interval that is varies based on the site of the pacemaker okay so this is the uh it's characterized by a pri of 0.12 to 0.20 seconds however it varies slightly mat is most often seen in patients with a lung disease or pulmonary hypertension coronary disease or some type of hypomagnesium it is also seen in patients undergoing themophylene therapy and treatment is not usually a pre-hospital level and therapies for svt are generally ineffective",
        "AV Junction Rhythms": "okay so now we're moving down we're going to move down now into the av junction so after the sa we go into the av the av junction should take over if the sa node fails to initiate that impulse and because the av junction is a secondary pacemaker its intrinsic rate is lower junctional rhythms normally have a rate of about 60 to 40 to 60 beats an impulse generated in the av junction travels down through the conduction system into the ventricles at the same time the impulse travels upward through the atria and internal pathways towards the sa node",
        "Premature Junctional Complexes": "this leads to three possible circumstances in which the qrs complex appears normal if the impulse begins moving upward through the atria before the other parts enter the ventricles the upside down p wave will slow will show followed immediately by the qrs complex the impulse moving through the atria occurs at the same time it travels through the ventricles the smaller inverted p wave will be hidden within the qrs complex giving the appearance of a missing p wave until a normal qrs complex begins if the impulse starts late through the atria it will result in an inverted p wave after the qrs complex okay so a premature junctional complex is not a dysrhythmia but rather an early complex that appears within a regular rhythm pjcs are also known as etopic complexes meaning they arise from a site other than the sa node the ray depends on the underlying rhythm and is irregular the p wave present the p wave if present will be inverted and may either proceed or follow the qrs complex pjcs are characterized by a pri if present less than 0.12 seconds and the qrs complex measures 0.11 seconds or less pjcs can be caused by many of the same factors that cause a pac pjcs do not normally require treatment and most people with the condition are asymptomatic possible symptoms are perceived skip beats lightheadedness or dizziness okay so junctional escape rhythm is a dysrhythmia that occurs when an sa node does not function and the av node takes over as the pacemaker it is also called the junctional rhythm the rate is going to be between 40 to 60 beats usually regular and with little variation between the r and r intervals so the p wave is inverted or and present before the qrs and junctional rhythm often accompanies sa no disease or increased vagal tone inferior wall mi or other conditions so it can occur after resuscitation from a cardiac arrest treatment depends on the underlying cause but may require a surgery or surgically planted pacemaker and the field atropine should be considered and the tcp may be necessary if the patient's condition is severely compromised accelerated junctional rhythm is present when the rate exceeds the normal rate of 60 beats per minute but remains less than 100 the rhythm is regular with little variation between the r and r intervals and the p wave is present if the p wave is present it's inverted or upside down before or after the qrs complex so it may be associated with digoxin toxicity hypoxia inferior wall and mine rheumatic fever recent cardiac surgery or an electrolyte imbalance and the rate is fast enough to maintain a reasonable co so the patient usually is asymptomatic nevertheless he or she should be closely monitored now junctional attack is accompanied with a rate that exceeds 100 beats the rhythm is regular with little variation between rmr intervals the ecg characteristics are the same as the accelerated junctional but the rate is faster at about 100 beats it's common in adults but it is associated uncommon in adults but is associated with an acute coronary syndrome heart failure or digoxin toxicity because a rate is fast enough to maintain that co it is seldom requires treatment in the pre-hospital setting if the rate exceeds 150 beats co2 or co could suffer so at the rapid ventricular rate distinguishing junctional attack from another narrow qrs tachycardia can be difficult so if the patient's symptomatic then treat in accordance with the tachycardia algorithm",
        "Ventricular Rhythms": "all right now we're moving right down the heart and we're going into the rhythms originating in the ventricles so then if the sa node fails to initiate an impulse then the av junction usually takes over however the there is a conversion to pacemaker so the ventricles may start originating their own impulses and become that pacemaker if the av junction does not take over right so you're going to have a y qrs and you're going to be missing p waves so premature ventricular complex once again pvc is not a dysrhythmia but rather an early complex that appears within another rhythm pvcs are atopic complexes because they originate from the site other than the sa node a pvc occurs either or earlier than the next expected sinus complex producing an irregular ventricular rhythm it is characterized by a lack of p wave and no pr interval the qrs complex associated with the pvc measures 0.12 seconds or more a fully compensatory pause usually follows the pvc to determine if one is present so you want to measure the rnr of the underlying rhythm next measure from the r wave to the qrs complex before the pvc to the r wave of the qrs complex and after the pvc a full compensatory pause has occurred if they are on our interval that includes a pvc measure twice that of the underlying rhythm the pvc may be unifocal or multifocal and so unifocal it originates from the same area or focus within the ventricle and look alike multifocal vary in appearance and more than one focus initiating the ventricular impulse and so you can see that on the to the left it's going to be unifocal and to the right you're going to see the multifocal complexes a ventricular couplet is two pvcs with no intervening pause a run of vtac is a term for three or more pvcs in a row also referred to as salvus or burst ventricular by gemini is a pattern that occurs when the complexes become so frequent that they begin to alternate with normal complexes generating a normal pvc than a normal beat then a pvc ventricular trigeminy is a pattern of every third beat being a pvc so it'd be normal normal pvc normal normal pvc and then pvcs can arise in the same ways as a premature atrial injunctional complexes but they most often originate from ischemia in the ventricle tissue they are generally characterized by more serious they're more serious than the premature atrial or junctional complex occasional pvcs are common and usually don't require treatment in otherwise healthy patients but pvcs that occur in patients with heart disease require close monitoring and search for underlying causes okay this next rhythm is the ideoventricular rhythm it occurs when the sa and av nodes fail and the ventricles must paste the heart usually regular with very little variation between the r and r intervals no p wave so no p r i interval the rate is 20 to 40 beats with little variation it's an agonal rhythm pattern created when the ventricular rates lose to the less of 20 beats it may or may not result in a palpable pause pulse treatment improving the co by increasing the rate and if possible treat the underlying cause",
        "Accelerated Idioventricular Rhythm": "accelerated idioventricular this rhythm occurs when the inner ventricular rate exceeds the normal upper rate of 40 beats but less than 100 the rhythm is regular with little variation p waves are absent the qrs complex is 0.12 seconds or more accelerated ventricular rhythm may be observed during the first 12 hours of an ami or after reperfusion therapy do not suppress these rhythms with ventricular anti-dysrhythmia agents",
        "Ventricular Tachycardia": "okay and this is ventricular attack v-tac is a ventricular rhythm that has a rate exceeding 100 beats the rhythm is regular with no variation between the r and r intervals p waves are absent so the pri does not exist qrs complex is 0.12 seconds or more this is considered a wide qrs complex occasionally the qrs complex will vary in height in an alternating pattern and that is polymorphic ventricular attack a wide irregular tachycardia is present in about 25 percent of out of hospital cardiorex cardiac arrest involving ventricular attack the most common is to recite the points it may convert spontaneously to a normal rhythm or it may degenerate into ventricular fib tac is extremely serious and requires treatment if the patient's stable emergency care should focus on treatment with antidysrhythmics if the patient is unstable electric therapy using synchronized cardioversion may be necessary",
        "Ventricular Fibrillation": "okay and then we have v-fib that rhythm in which the entire heart is just fibrillating okay so it occurs when many different cells become depolarized independently rather than from the sa node impulse there's no p waves there's no pr interval and or no complexes",
        "V-fib Defibrillation": "okay so when fibbing waves are greater than three millimeters in amplitude the dysrhythmia is called coarse and when the fib waves are less than three the dysrhythmia is called fine v fib defibrillation so it's effective for v-fib and pulseless v-tac it's a process by which a surge of electrical energy is generated and delivered to the heart defibrillation delivers a current that is powerful enough to depolarize all of the heart's component muscle competent muscle cells when the cells repolarize after the shock they should respond to an impulse from the sa node and begin to organize again",
        "Manual Defibrillation": "so an automatic external defibrillator so an aed interprets the cardiac rhythm to determine if defibrillation is needed in manual defibrillation the paramedic interprets the cardiac rhythm to determine if defibrillation is needed if you witness a cardiac arrest begin chest compressions and attach the defibrillator as soon as available for adults with an unmonitored cardiac arrest or situations where the defibrillator is not available start cpr while the machine is being retrieved and then perform defibrillation as soon as the device is ready aeds and manual defibrillations deliver energy and waveforms so there's monophasic waveforms and that delivers energy from the heart from one defibrillation pad to the other and then there's biphasic and that's when the energy travels from the heart from one defibrillation pad to the other and then reverses the direction flowing back through follow the same safety measures as you would for a manual defibrillation as you would for an aed make sure no one's touching the patient do not defibrillate the patient in water do not defibrillate the patient who is touching metal to avoid burns do not place the defibrillation pads on the medication patch inspect a defibrillator at the beginning of each shift and look for the defibrillation pads cables power supply and monitor to properly perform the manual defibrillation refer to skill drill 17-4 so there can be wearable cardio verter defibrillators and so those were designed for patients at a risk for sudden cardiac death but who are not immediate candidates for therapy with an implantable cardioverter defibrillator example life vest houses a non-adhesive sensing electrode and separate defibrillation electrodes and it constantly reads and records the patient's ecg and up to five biphasic energy shocks can be delivered okay so this is uh systole and a cysticly is the only true arrhythmia the entire heart no longer contracts and this shows no evidence of an organized activity so a systole is a complete absence of a ventricular electrical activity there's no p waves there's no qrs and there's no t waves a flat line on the ecg monitor may or may not indicate a systole so rule out causes of of um other than the systole a sicily is considered non-shockable cardiac arrest rhythm there is no electrical activity to reset and then you have pulseless electrical activity pea refers to an organized so that's the key thing organized cardiac rhythm not accompanied by a detectable pulse pea was formally called electromagnet electromechanical disassociation so mechanical ventricular activity is too weak to produce a palpable pulse as in cases of cardiogenic or hypovolemic shock cardiac tamponade massive pulmonary emboli electrolyte imbalance or disturbance or drug overdose the key to the treatment of pea is to underline or identify the underlying causes and to fix pea is a non-shockable cardiac arrest rhythm",
        "Conclusion": "okay so this is going to conclude chapter 17 cardiovascular emergencies and we just discussed part three we discussed dysrhythmia interpretation so go ahead and next we're going to do part four and that is going to be working the cardiac arrest and the algorithms for the management of the adult cardiac arrest okay thank you"
    },
    {
        "Introduction to Cardiovascular Emergencies": "chapter 18 cardiovascular emergencies according to the American Association an individual in the United States experiences an acute myocardial infarction or Ami approximately every 40 seconds heart disease has remained the leading cause of mortality among Americans since the early 1900s however mortality rates associated with cardiovascular disease can be reduced through several strategies these include enhancing public awareness ensuring Early Access to Emergency Medical Services increasing the number of lay persons trained and willing to perform CPR leveraging advancements in technology for dispatch and cardiac arrest response providing public access to defibrillation Services recognizing the importance of advanced life support and facilitating transportation to hospitals equipped to perform coronary catheterization and provide posteres care.",
        "Components of the Cardiovascular System": "The cardiovascular system is composed of three main components the heart the blood vessels and the blood these elements work together to maintain circulation delivering oxygen and nutrients to tissues while removing the waste products the heart functions as the central pump blood vessels serve as the conduits and blood carries the essential materialss necessary for sustaining life.",
        "Anatomy of the Heart": "The heart is a muscular cone-shaped organ that's primarily responsible for pumping blood throughout the body the muscle tissue of the heart is known as The myocardium surrounding the heart is the pericardium also referred to as the paracardial sac which is a thick fibrous membrane providing protection and Port the visceral layer of the pericardium known as the epicardium lies directly against the surface of the heart contributing to the overall structure and function of this vital organ the endocardium is the smooth inner lining of the heart's chambers and covers the surface of the valves providing a slick surface to minimize friction as blood flows through the heart that the Atria are the heart's upper chambers with each one responsible for receiving blood returning to the heart from various parts of the body the ventricles which are the lower Chambers are tasked with pumping blood out of the heart notably the left ventricle is the strongest and largest of the heart's chambers as it is responsible for pumping blood through the entire systemic circulation ensuring oxygenated blood reaches all tissues of the body the heart contains two main types of valves the atrio ventricular valve and semi lunar valves the atrio ventricular valves include the tricuspid valve which is located between the right atrium and right ventricle and the mitro valve which is situated between the left atrium and the left ventricle the semi lunar valves consist of the aortic valve which controls blood flow from the left ventricle into the aorta and the pulmonic valve which regulates blood flow from the right ventricle into the pulmonary artery papillary muscles which are located within the ventricles play a vital role by Contracting to tighten the cord a tendon which are tendonous cords that anchor the valve leaflets thereby preventing the valves from inverting during ventricular contraction the figure here illustrates the anatomy of the heart highlighting its Chambers major blood vessels and valves.",
        "Coronary Circulation": "Coronary circulation is the system of blood vessels that supplies the heart muscle with oxygen and essential nutrients this circulation originates from the left and right coronary arteries the left main coronary artery further divides into two branches the left anterior descending or L artery and the circumfluent tricle the interventricular septum and sometimes the atrio ventricular node the coronary artery also plays a key role in supplying blood to various parts of the heart ensuring that The myocardium receives adequate oxygenation to sustain its function the provided images depict both the anterior and posterior views of the heart illustrating the major structures that are involved in cordary circulation and overall cardiac function in the anterior View view we can observe the left coronary artery emerging from the aorta and quickly branching into the left anterior descending and circumlunar along the interventricular Groove supplying blood to the front of the left ventricle and the interventricular septum the lateral and posterior surfaces of the left ventricle also visible in this view is the right coronary artery which originates from the right side of the aorta and travels within the coronary sulcus this artery primarily supplies the right atrium left ventricle and the inferior portion of the left ventricle the coronary veins run parallel to the arteries collecting deoxygenated blood from The myocardium and returning it to the right atrium via the coronary sinus the posterior view highlights additional aspects of the coronary circulation the right coronary artery continues its path in the posterior interventricular Groove where it gives rise to the posterior descending artery or PDA this supplies the inferior wall of the left ventricle and the posterior part of the interventricular septum in this view the coronary sinus is more prominent collecting blood from the coronary veins and channeling it back into the right atrium this view also provides a clear visualization of the pulmonary circulation with the pulmonary veins returning oxygenated blood from the lungs to the left atrium and the pulmonary arteries carrying deoxygenated blood from the right ventricle to the lungs for oxygenation together these images emphasize the intricate work of coronary arteries and veins that ensure the heart muscle receives a constant supply of oxygenated blood.",
        "Blood Vessels and Circulation": "Blood vessels are integral to the circulatory system serving as the conduits through which blood is transported throughout the body the Journey of blood begins in the arteries with the aorta being the largest artery emerging directly from the heart from the arteries blood is carried to smaller arterioles and then to the capillaries which are the sites of nutrient and gas exchange with tissues after passing through the capillaries the blood enters venules which progressively merge to form veins deoxygenated blood from the body is returned to the heart via the superior and inferior vnea both of which empty into the right atrium from here the blood will eventually begin to be sent to the lungs for reoxygenation conversely oxygenated blood from the lungs is delivered back to the heart through the four pulmonary veins which empty into the left atrium preparing it for distribution to the rest of the body via the arterial system this cyclical process is fundamental to maintaining the body's homeostasis in ensuring that tissues receive the oxygen and nutrients they need while waste products are efficiently removed.",
        "Blood Flow and Gas Exchange": "The image on the left shows how oxygen poor blood which is already circulated through the body and delivered its oxygen to the tissues returns to the heart this deoxygenated blood enters the heart through the superior and inferior vnea which drain into the right atrium from the right atrium blood flows through the tricuspid valve into the right ventricle upon contraction of the right ventricle blood is pumped through the pulmonic valve into the pulmonary arteries which transport the blood to the lungs in the lungs the blood undergos gas exchange where it releases carbon dioxide and receives freshh oxygen the image on the right depicts the flow of oxygen-rich blood which has been oxygenated in the lungs this oxygenated blood is returned to the heart via the pulmonary veins which empty into the left atrium blood then passes through the mitro valve into the left ventricle the left ventricle being the strongest chamber of the heart contracts forcefully to pump blood through the aortic valve into the aorta from the aorta blood is distributed throughout the body via the arterial system delivering oxygen and nutrients to various tissues and organs this process ensures that the body continuously receives the oxygen it needs while removing carbon dioxide and other metabolic wastes thereby maintaining homeostasis the precise coordination of the heart's chambers and valves is vital for efficient blood circulation and any disruption in this flow can lead to significant cardiovascular complications.",
        "Components of Blood": "Blood is composed of two main components plasma and formed Elements which include red blood cells white blood cells and platelets plasma is the liquid portion of blood that carries nutrients hormones and waste products throughout the body the formed elements are the cellular components of blood each playing a unique and vital role red blood cells contain hemoglobin A protein that binds to oxygen in the lungs and transports it to tissues throughout the body this process is crucial for providing oxygen to cells and removing carbon dioxide as a waste product white blood cells or lucaites are an essential part of the immune system defending the body against infections and foreign Invaders platelets the smallest of the formed elements play a key role in homeostasis these components work together to maintain the body's homeostasis and ensure the effective delivery of oxygen defense against infections and prevention of excessive blood loss.",
        "Heart's Electrical Conduction System": "The heart's pumping action is regulated by an intricate electrical conduction system that initiates and coordinates each heartbeat this system begins with the Sino atrial node which is the primary pacemaker of the heart located in the right atrium the SA node generates electrical impulses at an intrinsic rate of 60 to 100 beats per minute setting the rhythm of the heart if the SA node fails to function properly the AV node can take over as the secondary pacemaker the AV node which is located at the junction between the Atria and the ventricles has an intrinsic rate of 40 to 60 beats per minute although slower than the SA node the AV node ensures that the heart continues to be in pump blood once the electrical impulse is generated it it spreads through the conduction system traveling from the Atria to the ventricles this propagation of nerve impulses causes the ventricles to contract a process known as syy the coordinated contraction of the ventricles is essential for Effective blood circulation as it ensures that blood is pumped out of the heart and into the arteries delivering oxygen and nutrients to the body.",
        "Electrical Properties of Cardiac Cells": "Cardiac cells possess unique electrical properties that are fundamental to the heart's ability to function as a pump these properties include excitability conductivity and automaticity excitability refers to the ability of cardiac cells to respond to electrical impulses when an electrical stimulus reaches these cells they can react by generating an action potential which is essential for initiating the contraction of the heart muscle conductivity is the ability of cardiac cells to transmit electrical impulses to neighboring cells this property ensures that the electrical signals generated by the SA node or other pacemaker cells are efficiently spread throughout the heart allowing for the coordinated contraction of the Atria and and the ventricles automaticity is the inherent ability of cardiac cells to contract without requiring a stimulus from an external nerve Source this property is particularly significant in pacemaker cells such as those in the SA node which can spontaneously generate electrical impulses thereby initiating the heart's rhythmic contractions independently of the nervous system to together these electrical properties enable the heart to maintain a consistent and effective pumping action.",
        "Regulation of Heart Function": "The regulation of heart function is a complex process involving multiple systems and mechanisms to ensure the heart operates effectively and responds to the body's varying needs key aspects of this regulation include chronotropic dromotropic and inotropic State which are influenced by the autonomic nervous system endocrine hormones and the heart's own tissue chronotropic refers to the heart rate which can be adjusted by the autonomic nervous system to increase or decrease based on the body's requirements dromotropic relates to the conduction velocity of electrical impulses through the heart which influences the timing of the heartbeat inotropic refers to the strength of the heart's contraction which can be modified to adjust the force with which the blood is pumped to maintain homeostasis various receptors located in blood vessels kidneys the brain and the Heart continuously monitor the body's internal environment Barrow receptors are specialized receptors that detect changes in blood pressure particularly within the heart and major arteries allowing the body to make necessary adjustments to maintain stable blood pressure levels chemo receptors monitor the chemical composition of the blood including oxygen carbon dioxide and pH levels and Trigger responses that help maintain the balance of these critical substances.",
        "Cardiac Cycle": "The cardiac cycle refers to the sequence of events that occur in the heart from the beginning of one heartbeat to the beginning of the next it is a continuous process that ensures the effective circulation of blood throughout the body the cycle begins with myocardial contraction which involves the heart muscle Contracting to pump blood this phase is followed by syy during which the ventricles contract forcing blood into the systemic circulation through the aorta and pulmonary circulation through the pulmonary artery syy is the period of active pumping when the heart expels blood from the chambers into the arteries following syy the heart enters diast a period of relaxation during diast the heart chambers relax allowing them to fill with blood in preparation for the next contraction this relaxation phase is crucial for ensuring that the heart has an adequate supply of blood to pump during the next cycle several key factors determine the efficiency and effectiveness of the heart's pumping ability preload refers to the amount of blood that is returned to the Heart during diasty before it is pumped out preload directly influences the the stretch of the ventricular walls and the subsequent force of contraction according to the Frank Starling mechanism it also plays a role in determining the afterload which is the pressure the left ventricle must overcome to eject blood into the aorta and through the peripheral circulation after load is influenced by the resistance of the blood vessels particularly the aorta and other large arteries stroke volume is the amount of blood ejected by the left ventricle with each contraction this volume is determined by preload after load and the contractility of the heart muscle cardiac output is the measure of the overall performance of the heart representing the total volume of blood pumped by the heart in 1 minute and it's calculated using the equation stroke volume time heart rate equals cardiac output this equation illustrates that cardiac output depends on both the volume of blood ejected with each beat and the number of heart beats per minute heart rate and stroke volume are critical determinants of cardiac output as I just mentioned any changes in either of these variables can significantly impact the amount of blood the heart pumps per minute thus affecting the delivery of oxygen and nutrients to the tissues.",
        "Starling Law and Ejection Fraction": "The Starling law of the heart describes how the heart adjusts its force of contraction in response to changes in Venus return when there is an increase in the volume of blood returning to the heart the ventricles are stretched to a greater extent this stretching leads to a more forceful contraction thereby increasing the stroke volume the in transic ability of the heart to adjust its force of contraction based on the volume of blood filling is crucial for maintaining effective circulation during varying levels of physical activity ejection fraction is another important measure of cardiac function as it represents the percentage of blood that is pumped out of the ventricles with each contraction relative to the total volume of blood in the ventricles at the end of diast a normal ejection fraction indicates efficient heart function while A reduced ejection fraction May signal heart failure or other cardiac conditions.",
        "Pathway of Blood Flow": "Blood flow within the heart follows a precise and organized Pathway to ensure efficient circulation throughout the body deoxygenated blood from the upper part of the body returns to the heart through the superior venne cava while blood from the lower part of the body returns via the inferior vena both of these large veins empty directly into the right atrium from there blood flows into the right ventricle and then it pumps into the pulmonary arteries leading to the lungs in the lungs via diffusion gas exchange occurs where the blood is oxygenated and carbon dioxide along with other waste products are removed oxygenated blood blood then returns to the heart entering the left atrium through the pulmonary veins at this point the blood moves into the left ventricle which pumps it out through the aorta to be distributed to the rest of the body.",
        "Pulmonary and Systemic Circulation": "Pulmonary circulation is the process by which blood is carried from the right side of the heart to the lungs and then back to the left side of the heart this circulation begins when de oxygenated blood is pumped from the right ventricle through the pulmonary arteries to the lungs and then in the lungs blood becomes oxygenated at which point it then returns to the left atrium of the heart via the pulmonary veins in contrast systemic circulation is responsible for Distributing blood to the rest of the body after the blood is oxygenated in the lungs it's pumped out of the left ventricle into the systemic arterial circulation systemic arterial circulation starts when the oxygen-rich blood leaves the heart through the aortic valve passing into the aorta the body's largest artery from there the blood is distributed via a network of arteries and arterioles to all parts of the body delivering oxygen nutrients to tissues and organs.",
        "Cardiac Ischemia and Myocardial Infarction": "Chest pain or discomfort associated with the heart often arises from cardiac cell esia a condition where the heart muscle is deprived of adequate blood flow this decrease in blood flow to the heart muscle means that the affected tissue does not receive sufficient oxygen and nutrients without prompt restoration of blood flow the tissue begins to suffer leading to Cellular starvation if the esea persists the heart tissue can sustain irreversible damage and eventually die a process known as myocardial infarction or heart attack this underscores the importance of early detection and treatment of esic events to preserve heart function and prevent serious complications.",
        "Atherosclerosis and Arteriosclerosis": "Atherosclerosis is a condition that significantly impairs blood flow to The myocardium this impairment is primarily caused by the accumulation of cholesterol and other fatty substances within the walls of blood vessels over time these substances build up to form plaque which Narrows the arterial Lumen and restricts blood flow as this progresses it can lead to arteriosclerosis a condition that's characterized by the thickening and hardening of the arterial walls this hardening further reduces the elasticity of the arteries making it more difficult for blood to flow through them the combined effects of plaque formation and arterial hardening can drastically diminish the amount of oxygen rich blood reaching the heart muscle which increases the risk of esea myocardial infarction and other cardiovascular conditions here we see the difference between a normal artery and an artery affected by atherosclerosis this highlights the impact of plaque formation on blood flow in the top image we see a normal artery the arterial wall is smooth and unobstructed allowing blood to flow freely the crosssection shows a clear wide Lumen through which blood can pass without resistance this normal blood blood flow ensures that oxygen nutrients are efficiently delivered to the tissues and organs throughout the body the narrowed artery on the bottom image demonstrates the effects of atherosclerosis in this artery plat composed of cholesterol fatty substances and other minerals has accumulated on the inner walls of the artery this buildup reduces the Lumen size significantly narrowing The Passage through which blood can flow the cross-section reveals how plaque has encroached upon the artery space leading to an abnormal and restricted blood flow.",
        "Thromboembolism and Acute Myocardial Infarction": "Thromboembolism occurs when a blood clot or thrombus forms in a blood vessel and then travels through the bloodstream becoming lodged in a narrower part of the circulatory system this blockage can significantly impede blood flow leading to tissue esea and potentially causing severe damage depending on the location of the clot if the clot obstructs a major artery it can prevent oxygen-rich blood from reaching vital organs leading to serious complications including stroke pulmonary embolism or myocardial infarction an acute myocardial infarction or Ami commonly known as a heart attack occurs when a blockage forms in one of the coronary arteries this blockage which is often caused by a thrombus formed due to ruptured atherosclerotic plaque prevents oxygenated blood from reaching a portion of the heart muscle without that adequate blood flow the affected heart tissue begins to die leading to the classic symptoms of a heart attack such as chest pain shortness of breath and fatigue.",
        "Controllable Risk Factors for Cardiovascular Disease": "The development and progression of cardiovascular diseases are heavily influenced by controllable factors including cigarette smoking hypertension hyperlipidemia diabetes lack of exercise and stress smoking damages arteries and promotes plaque formation increasing the risk of heart attacks and strokes while hypertension strains the cardiovascular system hyper lipidemia leads to atherosclerosis and uncontrolled diabetes accelerates this process raising coronary arter disease risk physical inactivity contributes to obesity and hypertension further exacerbating heart disease risk while chronic stress can lead to unhealthy behaviors and directly impacts cardiovascular health manag in these factors through lifestyle modifications such as quitting smoking maintaining a healthy diet exercising regularly and managing stress can significantly reduce the risk of heart disease.",
        "Uncontrollable Risk Factors for Cardiovascular Disease": "The major uncontrollable risk factors for cardiovascular disease include older age a family history of coronary arter disease race ethnicity and male sex these factors can can't be modified but they can increase an individual's predisposition to heart disease being aware of these risk factors is important for early detection and prevention efforts as individuals with these characteristics may need to take extra precautions and manage other modifiable risks more aggressively.",
        "Acute Coronary Syndrome": "Acute coronary syndrome or ACS is a term used to describe a range of symptoms that are consistent with acute myocardial esea this esea can lead to conditions such as angina pectoris characterized by chest pain or an Ami both angina and Ami are treated in a similar fashion under the ACs designation as they share the common underlying issue of insufficient blood supply to the heart muscle The Prompt recognition and treatment of ACS is vital to minimizing heart damage and improving patient outcomes.",
        "Angina Pectoris": "Angina PC taus is a condition characterized by a brief period during which the heart tissue does not receive enough oxygen which leads to discomfort or pain this discomfort typically has predictable characteristics such as a crushing or squeezing sensation often described as like somebody standing on my chest the pain is usually felt in the mid chest under the sternum but it can radiate to the jaw arms midback or epigram angina is most often a symptom of atherosclerotic coronary artery disease the pain or discomfort typically subsides quickly with rest supplemental oxygen or the administration of nitroglycerin all of which help increase the oxygen supply to the heart muscle.",
        "Types of Angina": "Angina Pectus can manifest in different forms each with varying implications for heart health a single episode of angina can simply be a warning of a potential myocardial infarction stable angina typically occurs at predictable times such as during physical exertion and is usually relieved by rest or medication like nitroglycerin in contrast unstable angina is more unpredictable occurring at irregular intervals and it may not always be alleviated by rest or medication indicating a higher risk of heart attack Progressive angina refers to either stable or unstable angina that is worsening in frequency and duration which suggests a deteriorating cardiac condition and an increased risk of severe cardiac event.",
        "Acute Myocardial Infarction": "An acute myocardial infarction commonly known as a heart attack occurs when blood flow to a part of the heart is blocked leading to the death of heart muscle cells in that area the pain associated with an Ami is a direct result of this cellular death most deaths from Ami are caused by dysrhythmia which is an AB normal heart rhythm that can lead to cardiac arrest if not prly treated the most effective treatment for AMI is angioplasty or PCI a procedure that opens blocked arteries and restores blood flow to the heart muscle significantly improving outcomes when performed quickly.",
        "Symptoms of Acute Myocardial Infarction": "The signs and symptoms of an Ami can vary but often include a sudden onset of weakness nausea and sweating without an obvious vious cause chest pain discomfort or even pressure are common symptoms typically described as crushing or squeezing and does not change with each breath this pain May radiate to other parts of the body including the lower jaw arms back abdomen or neck additionally an IR regular heartbeat and Syncopy may occur along with shortness of breath in some cases pink frothy sputum may be present indicating possible pulmonary edema the most common symptom of an Ami is chest pain though the chest pain associated with an Ami differs from that of angina in three significant ways first it can occur at any time not just during physical exertion or stress two it does not resolve within a few minutes but can last anywhere from 30 minutes to several hours and three it may or may not be relieved by rest or Nitro during an Ami the pain is typically felt just beneath the sternum and is often described as a heavy squeezing crushing or tight sensation several physical findings May accompany this pain the patient often appears frightened and anxious with an increased pulse as a normal response to the pain stress or injury to the heart muscle blood pressure may drop due to diminished cardiac output and difficulty breathing is common additionally patients may experience an overwhelming feeling of impending doom a physiological response that is often associated with severe cardiac events.",
        "Consequences of Acute Myocardial Infarction": "The consequences of an Ami can be severe and life-threatening sudden death is one of the most serious outcomes usually resulting from cardiac arrest other potential consequences include cardiogenic shock where the heart fails to pump enough blood to meet the body's needs and of course heart failure where the body's ability to pump blood is impaired in addition various dismas May develop following an Ami these can be lethal or non-lethal and include premature ventricular contractions teoc cardia bra cardia ventricular teoc cardia ventricular fibrillation and asy each of these dymas presents a unique Challenge and may require immediate medical intervention to prevent further complications or death.",
        "Cardiogenic Shock": "Cardiogenic shock is a severe condition often caused by a myocardial infarction where the heart is unable to pump sufficient blood to meet the body's needs this results in an inadequate circulation in oxygen delivery to tissues cardiogenic shock is distinguished from hypmic shock which is caused by blood loss by several Key signs and symptoms these include the chief complaints of chest pain breathing and tacac cardia the heart rate in cardiogenic shock may also present as braic cardia or excessive tacac cardia the heart rate in cardiogenic shock may also present as braic cardia or excessive tachicardia additional distinguishing features include peripheral edema dymas jugular vein distension and crackles heard in the lungs during oscilation this indicates Ates fluid buildup when evaluating and treating a patient in cardiogenic shock the initial approach is the same as for any patient presenting with chest pain focusing on rapid assessment and stabilization Key signs and symptoms to watch for include anxiety or restlessness a feeling of air hunger and pale clammy skin all of which are indicative ative of poor profusion the patient may also exhibit a high pulse rate rapid and shallow breathing nausea and vomiting and a decrease in body temp hypotension is a critical sign and reflects the body's inability to maintain adequate blood flow which is a Hallmark of cardiogenic shock.",
        "Treatment of Cardiogenic Shock": "Treatment for cardiogenic shock involves several critical steps to stabilize the patient and ensure adequate oxygenation and circulation first position the patient in a position of comfort usually sitting upright if they are conscious to ease breathing administer oxygen to maintain an spo2 of greater than 94% and assist with ventilation if necessary to ensure adequate respiratory function it's important to preserve the patient's body heat as hypothermia can worse the condition establish IV access to facilitate the administration of fluids and medications and then transport the patient to an appropriate medical facility as soon as possible if available and if needed call for paramedic backup to provide Advanced Care and Route.",
        "Heart Failure": "Heart failure occurs when the ventricular myocardium can no longer keep up with the return of blood flow from the aorta this condition can develop at any time following a myocardial infarction heart valve damage or as a result of long-standing high blood pressure heart failure often arises between the first few hours in the first few days after an Ami as the damaged heart muscle struggles to maintain effective circulation the inability of the heart to pump adequately leads to a buildup of fluid and blood in the lungs and other tissues which exacerbate their condition and require prompt clinical attention.",
        "Left-Sided Heart Failure": "Left-sided heart failure occurs when the left ventricle pumping function is compromised often due to coronary artery disease damaged heart valves or chronic hypertension in response to the heart's reduced deficiency the heart rate increases and the left ventricle enlarges to pump more blood with each beat however as the heart continues to struggle it may fail to pump blood effectively leading to congestive heart failure where fluid backs up into the lungs causing congestion and difficulty breathing.",
        "Right-Sided Heart Failure": "Right-sided heart failure occurs when the right ventricle of the heart cannot pump blood effectively leading to fluid accumulation in the body this fluid retention often manifests as swelling in the legs and feet this is known as dependent edema or pedal edema these terms describe the same phenomenon where gravity dependent areas like the lower extremities exhibit noticeable swelling due to fluid buildup right-sided heart failure is often a consequence of left-sided heart failure as the increased pressure from the left side of the heart backs up into the lungs and subsequently into the right side of the heart overloading its capacity.",
        "Signs and Symptoms of Heart Failure": "In cases of heart failure a variety of signs and symptoms may be present reflecting the body's struggle to manage the reduced cardiac output these include orthopnea where the patient experiences difficulty breathing when lying flat it must sit or stand to breathe more easily in agitation which reflects the distress caused by inadequate oxygenation chest pain may also occur due to the heart's inability to meet the body's oxygen demands distended neck veins indicate elevated Central Venus pressure commonly seen in right-sided heart failure while pedal edema or swelling of the ankles results from fluid accumulation the patient may also exhibit hypertension te a cardia and Topia as the body attempts to compensate for reduced cardiac function the use of accessory breathing muscles suggests increased worker breathing while crackles hurt in the lungs point to fluid buildup often a sign of pulmonary congestion additionally a productive cough may occur indicating fluid in the lungs and delayed capillary refill time suggests poor profusion and circulation signaling reduced cardiac output these symptoms and signs are critical in assessing the severity of heart failure and guiding appropriate treatment interventions.",
        "Treatment of Heart Failure": "Treatment for heart failure involves several critical steps first it's important to obtain Vital Signs monitor the heart rhythm and administer oxygen as needed the patient should be allowed to remain sitting in an upright position with their legs down which helps reduce the workload on the heart IV access should be gained to facilitate the administration of medications or fluids throughout this process it's important to be reassuring to the patient to help reduce anxiety if the patient has their medication with them it should be brought along and nitroglycerin can be administered if the patient's systolic pressure is above a 100 it's also recommended that patients should not receive Nitro without IV access finally the patient should be transported to a medical facility for further evaluation treatment.",
        "Pulmonary Edema": "Pulmonary edema is a common complication of myocardial esea which may or may not be associated with an Ami this condition involves the accumulation of fluid in the lungs leading to acute respiratory failure and if not promptly treated can result in death several precipitating factors can lead to pulmonary edema including heart failure Mi pulmonary embolism hypertension and cardiomegaly these conditions compromise the heart's ability to pump blood effectively Le the fluid back up in the lungs and subsequent respiratory distress the development of pulmonary edema is influenced by factors such as preload which is the amount of blood returning to the heart and afterload the resistance the heart must overcome to pump blood elevated preload or afterload can exacerbate fluid buildup in the lungs leading to pul ponary edema treatment will focus on maintaining the patient's air we breathing and circulation as well as ensuring prompt transport to a medical facility for further care.",
        "Hypertensive Emergencies": "Hypertensive emergencies occur when there's a significant and sudden increase in blood pressure typically defined as a systolic pressure greater than 180 mm of mercury or a diastolic pressure of 120 mm of mercury or higher these emergencies can lead to severe symptoms primarily due to the effects of elevated blood pressure on the body a common symptom is a sudden and severe headache in managing a hypertensive emergency it's important to position the patient with their head elevated rapidly transport them to a medical facility and establish IV access continuous monitoring of blood pressure is essential in order to assess the effectiveness of treatment and to guide further medical interventions.",
        "Aortic Aneurysm and Dissection": "An aortic aneurysm is characterized by a weakness in the wall of the aorta which can lead to a potentially life-threatening condition if it ruptures a dissecting aneurysm occurs when the inner layers of the aorta become separated allowing blood to flow between these layers which further weakens The Vessel and increases the risk of rupture the primary cause of these aneurysms is uncontrolled hypertension signs and symptoms of a dissecting aneurysm include sudden and severe chest pain which may be felt in the anterior chest or the back between the shoulder blades this pain typically comes on very quickly often reaching full intensity within a minute it's crucial to consider a dissecting aneurysm in any patient presenting with substantial hypertension as prompt diagnosis and intervention are vital in preventing fatal outcomes.",
        "Emergency Medical Care for Chest Pain": "Emergency medical care for chest pain or discomfort begins with proper positioning of the patient if a patient is unable to tolerate being positioned supine they should be allowed to sit up leaning back on the stretcher in a fers or semi position oxygen should be provided as needed to maintain an spo2 of 94% or higher an assistance with breathing should be given if necessary it's crucial to obtain a 12 Le ECG within 10 minutes of patient contact to assess the heart's electrical activity IV access should be gained as long as it doesn't delay transport depending on local protocol be prepared to administer aspirin and assist with prescribed nitroglycerin aspirin is effective in mi patients as it is an antiplatelet aggregate coating the red blood cells and stopping them from clumping together nitroglycerin relaxes the muscle of the blood vessel wall it also dilates coronary arteries increasing blood flow and oxygen supply to the heart muscle as well as decreasing the workload on the heart it also dilates blood vessels and other parts of the body which can sometimes lead to low blood pressure or severe headaches other side effects of nitro include changes in the patient's pulse rate such as tacac cardia or sometimes bra cardia.",
        "Administration of Nitroglycerin": "When administering nitroglycerin it's important to follow specific steps to ensure the medication's effectiveness and safety first always check the condition and expiration date of the medication before use wear gloves when handling Nitro to protect yourself as well as maintaining hygiene before administering the medication obtain permission from medical control especially espe when dealing with prescribed Nitro it is also essential to follow local protocols for administering additional doses of nitroglycerin as these can vary depending upon the situation.",
        "Heart Surgeries and Cardiac Assisted Devices": "Heart surgeries and cardiac assisted devices are critical interventions in managing severe cardiovascular conditions open heart procedures are commonly performed to bypass damage segments of coronary arteries these surgeries involve creating a new pathway for blood flow around the blocked or narrowed sections of the coronary arteries thereby restoring adequate blood flow to the heart muscle this procedure is often necessary for patients with severe coronary artery disease who have not responded to other treatments such as medication or less invasive procedures the goal of bypass surgery is to reduce syp symptoms improve quality of life and increase the chances of survival in patients with significant coronary artery disease in a coronary artery bypass graph or cabbage a blood fessel typically taken from the chest or leg is sewn from the aorta to a coordin artery beyond the point of obstruction allowing blood to bypass the block area and restore adequate blood flow flow to the heart muscle another procedure percutaneous translum coronary angioplasty or ptca involves dilating the coronary artery to improve blood flow by using a balloon or other device it is important to note that if a patient experiences chest pain after undergoing any of these procedures it should be treated with the same urgency in approach as chest pain in patients who have not had heart surgery as it still May indicate a serious underlying condition.",
        "Pacemakers and Defibrillators": "Pacemakers are used when the heart's electrical conduction system fails to function properly these devices deliver an electrical impulse through wires that are in direct contact with The myocardium helping to regulate the heart's Rhythm if a pacemaker malfunctions the patient may experience symptoms such as Syncopy dizziness or weakness which indicates that the device is not maintaining adequate heart function in such cases it's important to transport the patient promptly to a medical facility for evaluation and treatment automatic implantable cardiac defibrillators or acids are devices implanted in patients who have survived a cardiac arrest due to ventricular fibrillation these devices are attached directly to the heart and monitor for lifethreatening arrhythmias if a patient with an acid experiences symptoms of a myocardial infarction they should be treated like all other Ami patients if they go into cardiac arrest treatment should include performing CPR starting with chest compressions and using an automated external defibrillator if necessary external defibrillator vests are equipped with built-in monitoring electrodes and defibrillation pads alerting and guiding patients when a dangerous rhythm is detected before delivering a shock the vest should remain in place during CPR unless it interferes with compressions in which case the battery should be removed before the vest is taken off patients who have received a shock from the device should be transported to the hospital for further evaluation.",
        "Left Ventricular Assist Devices": "Left ventricular assist devices or lvads enhance the pumping function of the left ventricle in patients with severe heart failure El vads typically consist of an internal pump unit and an external battery pack with a characteristic hum indicating proper function in the event of an equipment failure troubleshooting should should include checking for alarm codes ensuring all cables are connected and verifying power supply replacing only one battery at a time assistance can also be sought from the manufacturer's hotline during transport caregivers should be utilized as a resource and all elad supplies and batteries should accompany the patient to the hospital.",
        "ECG Monitoring": "In some some EMS systems aemts permitted to place electrodes attach leads and obtain an ECG tracing before transport for the ECG to be reliable and provide useful information it's critical that the electrodes are placed in consistent positions on each patient when preparing a patient for ECG monitoring it may occasionally be necessary to shave body here from the electrod site to ensure proper adhesion before applying the electrodes the skin should be cleaned by briskly rubbing the site with an alcohol swab to remove oils and dead tissue attach the electrodes to the ECG cables before placement once all electrodes are in place switch on the Monitor and print a sample Rhythm strip if the strip shows any interference known as artifact check that the the electrodes are firmly applied to the skin and that the monitor cable is properly connected.",
        "Summary of Cardiovascular System and Health": "The cardiovascular system plays a vital role in maintaining homeostasis and includes key components such as the heart blood vessels and blood the heart structure consists of four chambers and valves that ensure unidirectional blood flow aided by the electrical conduction system that's responsible for synchronized cardiac Cycles blood is oxygenated in the lungs before being pumped throughout the body and coronary circulation supplies oxygen and nutrients directly to the heart muscle factors influencing cardiovascular health include both controllable and uncontrollable risk factors controllable factors like smoking hypertension high cholesterol diabetes lack of exercise and stress significantly impact the development of atherosclerosis which can lead to severe conditions such as myocardial infarction and heart failure uncontrollable factors including age family history race and sex also play a role in cardiovascular disease risk acute coronary syndrome encompasses a range of conditions associated with myocardia lmia which can lead to angina pectoris or an Ami emergency care for chest pain involves proper patient positioning oxygen Administration ECG monitoring and potentially the administration of medications such as aspirin and Nitro interventions such as angioplasty and coronary artery bypass graphs are critical in treating severe coronary artery disease for patients with Advanced heart failure devices like pacemakers implantable defibrillators and Lads provide essential support proper management and transport of patients with these devices require special considerations such as ensuring device functionality and maintaining battery power additionally conditions like cardiogenic shock hypert sens of emergencies and pulmonary edema require immediate intervention to prevent life-threatening outcomes with treatment focusing on stabilizing the patients Airway breathing and circulation as well as blood pressure"
    },
    {
        "Introduction to Shock": "chapter 14 shock shock or hypo profusion is characterized by the collapse and failure of the cardiovascular system in its initial stages the body engages compensatory mechanisms to sustain homeostasis which refers to the balance and stable function of bodily systems however as shock advances these mechanisms become inadequate leading to a progressive slowing of blood circulation which can ultimately result in the cessation of blood blood flow if left untreated shock can be precipitated by a variety of medical or traumatic events it's imperative for healthc care providers to maintain a high level of vigilance for the signs and symptoms of shock as early recognition and intervention are key to improving patient outcomes.",
        "Perfusion and Circulatory System": "perfusion refers to the circulation of blood within an organ or tissue in sufficient amounts to meet its metabolic needs this process is dependent on a properly functioning cardiovascular system blood profusion throughout the body occurs via the circulatory system which consists of two primary circuits systemic circulation which delivers blood throughout the body and pulmonary circulation which facilitates gas exchange in the lungs cardiac output is the volume of blood that the heart can pump per minute this output is determined by several factors including myocardial contractility which is the heart's ability to contract preload which refers to the volume of blood filling the heart before contraction and after load which is the resistance the heart must overcome to eject blood.",
        "Mean Arterial Pressure": "mean arterial pressure or map is a critical parameter in assessing a patient's hemodynamic status as it reflects the average pressure in a patient's arteries during a single cardiac cycle unlike systolic and diastolic pressures map provides a better overall indicator of profusion to vital organs this is particularly important in patients experiencing shock where maintaining adequate map is crucial for ensuring sufficient blood flow to organs such as the brain kidneys and heart the calculation of map is based on the observation that the heart spends more time in diast or the relaxation phase then in syy the contraction phase therefore the map is not simply the average of systolic and diastolic pressures but is instead weighted towards the diastolic pressure the commonly used formula for estimating map is diastolic pressure plus 1/3 times systolic pressure minus diastolic pressure in this formula the difference between systolic and diastolic blood pressures is known as the pulse pressure by adding 1/3 of the pulse pressure to the diastolic blood pressure the map calc calculation accounts for the longer duration of the diastolic phase clinically a map of at least 65 is often targeted in the management of shock to ensure that there is adequate profusion of vital organs however the target map may vary depending upon the individual patient factors and the underlying cause of shock continuous monitoring of map along with other hemodynamic parameters is integral in guiding therapeutic interventions such as fluid resuscitation vasopressor therapy and inotropic support to maintain adequate organ profusion.",
        "Autonomic Nervous System and Cardiovascular Regulation": "the regulation of the cardiovascular system is governed by the autonomic nervous system which operates largely outside of conscious control the autonomic ner system is primarily managed by the medulla oblongata which is located in the brain stem and acts as the command center for autonomic or automatic function the system is further divided into two main branches the sympathetic and parasympathetic nervous system the sympathetic nervous system is responsible for preparing the body for physical activity particularly in response to stressful situations it triggers the fight ORF flight response increasing heart rate dilating broiles and redirecting blood flow towards muscles thereby preparing the body for Action in contrast the parasympathetic nervous system plays a key role in maintaining homeostasis during restful periods it promotes the rest and digest or feed or breed activities such as reducing heart rate enhancing digestion and facilitating the Regeneration and Recovery together these two systems work in concert to maintain cardiovascular stability and adjusting bodily functions based on the current demands and conditions faced by the individual.",
        "Sympathetic vs. Parasympathetic Effects": "this image illustrates the contrasting effects of the sympathetic and parasympathetic nervous systems on various organs the sympathetic nervous system which you can see depicted on the left prepares the body for stressful situations by dilating pupils constricting arteries relaxing the bronchial muscles increasing heart rate enhancing the force of heart contractions and slowing the GI tract activity in contrast the parasympathetic nervous system which you can see on the right promotes restful activities by constricting pupils decreasing heart rate and contractility and increasing salivation and G trct motility these systems work antagonistically to maintain the physiological balance depending on the body's needs.",
        "Blood Flow Regulation": "the regulation of blood flow is primarily managed by sphincters which control the the passage of blood through the capillary beds and are regulated by the autonomic nervous system blood flow is adjusted based on the needs of the cells with vessels either constricting or dilating to increase or decrease flow as necessary the maintenance of adequate blood flow or profusion is a coordinated effort that involves the heart blood vessels and the blood itself self all working together to ensure that tissues receive the oxygen and nutrients that they require during respiration each breath brings oxygen-rich air into the Alvi the small air sacs and the lungs oxygen then defuses through the Alvar walls into the pulmonary capillaries where it enters the blood stream this oxygenated blood must be effectively circulated throughout the body to prevent cellular death which can occur if tissues do not receive adequate oxygen the process of diffusion which is the passive movement of molecules from an area of higher concentration to one of lower concentration facilitates the transfer of oxygen from the Alvi into the blood additionally carbonic acid in the blood is broken down in the lungs leading to the exhalation of carbon dioxide this process helps maintain the balance between gases in the body and regulates the body's pH ensuring proper physiological breakdown.",
        "Causes and Effects of Shock": "shock can occur due to inadequate cardiac output reduced systemic vascular resistance or the inability of red blood cells to effectively deliver oxygen to tissues if the shock State continues without intervention it will ultimately lead to the death of the organism in an attempt to survive the body tries to compensate by redirecting blood flow from the less vital organs such as the skin and intestines to more critical organs like the heart brain and lungs this shunting mechanism is the body's effort to preserve vital functions in the face of circulatory failure it's a key reason why skin color changes are one of the first signs of hypo profusion in a patient.",
        "Perfusion Triangle": "the cardiovascular system is composed of three essential components the pump which is the heart the set of pipes referring to the blood vessels or arteries that serve as the container for the blood and then the contents of the container itself which is simply the fluid or blood these three elements work together to ensure the continuous circulation of blood throughout the body which in turn supplies oxygen and nutrients to tissues while removing all waste products the profusion triangle illustrates the three key components that are necessary for adequate profusion the heart or pump function the blood vessels or container function and the blood or content function the heart must effectively pump blood to sustain circulation damage to the heart impairs its ability to function as a pump reducing blood flow blood vessels must maintain proper tone if they dilate excessively the available blood volume may not be sufficient to fill the system this leads to an adequate  profusion finally the blood itself must be present in adequate volume significant loss of blood or plasma decreases the available fluid in the system compromising the body's ability to maintain effective profusion all three components must work together to ensure proper blood flow and oxygen delivery to the tissues.",
        "Blood Composition and Clotting": "blood serves as the primary vehicle for transporting oxygen and nutrients throughout the body it consists of red blood cells white blood cells platelets and plasma blood clotting is a vital mechanism to control blood loss with clots forming due to factors such as blood stasis changes in the vessel wall from injury or alterations in the blood's clotting ability due to disease or medication when an injury occurs platelets gather at the site causing red blood cells to become sticky and clumped together fibrinogen which is a protein reinforces this Clump stabilizing the clot however these clots can become unstable and may be prone to rupture which can lead to further complications.",
        "Compensatory Mechanisms in Shock": "when the body detects a drop in systemic pressure neural and hormonal mechanisms are activated to restore equilibrium the sympathetic nervous system increases its control over bodily functions during the shock enhancing heart rate and constricting blood vessels in order to maintain profusion to vital organs conversely the parasympathetic nervous system which again typically regulates involuntary functions such as cardiac and glandular activity during non-stressful situations recedes in influence Additionally the body initiates a fluid shift to help stabilize blood pressure within the circulatory system which further supports the body's efforts to maintain homeostasis during critical periods.",
        "Baroreceptors and Chemoreceptors": "when perfusion decreases the body activates compensatory mechanisms to restore blood pressure in flow Barrow receptors which are sensitive to changes in blood pressure detect the decrease and stimulate the vasomotor center of the medulla oblongata in order to increase blood pressure chemo receptors on the other hand monitor subtle changes in the levels of carbon dioxide in arterial blood adjusting respiratory and cardiovascular responses accordingly these compensatory responses are particularly triggered when systolic pressures Falls between 60 and 80 millimeters of mercury in adults and potentially even lower in children as the body attempts to maintain adequate profusion to vital organs.",
        "Renin-Angiotensin-Aldosterone System": "in response to hypo perfusion the body activates the renin Angiotensin aldosterone system in the kidneys along with the release of antidiuretic hormone from the pituitary gland these mechanisms lead to an increase in blood pressure to help maintain cardiac output the initial compensatory response aims to increase preload stroke volume and pulse rate which typically results in an elevated cardiac output Additionally the autot transfusion effect which involves the movement of fluid from the interstitial space into the vascular compartment along with other subtle physiological responses allows the body to effectively compensate for a blood volume loss of up to 25%.",
        "Failure of Compensatory Mechanisms": "as hypo perfusion continues the body's compens Tor mechanisms begin to fail leading to a worsening of myocardial function characterized by decreased cardiac output and ejection fraction this decline in cardiac function results in reduced tissue profusion additionally fluid May begin to leak from the blood vessels causing systemic and pulmonary edema as the patient further decompensates profusion to critical areas such as the brain and coronary arteries diminishes putting these vital organs at risk.",
        "Cellular Metabolism in Shock": "at the cellular level a shift occurs from aerobic metabolism which relies on adequate oxygen supply to anerobic metabolism where cellular processes continue in the absence of oxygen this shift is less efficient and leads to the production of lactic acid which contributes to Cellular damage in response to the ongoing hypo profusion the adrenal gland secrete epinephrine and norepinephrine which are catacol amines hormones that attempt to sustain blood pressure and cardiac output despite the deteriorating conditions the body strategic redistribution of blood from areas of lesser need to areas of Greater necess necessity is known as the pecking order this process prioritizes vital organs such as the heart and brain over the less critical areas during the so-called golden hour or golden period This Is The crucial time frame for preventing irreversible damage following an injury or shock however if the compensatory mechanisms fail to maintain adequate profusion there will be a decrease inrease in preload and cardiac output which will further compromise the body's ability to sustain vital function.",
        "ATP and Sodium-Potassium Pump": "when the body experiences shock the reduction in blood flow and oxygen delivery to tissues leads to a Cascade of cellular and metabolic disturbances particularly at the capillary and microcirculatory levels one of the most significant effects is the reduction of adenosin triop phosphate or ATP production ATP remember is the primary energy currency of the cell and its availability is critical for maintaining normal cellular functions including the operation of the sodium pottassium pump this pump is essential for cellular membrane protein and helps maintain the electrochemical gradient across the cell membrane by actively transporting sodium ions out of the cell and potassium ions into the cell this gradiate is vital for numerous cellular processes including maintaining the cell's osmotic balance nerve impulse transmission and muscle contraction.",
        "Anaerobic Metabolism and Cellular Damage": "in the context of shock as perfusion decreases cells are deprived of oxygen and nutrients forcing them to rely on anerobic metabolism anerobic metabolism is far less efficient than aerobic metabolism because it produces only a fraction of the ATP that is generated in the presence of oxygen as a result the ATP levels within the cells drop significantly with insufficient ATP the sodium potassium pump becomes dysfunctional and this leads to an accumulation of sodium ions inside the cell and a corresponding loss of potassium ions the accumulation of sodium within the cell causes water to enter the cell leading to Cellular swelling if this process continues unchecked it can result in cellular injury and death moreover the disruption of the sodium potassium pump further exacerbates the metabolic disturbances already present in shock the loss of the electrochemical gradient can impair other ion pumps and channels leading to further disregulation of intracellular processes this can increase the likelihood of arrhythmias in cardiac cells and impair nerve and muscle function throughout the body Additionally the ongoing shift to anerobic metabolism and the resultant production of lactic acid contribute to sustain iic acidosis this acidosis further impairs enzyme activity and cellular metabolism this creates a vicious cycle that accelerates cellular damage and ultimately organ dysfunction.",
        "Systemic Effects of Shock": "as shock progresses several detrimental cellular and systemic effects unfold cellular flooding which is a result of severe osmotic balance leads to the rupture of lysomal membranes this rupture releases lysomal enzymes into the cell which then autodigest cellular components which ultimately contributes to organ failure the reduced blood supply to the vasom motor center of the brain causes a decrease in sympathetic nervous system activity initially slowing it down and eventually leading to its cessation this loss of sympathetic tone further exacerbates circulatory collapse the ongoing accumulation of lactic acid and carbon dioxide within the body acts as a potent vasodilator further impairing vascular tone and worsening the shock State this vasod dilation leads to a vicious cycle of decreasing blood pressure and profusion further aggravating cellular and tissue damage.",
        "Disseminated Intravascular Coagulation": "compounding these issues the shock State also impairs the function of white blood cells and the blood clotting system this impairment can lead to disseminated intravascular coagulation or DSC which is a condition where widespread clotting occurs within the blood vessels this paradoxically leads to both clotting and bleeding complications DC is particular dangerous and has been frequently associated with septic shock which further complicates the management of these critically ill patients the combination of these events cellular autodigestion impaired neural regulation systemic acidosis and coagulopathy leads to a highly detrimental environment that will then lead to multi-organ failure and significant challenges in clinical management.",
        "Multiple Organ Dysfunction Syndrome": "multiple organ dysfunction syndrome or mods represents a severe life-threatening phase in the Continuum of critical illness where the failure of multiple organ systems occurs simultaneously or in Rapid succession this condition is often precipitated by a triggering event such as sepsis severe trauma or extensive Burns all of which overwhelms the body natural homeostatic mechanisms the pathophysiology of mods is complex and involves a Cascade of interconnected biological processes when the body experiences a significant insult such as an overwhelming infection or severe injury it triggers a massive systemic response involving the immune inflammatory and coagulation systems this resp response is designed to localize and eliminate the threat but in the case of mods becomes disregulated and widespread.",
        "Pathophysiology of MODS": "the initial immune response to injury or infection is intended to protect the body by fighting off pathogens or repairing tissue damage however in mods this response becomes excessive and uncontained immune cells such as macras and neutrophils release large amounts of pro-inflammatory cyto kindes into the bloodstream these cyto amplify inflammatory response leading to the widespread inflammation which can then damage tissues and organs that were not initially affected by the primary insult the complement system which is part of the innate immune response is also activated this system comprising a series of of proteins enhances the ability of antibodies and fosic cells to clear microbes and damage cells from an organism promotes inflammation and attacks the pathogen's cell membrane in mods uncontrolled activation of the compliment system contributes to further tissue damage and organ dysfunction.",
        "Coagulation and Inflammation in MODS": "alongside the inflammatory response the coagulation system is also activated leading to the the formation of microthrombi in these small blood vessels throughout the body this widespread clotting which we call disseminated intravascular coagulation paradoxically leads to both clotting and bleeding the clots can obstruct blood flow to organs exacerbating esema and contributing to organ failure meanwhile the consumption of clotting factors in the formation of microthrombi increases the risk of severe bleeding elsewhere in the body the activation of the cicr Kinnon system which regulates blood pressure and inflammation leads to the production of Brinnon which is a potent vasodilator Brady Kinnon increases vascular permeability which leads to fluid leakage from the blood vessels into the surrounding tissues which results in edema this fluid shift further compromises organ function F by reducing blood flow and oxygen delivery to vital organs.",
        "Progression and Impact of MODS": "as these processes continue unchecked they lead to Progressive organ dysfunction the organs most commonly affected in mods include the lungs kidneys and GI tract a failure of one organ system can precipitate the failure of others creating a vicious cycle that's difficult to reverse mods typically develops within hours to days following the initial result the speed at which it progresses depends on several factors including the severity of the injury or infection as well as the patients's underlying health and the effectiveness of the resuscitation and early therapeutic interventions early identification of patients at risk for mods along with prompt and aggressive management is crucial for improving outcomes.",
        "Signs and Symptoms of MODS": "multiple organ dysfunction syndrome presents with several critical signs and symptoms including hypotension which indicates a failure of the cardiovascular system to maintain adequate blood flow leading to insufficient tissue profusion and resulting in cellular dysfunction and death uncontrollable bleeding can occur due to disseminated intravascular coagulation as hypoxia prist exists multi-organ failure ensues affecting vital organs like the lungs kidneys liver and heart tissue acidosis develops as a result of anob metabolism where the lactic acid accumulates lowering the body's pH and further impairing cellular functions additionally severe local alterations of metabolism occur within affected tissues contributing to the progress cellular injury that characterizes mods.",
        "Respiratory Impairment and Shock": "respitory impairment can lead to shock as quickly as vascular cases when there's an insufficient concentration of oxygen in the blood as oxygen is essential for the survival of organs certain types of poisoning such as carb monoxide and cyanide poisoning can disrupt the ability of cells to metabolize or transport oxygen effectively additionally anemia which we would characterize as an abnormally low number of red blood cells can result from chronic or acute bleeding when it's severe it can cause tissue hypoxia further compromising organ function and contributing to the development of shock.",
        "Causes of Shock": "shock can be caused by various factors including significant bleeding which reduces the volume of circulating blood and leads to an adequate tissue profusion respiratory failure can also precipitate Shock by impairing the body's ability to oxygenate blood effectively acute allergic reactions such as anaphylaxis can cause widespread vasod dilation and capillary permeability resulting in shock additionally overwhelming infections particularly sepsis can trigger a systemic inflammatory response that leads to profound circulatory and metabolic disturbances ultimately causing shock.",
        "Risk Factors for Shock": "shock should be anticipated in patients presenting with multiple severe fractures as these injuries can lead to significant blood loss and compensated circulation abdominal or chest injuries may cause internal bleeding or damage to vital organs further increasing the risk of shock spinal injuries can disrupt the autonomic nervous system leading to neurogenic shock severe infections particularly sepsis can trigger systemic inflammation and septic shock a major heart attack can severely impair cardiac output leading to cardiogenic shock and lastly anaphylaxis can cause rapid vasod dilation and fluid shifts.",
        "Types of Shock": "shock can arise from a variety of causes with hypovolemia due to blood or fluid loss being a common cause hypmic shock specifically refers to shock resulting from inadequate blood volume which can occur due to hemorragic causes such as external or internal bleeding or non-hemorrhagic causes such as dehydration or Burns non-hemorrhagic hypothalmic shock occurs when fluid loss is contained within the body such as in cases of severe dehydration where fluids are lost through the GI tract or skin rather than through bleeding understanding the distinctions between hypothalmic shock and other types of shock is crucial for appropriate diagnosis treatment.",
        "Dehydration and Fluid Loss": "dehydration characterized by abnormal losses of fluids and electrolytes can occur through various mechanisms GI losses such as those resulting from vomiting and diarrhea are common fluid loss can also be exacerbated by fever hyperventilation or exposure to high environmental temperatures which increase fluid loss to the lungs excessive sweating is another significant contributor to dehydration internal losses or third space losses occur when fluid shifts into nonfunctional spaces within the body such as in cases of peritonitis pancreatitis or ilas additionally plasma can be lost through Burns surgical drains and granulating wounds other condition that can lead to dehydration include aites diabetes and citus and osmotic diuresis particularly if the patient is in a hyperosmolar state these various forms of fluid loss can severely compromise the body's ability to maintain adequate hydration and electrolyte balance this leads to some potentially life-threatening conditions.",
        "Early Signs of Shock": "the earliest signs of shock often include restlessness and anxiety with patients potentially reporting thirst if they are alert nausea and vomiting may occur and the skin can become pale cold and clammy it can even sometimes show modeling Additionally the heart rate increases as the body attempts to compensate for the decreasing blood volume symptoms of dehydration can include include a loss of appetite nausea vomiting and occasionally fainting when standing up known as postural Syncopy as bleeding or fluid loss progresses a drop in blood pressure is a late sign of shock it's important not to wait for this drop in blood pressure before suspecting and treating shock as early intervention is the key to saving vital organs particularly the brain lungs and kidneys the the best indicator of adequate brain profusion is the patient's level of Consciousness making it an essential parameter to monitor during treatment.",
        "Cardiogenic Shock": "cardiogenic shock occurs when the heart's ability to function as a pump is inadequate leading to insufficient blood circulation to meet the body's needs this condition is often associated with the presence of Edema which is the abnormal AC accumulation of fluid between the cells and body tissues pulmonary edema in particular impairs ventilation and further complicates the condition for blood to circulate effectively there must be adequate pressure and an appropriate heart rate cardiogenic shock develops when the heart fails to maintain sufficient cardiac output due to factors such as increased afterload low preload or poor contractility of the heart these factors either alone or in combination result in a decreased ability of the heart to pump blood which leads to the progression of cardiogenic shock.",
        "Obstructive Shock": "obstructive shock occurs when mechanical obstructions impede the heart's ability to function as an effective pump this type of shock can result from conditions such as cardiac tanod where blood accumulates in the pericardium creating pressure that restricts the heart's movement another cause is tension Numa thorax which arises from damage to lung tissue in tension Numa thorax air escapes into the plural space causing increased heart and respiratory rates shallower breathing and a decrease in blood pressure tracheal deviation which is a shift of the trachea to one side is a late sign of this condition pulmonary embolism which is a blockage in the pulmonary circulation caused by a blood clot can also lead to obstructive Shock by preventing blood from being pumped from the right side of the heart to the left which severely compromises circulation these conditions require prompt recognition and intervention to prevent the progression to life-threatening shock.",
        "Distributive Shock": "distributive shock occurs when there's a widespread dilation of small arterioles small venules or both leading to a relative deficiency in blood volume and impaired profusion despite adequate fluid levels a common subtype of distributive shock is septic shock which results from severe infections typically bacterial in septic shock bacterial toxins damage the vessel walls increasing cellular permeability and causing fluid leakage into the surrounding tissues this condition presents in a similar fashion to hemorrhagic shock with signs such as a weak threat puls shallow and Rapid respirations altered mentation and skin that is warm or hot to the touch these symptoms reflect the body's systemic response to infection and the subsequent failure to maintain adequate circulation and oxygen delivery to the tissues.",
        "Neurogenic Shock": "neurogenic shock occurs when there is damage to the nervous system particularly the pathway that control the size and muscular tone of blood vessels this damage disrupts the connection between the sympathetic nervous system and the muscles in the walls of blood vessels preventing the vessels from Contracting as a normally would as a result all blood vessels below the level of the spinal injury dilate widely significantly increasing the size and capacity of the vascular system this leads to relative hypovolemia characteristic signs of neurogenic shock include the absence of sweating below the level of injury normal warm skin in contrast to the cool clammy skin as seen in other types of shock and a lack of an elevated pulse as the usual compensatory mechanisms are impaired this type of shock requires specific management to address the underlying nervous system injury and support circulation.",
        "Anaphylactic Shock": "anaphylactic shock is a severe and life-threatening allergic reaction that occurs when an individual is exposed to a substance to which they have been sensitized unlike other forms of shock this does not involve blood loss or mechanical vascular damage and there's actually minimal risk of direct cardiac muscle injury this reaction leads to widespread vascular dilation though and increase capillary permeability as well as Bronco constriction all of which will contribute to the rapid onset of shock symptoms common triggers include injections stings the ingestion of allergens or the inhalation of allergens anaphylactic shock can develop within minutes or even seconds after exposure to the allergen cyanosis or a bluish discoloration of the skin is a late sign of this condition and indicates severe hypoxia.",
        "Psychogenic Shock": "sometimes mistakenly called psychological shock psychogenic shock occurs when a sudden reaction of the nervous system leads to Temporary generalized vascular dilation which results in fainting or Syncopy this type of shock is typically not life-threatening but it can be triggered by serious underlying conditions such as arhythmia or brain aneurysm with psychogenic shock it's important to remember that these patients typically are not faking it and they definitely require immediate medical attention and transport.",
        "Stages of Shock": "shock progresses through two primary stages compensated and decompensated in the compensated stage the body still manages to maintain adequate profusion despite the underlying issues such as blood loss this early stage is characterized by the body's compensatory mechanisms including the release of chemical mediators by the autonomic nervous system which increases the rate in depth of respirations during this stage blood pressure remains relatively stable although there is often a narrowing of pulse pressures remember a pulse pressure is the difference between the systolic and diastolic pressures the level of responsiveness in a patient is a much more reliable indicator of tissue profusion at this stage than all other Vital Signs particularly blood pressure patients may show positive orthostatic vital signs indicating that they can still compensate when changing positions if treatment is initiated during the compensated stage recovery is very likely however as shock progresses to the decompensated stage the body's compensatory mechanisms begin to fail leading to a drop in blood pressure if left untreated shock can progress or will progress to irreversible stages where the damage is so extensive that recovery is no longer possible this terminal stage marks the point where shock has caused widespread cellular and tissue death leading to the failure of multiple organ systems unfortunately it can be very difficult to tell where decompensated shock ends and irreversible shock begins this is why it's so important to aggressively treat compensated shock as early as possible.",
        "Decompensated and Irreversible Shock": "in the decompensated stage of shock the bodies compens to mechanisms start to fail leading to a significant drop in blood pressure and a decrease in blood volume by more than 30% as a result cardiac output Falls dramatically and the signs and symptoms of shock become more apparent if Vaso constriction a compensatory mechanism continues unchecked it can lead to disastrous outcomes by further compromising blood flow to vital organs although treatment at the stage may still be in recovery the chances diminish as the shock progresses as stated earlier irreversible shock represents the final stage where the condition becomes terminal here arterial blood pressure is abnormally low and there is a rapid and irreversible deterioration of the cardiovascular system this leads to life-threatening reductions in cardiac output blood pressure and tissue perfusion the distinction between decompensated shock and irreversible shock is primarily based on whether the shock State can be reversed with treatment however it's often challenging to even differentiate between irreversible shock and severe decompensated shock in a prehospital environment making early and aggressive intervention important even crucial to improving patient outcomes.",
        "Emergency Medical Care for Shock": "emergency medical care for shock begins immediately during the assessment process the first priority is to control any obvious external bleeding the patient should then be positioned according to local protocols specific to shock treatment it's crucial to provide warmth for the patient by placing blankets both under and over them but care must be taken not to overheat the body external heat sources such as hot water bottles or heating pads should be avoided to prevent further comp complications IV access should be gained and fluids should be administered as needed after stabilizing the patient transport should be initiated promptly with additional treatments provided in route the first 60 minutes after injury known as the golden hour is critical for patient survival emphasizing the importance of Swift and effective care to alleviate the intense thirst that often accompanies shock offering the patient a moistened piece of gauze to chew or suck can provide some comfort without exacerbating their condition be advised if the patient has any form of altered mental status this should be avoided.",
        "Initial Management of Shock": "initial management of shock involves several critical steps to stabilize the patient first the airway must be managed to ensure it's open and unobstructed followed by the administration of supplemental oxygen to enhance tissue oxygenation the patient should be placed in a position of comfort which is often dictated by their condition and local protocols Vital Signs should be obtained to assess the patient status and guide further treatment it is also essential to establish IV or intra OAS access to administer medications or a fluid bolus if necessary finally maintaining the patient's body heat is critical to prevent hypothermia which can exacerbate shock and lead to further complications.",
        "IV Therapy in Shock Management": "IV therapy is a critical component of managing patients in shock particularly those in hypmic shock IV lines should be inserted to provide a route for immediate fluid replacement it should also be used as a potential route for blood replacement if the patient is at risk of substantial losses as well as for the administration of medications all patients in hypoy liic shock require IV fluid replacement and in cases where there is a need for emergency medication administration the line should be maintained at a kvo rate most treatment protocols recommend administering fluids in boluses of 20 MLS per kg with increments up to 30 MLS per kg typically in 250 ml doses or until radial pulses return which would indicate improved circulation once the patient's Vital Signs return to Norm normal or at least the desired status is achieved IV fluid administration should be reduced to a kvo rate with frequent reassessment if the patient does not respond adequately to fluids early intervention by paramedics to administer vase oppressors such as norepinephrine may be necessary to support blood pressure and cardiac output.",
        "Fluid Resuscitation Considerations": "when admin ing fluid resuscitation special considerations must be taken into account to avoid causing harm in cases where increasing blood pressure could be detrimental such as in cardiogenic shock or when there's a risk of exacerbating internal bleeding fluids should be administered conservatively just enough to maintain radial pulses in children and infants temperature control is crucial for maintaining effective profusion and using tools like brzo tape can help ensure correct dosing and monitoring of vital signs a standard approach involves infusing a 20 ml per kg bolus of warm isotonic crystalloid solution with the possibility of a second infusion if the patient does not respond appropriately to the first in patients with uncontrolled Hemorrhage fluid administration should be carefully mon monitored and a conservative approach is recommended to avoid worsening the bleeding for patients with chronic hypertension a higher blood pressure may be required to achieve adequate end organ profusion so treatment goals may need adjustment in pregnant patients the only way to maintain fetal profusion is to treat the mother aggressively as maternal shock directly affects the fetus PR patients should be placed in a left lateral recumbent position to optimize blood flow and prevent compression of the inferior vena which can further compromise circulation these considerations help tailor fluid resuscitation to the specific needs of different patient groups.",
        "Hypovolemic Shock Treatment": "when treating hypovolemic shock immediate steps should be taken to stabilize the patient first control any obvious external bleeding to prevent further blood loss while in route to the emergency department establish at least one 18 gauge peripheral IV line using an over the needle catheter to facilitate fluid resuscitation and medication administration it's important to recognize the signs of internal bleeding and provide aggressive General support including securing and maintaining an open Airway and providing respiratory assistance as needed it should go without saying but patience in shock should not be given anything by mouth in order to prevent aspiration and complications during potential surgery as a matter of fact it's often not out of the question to give the patient anti medic such as Zofran continuous monitoring of the patient's mental status pulse rate blood pressure spo2 and if indicated entitled carbon dioxide levels is critical in order to assess their response to treatment we should also ensure rapid transport to the closest most appropriate medical facility where further definitive care can be provided.",
        "Cardiogenic Shock Treatment": "when treating cardiogenic shock it's important to follow specific steps to stabilize the patient and prevent further deterioration first before administering nitroglycerin ensure that the patient's systolic blood pressure is greater than 90 and consult with medical control for guidance assess the patient's blood pressure and establish IV access before proceeding with nitroglycerin Administration the patient should be placed in a position of comfort and high flow oxygen should be administered to improve oxygenation prompt transport to the Ed is critical during transport IV access should be maintained and fluids should be administered as discussed earlier it's important to make sure that we're not overloading the heart with fluids for un responsive patients it's vital to frequently check for a pulse to determine if an automated external defibrillator is needed as cardiak arest can occur suddenly in cases of cardiogenic shock.",
        "Obstructive Shock Treatment": "when treating obstructive shock caused by cardiac tampon or attention to a thorax the priority is to stabilize the patient and ensure rapid transport for definitive care for cardiac tamponade increasing cardiac output is essential and is achieved by administering High flow oxygen and carefully considering the use of positive pressure ventilations this must be carefully considered because it may reduce Venus return definitive treatment such as a paric cardio centesis is now only available in a hospital setting so prehospital care focuses on early recognition and transport in the case of attenion Numa thorax early application of high flow oxygen via nonar breather is critical followed by needle chest decompression to relieve pressure IV access should be established to administer fluids quick identification and transport are also critical in both scenarios so that we can ensure the patient receives a necessary Advanced Care.",
        "Pulmonary Embolism Treatment": "when treating a pulmonary embolis is essential to assess blood pressure and administer a 250 ml bolus of a crystalloid solution followed by reassessment of blood pressure the patient may find it more comfortable to breathe in an upright or at least partially upright position since definitive treatment which includes anti-coagulation ventilatory and circulatory support and sometimes thrombolytic therapy or clot retrieval is not possible in AE hospital setting so rapid transport to an appropriate facility is crucial.",
        "Septic Shock Treatment": "for septic shock complex Hospital management is required including antibiotics prehospital care should involve using standard precautions transporting the patient as quickly as possible administering highflow oxygen during transport and establishing IV access that additionally in some areas aemts are allowed to draw labs for the hospital as well as administer prehosp antibiotics make sure you check with your local protocols.",
        "Neurogenic Shock Treatment": "neurogenic shock is best managed with a combination of all available supportive measures emergency treatment should focus on obtaining and maintaining a proper Airway ensuring spinal motion restriction and assisting with breathing if it becomes inadequate it's also important to conserve body heat and support circulation as effectively as possible prompt transport to a medical facility is essential to ensure the patient receives further definitive care this comprehensive approach is necessary to stabilize the patient and prevent further complications.",
        "Anaphylactic Shock Treatment": "when treating anaphylactic shock the first step is to administer epinephrine via subcutaneous or intramuscular injection patients who are aware of their specific sensitivities may carry a beIN kit containing epinephrine for this purpose if the patient's condition deteriorates or symptoms reoccur a repeat injection may be necessary after Consulting with medical control the patient should be promtly transported to the emergency department while providing all possible support in route it's important to identify the agent that triggered the reaction and how it was introduced to the patient always remember that even a mild reaction can escalate so ongoing assessment is essential.",
        "Psychogenic Shock Treatment": "when treating psychogenic shock it's important to recognize that it can significantly exacerbate other types of shock Begin by recording your initial observations of the patient's Vital Signs and level of Consciousness gathering information from bystanders is also critical ask them if the patient reported any issues before figing and how long the patient was unresponsive this information can help guide further assessment and management ensuring that the underlying cause of shock is appropriately addressed.",
        "General Shock Management": "in managing the various types of shock the approach must be tailored to the spefic specific underlying calls while ensuring rapid stabilization and transport for conditions like hypothalmic and cardiogenic shock key steps include controlling external bleeding administering fluids through IV access and providing oxygen in cardiogenic shock particular caution is needed with fluid administration and nitroglycerin should only be given if the systolic pressure is is above 90 obstructive shock such as that caused by cardiac tanod or tension num thorax requires immediate interventions Like Oxygen Administration and in the case of pneumothorax needle decompression for conditions like anaphylactic shock administering epinephrine is the first line of treatment and repeated doses may be necessary under medical guidance rapid identification and transport to a facility where definitive care such as surgery or Advanced medications can be provided is critical in septic shock supportive care including fluids and oxygen is necessary in route to the hospital where antibiotics and other complex treatments will be administered psychogenic shock while less physically damaging in itself can complicate other shock types and must be managed carefully recording initial observations and gathering information from witnesses can provide valuable context for treatment across all types of shock maintaining your Airway breathing and circulation as well as body heat are fundamental along with ensuring rapid transport to an appropriate facility for further treatment"
    },
    {
        "Introduction to Shock, Sepsis, and MODS": "introduction shock sepsis and multiple organ dysfunction syndrome or mods are complex medical conditions marked by disruptions in the equilibrium of oxygen supply and demand within the body shock often initiated by localized tissue damage can evolve into organ failure and fatality due to inadequate tissue profusion sepsis triggers a systemic inflammatory response potentially leading to distributive shock where improper blood flow distribution hinders oxygen delivery mods often stemming from conditions like sepsis or severe shock involves the simultaneous failure of multiple organ systems exacerbating oxygen supply demand imbalances understanding microcirculation in cellular phys ology is essential for critical care transport professionals knowledge of microcirculation helps identify early tissue hypoxia signs and facilitates interventions to enhance tissue profusion while comprehending cellular physiology sheds light on cellular oxygen and nutrient utilization impacting the progression of these lifethreatening",
        "Cellular Respiration": "conditions cellular respiration all cells in the human body require a continuous and essential supply of oxygen glucose and various other nutrients to maintain their normal metabolic function and uphold homeostasis energy is a fundamental requirement to power these cellular metabolic processes one of the key players in generating cellular energy is the mitochondria often referred to as the PowerHouse of the cell within these mitochondria nutrients are processed and converted into energy in the form of a Denine triop phosphate or ATP which serves as the primary energy carrying molecule in the body this energy production occurs through a highly intricate process known as cellular respiration cular respiration comprises three main stages glycolysis the kreb cycle which is also known as the citric acid cycle and the electron transport chain glycolysis initiates the breakdown of glucose generating pyruvate and a small amount of ATP in the absence of oxygen however the kreb cycle and the electron transport chain which are the subsequent stages in cellular respiration are reliant on the presence of oxygen these stages function optimally only in an oxygen enrich environment allowing for the efficient breakdown of glucose and the production of a significantly greater amount of ATP in essence oxygen acts as the essential final electron acceptor in the electron transport chain enabling the transfer of electrons and the synthesis of ATP this process underscores the role of Oxygen in cellular energy production demonstrating the interconnectedness between cellular metabolism and oxygen availability glycolysis can occur in both aerobic and anerobic environments this adaptability is critical for cells as it allows them to generate energy from gluc glucose under varying oxygen conditions in Aerobic environments where oxygen is present lsis is just the initial step in a more comprehensive energy production process it yields a moderate amount of ATP which serves as a primary energy currency in cells however when cells find themselves in an anerobic environment meaning it lacks sufficient oxygen gly G olysis becomes a more prominent source of energy production in this situation glycolysis is a Lifeline for cells to continue generating ATP albeit at a reduced rate compared to aerobic conditions the downside of anobi glycolysis is that it leads to the accumulation of lactic acid as a byproduct this buildup can have a detrimental effect on cellular pH levels potentially causing acidosis and impairing normal cellular function the conversion from ATP to adenosine Diop phosphate or ADP and vice versa is a critical process in cellular bioenergetics ATP stores energy in its phosphate bonds and when cells require energy for various biological functions such as muscle contraction active transport or biochemical reactions ATP releases energy by converting into a DP this release of Energy Fuels the cellular processes necessary for Life conversely when cells have excess energy and need to store it a DP can be converted back into a TP through the process such as oxidative phosphorilation in in the presence of oxygen this Dynamic inter conversion of ATP and ADP is fundamental for the continuous supply of energy that is required to drive various biologic functions in the cell ensuring its viability and proper functioning aerobic metabolism is a highly efficient process occurring within the mitochondria of the cells where various fuel sources such as glucose amino acids and fatty acids combined with oxygen and ADP to produce several products first and foremost arobic metabolism yields adenosine triop phosphate or ATP the primary energy currency of the cell as stated before ATP provides the energy needed for various cellular functions including muscle contraction active transport and biochemical reactions additionally aerobic metabolism generates carbon dioxide or CO2 as a waste product which is subsequently eliminated from the body through the respiratory tract furthermore water and heat are produced as byproducts of this process the heat generated plays a role in maintaining body temperature and ensuring that enatic reaction proceed optimally in contrast anerobic metabolism serves as an alternative pathway for energy production when oxygen availability is limited this process involves the conversion of glucose to pyruvic acid and results in the production of ATP however it's important to note that anerobic metabolism is less efficient efficient than its aerobic counterpart in terms of ATP production consequently fewer ATP molecules are generated during anerobic metabolism compared to aerobic metabolism this can lead to a decreased capacity for sustained energy production and may result in fatigue during intense physical activities moreover anerobic metabolism does not involve the complete breakdown of glucose and lactic acid can accumulate as a byproduct this buildup of lactic acid can lower cellular pH leading to acidosis and",
        "The Microcirculation and the Cell: Oxygen Transport and Utilization": "discomfort the microcirculation and the cell oxygen transport and utilization comprehending the intricacies of the balance between oxygen supply and demand is of Paramount importance in understanding the pathophysiology of shock sepsis and mods that's because this knowledge can be likened to understanding the mechanisms of injury and Trauma as it allows providers to grasp the underlying processes driving these life-threatening conditions one key aspect of this understanding is the appreciation of microcirculation which acts as the critical Nexus between arterioles and venules comprising the capillaries that intricately course between the cells within various organs these microscopic vessels serve as the conduit for oxygen and nutrient delivery to individual cells ensuring that the body's metabolic demands are met remarkably the size of these microcirculatory conduits is just large large enough to permit the passage of a single red blood cell highlighting the Precision and delicacy of this system in the context of shock sepsis and mods the crash site where the devastating consequences begin is often concealed deep within the cellular level while the macroscopic signs of these conditions May manifest as systemic symptoms the true origins of their pathophysiology lie within the malfunctioning microcirculation and cellular processes it is at this level that the balance between oxygen supply and demand is disrupted setting off a Cascade of events that can lead to organ dysfunction and eventual failure oxygen transport and utilization are essential components of maintaining physiological homeostasis within the human body to achieve this a sufficient supply of oxygen must be available to meet the cellular demands of each body system this process involves several critical aspects of the body's physiology working together seamlessly first for homeostasis to be maintained each of the body's systems must be intact and functioning normally this includes not only the respiratory system but also the cardiovascular system which plays a vital role in transporting oxygen-rich blood to tissues the respiratory system enables the exchange of oxygen and carbon dioxide across the Alvar capillary membrane within the lungs this exchange ensures that oxygen is adequately loaded onto red blood cells while carbon dioxide a waste product of cellular metabolism is expelled from the body during exhalation once oxygen is bound to hemoglobin with the red blood cells arterial blood transports it to the various tissues and organs throughout the body hemoglobin is a critical molecule in this process with each gram of hemoglobin capable of carrying approximately 139 milliliters of oxygen therefore the oxygen carrying capacity of blood is directly related to the level of hemoglobin present in cases where the hemoglobin level is low such as present anemia or acute blood loss it is imperative to administer blood transfusions to optimize the blood's oxygen carrying capacity to assess the oxygen content in arterial blood providers should use the arterial oxygen content or cao2 formula this formula takes into account both the oxygen bound to hemoglobin and the dissolved oxygen in plasma by calculating coo2 clinicians can gauge the oxygen carrying capacity of the blood as well as the adequacy of oxygen delivery to the body's tissues the primary determinants of this oxygen transport are blood pressure and cardiac output systolic blood pressure which represents the pressure in the arteries during the heart's contraction is primarily dependent on cardiac output cardiac output in turn relies on heart rate and stroke volume which includes the amount of blood ejected from the heart with each beat diastolic blood pressure representing arterial pressure during the heart's relaxation phase is determined largely by peripheral resistance this resistance results from arteriolar Vaso constriction and influences the force with which blood is pushed through the circulatory system calculating the mean arterial pressure is essential as it reflects blood pressures pulsatile nature and helps evaluate overall profusion the oxygen-rich hemoglobin carried by red blood cells reaches the capillaries where it undergos an exchange oxygen is released from hemoglobin to the surrounding cells in exchange for cellular waste products like carbon dioxide the amount of oxygen used by these cells and tissues is denoted as oxygen consumption or V O2 under specific circumstances oxygen may be more readily extracted from hemoglobin or tightly bound to it depending on hemoglobin's affinity for oxygen this Affinity is influenced by factors such as the partial pressure of oxygen blood pH levels of carbon dioxide in the blood ambient temperature and the effects of bif phosphoglycerate molecule that regulates oxygen binding and release from hemoglobin ultimately the responsibility of utilizing the oxygen delivered by the cardiovascular system falls to the cells the oxygen extraction ratio which represents the amount of oxygen extracted from the blood by the tissues typically ranges from around 25% even in normal conditions only a quarter of the delivered oxygen is extracted this can be assessed by measuring mixed Venus oxygen saturation or sv2 when sampled in the pulmonary artery which is typically around 75% in normal circumstances monitoring these parameters and understanding the intricate interplay between oxygen transport delivery and utilization is essential for assessing tissue profusion and overall health particularly in critically ill",
        "Shock": "patients shock shock is a comprehensive physiological response that the body initiates when there is an inadequate supply of oxygen to cells tissues and organs often resulting from one or multiple underlying causes this response begins at the cellular level and progresses through distinct stages classically categorized into three phases compensatory decompensated and refractory at the onset of shock blood flow into the microcirculatory beds starts to diminish to a point where oxygen delivery to the cells Falls below the threshold required for maintaining normal aerobic cellular function in response to this oxygen deficit tissu attempt to compensate by increasing oxygen consumption however this heightened oxygen consumption leads to the development of hypoxia where the supply of oxygen no longer meets the cellular demand as a result lactate and carbon dioxide levels rise within the body the inability of cells to maintain their homeostasis during the stage impairs microcirculatory flow to vital organs such as the heart brain and adrenal glands while signs and symptoms of hypo profusion may be subtle in the compensatory stage they often include an increase in heart rate and respiratory rate Additionally the mean arterial pressure may drop somewhat but compensatory mechanisms work diligently to return these values to Baseline an essential early marker of shock during the stage is the elevation of serum lactate levels signaling cellular distress the body deploys various physiologic mechanisms to maintain cellular homeostasis during shock which can be categorized into neural hormonal and chemical responses as oxygen delivery to tissues become severely reduced the patient may become tohnic in an attempt to take in more oxygen while exhaling excess carbon dioxide simultaneously the heart and circulatory system work together to preserve cardiac output ensuring that vital organs continue to receive blood flow the renin Angiotensin aldosterone system is activated in response to low arterial pressures helping to conserve fluid and maintain blood pressure low arterial pressures also trigger the posterior pituitary gland to release anti-diuretic hormone to conserve water and maintain blood volume despite the body's remarkable ability to compensate for shock these compens short mechanisms can often Mass the severity of what is occurring at the cellular level for example a patient in shock May exhibit low circulatory volume poor stroke volume or inadequate cardiac output but these deficits may not be readily apparent in the early stages of shock understanding the progression of shock through its stages assist providers in the initiation of timely interventions and prevent the condition from advancing to more severe and potentially irreversible phases the decompensated stage of sh is a critical phase in the progression of this life-threatening condition if the underlying cause of shock remains untreated it will inevitably advance to an uncompensated state where the body's compensatory mechanisms can no longer provide the much needed oxygen to cells during this stage patients exhibit more pronounced signs of shock and the clinical picture becomes increasingly severe several factors contribute to to the clinical deterioration seen in the decompensated stage of shock hypotension or low blood pressure becomes more prominent leading to inadequate profusion of vital organs elevated hydrostatic pressure can result in the accumulation of fluid and tissues causing edema in third spacing this further impairs tissue profusion and can lead to organ dysfunction micro imoli May develop inhibiting cellular respiration and causing cellular damage in tissues and organs this can exacerbate tissue hypoxia in some critically ill patients particularly those with sepsis diic may occur this is a complex condition characterized by both excessive bleeding and clotting it can further disrupt tissue profusion in oxygen delivery as oxygen supply continues to decrease Anor robic metabolism becomes more pronounced this metabolic pathway produces lactic acid leading to an acidic environment within the body cells begin to die due to prolonged oxygen deprivation and release toxins into the microcirculation further contributing to systemic dysfunction these factors collectively result in persistent hypotension as blood vessels lose their ability to constrict effectively smooth muscle tone decreases and tissue permeability increases patients in the decompensated stage typically present with severe clinical manifestations including hypotension teoc cardia tpia oliguria and frequently altered mentation this stage of shock is a lifeat threatening emergency which requires immediate intervention to address the underlying cause and restore tissue profusion in contrast the refractory stage represents the most advanced and critical phase of shock here compensatory mechanisms have failed entirely and permanent organ dysfunction has occurred patients in the refractory stage are often minimally responsive or unresponsive severely hypotensive exhibit cold cytic and modeled skin and may have weak or absent peripheral pulses survival rates in the refractory stage are generally poor with a mortality rate of approximately 60% because of this timely recognition and intervention is essential in order to prevent the progression of shock to this dire stage and improve patient outcomes mods is a severe and life-threatening condition diagnosed when two or more organs in the body stop functioning adequately it is a complex and challenging medical issue with distinct types and high mortality rates mods can manifest in two primary types primary mods results from a direct insult to the organs often due to severe trauma or injury it can develop rapidly and is characterized by the simultaneous dysfunction of multiple organs secondary mods is typically a slower and more Progressive condition it occurs as a consequence of a systemic insult most commonly seen in cases of severe sepsis the Cascade of events in sepsis involving widespread inflammation and an uncontrolled immune response can eventually lead to the progressive dysfunction of multiple organs the mortality rates associated with mods are alarmingly high ranging from 44 to 76% depending on the source the prognosis is closely related to the number of organ failures with mortality rates increasing as more organs become compromised for instance between 10 and % of patients with failure of two to four organs may not survive and up to 50% of patients with five organ failures face a grim prognosis in cases where seven organs are failing survival is extremely rare with a mortality rate of almost 98% mods can affect virtually all organs in the body decreased map can lead to reduced renal profusion and function resulting in oliguria many patients with mods require temporary continuous bedside dialysis to support renal function liver damage can impair detoxification capacity decrease clotting ability and reduce the production of essential oncotic proteins which affects overall homeostasis a emia in the brain may lead to anoxic brain injury causing neurological deficits cardiac effects include hypotension and arrhythmias further complicating the condition Additionally the pancreas can release a myocardial depressant Factor potentially exacerbating cardiac dysfunction in",
        "Classification of Shock": "mods classification of shock cardiogenic shock is a critical medical condition characterized by the failure of the heart to pump effectively resulting in inadequate oxygen delivery to the body's organs and tissues it is diagnosed based on specific criteria including a sustained systolic blood pressure of 80 to 90 millim of mercury for more than 30 minutes a cardiac index of less than 2.2 and a pulmonary capillary wedge pressure greater than 15 mm of mercury often accompanied by evidence of end organ damage such as altered mental status reduced urine output cool extremities and modeled skin the diagnosis of cardiogenic shock typically relies on a combination of clinical presentation laboratory studies Echo card cardiography and an ECG there are both intrinsic and extrinsic causes of cardiogenic shock intrinsic causes may include left ventricular failure resulting from a large myocardial infarction right ventricular failure valvular disorders cardiomyopathies sepal defects papillary muscle rupture and sustained arrhythmias extrinsic causes May Encompass conditions like pericardial tampeno effusion pulmonary emili and tension pneumothorax certain populations are at a higher risk of developing cardiogenic shock including elderly patients patients with a history of diabetes metis and individuals who have experienced a myocardial infarction with an ejection fraction of less than 35% mortality rates for cardiogenic shock have historically been very high often exceeding 80% that being said newer treatment modalities have significantly improved risk stratification leading to A reduced mortality rate of approximately 50% five major determinants of myio cardio oxygen consumption are critical in managing cardiogenic shock these are contractility preload wall tension afterload and heart rate manifestations of cardiogenic shock can vary depending on the underlying cause but often include poor cardiac output low blood pressure altered mental status cool and pale skin decreased urine output and a weak and threy pulse treatment for cardiogenic shock involves a multifaceted approach which includes providing high flow oxygen supporting therapy to alleviate chest pain and reduce anxiety administering anti- rhythmics if necessary judicious fluid therapy anatrophic within physician ordered parameters agents to decrease afterload such as vasodilators and diuretics may also be employed additionally providers must address the underlying causes of cardiogenic shock when known for example pericardiocentesis may be performed for cardiac tamponade if protocols allow and needle decompression may be considered in specific cases when pharmacologic intervention prove inadequate in supporting the failing heart temporary and durable mechanical circulatory support devices can be considered these devices include the iabp impella the tandem heart ECMO or lvads these Advanced interventions aimed to provide additional circulatory support and improve cardiac output in patients with severe cardiogenic shock potentially serving as a bridge to further treatment or recovery hypovolemic shock is a condition that arises due to an insufficient circulating blood volume within the vascular system resulting in hypotension this condition can occur when there is a loss of blood or fluids either internally or externally various medical conditions and situations can lead to hypothalmic shock including fever severe vomiting and diarrhea Hemorrhage Burns and excessive third spacing which is fluid accumulation in body cavities or interstitial spaces the signs and symptoms of hypmic shock are indicative of poor tissue profusion and can include teoc cardia hypotension poer delayed capillary refill confusion anxiety cold and modeled extremities and pulselessness in severe cases the patient's mental status May deteriorate as the condition progresses one of the laboratory indicators of hypovolemic shock is a decrease in the hermit value especially in cases involving hemorrhage when hypovolemic shock is caused by hemorrhagic trauma it can be classified into four classes according to the American College of Surgeons committee on trauma guidelines each class has its specific characteristics and treatments helping guide healthc care providers in managing the condition effectively class one is a volume loss up to 15% of total blood volume or approximately 750 ml Class 2 is a volume loss between 15 to 30% of total blood volume or 750 to 1500 MLS class three is a volume loss of 30 to 40% of total blood volume or500 MLS to 2,000 MLS and lastly class 4 is a volume loss of over 40% of total blood volume in terms of treatment and transport management of hypovolemic shock the primary goal is to treat the underlying cause of hypovolemia such as controlling bleeding or addressing the condition responsible for fluid loss patients in hypovolemic shock often require supplemental oxygen to support tissue oxygenation intravenous volume replacement is a critical intervention as well normal saline or lactated ringer solution is preferred administered in 250 to 500 mm increments this helps restore intravascular volume and improve blood pressure in cases where Hemorrhage is suspected or confirmed early administration of blood products such as packed red blood cells and fresh frozen plasma may be necessary to replace lost blood components and improve oxygen carrying capacity distributive shock encompasses several subtypes and one of them is neurogenic shock neurogenic shock occurs due to the loss of sympathetic tone leading to vasod dilation and reduced systemic vascular resistance it can be caused by various factors including trauma to the brain or spinal cord above the thoro lumbar t level and the administration of certain pharmacologic agents the signs and symptoms of neurogenic shock are characterized by relative hypovolemia due to widespread Vaso dilation this dilation results in a significant drop in systemate vascular resistance and blood pressure interestingly neurogenic shock often presents with braic cardia in the face of hypotension which is an unusual feature compar compared to other forms of shock in terms of treatment and transport management of neurogenic shock immediate intervention is key to address hypotension and stabilize the patient's blood pressure providers should work to maintain a map of 855 to 90 millimet of mercury for the first s days following the injury that caused neurogenic shock this helps ensure adequate profusion to vital organs intravenous fluid therapy with isotonic crystalloids is often initiated to restore intravascular volume in blood pressure the goal is to provide adequate fluid resuscitation while closely monitoring the patient's response in some cases Vaso pressor medications may be necessary to augment blood pressure and counteract the vasodilatory effect seen in neurogenic shock given the presence of bradicardia maintaining an appropriate heart rate is required this may involve interventions such as pacemaker therapy or the administration of atropine to increase the heart rate anaphylactic shock is a severe and life-threatening allergic reaction that triggers systemic vasodilation in response to the release of histamine and other inflammatory mediators this condition can occur in response to a wide range of antigens including diagnostic agents Foods insect bites or stings chemical agents and various classes of medications you can classify anaphylactic reactions into two main categories true anaphylaxis and anaphylactoid reactions in true anaphylaxis an allergen binds to imunoglobulin e or IG on the cell membranes of basophils and mass cells this binding stimulates the release of histamine from these cells which leads to widespread vasad dilation and other allergic responses anaphylactoid reactions are non-ig mediated responses that can also result in the release of histamine and other defense mediators importantly these reactions can produce the same severe symptoms as true anaphylaxis without prior exposure to the allergen the signs and symptoms of anaphylactic shock are characterized by vasod dilation and relative hypovolemia which can lead to a drop in blood pressure patients may also experience orofer gal and lenial edema Bronco constriction and Rapid life-threatening Airway compromise providing supplemental oxygen is essential to support oxygenation and tissue profusion as well as ensuring that the patient's Airway is Paton as anaphylaxis can lead to swelling of the Ora ferx and Linex potentially causing Airway obstruction whenever possible identify and remove the allergen that triggered the reaction to prevent further exposure epinephrine is the Cornerstone of anaphylaxis treatment and acts as a potent vasoconstrictor and bronchodilator counteracting the effects of vas of dilation and Bronco constriction epinephrine is typically administered intramuscularly for patients taking beta blocker medications which can blunt the effectiveness of epinephrine glucagon may be administered to counteract this effect early initiation of fluid therapy with normal saline is essential to maintain a map of greater than 65 mm of mercury or simply a systolic blood pressure of greater than 90 if crystalloid therapy alone is insufficient to maintain cardiac output Vasa pressure medications may be necessary to support blood pressure depending on the patient's response and the severity of symptoms additional medications such as antihistamines and C steroids may be administered it's important to observe patients with anaphylaxis for a possible second phase reaction which can occur after the initial treatment in addition to anaphylactic shock there are other forms of distributive shock including addisonian Crisis memac crisis thyrotoxicosis and septic",
        "Sepsis": "shock sepsis sepsis is a life-threatening medical condition characterized by organ dysfunction resulting from a disregulated host response to infection the European Society of intensive care medicine and the Society of Critical Care Medicine have established classifications and treatment approaches for sepsis with the most recent updates in 2016 there are several types of sepsis with systemic inflammatory response syndrome or Sears being a key component Sears represents a widespread inflammatory process that can occur in response to both infectious and non-infectious causes it can be triggered by various factors such as acute respiratory distress syndrome severe burns pancreatitis exposure to interstial endotoxins and major trauma Sears is diagnosed using four variables temperature heart rate respiratory rate and white blood cell count current definitions of sepsis also involve the presence of organ dysfunction in the context of infection for a quick assessment the quick sequential organ failure assessment or qofa score is used which assigns two points or more for certain criteria including a respiratory rate of 22 breasts per minute or greater altered mentation or a systolic blood pressure of 100 MIM of mercury or less another scoring system called the national early warning score or news evaluates six physiologic parameters including respiratory rate ox oxygen saturation systolic blood pressure pulse rate level of Consciousness or new confusion and temperature septic shock is a severe form of sepsis characterized by fluid unresponsive hypotension that requires the use of vasopressor medications to maintain a mean arterial pressure of 65 mm or Mercury or greater additionally patients with septic shock often have elevated serum lactate levels greater than 22 mes per liter or greater than 18 mg per deiler in the absence of hypovolemia these patients are critically ill and face a mortality rate that exceeds 40% making septic shock highly lethal sepsis related infections have been on the rise in recent years according to the CDC an estimated 1.7 million cases of sepsis occur annually in the United States this alarming increase may be attributed to factors such as an aging population the emergence of antibiotic resistant bacteria or simply improved recognition and reporting of sepsis cases sepsis can affect all populations and age groups it does not discriminate based on age gender or background making it a significant Public Health concern that can impact anyone regardless of their demographic characteristics it is a serious and potentially life-threatening condition and despite advances in medical care and treatment the mortality rates for sepsis remain substantial with an approximate rate of 20% this emphasizes the urgency of early detection and effective management to improve patient outcomes and reduce the risk of death prolonged hospitalization is a known risk factor for the development of sepsis in individuals of any age during extended hospital stays patients may be exposed to healthare Associated infections invasive procedures and a compromised immune system all of which increase the likelihood of developing sepsis healthc care facilities have implemented various strategies and protocols to reduce the incidence of Hospital acquired infections and sepsis in an effort to protect patients during their hospitalization the pathophysiology of sepsis involves complex interactions between the immune system and invaded pathogens leading to a Cascade of events that can result in lifethreatening organ dysfunction here's a detailed expansion of the key as aspects of sep's pathophysiology the innate immune system serves as the body's first ler defense against pathogens and provides a generalized and fast acting response to the recognition of antigens which are molecular markers found on the surface of pathogens this initial response is needed for Rapid protection in contrast to the na immune system the Adaptive immune system offers a more precise in specific response to antigens however it requires more time to mobilize its defense mechanisms when encountering an unknown pathogen this response relies on previous exposure which allows the immune system to create memory cells for future encounters pathogens are microorganisms that are responsible for activating the immune system while various types can cause sepsis bacteria are the most commonly associated with this development others include fungi viruses and parasites which can all lead to sepsis the recognition of a pathogen within the body occurs when its antigen binds to specialize cells within the immune system antigens can be categorized as self antigens as in related to normal flora or non-self antigens infection occurs when the pathogen or multiple pathogens invade the host body this Invasion can result in bacteremia which is the presence of viable bacteria in the bloodstream the body's natural barriers such as the skin mucous membranes and the GI tract serve as the first line of defense against infection when infection is detected the innate immune system is activated which initiates the inflammatory response the inflammatory process is a key component of the innate immune response it involves a series of events to contain and eliminate the infection blood vessels dilate to increase blood flow to the affected area and Vascular permeability increases allowing fluid and plasma cells to enter the site of infection white blood cells particularly nutrifil adhere to the inner walls of blood vessels and migrate through vessel walls to the side of injury inflammatory processes are triggered by chemical mediators called cyto which released from injured cells in response to tissue insult inflammation helps contain the injury allowing fyes cells that engulf and digest pathogens and the complement system which is a group of proteins that Aid an immune responses to clean up the area during the inflammatory response vasod dilation and increased capillary permeability occur this activation of clotting Pathways is a protective mechanism to limit the spread of infection and repair damaged tissues in sepsis this immune response becomes disregulated leading to a systemic and exaggerated inflammatory reaction that can ultimately result in organ dysfunction the release of toxins by infectious agents can further contribute to host cell damage the pathophysiology of sepsis is a dynamic and complex process and requires timely intervention and effective management to prevent severe organ dysfunction immortality systemic infection particularly in the context of sepsis triggers a Cascade of events that leads to a widespread and overwhelming inflammatory response throughout the body this response can disrupt normal immune system functioning and have profound effects on various physiological processes essentially systemic infection completely overwhelms and confuses the immune system the body's normal inflammator modulators are disrupted in conditions like Sears key mediators of inflammation including tumor necrosis factors inter lucans and other cyto kindes are released in large quantities these mediators can activate neutrophils while inhibiting the body's ability to regulate and modulate the immune response the inflammatory process and activation of the complement Cascade can cause damage to the endothelium or the interlining of the blood vessel this damage can result in small clots forming in the capillaries inhibiting cellular respiration and causing further damage to surrounding cells these microemboli can lead to a condition called disseminated intravascular coagulation or DIC which is characterized by excessive clotting and bleeding the overall result of these processes is microvascular disruption and injury which are responsible for hypo profusion and the shunting of oxygen this leads to a decreased delivery of oxygen to the tissues resulting in cellular and tissue hypoxia the profound imbalance between oxygen delivery and consumption within the cells and tissues is a Hallmark of sepsis this imbalance causes hypoxia within the cells and tissues ultimately leading to organ dysfunction and failure the complex Cascade of events triggered by a systemic infection is the primary cause of severe sepsis and its progression to organ dysfunction and failure assessing distributive shock caused by sepsis is essential for early intervention ion and effective management this form of shock differs from other shock States in that it typically presents in two distinct phases phase one is the hyperdynamic state or warm shock this initial phase of septic shock is characterized by a high cardiac output state that may persist for hours or even days during this phase the patient's condition May initially appear stable however it's important to note that this hyperdynamic state can progress rapidly into the next phase phase two is the hypodynamic state or cold shock here the patient's condition deteriorates with a sudden drop in cardiac output it is often associated with a worse prognosis compared to the hyperdynamic phase during cold shock the patient's Vital Signs May worsen significantly and organ dysfunction becomes more pronounced when assessing a patient for sepsis maintaining a high index of Suspicion is Paramount obtain a thorough patient history and correlate it with the patient's presentation while an infectious cause is often suspected it's important to acknowledge that the pathogen may not always be identified when possible collect specimen cultures to to identify the causitive pathogen if identified initiate direct antimicrobial therapy fever may be an indicator of infection but it may not be present in all patient populations such as geriatric patients newborns infants those with chronic renal failure are individuals taking anti-inflammatory drugs remember hypothermia can also be present in later stages of seps cardiovascular and respiratory organs are particularly affected in severe sepsis and septic shock patients with septic shock typically exhibit the following signs and symptoms a significantly lowered systemic vascular resistance teoc cardia initially normal to low normal blood pressure which can progress to hypotension once in septic shock initially warms skin with normal skin and mucous membrane color but can progress to cold clammy skin with poor or cyanosis as sepsis advances petii oozing of blood from mucous membranes and procedure sites decreased pulse pressure increased respiratory rate and depth respiratory alcalosis and ards characterized by bilateral lung infiltrates on a chest x-ray monitoring lactate levels is required to assess sepsis severity a rising lactate level is considered one of the most ominous signs and can be used as a marker of disease severity speaking of ards when assessing for acute lung injury and ards specific criteria should include acute onset of respiratory failure diffuse bilateral infil traits on chest x-ray respiratory failure not fully explained by cardiac failure or fluid overload and hypoxemia defined by specific pao2 F2 ratios for different Arts severity categories sepsis management is a complex and multifaceted process aimed at preventing organ dysfunction and optimizing patient outcomes early recognition and intervention is important to ensure a positive outcome for septic patients the primary goal of management is to maintain organ profusion while enhancing tissue oxygenation which involves a delicate balance of preload afterload and contractility to achieve an optimal level of homeostasis the surviving sepsis campaign recommends a a series of actions to be taken within the first hour of identifying sepsis one measure the patient's lactate level with remeasurement if the initial level is greater than 2 milles per liter two obtain blood cultures before administering antibiotics to identify the causitive pathogen three administer broadspectrum antibiotics to Target the infectious agent four initiate rapid administration of 30 ml per kg of crystalloid solution for patients with hypotension or a lactate level of greater than or equal to 4 milles per liter and five apply vas supressors if the patient remains hypotensive during or after fluid resuscitation to maintain a map of 65 5 mm of mercury are greater initial fluid resuscitation involves volume expansion to optimize cardiac output isotonic crystalloids are typically used for this purpose impacted red blood cells may be infused if the hemoglobin level drops below 7 gram per deciliter lactate trending can be a useful guide to assess the patient's response to this treatment in some cas cases though fluid therapy alone may be insufficient to maintain blood pressure Vaso pressures should be initiated if the 30 ml per kg fluid challenge does not effectively support blood pressure nor epinephrine is the vasopressor of choice while dopamine is no longer recommended for routine use other pressors such as vasopressin or epinephrine may be administered as secondary option if hypotension is refractory to nor epinephrine epinephrine is a non-selective adrenic activator that can be used in such cases dobutamine an inotropic agent may be beneficial in treating cardiac depression associated with sepsis and is often used in conjunction with norepinephrine cultures of potential infection sources such as blood urine speu and wounds should be obtained ideally before antibotic Administration while obtaining cultures should not delay antibiotic treatment it is essential to identify the causitive microorganisms initial therapy typically involves broadspectrum antibiotics and specific antibiotics are administered once the microorganisms are identified antibiotics should be initiated within the first hour of suspecting sepsis to minimize mortality additionally therapy may involve procedures like wound de bment abscess drainage or device removal to remove potential sources of infection corticosteroids have shown mixed outcomes on mortality of sepsis the 2016 surviving sepsis guidelines recommend their use only when hypotension is refractory to fluid challenges and vasopressors in such cases intravenous hydrocortisone at 200 milligram per day is recommended postresuscitation management is also essential with ongoing monitoring and targeted interventions as needed such as cardiac assessments and temperature management for comos patients following cardiac",
        "Blood Administration": "restr blood Administration blood Administration is a critical aspect of patient care especially in critical care transport situations several considerations must be taken into account to ensure the safe and effective use of blood products before administering blood products providers must conduct a risk benefit analysis taking into account factors such as the urgency of transfusion the time spent out of the hospital the availability of blood products type and crossmatch information as well as the appropriate transport and care of the products themselves this analysis helps determine if blood transfusion is the right treatment for the right patient at the right time blood Administration may be required to restore circulating blood volume improve oxygen carrying capacity or correct specific coagulation components depending depending on the patient's condition and needs various forms are available including whole blood although less common due to expense and availability red blood cells white blood cells platelets cryoprecipitate and other specialized products each with specific indications and components blood Administration may be considered in cases of hemorrhagic blood loss due to trauma internal bleeding peroperative and post-operative complications or specific disease entities such as leukemia anemia related to illness or coagulation disorders in critical care transport many programs carry typo blood for field pickups or transport patients with match blood from outlying hospitals particularly in rural areas with limited resources time becomes a factor when deciding to wait for blood products as delays may impact the time to reach a tertiary Care Center blood Administration carries the risk of undesirable complications including transfusion reactions underscoring the need for careful monitoring and adherence to protocols in some states the transfusion of blood or blood products is considered a form of human tissue transplantation and is subject to regulation and oversight proper care of blood products is essential particularly if transfusion is not initiated before transport blood and blood products must be kept cold and blood banks have strict policies to ensure their integrity wasting these scarce resources should be avoided whenever possible transfusion requires skilled healthcare providers ERS with knowledge and experience in blood Administration in order to ensure safety and Effectiveness the blood group system is a critical component of blood compatibility involving specific antigens found on the surface of red blood cells blood contains antigens which are substances that can trigger an immune response when introduced into the body in the context of blood transfusions these antigens play a role in determining the compatibility of blood between different individuals to date more than 400 RBC antigens have been identified but the blood group system is one of the most well-known and clinically significant there are three main blood antigens that are of primary importance when considering blood compatibility the system is perhaps the most familiar to people and is determined by the presence or absence of two antigens A and B on the surface of red blood cells there are four main blood types based on the system type A are individuals that have a antigens on their rbcs type B are individuals that have b antigens on their rbcs type AB are individuals that have both A and B antigens on their rbcs and type O are individuals that have neither a nor B antigens on their rbcs this is the most common blood type in the population Rh factor is another critical antigen individuals who have the RH antigen on their rbc's are considered RH positive Ergo a positive or B positive while those that lactus antigen are RH negative the Rh factor can be a significant consideration in blood transfusions and during pregnancy as RH incompatibility can lead to hemolytic disease of the newborn the human Lucy antigen blood group also known as the HLA system is a complex group of antigens that play a role in immune responses and tissue compatibility particularly in organ transplantation while not typically a primary concern in blood transfusions HLA matching becomes critical in organ and tissue transplantation when determining the compatibility of blood for transfusion the type and crossmatch process is employed this Laboratory Testing focuses on identifying the antigen group characteristics of both the donors and recipients blood the goal is to ensure compatibility by matching the and Rh blood types among other factors incompatibility between donor and recipient blood can lead to acute hemalis which is a dangerous reaction where the immune system destroys the transfused blood cells if a person has antigens A or B specific to a particular blood type then they can safely receive blood of that type without an adverse reaction AO incompatible trans Fusion reactions occur when there is a mismatch between the donor's blood type and the recipient's blood type for example if a person with blood type A receives type B or type AB blood their immune system recognizes the foreign antigens as threats and mounts an immune response this can lead to severe and potentially life-threatening transfusion reactions such as hemalis fever chills and organ damage providers must avoid incompatible transfusions by carefully matching blood types individuals with blood type AB are often referred to as universal recipients because they do not have naturally occurring antibodies against A or B antigens this means that they can receive blood from donors with with any  blood type without experiencing a transfusion reaction related to incompatibility their immune systems do not recognize a orb antigens as foreign making them highly compatible with a wide range of blood types individuals with type O blood are often considered universal donors for red blood cell transfusions because they do not have a orb antigens on their rbc's this makes their blood compatible with individuals of blood types A B and ab as their immune systems do not recognize A or B antigens as foreign however individuals with blood type O can only receive typo blood themselves as they may have antibodies against both A and B antigens in their plasma to minimize the risk of transfusion reactions patients should receive transfusions of their own blood type whenever possible this practice ensures compatibility between donor and recipient blood for instance a person with blood type A should receive type A blood whenever feasible however in emergencies or situations where an exact match is not readily available type O RH negative blood or plasma can be transfused temporarily as a un blood type until crossmatch blood of the recipient's specific type becomes available while this approach can help in emergencies it is not a substitute for matching blood types as closely as possible to reduce the risk of adverse reactions during transfusion individuals who have Rh antigens on the surface of their rbcs are considered RH positive this is quite common with approximately 85% of the US population having RH positive blood conversely individuals who do not possess these RH antigens on their rbcs are considered Rh negative unlike the blood group system which naturally produces antibodies against ARB antigens if absent individuals with Rh negative blood do not naturally produce antibodies against RH antigens an Rh negative patient can become sensitized to RH if they are exposed to RH positive blood either through transfusion or even during pregnancy during the first exposure to RH positive blood the immune system may become sensitized and produce antibodies against RH antigens subsequent exposure Ure to RH positive blood such as in a second transfusion or a subsequent RH positive pregnancy can lead to a severe and potentially fatal hemolytic reaction this reaction is due to the antibodies targeting and destroying RH positive rbcs human Lucy antigen or HLA is a group of antigens found on the cell membrane surface of circulating platelets white blood cells and most tissue cells in the body they play a role in the immune system and are involved in immune response regulation in some cases patients who receive platelets from multiple donors may experience fee transfusion reactions related to HLA mismatches febr transfusion reactions are characterized by the development of fever during or after blood transfusion these reactions are often associated with the patient's immune response to antigens present on the transfused platelets to mitigate febril transfusion reactions related to HLA incompatibility HLA match platelet transfusions may be used these platelet transfusions involve selecting donors with matching HLA antigens to reduce the likelihood of an immune response and minimize transfusion reactions HLA match platelet transfusions can significantly decrease the risk of febrile reactions and improve the compatibility of the transfused platelets with the recipient's immune system the possibility of blood transfusions began to emerge in the early 1900s after the discovery of the blood types by Carl liner the first First Blood Bank in the United States was established in 1937 marking a significant milestone in blood transfusion Medicine by the 1970s blood component therapy had largely surpassed the use of whole blood in clinical practice this transition allowed providers to manage more targeted treatment to patients by administering specific blood components rather than whole blood whole blood contains all the components components of blood such as rbc's wbc's platelets plasma and clotting factors it's typically considered for transfusion in patients who have lost at least 25% of their total blood volume such as in cases of massive Hemorrhage it is less commonly used today due to the potential for fluid volume overload in patients with cardiac compromise and its relatively short shelf life as it degrades after approximately 24 hours of storage additionally whole blood transfusions must be matched with the recipient due to the presence of antibodies packed red blood cells are a blood component that retain all the characteristics of whole blood except for approximately 250 ml of platelet rich plasma these transfusions are commonly used to treat anemia blood loss or to improve oxygen carrying capacity in patients washed blood products such as washed rbcs or platelet products involve the removal of the small amount of non-cellular fluid from the blood component typically replacing it with saline this process helps reduce the risk of severe allerg reactions in recipients and decreases the likelihood of hyperemia in the transfused blood products luuc reduced blood products undergo a filtration process to remove white blood cells and platelet fragments from the blood component this filtration step significantly reduces the risk of febril non-hemolytic transfusion reactions which can be associated with white blood cells and also decreases the risk of HLA Alo immunization in patients awaiting organ transplantation these products are commonly used to improve the safety of blood transfusions as well as to minimize adverse reactions platelets are produced in the bone marrow specifically by Mega caros sites these small disk-shaped cell fragments are released into the bloodstream where they circulate as part of the blood's cellular components platelets contain a variety of cytoplasmic fragments that are rich in enzymes necessary for the normal clotting response when a blood vessel is injured platelets are among the First Responders to the site injury they adhere to the exposed collagen in the damaged blood vessel wall becoming activated and initiate the formation of a platelet plug this plug helps prevent excessive bleeding and serves as the initial step in the clotting Cascade let's look at a few indications for platelet transfusion bleeding from thrombocytopenia platelet transfusions are commonly administered to individuals with low platelet counts also known as thrombocytopenia who are at risk of bleeding due to insufficient playlet numbers abnormally functioning platelets in some cases individuals may have platelets with abnormal function leading to a bleeding tendency platelet transfusions may be considered in these rare cases low platelet CS prior to surgery or invasive procedures patients with low platelet counts may receive platelet transfusions before surgery or extensive invasive procedures to reduce the risk of bleeding complications situations involving chemotherapy diic and massive transfusion platelet transfusions may be required in various medical conditions including chemotherapy induced thrombocytopenia DIC in situations involving massive blood transfusions that can deplete platelet levels platelet transfusions are typically administered through a filtered component intravenous drip set with a normal sailing solution the use of a filter is essential to prevent any potential small clots or debris from entering the patient's circulation during the transfusion this filtration step ensures the safety and integrity of the transfusion fresh frozen plasma is a blood product that consists of uncoagulated plasma separated from rbcs and it contains a variety of clotting factors and proteins necessary for coagulation indications for ffp transfusion include the management of significant blood loss due to surgery or trauma correction of coagulation deficiency disease which may occur in conditions such as liver disease reversal of the anti-coagulant effects of medications such as werin and treatment of thrombotic thrombocytopenia propura or TTP which is a rare blood disorder characterized by abnormal blood clotting and low platelet counts ffp provides the necessary coagulation factors to help restore or maintain proper blood clotting function making it a valuable component in managing bleeding disorders or related conditions cryoprecipitate is a frozen blood product that is Created from the plasma of blood donors it is rich in various coagulation factors and proteins and is used to treat specific coagulation disorders indications for transfusion include hemophilia a cryoprecipitate is an essential component in the treatment of Hemophilia a a genetic bleeding disorder characterized by a deficiency and clotting factor eight it provides the missing factor eight which is necessary for blood clotting fibrinogen deficiency cryoprecipitate is also used to manage fibrinogen def efficiency which can result from various medical conditions or medications fibrinogen is a component in the blood clotting process and cryoprecipitate contains high levels of fibrinogen vond willin disease this inherited bleeding disorder is characterized by deficiency or dysfunction of Von willburn Factor A protein that plays a key role in blood clotting cryor precipitate it may be used to provide additional clotting factors and support hemostasis in patients with Von willbrand disease factor eight deficiency factor eight is an important clotting factor and cryoprecipitate can be used to treat individuals with this deficiency though it is a rare coagulation disorder albumin is a blood product that is prepared by fractionation of pulled plas Asma unlike blood components and Rh compatibility are not significant considerations with administering albumin and it is primarily used for volume expansion and in patients with hypo pronia indications for alumin include volume expansion alumin is used to expand blood volume in patients with hypovolemia which can result from various causes including surgery trauma or severe dehydration it helps restore blood pressure and profusion hypoproteinemia in cases of low blood protein levels albumin can be administered to increase the overall protein content in the bloodstream albumin is commonly used in clinical settings such as shock management and the treatment of burn patients at it aids in maintaining adequate blood volume and circulation plasma protein fraction plasma protein fraction is a blood product that contains approximately 83% albumin and 177% globulins it serves specific medical purposes related to volume expansion and protein support indications include volume expansion similar to albumin plasma protein fraction can be used to expand blood volume in patients with hypovolemia especially in clinical scenarios where the preservation of colloid osmotic pressure is important shock and burn patients plasma protein fraction is often employed in the management of patients experiencing shock particularly those with Burns as it contributes to stabilizing blood pressure and supporting circulation and these critical situations the development of synthetic blood substitutes has been an ongoing quest in the field of medicine aimed at addressing critical situations where traditional blood transfusions may not be readily available or or even contraindicated one such synthetic blood substitute is hemopure hemopure is a synthetic blood substitute made from from purify Bine hemoglobin it is designed to serve as an alternative to traditional blood infusions it has found limited compassionate use in patients with critical anemia who are unable to receive blood products due to various reasons including religious beliefs refusal or simply the unavailability of compatible blood it does provide an option to increase oxygen carrying capacity in these patients and has been explored in various clinical scenarios where blood transfusions are not feasible or simply just pose a significant risk trans exic acid or txa is a synthetic antii linic agent with several applications in medicine it works by inhibiting the activation of plasminogen an enzyme responsible for breaking down fiber and clots by preventing fibrin clot breakdown txa promotes clot stability and supports hemostasis this drug has a wide range for clinical use including its role in trauma management where it helps control bleeding by stabilizing clots it has also demonstrated an effectiveness at managing conditions such as nose bleeds coughing up blood and postpartum Hemorrhage anti-coagulants or medications that prevent or slow down blood clot formation making them essential in various medical scenarios two main categories have been used over the years werin and Hein werin is an oral anti-coagulant that has been widely used for the prophylaxis and treatment of thromboembolic disorders such as dvts and atal fibrillation Hein is administered parenterally and used in various clinical settings including surgical procedures to prevent clot formation both drugs work by interfering with the body's coagulation Cascade conversely direct acting oral anti-coagulants have gained prominence in clinical practice in recent years these medications have become increasingly prevalent due to their effectiveness convenience and safety profiles these drugs are often administered to prevent thromboembolic events in patients with conditions such as atrial fibrillation or mechanical heart valves they work by directly inhibiting specific coagulation factors such as thrombin or factor XA thus interrupting the clotting process more directly than traditional anti-coagulants blood transfusions are indicated for various medical conditions including significant hypovolemia resulting from acute blood loss symptomatic anemia decreasing hemoglobin and hematocrit values the need to increase the oxygen carrying capacity of the blood and situations where clotting factors are deficient in some cases blood transfusions are administered is part of pre-surgical care especially when a patient's hemoglobin levels need optimization prior to surgery the necessary equipment for a blood transfusion procedure includes a physician's orders specifying the type and quantity of blood product required the actual product itself that has been typed and crossmatched for compatibility a dedicated Venus access line typically using at minimum an 18 gauge or larger IV to accommodate blood flow a filtered Administration set to prevent clots and debris from entering circulation normal saline solution to flush the line and facilitate blood product infusion and a thermometer to monitor the patient's temperature during and after the transfusion while blood transfusions are generally safe they can lead to complications including anaphylaxis hemolytic reactions disseminated intravascular coagulation transfusion reactions and infections these complications can be serious and must be closely monitored for and managed promptly healthc care providers involved in administering blood transfusions should be vigilant for signs of potential complications these include a significant ific increase in body temperature such as 2\u00b0 F or more above the Baseline skin reactions such as hives itching or ratch localized symptoms like swelling soreness or hematoma at the Venus access site flank pain tacac cardia respiratory distress characterized by wheezing and disia hypotension unexpected bleeding from various sites or previously clotted wounds blood in the urine and severe allergic reactions leading to anaphylaxis which may manifest as nausea vomiting and cardiovascular instability allergic reactions during blood transfusions are typically triggered by allergens present in the donated blood these allergens can include proteins or other substances to which the recipient's immune system reacts these reactions can manifest with a range of symptoms including anaphylaxis puitis ticaria wheezing fever GI upset or other signs of systemic hypers sensitivity managing these reactions during blood transfusions involve several steps providers should discontinue the transfusion immediately and initiate supportive care this may include administering antihistamines to alleviate allergic symptoms in severe cases especially when anaphylaxis occurs epinephrine and corticosteroids may be necessary to manage the reaction effectively bacterial contamination during blood transfusions is relatively uncommon but can have serious consequences contamin mination can occur at various points in the blood collection and processing chain such as during photomy component preparation or processing and the Tha of blood components typically contaminating bacteria originate from donors or from environmental sources this can lead to a rapid onset of symptoms including chills fever vomiting abdominal cramping bloody diarrhea the presence of hemoglobin in the urine shock renal failure disseminated intravascular coagulation and in severe cases death the transfusion should be stopped immediately and a protocol for managing transfusion reactions should be initiated febril transfusion reactions are Adverse Events that can occur during or after a blood transfusion and they are characterized by the development of a fever they are usually less severe than other reactions but can still cause discomfort and concern they are primarily caused by the recipient's immune response to certain components in the transfused blood the Hallmark symptom is an unexplained fever either during or after the transfusion this fever typically occurs within the first few hours after starting the transfusion other Associated symptoms may include chills shivering and a general discomfort febr transfusion reactions are usually managed by administering antipiretico and antihistamines to alleviate Associated symptoms in some cases the transfus Fusion may be temporarily halted until the patient symptoms are under control hemolytic transfusion reactions are severe and they are potentially life-threatening complications of blood transfusions they result from the destruction of rbcs within the recipient's bloodstream they can be caused by various factors including or RH incompatibility these reactions occur rapidly after the transfusion of incompatible rbcs and manifest with severe symptoms including fever chills chest pain back pain flake pain the presence of hemoglobin in the urine hypotension and Di delayed hemolytic transfusion reactions occur in sensitized patients who have been previously exposed to foreign blood antigens often through prior transfusions pregnancy or organ transplantation the patient may develop antibodies against specific blood antigens which may not be detectable by standard pre-transfusion testings the antibodies can then react with transfused rbcs causing their destruction symptoms of delayed reactions include fever jaundice and anemia transfusion reactions related to plasma protein incompatibility involve an adverse response to specific components in the plasma portion of the blood product particularly imunoglobulin a or IG these reactions are relatively rare but can occur in certain individuals who have antibodies against IGA or a deficiency in IGA IGA is a type of antibody found in plasma and most people have this antibody naturally however in rare cases individuals may develop antibodies against IGA or have an IGA deficiency themselves when blood products containing IGA are transfused used into these individuals it can trigger an immune response management includes immediate cessation of the transfusion and providing appropriate medical treatment based on the severity of the reaction other causes of transfusion reactions bleeding tendencies in some cases patients with underlying bleeding disorders or coagulation abnormalities may experience exacerbation of their condition following a blood transfusion this may disrupt the balance of clotting factors in the recipient's blood circulatory overload this can occur when blood is transfused too rapidly or when large volumes of blood are administered to a patient with compromised cardiac function these patients May complain of shortness of breath hypertension and congestive heart failure hypocalcemia hypocalcemia or low levels of calcium in the blood can be associated with citrate toxicity due to the anti-coagulant used in blood products it can manifest as symptoms such as tingling or numbness muscle cramps and cardiac arrhythmias hypo hypothermia blood products that are stored at cold temperatures can lead to hypothermia in the recipient potassium intoxication this can occur if a large volume of blood with high potassium levels is rapidly transfused this can lead to cardiac arrhythmias or other serious",
        "Flight Considerations": "complications flight considerations when providing care to patients with shock sepsis or mods during Air transport several critical considerations must be taken into account these patients are typically highly unstable their Vital Signs and clinical condition can change rapidly necessitating Vigilant monitoring and immediate intervention when necessary Air transport can introduce additional stressors such as changes in altitude and cabin pressure continuous monitoring of Vital Signs including blood pressure heart rate respiratory rate oxygen saturation and entitle carbon dioxide levels is essential providers should be prepared to make rapid adjustments to therapy to maintain adequate oxygenation and hemodynamic stability this may involve titrating vasoactive medications adjusting ventilator settings and ensuring proper fluid management infusions of medications and fluids should be administered with Precision careful attention must be paid to dosages and compatibility to avoid complications incompatibilities between medications or fluids can lead to adverse reactions or compromise patient safety patients who require mechanical ventilation must have their ventilator settings closely monitored and adjusted as needed during transport changes in altitude and cabin pressure can affect the performance of the ventilator and the patient's respiratory status providers should be prepared to modify ventilator settings to compensate for these environmental factors and maintain appropriate oxygenation and ventilation as the aircraft ascends or descends there are changes to atmospheric pressure and oxygen levels ventilator settings such as oxygen concentration and Peep may need to be modified to ensure adequate oxygen delivery to the patient's lungs providers must be knowledgeable about altitude effects and be ready to adapt to the changing conditions overall the management of critically ill patient with shock sepsis or mods during a Air transport demands a high level of expertise experience and adaptability the medical team must be well prepared to respond to the unique challenges of Air transport including maintaining patient stability in a dynamic environment and optimizing therapies to ensure safe and effective care throughout the journey"
    },
    {
        "Introduction to Hemodynamic Monitoring": "chapter 15 hemodynamic\n\nIntroduction\nmonitoring introduction hemodynamic monitoring plays a pivotal role in critical care by focusing on the correction of profusion deficits ensuring that patients receive adequate blood flow and oxygen delivery to vital organs in recent years there has been a remarkable shift towards safer more portable and less invasive Technologies for monitoring hemodynamic parameters this evolution of monitoring tools has expanded beyond the Intensive Care Unit allowing healthc Care Professionals to utilize these Technologies on medical surgical Wards during patient transport in long-term care facilities and even in some cases within the familiar and comforting environment of patients homes this broader accessibility to hemodynamic monitoring not only facilitates early protection and intervention for patients at risk of circulatory compromise but also promotes patient centered Care by extending the benefits of advanced monitoring to a wider range of healthcare settings traditional physical assessments of vital signs and clinical parameters like mentation skin color and urine output are valuable but may not reveal subtle signs of poor profusion potentially leading clinicians to mistakenly believe that profusion is adequate however with the advancement of technology and a deeper understanding of profusion hemodynamic monitoring has shifted its focus from Central measurements to the assessment of tissue level circulation and microcirculation allowing for more accurate and timely identification of profusion deficits over the past 50 years evolving monitoring technologies have imparted crucial lessons first no single measurement on its own can provide a comprehensive hemodynamic assessment of a critically ill patient second that Critical Care interventions must be personalized according to the individual's specific needs and third that personalized care necessitates the use of multiple mon monitoring devices and dynamic variables sensitive to changes in the patient's condition over time these lessons underscore the importance of a multifaceted approach enabling Health Care Providers to offer tailored and effective care to their",
        "Cardiovascular Anatomy and Physiology": "patients cardiovascular anatomy and physiology the human heart is positioned in the thoracic cavity beneath the sternum with the majority of it situated to the left of the midsternal line it's a vital organ responsible for pumping blood throughout the body within the heart there are four crucial valves that play a fundamental role in regulating blood flow the atrio ventricular valves better known as the AV valves including the mitro valve on the left side and the tricuspid valve on the right side which are positioned between the Atria and the ventricles also the semi lunar valves consisting of the aortic valve on the left and the pulmonic valve on the right these valves serve the critical function of preventing the backward flow of blood within the heart ensuring that blood moves efficiently from one cardiac chamber to another and then out out to the body or lungs this unidirectional flow is essential for maintaining proper circulation and ensuring that oxygenated blood is delivered to the body's tissues while deoxygenated blood is sent from the lungs for reoxygenation the coronary arteries play a vital role in supplying the heart muscle with the oxygen it requires to function properly these arteries have openings known as osta located in the base of the aorta just coddle to the attachment points of the aortic valve leaflets this anatomical Arrangement is of great significance because it means that the ostea are obstructed when the aortic valve is in the open position thus preventing the backflow of blood into the coronary arteries during ventricular contraction furthermore it is essential to note that the majority of coronary profusion occurs during diast the resting phase of the cardiac cycle when the heart muscle relaxes and the coronary arteries can fill with oxygenated blood blood returns to the heart through the two major veins the inferior and Superior vnea which confer in the right atrium from there the blood passes through the tricuspid valve into the right ventricle upon exiting the right ventricle the blood travels through the outflow tract passes through the pulmonic valve and enters the pulmonary arteries leading to the lungs for oxygenation it is important to note that the pulmonary arteries carry the most deoxygenated blood found in the body once oxygenated in the lungs blood returns to the left atrium traverses through the mitro valve and proceeds to the left ventricle from the left ventricle blood exits via an outflow tract leading to the aortic valve and then it enters the central circulation to be distributed throughout the body The myocardium or the heart muscle itself exhibits distinct anatomical and functional characteristics the heart functions as a b ventricular system with much lower pressures on the right side compared to the left side this difference in pressure is necessary to ensure proper profusion of the brain and splanchnic organs which require higher pressures than those needed to deliver blood just a few inches from the heart to the lungs the left ventricle is notably more muscular than the right ventricle reflecting the difference in the workload required to pump oxygenated blood throughout the systemic circulation compared to deoxygenated blood to the pulmonary circulation despite the differences in ventricular muscle mass and pressure there is relatively little variation in cardiac output between the right and left sides of the heart highlighting the remarkable balance and coordination that exists within the cardiovascular system to maintain overall circulatory efficiency invasive hemodynamic monitoring is a valuable tool that capitalizes on the lower pressures that are characteristic of the right side of the heart by placing catheters within this low pressure system by doing so clinicians can gain valuable insights into the Dynamics of the cardiovascular system however there are critical considerations related to hemo Dynamic monitoring one of which is coronary profusion the heart is supplied with oxygenated blood by two main coronary arteries the right coronary artery and the left main coronary artery the right coronary artery primarily supplies the right ventricle and in most people also feeds the ventricular septum including the cardiac conduction system it is a essential to recognize that the heart receives its blood supply primarily during diast the resting phase of the cardiac cycle therefore maintaining an adequate diastolic blood pressure is of utmost importance for ensuring proper coronary profusion and subsequently myocardial oxygenation considering the anatomical positioning of The myocardium there are several implications patients who have experienced chest wall injuries such as trauma or impact should be closely monitored for the development of arrhythmias when there is suspicion of myocardial contusion chest wall injuries can lead to myocardial contusion which can disrupt the electrical Pathways within the heart and result in arrhythmias additionally for patients presenting with significant arrhythmias it is often advisable to conduct a cardiac catherization to assess the the patency of their right coronary arteries this procedure can help determine if there are any blockages or abnormalities in the RCA that might be contributing to the arrhythmias ensuring that prompt and appropriate treatment can be administered to optimize coronary profusion and maintain cardiac function the cardiac cycle is a dynamic proc process that can be divided into two main stages syy and diast each of these stages can be further broken down into five distinct phases providing a comprehensive view of the heart's functioning one syy and diast the cardiac cycle encompasses syy which represents the contraction of the heart and diast the relaxation phase two phases of the cardiac cycle atrial Cy atrial Cy initiates with the electrical impulse from the sinoatrial node and is reflected as the p-wave on an ECG during this phase The Atrium depolarizes and contracts contributing approximately 20 to 30% of the ventricular filling volume also known as preload this atrial kick is vital in raising ventricular volume and pressure impacting the force of ventricular contraction through the Frank Starling mechanism something we will talk about later in the lecture three isov volumetric contraction after the electric impulse from the Atria moves through the atrio ventricular node to the ventricular conduction system the ventricles depolarize and contract ventricular pressure Rises abruptly leading to the closure of the AV valves the volume of blood in the ventricles just before this valve closure is known as the ventricular preload during this phase the pressure within the ventricles continues to rise but since the cardiac valves are closed no change in ventricular blood volume occurs four ventricular syy as the pressure in the ventricles surpasses the arterial pressure the aortic and Pulmonary valves open allowing the ventricles to eject blood into the aorta and pulmonary artery ventricular ejection commences with the aortic valve opening slightly after the pulmonary valve due to differences in the pressure gradient in the pulmonary circulation that being said during this phase no coronary perfusion takes place as the aortic valve leaflets are blocking the coronary arteries five isov volumetric relaxation near the end of ventricular ejection as the ventricles begin to relax and ventricular tissue repolarizes the pressure within the ventricles Falls below arterial pressure this results in the closure of the semilunar valves to prevent the backward flow of blood into the heart the atrioventricular valves remain closed during this isov volumetric relaxation phase six ventricular filling ventricular filling starts when the pressure in the ventricles drops below the pressure in the Atria causing the mital and tricuspid valves to open blood then flows passively from the Atria through the AV valves into the ventricles the SA node produc produces an electrical impulse to initiate atrial syy and the cardiac cycle restarts understanding these phases of the cardiac cycle is extremely important when evaluating and interpreting cardiovascular function especially in conditions where this Dynamic process may be compromised such as heart failure arrhythmias or valve disorders cardiac output is a fundamental parameter in cardiovascular physiology that describes the volume of blood the heart pumps in one minute it's calculated as the product of stroke volume and heart rate often expressed by the formula Co equal SV * HR this essential metric helps assess the heart's Effectiveness in meeting the body's circulatory demands stroke volume represents the volume of blood ejected from the left ventricle with each heartbeat and as a crucial determinant of cardiac output stroke volume is intricately regulated by three main factors preload afterload and contractility we will go more in depth on these three factors later in the lecture but for now we will briefly Define them preload signifies the volume of blood in the ventricles at the end of diast immediately before systolic contraction the greater the preload The More The myocardium stretches leading to Stronger contractile force and a higher stroke volume preload is often measured as end diastolic volume or enddiastolic pressure in conditions like hypervolemia The increased preload May Elevate stroke volume after load relates to the resistance the ventricles face when ejecting blood into the arterial system elevated afterload as seen as hypertension or conditions like aortic stenosis can reduce stroke volume by imposing extra work on the heart making it harder to eject blood and contrast a decrease in afterload typically due to Vaso dilation can enhance stroke volume contractility pertains to the strength of myocardial contractions and is influenced by factors such as hormones autonomic nervous system activity and medications an increase in contractility leads to a stronger ventricular contraction and a higher stroke volume in heart failure impaired contractility can reduce stroke volume monitoring cardiac output is crucial in assessing cardiac function and overall circulatory status as it reflects how effectively the heart meets the body's oxygen and nutrient demands alterations in cardiac output can signal underlying cardiovascular issues fluid imbalances and hemodynamic changes in critically ill patients accurate measurement and interpretations of cardiac output are vital in clinical practice guiding decisions related to patient management such as adjusting medications or initiating supportive therapies to optimize cardiac output and tissue profusion when face with the low cardiac output in a critical care transport setting the initial assessment for the critical care transport professional should focus on the patient's heart rate this rapid evaluation of heart rate provides valuable preliminary information about the patient's circulatory status allowing for quick decision making and intervention a significantly elevated heart rate may indicate the heart's attempt to compensate for a reduced cardiac output by pumping blood at a faster Pace conversely a braic cartic State might suggest a primary issue related to the heart's inability to generate a sufficient cardiac output once the heart rate is assessed the provider can delve further into the evaluation of stroke volume constituents including preload afterload and contractility in order to pinpoint the underlying causes of the low cardiac output and determine the most appropriate therapeutic interventions for the patient's condition the heart rate plays a pivotal role in determining a patient's cardiac output and is a vital factor in regulating overall cardiovascular performance increasing the heart rate is one of the most efficient methods of enhancing ing cardiac output rapidly this acceleration in heart rate allows the heart to pump more blood in a shorter period which can be crucial during states of hypo profusion or decreased cardiac output that being said it's essential to recognize that there are limits to the benefits gained from elevating a patient's heart rate when the heart rate becomes excessively rapid ventricular filling time is shortened significantly and this can adversely affect cardiac output these specific thresholds for heart rate limits may vary among individuals and it's imperative for health care providers to assess the patients hemodynamic status and tailor interventions accordingly to optimize cardiac output without exceeding these individualized limits heart rate thresholds represent essential guidelines for health care providers when assessing and managing patients with abnormal heart rates these thresholds are crucial in optimizing cardiac output while avoiding potential complications for adult patients a medical legal ceiling of an acceptable heart rate at or below 120 beats per minute has been established when encountering a sustained heart rate exceeding this limit providers should focus on identifying the underlying cause it's important to recognize that heart rates exceeding 120 beats per minute can Elevate myocardial oxygen consumption potentially compromising cardiac output and coronary profusion this can lead to a vicious cycle of deteriorating cardiovascular function conversely heart rates below 50 beats per minute can have their own set of challenges while slower heart rates can provide increased ventricular filling time and prolonged diastolic intervals promoting improved preload in coronary blood flow when the heart rate drops below 50 beats per minute hemodynamic improvements are offset by a subsequent decrease in cardiac output therefore 50 beats per minute is generally considered the lower thresold for acceptable heart rates in adults balancing the benefits of prolonged diastolic intervals with the need to maintain an adequate cardiac output heart rate regulation involves a complex interplay of mechanisms or orchestrated by the autonomic nervous system various receptors and metabolic demands the autonomic nervous system consisting of the sympathetic and parasympathetic branches plays out a fundamental role in modulating heart rate sympathetic stimulation of the autonomic system triggers the release of norepinephrine which acts on beta of generic receptors in the heart leading to an increase in heart rate and thus cardiac output particularly during fight ORF flight responses conversely the parasympathetic Branch predominantly via the vagus nerve releases acetycholine which influences receptors in the heart slowing down the heart rate additionally various receptors throughout the body Monitor and relay information about oxygen levels blood pressure and pH to the central nervous system which can then adjust heart rate to meet the body's oxygen and profusion needs furthermore metabolic demands driven by the body's need for oxygen and nutrient delivery can also trigger changes in heart rate ensuring that the cardiovascular system adapts to the body's constantly shifting requirements this intricate system of heart rate regulation serves as a critical component of overall homeostasis and the ability of the cardiovascular system to respond to changing circumstances the body's intricate network of receptors significantly impact heart rate with some of the most influential ones being the Barrow receptors primarily located in the cored body IES and the aortic Arch these Barrel receptors act as Vigilant monitors of blood pressure responding to deviations from the body's normal range when blood pressure drops such as during orthostatic changes or sudden postural shifts be receptors swiftly trigger an increase in heart rate to help maintain sufficient profusion and oxygen delivery to vital organs conversely when blood pressure surges the beer receptors act by decreasing the heart rate to prevent excessive strain on the cardiovascular system furthermore chemoreceptors while exerting a somewhat lesser influence on the heart rate are still essential in responding to changes in blood chemistry particularly pH and oxygen saturation when faced with a decrease in PH or lowered oxygen saturation chemo receptors stimulate an elevation and heart rate to enhance oxygen delivery conversely when pH or oxygen saturation Rises these receptors guide a decrease in heart rate optimizing the balance between oxygen supply and demand within the body all of which collectively ensures the finally tuned regulation of heart rate measuring heart rate is a vital component of assessing a patient's hemodynamic status especially in emergency and critical care situations where Swift and accurate information is essential for timely interventions in such high stress environments obtaining an accurate heart rate is often challeng alling due to various factors including noise and other distractions here the heart rate derived from a pulse oximeter emerges as a reliable and practical tool the pulse oximeter ability to non-invasively monitor heart rate by detecting pulsatile changes in blood flow provides a realtime and continuous assessment significantly enhancing the clinician situational awareness furthermore to ensure the utmost Precision the heart rate obtain from the puls oximeter can be cross referenced with an ECG display or the pleth waveform from the monitor's pulo Symmetry thereby reinforcing the accuracy of the measurement and allowing for timely detection of any discrepancies or arrhythmias preload a crucial aspect of cardiac physiology refers to the degree of stretch that myocardial fibers experience as a result of the volume of blood present in The ventricle at the end of diast just before ventricular contraction preload signifies the ventricular filling pressure at the onset of syy and is often synonymous with two important parameters indolic volume and indolic pressure this parameter plays a pivotal role in determining the heart's capacity to pump blood effectively several key factors influence preload including total blood volume the distribution of blood within the circulatory system and atrio ventri synchrony when preload decreases such as in cases of hemorrhage dehydration vomiting gastric suction profuse sweating diarrhea or significant fluid shifts that result in the loss of fluid to areas like the intertial space patients may experience a reduction in myocardial fiber stretch in contrast preload increases in conditions marked by excessive blood volume or hyper volic states such as those seen in patients with fluid overload renal failure and elevated Venus return understanding in managing preload is critical in maintaining cardiac output and ensuring optimal circulation especially in critically ill patients where preload alterations can have profound implications for the patient's hemodynamic stability and overall well-being the Frank Starling law often represented as the Starling curve elucidates a fundamental principle of cardiac physiology it describes the relationship between the stroke volume and the volume of blood filling the heart known as preload according to this law an increase in preload initially leads to an increase in stroke volume and consequently to cardiac output the reason behind this relationship lies in the stretching of myocardial fibers within the ventricles when the heart fills with blood during diast as the myocardial fibers are stretched they develop a greater force of contraction resulting in a more forceful ejection of blood during diast this phenomenon signifies an optimal range where stroke volume and cardiac output are maximized indicating the heart's efficiency in pumping blood however Beyond a certain point of optimal preload further increases in preload lead to a decline in stroke volume and cardiac output this downturn occurs when the myocardial fibers become excessively stretched causing the force of contraction to decrease and ultimately impairing the heart's ability to effectively pump blood in essence the Frank Starling law emphasizes that every patient has an individualized point of optimal preload at which their cardiac output is at its highest and most efficient when a patient's preload deviates from its optimal range either by being too low or too high it results in a decline in cardiac output this concept is essential for clinicians especially in critical care settings as understanding and managing preload can significantly impact a patient's hemodynamic stability and guide therapeutic interventions it underscores the significance of maintaining a delicate balance in the volume of blood returning to the Heart during diast to ensure optimal cardiac performance and ultimately adequate tissue profusion measurement of preload is a crucial aspect of assessing the patient's cardiac function and hemodynamics status preload refers to the degree of myocardial fiber stretch induced by the volume of blood present in The ventricle during the end of diast and it is essential for determining the heart's ability to effectively pump blood there are several methods that are employed to assess preload right ventricular preload or CVP the central Venus pressure is used to estimate right atrial pressure serving as an indicator of right ventricular preload CVP measurement provides insights into the blood volume returning to the right side of the heart reflecting the ability to pump blood into pulmonary circulation left ventricular preload left ventricular preload is typically measured by assessing the pulmonary capillary wedge pressure or pcwp or in specific cases the pulmonary artery diastolic pressure pcwp in particular was once regarded as the gold standard for evaluating left ventricular preload a pcwp measurement exceeding 18 millim of Mercury is often indicative of decompensated left ventricular failure or heart failure however it's important to note that both CVP and pcwp are static pressure measurements providing limited information about the circulating blood volume increasingly however clinicians are turning to Dynamic parameters to assess preload these include stroke volume variation pulse pressure variation or ppv and the pleth variability index or pvi these Dynamic parameters offer more accurate and real-time assessments of preload status helping to differentiate between patients with adequate preload who may not respond well to fluids and those with low preload who would benefit from fluid resuscitation the commonly used memonic high is dry emphasizes that high values of these Dynamic parameters May indicate a patient with inadequate preload another practical method to assess fluid responsiveness and preload is the passive leg raise or plr test this test involves raising the patient's legs to mimic a fluid is effect on increasing preload by monitoring changes in cardiac output or other hemodynamic parameters in response to plr Providers can quickly determine a patient's fluid responsiveness without the need for invasive monitoring assessing preload is a critical component of evaluating a patient's hemodynamic status and it can be achieved through various methods in including static pressure measurements like CVP and pcwp dynamic parameters and functional tests such as plr these measurements help guide clinical decisions regarding fluid management and cardiovascular support in different patient scenarios afterload is a fundamental Concept in cardiovascular physiology that reflects the resistance the ventricles must overcome to effectively eject blood into the circulatory system understanding afterload is crucial because it directly impacts ventricular function and cardiac output afterload can be thought of as the pressure or resistance the ventricles must work against to open the aortic or pulmonary valve and eject blood into the arterial system it is the resistance that The myocardium encounters during the ejection phase of the cardiac cycle an increase in afterload whether due to hypertension outflow obstructions or other factors results in a greater resistance to ventricular ejection this increased resistance makes it more challenging for the ventricles to expel blood effectively leading to a decrease and ventricular function and cardiac output ventricles must generate higher pressures to overcome elevated afterload which can lead to hypertrophy and in the longterm heart failure conditions such as aortic stenosis or pulmonary stenosis create mechanical obstructions at the outflow of the left or right ventricle increasing the pressure the ventricles must generate to eject blood against the narrowed valves the degree of Vaso constriction or vasod dilation in the systemic and pulmonary circulation affects afterload elevated vascular tone as seen in hypertension raises systemic afterload making it more challenging for the left ventricle to pump blood into the high press arterial system blood viscosity can influence after load increase blood viscosity due to conditions like polycythemia can raise afterload because thicker blood resists flow more requiring greater force for ejection conditions that lead to ventricular dilation like dilated cardiomyopathy can increase after load a dilated ventricle May face higher pressure requirements for Effective ejection after load of the left ventricle is typically assessed by measuring systemic vascular resistance which reflects the overall resistance encountered during ejection changes in systemic vascular resistance can significantly affect systemic circulation and consequently cardiac output therefore evaluating left ventricular afterload is crucial when addressing issues rela to cardiac output and systemic profusion after load of the right ventricle is commonly evaluated by assessing pulmonary vascular resistance this measurement helps determine the resistance the right ventricle faces when pumping blood into the pulmonary circulation right ventricular afterload is particularly relevant when assessing patients with suspected heart disease correlating pulmonary artery diastolic pressure with pulmonary capillary wedge pressure or evaluating individuals for heart transplantation understanding and managing afterload are critical aspects of cardiovascular care as they directly impact ventricular performance and overall hemodynamic function by recognizing factors affecting afterload and appropriately measuring it through systemic vascular resistance and pulon AR vascular resistance healthc care providers can better assess diagnose and manage conditions related to ventricular ejection resistance ultimately optimizing cardiac function and patient outcomes contractility also known as inotropic state is a fundamental aspect of cardiac function that refers to the intrinsic ability of the heart muscle to contract and generate force it plays a crucial role in regulating stroke volume and consequently cardiac output understanding contractility is essential for addressing and managing cardiac function contractility represents the force and vigor with which The myocardium contracts during syy it directly affects the amount of blood expelled by the heart with with each beat and therefore influences cardiac output unlike preload and after load which can be measured using various hemodynamic parameters contractility is not directly measurable through conventional monitoring methods traditional monitoring tools provide information about pressures and volumes but not the actual force of contraction so to assess contractility Healthcare Providers often rely on newer Technologies such as Doppler electrocardiography and ultrasonography these Imaging techniques enable clinicians to visualize and assess the heart's contraction strength and function there are several factors that influence contractility the first is myocardial Health the overall health of the heart muscle significantly affects contractility so conditions such as esic heart disease cardiomyopathies and heart failure can impair contractile function the autonomic nervous system specifically the sympathetic and parasympathetic inputs play a crucial role in regulating contractility sympathetic stimulation increases contractility while while parasympathetic input has an inhibitory effect alterations in metabolic states such as changes in oxygen supply and demand can influence contractility for example increased demand during exercise can enhance contractility the concentration of ions particularly calcium inside cardiac myocytes affects the force of contraction changes in ion levels can modify contractility pharmacologic agents such as inotropic drugs can directly modulate contractility remember positive inotropes will increase cardiac contractility while negative inotropes will decrease it lastly the heart rate is closely linked to contractility an increased heart rate at least up to a certain point can have a positive anatropin stronger contractions however excessively rapid heart rates can reduce ventricular filling time and potentially diminish contractility myocardial muscle injury or esea often due to conditions like myocardial infarction can significantly decrease contractility these injuries impair the heart's ability to contract forcefully leading to reduced stroke volume and cardiac output the impact of es schea on contractility is particularly concerning as it can lead to inadequate blood supply to vital organs the regulation of contractility involves essential ions with calcium playing essential role calcium ions are integral for the excitation contraction coupling process allowing myocytes to contract sodium and potassium ions also influence contractility contributing to the action potential and electrical excitability of the myocard an imbalance or disruption in these ions homeostasis can have a profound effect on the heart's ability to contract effectively further highlighting the critical role that these ions play in maintaining cardiac function multiple pharmacologic agents can influence myocardial contractility through various mechanisms dexin is a cardiac glycoside derived from the Fox Glove plant its primary mechanism of action involves inhibiting the sodium potassium pump in cardiac mosites by doing so it increases intracellular sodium levels which subsequently reduce the activity of the sodium calcium exchanger this leads to an accumulation of intracellular calcium enhancing contractility dexin also has a Vago mtic effect reducing heart rate and improving the heart's efficiency in cases of atal fibrillation do dopamine is a catacol amine that can influence myocardial contractility its effects are dose dependent at lower doses it stimulates dopamine receptors causing vasodilation in the renal mesenteric and coronary vasculature higher doses stimulate beta 1 adrenic receptors in the heart leading to increased contractility dopamine's ability to Target different receptors makes it a versatile medication for managing cardiac output and blood pressure debam is another catacol amine primarily affecting beta 1 adrenic receptors it has a more specific inotropic effect compared to dopamine and is frequently used to improve myocardial contractility in patients with heart failure dobutamine increases cardiac output by enhancing the force of contraction without significantly increasing heart rate mil renon is a phosphodiesterase inhibitor it works by inhibiting the breakdown of cyclic adenosine monophosphate leading to increased levels in cardiac myocytes elevated cyclic adenosin monophosphate levels enhance intracellular calcium release and subsequently myocardial contractility mil Renown is particularly useful in patients with heart failure or those undergoing cardiac surgery calcium itself can be administered intravenously to increase myocardial contractility it plays a crucial role in excitation contraction coupling with cardiac myocytes while calcium infusion can enhance contractility it is used with caution due to the risk of arrhythmias and increased myocardial o oxygen consumption epinephrine is a potent catacol amine stimulating both Alpha and beta adrenic receptors its positive inotropic effects stem from its stimulation of beta 1 adrenic receptors in the heart increasing contractility and heart rate epinephrine is often used in ALS support for patients with severe cardiac compromise and then lastly we have glucagon a hormone that acts through G protein coupled receptors glucagon increases myocardial contractility by elevating cyclic adenosine monophosphate levels in cardiac myocytes it leads to increased calcium entry into the cells subsequently enhancing contractility glucagon is sometimes employed in situations of beta blocker overdose when patients experience severe bardia or heart failure each of these pharmacologic agents offers specific advantages and considerations for modifying myocardial contractility providing clinicians with a range of tools to address various cardiac conditions the choice of agent depends on the patient's clinical presentation the underlying pathology and the desired hemodynamic outcomes negative inotropic agents decrease contractility and can be essential in specific clinical scenarios beta blockers for example work by blocking beta or generic receptors on cardiac myocytes reducing the effects of of catacol amines like epinephrine and norepinephrine by doing so they lower heart rate and contractility making them valuable in conditions like hypertension arrhythmias and heart failure in similar fashion anti-ar rythmics like quinidine and propanamide can exert negative inotropic effects as part of their anti- rythmic action calcium Chanel blockers particularly those that affect the heart decrease the entry of calcium into cardiac myocytes reducing contractility these agents are used in various cardiac conditions to slow heart rate and simultaneously lower blood pressure as stated earlier heart rate plays a crucial role in determining contractility an El elevated heart rate can reduce diastolic filling time limiting the ventricles ability to fill adequately this can lead to decreased preload reducing stroke volume and ultimately cardiac output additionally an extremely high heart rate can decrease coronary artery profusion time potentially leading to myocardial esmia in contrast lower heart rates provide more time for rric filling allowing for optimal diastolic preload which can enhance contractility contractility can be inferred through the various hemodynamic parameters these include the stroke volume index left ventricular stroke work index and the right ventricular stroke work index stroke volume index reflects the amount of blood ejected from the left ventricle per heartbeat while the left ventricular stroke work index and the right ventricular stroke work index assess the work performed by the left and right ventricles respectively changes in these parameters can indicate alterations in contractility electrocardiography is another essential tool for assessing contractility where the ejection fraction is commonly used remember the ejection fraction represents the percentage of blood ejected from the left ventricle during each cardiac cycle a decreased ejection fraction can indicate reduced contractility as seen in heart failure blood pressure a fundamental component of hemodynamic monitoring can be assessed through various methods including both direct and indirect monitoring direct monitoring involves the insertion of an arterial line which allows for continuous measurement of blood pressure this method provides precise data and is particularly valuable in clinical care settings in contrast indirect monitoring a more common approach involves the use of a blood pressure cuff this method provides intermittent measurements and is typically performed using automated electronic blood pressure cuffs blood pressure is expressed as two values systolic blood pressure and diastolic blood pressure systolic blood pressure represents the arterial pressure during syy when the heart contracts and ejects blood into the the circulation in contrast diastolic blood pressure is the measurement of arterial pressure during diasti when the heart is in a relaxed State allowing it to fill with blood these values offer insights into the condition of a patient's cardiovascular system and are vital for diagnosing and managing hypertension hypotension and other cardiovascular conditions various indirect methods for monitoring blood pressure exist including assessing pulses utilizing electronic blood pressure cuffs and employing Doppler ultrasonography machines automatic blood pressure units are frequently integrated into transport monitors and can automatically measure blood pressure at predetermined intervals they typically provide data on heart rate and mean arterial pressure because mean arterial pressure is considered a critical indicator of profusion it is often used as a key parameter in making clinical decisions and guiding treatment strategies ensuring the accuracy of blood pressure measurements involves selecting the appropriate cuff size and ensuring the extremities position is correct as these factors can significantly affect the reliability of the reading overall the monitoring of blood pressure is essential for evaluating a patient's cardiovascular status identifying potential issues and guiding clinical interventions automatic blood pressure units measure two primary parameters heart rate and mean arterial pressure heart rate recorded in beats per minute reflects the rate at which the heart contracts and plays a crucial role in understanding the patient's cardiac function abnormal rates can signify various underlying conditions from arhythmia to life-threatening teoc cardia or bra cardia therefore tracking heart rate is essential for diagnosing and managing these cardiac issues map on the other hand is a vital hemodynamic parameter calculated based B on the systolic and diastolic blood pressure values it represents the average pressure within the arterial system over the entire cardiac cycle because it reflects both the profusion pressure to vital organs and the balance between diastolic and systolic pressures map is a critical parameter for assessing tissue profusion and oxygen delivery when using patient care care and treatment decisions healthc care providers often rely on map values as they offer a more comprehensive picture of a patient's circulatory State compared to isolated systolic or diastolic blood pressure measurements maintaining an adequate map is essential to ensure that vital organs receive sufficient blood flow and oxygen but how does mean arterial pressure work a critical care transport professional may use mean arterial pressure to assess a patient's circulatory status in a variety of scenarios particularly when managing critically ill patients here's an example of how mean arterial pressure can be a valuable parameter in such a situation imagine a critical care paramedic responding to a call for a patient in severe shock the patient is hypotensive lethar IC and displaying other signs of poor profusion the paramedic knows that sepsis can lead to distributive shock causing systemic vasodilation and a significant drop in blood pressure in this case the patient mean arterial pressure is a key indicator of their circulatory status and their ability to profuse vital organs effectively the paramedic first measures the patient's blood pressure finding it to be significantly low however they also assess mean arterial pressure because they can gain a more comprehensive understanding of the patient's profusion mean arterial pressure is calculated by taking the average of the patients systolic and diastolic blood pressure values and is a more accurate indicator of profusion pressure compared to isolated blood pressure readings in this context a reading below the normal range which is typically between 70 and 100 millim of mercury suggests that the patient's organs are probably not receiving sufficient blood flow recognizing the significance of a low mean arterial pressure the paramedic can then initiate appropriate interventions including intravenous fluids vasopressors and initiating other lepsis management protocols as the patient's mean arterial pressure increases it indicates an improved perfusion pressure and a positive response to treatment continuous monitoring of me arterial pressure allows the paramedic to titrate interventions ensuring that the patient's circulatory status improves and that vital organs receive adequate blood flow in summary a critical care trans transport professional can use mean arterial pressure as a vital tool to assess circulatory status especially in situations like septic shock where profusion is a critical concern by calculating and monitoring me arterial pressure paramedics can guide their treatment decisions optimize patient care and respond effectively to life-threatening",
        "Arterial Lines": "conditions arterial lines arterial lines serve as invaluable Tools in critical care settings enabling continuous and direct monitoring of a patients arterial blood pressure these lines are typically inserted into major arteries with the radial artery being the preferred site due to its accessibility and lower risk of complications once in place the arterial line provides real-time data on blood pressure enabling Health Care Providers to make precise adjustments in medication or interventions this continuous data stream is particularly beneficial when titrating vasoactive agents or managing patients with rapidly changing hemodynamics such as those in septic shock or undergoing cardiac surgery by displaying arterial pressure waveforms and corresponding values Healthcare Providers can promptly identify Trends or aberations allowing for timely intervention the presence of an arterial line confirms the existence of pulsatile blood flow which is a crucial indicator of cardiovascular health and function in cases where peripheral pulses may be weak or challenging to assess by traditional methods an arterial line serves as a reliable alternative additionally arterial lines offer a means to obtain arterial blood samples for arterial blood gas analysis ABG values including pH partial pressures of oxygen and carbon dioxide and bicarbonate levels are essential in assessing a patient's oxygenation and acid base balance this is especially important for patients with respiratory stress or metabolic imbalances where quick and accurate ABG results can guide treatment decisions here are some key indications for the use of arterial lines patients requiring constant blood pressure monitoring one of the primary indications for arterial lines is the need for continuous blood blood pressure monitoring this applies to critically ill patients in intensive care units or operating rooms where minute to- minute changes in blood pressure can significantly impact patient care for instance patients undergoing complex surgeries like cardiac or Neurosurgical procedures May benefit from arterial lines to closely track blood pressure fluctuations during the operation and immediate post-operative period shock and hemodynamic instability arterial lines play a crucial role in the assessment and management of patients in shock or those with hemodynamic instability patients in shock may not respond adequately to initial resuscitation measures and an arterial line allows Health Care Providers to closely monitor blood pressure Trends assess the effectiveness of interventions and make timely adjustments to treatment plans this is valuable in cases of septic shock cardiogenic shock or traumatic injuries where rapid and precise blood pressure measurement is vital and lastly vasoactive or anti-hypertensive infusions patients who require vasoactive medications to support or regulate their blood pressure such as those with severe sepsis or postcardiac surgery will benefit fit from an arterial line these lines enable continuous monitoring of response to vasoactive agents allowing clinicians to adjust medication doses based on real-time blood pressure data conversely these lines are equally valuable for patients receiving anti-hypertensive medications as again they help ensure that blood pressure is lowered at an appropriate rate avoiding abrupt potentially harmful drops in blood pressure contraindications to arterial lines are vital considerations in clinical practice to ensure patient safety and minimize potential complications associated with this invasive procedure here we'll take a look at each of these Contra indications aeia which results from insufficient blood flow to tissues can be exacerbated by arterial line insertion if the extremity where the arterial line is to be placed is already experiencing esea due to conditions like arterial blockages or severe vascular disease the procedure May further compromise blood supply potentially leading to tissue damage necrosis or impaired wound healing in such cases alternative methods for monitoring blood pressure which would not require arterial access should be considered inserting an arterial line through infected or inflamed tissue is strongly contraindicated infection at the puncture site can lead to the introduction of bacteria into the bloodstream during the procedure potentially causing systemic infections health providers must ensure that the insertion site is free from signs of infection including redness warmth swelling and tenderness ral's disease is a vasospastic disorder that leads to exaggerated episodic narrowing of blood vessels in response to cold temperatures or emotional stress this extreme Vaso constriction can result in compromised blood blood flow to the extremities patients with brainal disease are at a higher risk for vascular complications making arterial line insertion contraindicated the reason being is this procedure could trigger a vasospastic attack further reducing blood flow and potentially causing severe pain and tissue damage previous vascular surgery or interventions in the vicinity of the proposed arterial line insertion site can complicate the procedure Scar Tissue altered vascular Anatomy or residual vascular abnormalities may increase the risk of complications such as bleeding vessel damage or catheter misplacement in such cases alternative monitoring methods or the consideration of a different insertion site may be necessary to avoid potential hazards contraindications to arterial line placement are critical for health care providers to consider in order to ensure patient safety and reduce the risk of Adverse Events a thorough assessment of the patient's medical history clinical condition and Vascular status is essential before proceeding with arterial line insertion if contraindications are present Healthcare team should explore alternative monitoring methods and strategies to manage the patient effectively while minimizing potential risks and complications complications associated with arterial lines though relatively rare are important to be aware of to ensure the safety of patients and the effectiveness of the procedure let's look at a few of the most common complications one arterial line thrombosis this complication involves the formation of a blood clot within the arterial line or the artery itself potentially obstructing blood flow thrombosis can hinder accurate pressure monitoring and lead to distal tissue esea two in imization embolization occurs when a clot or debris dislodges from the arterial line or catheter and travels Downstream potentially causing vascular occlusion or ES schic events in distal tissues three hematoma hematomas are collections of blood that can develop at the insertion site sometimes resulting in injury to the surrounding vessels during the procedure four insertion sight infection localized infection at the insertion site can lead to systemic infections or sepsis if not promptly addressed five median nerve neuropathy insertion of an arterial line into the radial artery carries the risk of damaging the median nerve poten leading to neuropathy or sensory motor deficits six pseudoaneurysm of the artery these can develop when a leak occurs from the arterial wall causing blood to accumulate outside the artery these may require intervention to prevent complications seven esic necrosis severe complications may lead to localized tissue necrosis due to impaired blood supply eight digit hand leg or foot esea this outcome can occur if the arterial line or catheter disrupts blood flow to these areas nine Hemorrhage excessive bleeding at the insertion site or along the catheter tract can lead to hypovolemia hemodynamic instability and an increased risk of infection 10 air embolism the introduction of air into the arterial system can lead to an air embolism which can block blood flow and be life-threatening 11 arterovenous fistula this is an abnormal connection between an artery and a vein that can develop as a result of arterial line insertion this can lead to hemodynamic disturbances and does require surgical intervention 12 arterial aneurysm in rare instances the arterial wall May weaken and dilate forming an aneurysm providers should be well versed in the prevention recognition and management of these complications in order to minimize risks associated with arterial line placement procedural expertise aseptic technique and Vigilant monitoring are crucial to reduce the incidence of these potential issues and ensure patient safety the Allen test is a crucial pre-procedure assessment performed before radial artery arterial line catherization to evaluate extremity profusion and the function of the oler artery this test involves several key steps firstly The Examiner compresses both the radial and oler arteries to temporarily block blood flow to the hand subsequently The Examiner releases pressure on the oler artery while maintaining radio artery compression during this release the examiner observes the hand closely for color changes if adequate collateral circulation is present the hand should quickly regain its normal color within approximately 6 seconds the Allen test is essential to ensure that the radial artery can be safely canulated as it assesses the viability of the owner artery as a collateral blood supply appli to the hand this step helps prevent complications and esea in the event of radial artery catherization as it ensures that alternative circulation pathways are available in case of potential issues let's look at a quick video Allen's test is used to assess arterial sufficiency to the hand to perform this test ask the patient to clench her fist while you clamp down firmly on both the olner and Radial arteries once the patient has clenched her fist for a period of approximately 30 seconds release one of the arteries return of color to the hand indicates that the blood flow is adequate from that arterial Supply you can repeat the test for the other artery obtaining invasive hemodynamic measurements involves several important steps once the arterial catheter is correctly placed into the patient it needs to be connected to a pressure monitoring transducer via a rigid pressure monitoring tubing system this connection ensures that the realtime arterial pressure measurements can be accurately transmitted to the monitoring equipment the transducer acts as a crucial intermediary converting the pressure waveform into an electrical signal that can be displayed in monitor in real time to maintain the patency and accuracy of the pressure monitoring line and the fluid filled system a continuous flush solution system is essential this system is typically placed into a disposable pressure bag that is filled with sterile normal saline or a similar solution maintaining a continuous flush is crucial to prevent the catheter from becoming obstructed or or clogged ensuring accurate and reliable pressure measurements this pressurized system helps to keep the catheter's Lumen open and clear of any potential clots or debris which could otherwise lead to inaccurate or delayed measurements once the monitoring system is connected to the patient and the transducer the pressure bag is inflated to a standardized pressure typically set at 300 mm of mercury or slightly higher than the patient's blood pressure this inflation of the pressure bag ensures a continuous and stable flow of flush solution through the catheter maintaining its patency and the accuracy of the pressure readings when the pressure in the monitoring system surpasses the patient's actual blood pressure the transducer functions to release a controlled volume of flush solution into the patient's arterial catheter in most cases each transducer will release approximately 3 MLS of flush solution per hour this mechanism serves two essential purposes firstly it helps to prevent clot formation or any potential obstruction within the catheter which could obstruct the blood flow or cause inaccuracies in the pressure findings secondly The Continuous flush of solution serves as a barrier preventing blood from flowing back into the catheter and the monitoring system this not only maintains the patency of the catheter but also prevents retrograde contamination of the monitoring equipment The Continuous flush system is instrumental in maintaining the patency of the arterial catheter while also safeguarding the Integrity of the pressure monitoring system it acts as a reliable and consistent method to ensure that the catheter remains clear of any obstructions and clot formation which could disrupt the flow of blood or compromise the accuracy of pressure measurements moreover the flow of flush solution serves as a dynamic seal that prevents any retrograde flow of blood effectively isolating the monitoring system from the patient's arterial system this preventive measure helps to ensure that the monitoring system remains free of any contamination keeping the measurements accurate and the patient safety a top priority during the entire monitoring process when preparing for air Medical Transport several important measures should be taken to ensure the accuracy and reliability of invasive hemo Dynamic monitoring first and foremost it's crucial to expel all air from the pressure bag to prevent any potential expansion during flight which could lead to inaccurate pressure readings additionally after the pressure bag is correctly inflated it's essential to turn off the air supply to avoid accidental deflation and periodic checks should be conducted throughout the journey to maintain proper inflation levels moreover setting monitoring alarms at the appropriate thresholds is a fundamental protective measure against potential issues such as catheter dislodgment or dislocation which could compromise the Integrity of the monitoring system by establishing and adhering to these best practices healthc care providers can ensure the reliability of invasive hemodynamic measurements during air Medical Transport obtaining accurate direct hemodynamic pressure measurements is important for making informed clinical decisions and one of the most prevalent sources of error in this process is the incorrect leveling of the transducer proper alignment of the transducer at Mid Heart level is essential as any deviation whether it's higher or lower can result in inaccurate pressure readings due to the influence of hydrostatic pressure on the fluid filled pressure tubing in cases where the transducer is positioned above the midlevel heart it can underestimate the true pressure values while placement below this level can lead to overestimation these errors can have significant clinical consequences but potentially leading to incorrect diagnosis or treatment decisions meticulous attention to transducer leveling is Paramount to ensure the reliability and precision of hemodynamic pressure measurements in critical care settings leveling the hemodynamic pressure transducer to match the level of the left atrium is a critical procedure in the AC accurate measurement of invasive pressures as it helps to negate the influence of hydrostatic pressure in the fluid filled monitoring system it's important to emphasize that this leveling must be meticulously maintained especially during patient position changes to ensure consistent and reliable pressure readings one practical approach to maintaining proper transducer alignment particularly during patient transport is to secure the transducer to the fipo static axis a point on the chest wall that approximates the level of the left atrium by fixing the transducer to this anatomical reference clinicians can help mitigate errors related to Patient positioning enhancing the Precision of hemodynamic monitoring and ultimately facilitating more informed clinical decisions and critical care and emergency settings leveling the hemodynamic pressure transducer should be conducted using precise tools such as a carpenter's level or specialized leveling instruments tailored for hemodynamic monitoring this process ensures that the transducer accurately reflects the level of the left atrium enhancing the Fidelity of pressure readings zeroing the pressure transducer is a crucial step to eliminate any impact of atmospheric pressure on the measurements this procedure effectively establishes a baseline for pressure readings ensuring that changes in pressure are due to physiological factors rather than external atmospheric variations combined proper leveling and zeroing are vital in providing accurate reliable hemodynamic data various transducer brands with unique fast flush systems are accessible for hemodynamic monitoring and are often categorized into two common Styles the squeezable style and the pull style the inclusion of fast flush mechanisms is integral to these systems permitting healthc care providers to temporarily bypass the standard delivery of 3 MLS an hour of flush solution this feature is particularly valuable when confronting issues such as dampened or absent pressure waveforms by engaging the fast flush option clinicians can swiftly and forcefully introduce flush solution to clear potential obstructions or ensure unimpeded communication between the patients's arterial catheter and the monitoring equipment a critical care transport professional should acquire a strong familiarity with transport monitors and the accompanying cables required to establish connections with pressure monitoring equipment and transducers these cables serve as the essential bridge between the patients's arterial catheter and the monitoring equipment ensuring the accurate and continuous hemodynamic data is relayed for prompt assessment and intervention moreover it is imperative that these cables are compatible with the equipment used both by the referring facility and the Receiving Hospital to guarantee seamless and uninterrupted monitoring during patient transfer asepsis stands as a Cornerstone of patient care particularly when dealing with the insertion of catheters which compose a substantial risk of introducing bacterial and fungal infections from central line Associated bloodstream infection one of the pivotal aspects of the prevention of central line Associated bloodstream infections is the recognition that it is entirely preventable through the application of evidence-based practices these practices Encompass a multifaceted approach aimed at reducing the risk of infection at every stage of catherization to ensure the highest level of asepsis Health Care Providers must adhere to strict aseptic techniques and guidelines this involves maximizing sterile barrier precautions which may include removing any unnecessary Personnel from the room ensuring that healthcare workers wear masks caps gowns and sterile gloves while employing full body draping to create a controlled and sterile environment for the procedure hand hygiene plays a fundamental role in preventing central line Associated bloodstream infections emphasizing the importance of healthc care workers maintaining strict cleanliness the use of chlorohexidine for skin antisepsis is another crucial element in reducing infection risk careful selection of the catheter insertion site is also important as certain areas are more prone to infection than others additionally after catheter insertion it's essential to follow best practices for dressing the catheter site notably one of the key strategies in prevention is the use of catheter tubing with multiple ports which allows for various therapeutic interventions without the need for reinsertion adding multiple port adapters to catheter hubs facilitates the management of central lines streamlining the care process and further reducing the risk of infection transmission during any",
        "Central Venous Lines": "insertions Central Venus lines Central Venus lines also known as C Central Venus catheters are indispensable medical devices that find application in a wide range of clinical settings they are inserted into the central Venus system affording Health Care Providers access to the core vessels of the body which include the superior vena inferior vena and the right atrium these lines play a pivotal role in the administration of various therapies including intravenous medic medications blood products and parental nutrition moreover they serve as crucial conduits for hemodynamic monitoring and blood sampling the right internal jugular vein stands out as the preferred site for Central Venus line insertion due to its relatively straightforward accessibility making it a favorable choice for health care providers seeking to efficiently establish Central Venus access while minimizing patient discomfort and procedural complexity aside from the right internal jugular vein subclavian sites are also commonly preferred due to their Associated lower infection risk when compared to other options this is because the subclavian approach minimizes the likelihood of contamination from orifices such as the mouth which is a concern with internal jugular or femoral sites while subclavian sites are often the top choice for Central Venus line insertion other locations are utilized when necessary or when a specific clinical condition dictates among these femoral and brachial veins are commonly used it is important to note that femoral lines despite their convenience are strongly discouraged for adults due to their higher higher risk of infection the ideal placement of the catheter involves advancing it until the tip resides just outside the right atrium specifically inside the superior vnea this positioning is critical for accurate Central fenus pressure or CVP monitoring CVP measurements are valuable in assessing right ventricular preload intravascular volume status and right heart function the normal range for CVP is typically considered to be 0 to -2 mm of mercury but it's essential to interpret these values in the context of the patients overall condition and clinical presentation most monitors designed for critical care patients measure CVP with the presumption that the patient is mechanically ventilated ensuring that the readings accurately reflect the patient's hemodynamic status let's take a look at the wide range of clinical indications for Central Venus lines one rapid fluid replacement one of the primary indications for Central Venus lines is the need for Rapid fluid replacement in emergency situation such as severe hypovolemia septic shock or trauma Central Venus access allows for the Swift administration of large volumes of intravenous fluids directly into the central circulation providing rapid resuscitation to stabilize a patient's hemodynamic status two medication administration Central Venus lines offer an efficient means of administering medications especially those that can be harsh on peripheral veins irritate vessel walls or require precise dosing they also facilitate the administration of drugs that need to be administered slowly or continuously making them ideal for patients receiving vasoactive agents chemotherapy or parental nutrition three rapid access to Central circulation in critical care scenarios gaining rapid access to Central circulation is crucial Central Venus lines can be inserted promptly and critically ill patients to facilitate blood draws hemodynamic monitoring or the introduction of life-saving interventions such as inotropes or vasor pressors and four invasive monitoring Central Venus lines provide an ideal conduit for invasive hemodynamic monitoring enabling healthc care providers to directly measure Central Venus pressure pulmonary artery pressure or other important hemodynamic parameters this information is invaluable in managing patients with complex cardiovascular conditions heart failure and those undergoing major surgeries Central Venus lines while valuable in VAR clinical situations have specific contraindications that healthc care providers must consider to ensure patient safety one significant coagulopathy coagulopathy refers to a disorder of blood clotting where a patient's ability to form clots is impaired this is a contraindication because the insertion of a central Venus line May pose a risk of significant bleeding hematoma formation or other bleeding complications in patients with coagulopathy these risks are heightened and alternative access routes or correction of the coagulation disorder may be necessary before considering Central Venus access two trauma to the insertion site if the chosen site has sustained recent trauma or injury it may not be suitable for Central Venus line placement trauma to the surrounding tissues can result in local inflammation tissue damage or infection which can increase the risk of complications during and after the procedure providers should assess the insertion site carefully and choose a location that is free from recent injury or trauma and three infection of the site of insertion in me sign of infection at the intended insertion site is a clear contraindication inserting a central Venus line in an area with an existing infection increases the risk of introducing bacteria into the bloodstream potentially leading to a serious infection such as central line Associated bloodstream infections patients with local signs of infection such as redness swelling warmth or drainage at the site should have the infection treated and resolved before the central Venus line is considered Central Venus lines are valuable for various indications but just like any medical procedure they come with potential complications that healthc care providers must be aware of one Numa thorax and hemothorax ATT attempting subclavian vein insertion can lead to a pnea thorax or a hemothorax if there is inadvertent lung or blood vessel puncture these complications can result in respiratory distress chest pain or other lifethreatening conditions making careful placement essential two air embolism an air embolism occurs when air enters the central Venus system and travels to the heart and lungs this can cause significant problems including cardiac arrhythmias trouble breathing and even sudden death preventing air entry into the line during insertion and maintenance is critical three infection infections can occur at the insertion site or within the central line central line Associated bloodstream infections are a particularly severe concern and can lead to sepsis and increase mortality if not managed promly number four thrombosis blood clots can form around or within the catheter potentially leading to vessel blockage embolism and catheter malfunction this may necessitate anti-coagulation or thrombotic therapy five fitis inflammation of the vein called fitis can result from catheter irritation or infection symptoms include redness warmth swelling and pain at the insertion site six limb esea in rare cases the catheter May compromise arterial circulation leading to Lim esea which would necessitate immediate removal or repositioning of the line seven arterial puncture misplacement of the catheter can lead to inadvertent arterial puncture increasing the risk of bleeding complications hematoma formation and thrombosis eight improper placement catheter misplacement can occur within the vessel leading to inadequate Central Venus access or incorrect positioning affecting the utility of the line nine myocardial perforation while rare this is very serious myocardial perforation can occur during insertion potentially causing pericardial affusion and cardiac tampeno 10 thoracic duck injury thoracic duct injury although infrequent can result from catheter placement in the subclavian or jugular veins this can lead to kylo thorax a condition characterized by Kyle or lymphatic fluid leaking into the plural space 11 nerve injury in cases of brachial or subclavian vein insertion nerve injury is a rare possibility and can cause sensory or motor deficits in the upper extremity 12 catheter occlusion catheter occlusion May hinder medication or fluid therapy this requires prompt intervention such as flushing or catheter replacement 13 sluggish infusion catheter related factors can result in sluggish infusion affecting the timely administration of medications or fluids 14 catheter damage catheter damage can occur during placement or manipulation necessitating removal and replacement to prevent leakage or further complications lastly 15 blood withdrawal problems issues with blood withdrawal from the central Venus line can affect diagnostic testing making regular catheter maintenance and flushing crucial healthc care providers must be Vig in assessing patients using proper insertion techniques adhering to aseptic guidelines and monitoring for early science of complications in order to minimize the risks associated with Central Venus lines and optimize patient outcomes there are several different types of central Venus catheters available each designed to meet specific specific clinical needs triple Lumen catheters are versatile devices with three separate lumens or channels that can be used for various purposes each Lumen can be employed for photomy or the administration of fluids and medications this flexibility makes them particularly valuable in settings where multiple intravenous treatments are required simultaneously in critical care in emergency scenarios two lumens can be used for fluid administration while the third can be utilized for monitoring Central Venus pressure aiding in hemodynamic assessments the Hickman catheter is a long-term catheter designed for both Venus access and blood withdrawal it can be inserted into veins like the calic subclavian or external and internal jugular veins allowing for physician preference or patient specific factors to guide the choice of insertion site the catheter exits the lower part of the Interior chest wall through a subcutaneous tunnel to maintain patency and prevent clotting routine flushing is essential especially after each use or when blood is drawn potential complication s include line clotting catheter breakage and infection catheter related infections can manifest potentially progressing antiseptic shock gron catheters are thinner and more flexible than some other catheters making them a preferred choice for certain patients these catheters often feature up to three lumens and incorporate a subcutaneous cff unlike traditional catheters gon catheters are designed with a pressure sensitive two-way valve on the lateral wall this Innovative feature minimizes blood backflow into the catheter thus reducing the need for regular clamping and frequent flushing typically a saline flush is required after each use or once daily to maintain line integrity the porath is a unique catheter consisting of a titanium chamber with a catheter the device threads under the patient's skin directly accessing the subclavian vein and terminating in the right atrium this design enables the administration of fluids medications and blood draws without daily care or maintenance A specialized Huber need needle is used to access the port which is self-sealing with a rubberlike top portic caths can remain in place for extended periods allowing patients to maintain an active lifestyle however potential disadvantages include the rare occurrence of Kinks ruptures and infections lastly we have the pick line pick lines are suitable for patients requiring medium duration to long-term Venus access they are inserted through veins in the arm such as the brachial vein and advanced until the catheter tip reaches the superior vnea just outside the atrium pick lines provide a reliable route for medications and fluids as well as blood withdrawal making them suitable for patients with extended treatment needs to prevent clotting pick lines require regular flushing with a saline solution and low dose werin may be prescribed in cases of recurrent clotting issues nonetheless pick lines do come with some restrictions as they can limit arm mobility and may preclude intense physical activities such as swimming each type of central Venus catheter offers distinct advantages and may be chosen based on the patient's clinical requirements expected duration of use and other considerations Central Venus catheter placement is a medical procedure that is typically carried out by physicians nurses or specially trained Health Care Providers while Critical Care transport professionals might not commonly perform this procedure understanding the process and Equipment involved is valuable for background knowledge the following outlines the steps involved in central Venus catheter placement to perform a central Venus catheter insertion a variety of equipment is needed including catheters of different sizes and lengths syringes both a 5 and 10 mL for medication at Administration and blood withdrawal saline flush solution for line maintenance chlorohexidine solution for skin antisepsis a j tipped guide wire to navigate the vasculature intravenous tubing and fluids for patient hydration suture materials for wound closure occlusive dressings to secure the catheter site sterile drape AP for maintaining a sepsis tape for catheter stabilization and a local anesthetic to numb the insertion site during and after placement providers need to be prepared to troubleshoot potential issues some common problems that may arise include sluggish infusion making it difficult to administer medications or fluids an inability to withdraw blood from the cathet which can hinder diagnostic tests and catheter damage which might necessitate device removal or replacement proper technique and adherence to aseptic guidelines are essential to prevent these complications it's important to note that Central Venus catheter placement is a complex procedure that requires thorough training and expertise to ensure patient safety and the successful delivery of Medical Care Critical Care transport providers typically work in collaboration with medical teams and their roles primarily focus on Patient Care Transportation and monitoring rather than performing these invasive procedures",
        "Pulmonary Artery Catheters": "themselves pulmonary artery catheters the pulmonary artery catheter or PAC is a specialized catheter used in critical care and invasive hemodynamic monitoring it is designed with a balloon at its tip which when inflated allows the pressure of the flowing blood to carry the catheter through the heart and into the pulmonary artery this invasive monitoring tool provides valuable information about the patient's cardiac function and fluid status by measuring various pressures within the heart and pulmonary circulation while the use of pac's has evolved over the years they remain a vital component of managing critically ill patients allowing healthc Care Professionals to make informed decisions about treatment and interventions to optimize patient care the pulmonary artery Cath often referred to as the swan Gans catheter is named after the Physicians Harold Jeremy Swan and William Gans who introduced it in 1970 it's important to note that the PAC is primarily a diagnostic device not a therapeutic one and interpreting the data it provides requires substantial knowledge and expertise this Advanced monitoring tool is typically used in intensive care settings by Health Care Professionals with specialized training as its usage carries inherent risks and necessitates a deep understanding of hemodynamics and cardiac physiology the PAC is introduced into the patient's vascular system through the same access routes as a central line typically entering through a large vein and advancing through the right atrium into the pulmonary artery once the catheter has passed the Lumen of the introducer sheath the catheter's tip balloon is inflated with 1.5 MLS of air aiding in its further advancement with the balloon inflated the catheter is gently guided through the right atrium and into the right ventricle before ultimately wedging into a proximal branch of the pulmonary artery after reaching its desired location the balloon is deflated to allow blood to flow unimpeded around the catheter the PAC is approximately 43 in long and contains multiple lumens that terminate at various points along its length corresponding to different locations within the heart two of these lumens are connected to pressure transducers contain continuously displaying readings the first reading obtained is the right atrial pressure with the second reading being the pulmonary artery pressure providing valuable insights into the patient's hemodynamic status complications of pulmonary artery catheter insertion closely resemble those of central line ins insertion and include issues such as pneumothorax hemothorax infection thrombosis and so on since we've already covered these we're not going to go back through them again however Pac insertion presents additional risks including pulmonary artery perforation or rupture pulmonary infarction arrhythmias tricuspid and pulmonic valve injury tanod and catheter nodding of particular concern is the potential for misinterpretation of data by clinicians which can lead to inappropriate therapy and worsened patient outcomes accurate interpretation of Pac data is crucial due to the invasive nature of the device and the complexity of the information it provides making proper training and expertise essential a thermore is a crucial component connected to the distal end of a pulmonary artery catheter when it's used for thermodilution cardiac output measurement the thermore serves the dual purpose of providing both continuous readings of pulmonary artery temperature and serving as the primary indicator of core body temperature this continuous temperature monitoring is essential for accurate Co measurement through the thermodilution method as changes in blood temperature are used to calculate the cardiac output making the thermore an integral part of hemodynamic monitoring during Critical Care interventions a quick word on Thermo dilution this is a technique used to me measure cardiac output which is the amount of blood pumped by the heart per minute in thermodilution a known volume of cold or room temperature saline which is the delusion is rapidly injected into the right atrium or a proximal part of the pulmonary artery through a catheter typically a pulmonary artery catheter this Bolis a saline then mixes with the warmer blood in the heart's chambers and in the pulmonary artery by measuring the temperature changes in the blood as it passes to the pulmonary artery a computerized monitoring system can calculate the cardiac output the rate of temperature change the temperature difference between the dilution and the blood and the volume of the injected dilution are all factors used in this calculation thermodilution provides valuable data on cardiac function making it an essential tool in assessing and managing patients with various cardiovascular conditions the use of a pulmonary artery catheter is typically considered when clinicians encounter complex clinical scenarios in which non-invasive assessment alone does not provide sufficient information to answer critical questions about a patient's hemodynamic status the PAC plays a valuable role in the following key indications one the differentiation among causes of shock when a patient presents with shock which can result from various underlying causes the PAC can help differentiate between these causes for example it can assist in distinguishing between cardiogenic shock caused by heart dis function hypovolemic shock due to fluid loss or distributive shock as seen in sepsis this is crucial for tailoring specific treatment strategies to the underlying cause two determining mechanisms responsible for pulmonary edema pulmonary edema is a condition characterized by the accumulation of fluid in the lungs the PAC is use for identifying the mechanisms contributing to pulmonary edema it can distinguish between cardiogenic pulmonary edema which is often caused by heart failure and non-cardiogenic pulmonary edema which can result from conditions like acute respiratory distress syndrome or Arts three evaluation or diagnosis of intracardiac shunts intracardiac shunts involve abnormal blood flow patterns within the heart such as in atrial sepal defects or ventricular sepal defects the PAC can help in diagnosing the presence of these shunts and assessing their hemodynamic impact four evaluation and treatment of pulmonary hypertension pulmonary hypertension characterized by high blood pressure in the pulmonary arteries can be caused by a variety of conditions the PAC is instrumental in evaluating the severity of pulmonary hypertension and guiding treatment Decisions by providing accurate measurements of pulmonary artery pressure and Pulmonary vascular resistance five peroperative and post-operative management of patients with unstable cardiac status in surgical settings especially complex cardiac procedures it's essential to closely monitor a patient's hemodynamics cardiac output and pulmonary artery pressures the PAC can help guide therapeutic interventions optimize fluid balance and ensure the patients cardiovascular stability through the peroperative and post-operative periods six management of complex myocardial infarction the PAC is valuable in the management of complex myocardial infarction patients who experience severe Mis often face hemodynamic instability and the PAC can provide real-time data on cardiac output pulmonary artery pressures and other relevant parameters this information assists clinicians in tailoring treatment strategies including the administration of medications or interventions like intraaortic Bloom pump placement to enhance coronary profusion and support the patient's cardiovascular function seven care of patients undergoing cardiac operations in patients undergoing cardiac operations especially those with complex surgical needs the PAC offers crucial insights into hemodynamics helping surgical teams make informed decisions during the procedure and in the early post operative period to optimize patient outcomes the PAC AIDS in monitoring cardiac function assessing fluid status and guiding the use of inotropic or vasoactive agents to maintain cardiovascular stability in these critical situations eight guidance for titration of inotropic vasopressor or vasodilator therapy in cases of hemodynamic instability or shock the PAC can provide realtime data on cardiac output pulmonary artery pressures and other parameters this information helps clinicians optimize the dosing of inotropic Agents such as tiamin and epinephrine vasopressors such as nor epinephrine and vasopressin or vasodilators such as nitroglycerin to improve cardiac function and systemic vascular resistance ensuring appropriate profusion and blood pressure nine complex fluid volume status Management in patients with complex fluid management needs such as those with acute kidney injury the PAC can assist in assessing fluid responsiveness it provides information on right atrial pressure which helps guide the administration of fluids diuretics or renal replacement therapy 10 assessment of cardiac performance the PAC offers valuable data for evaluating cardiac performance including parameters like cardiac output and pulmonary artery wedge pressure clinicians can assess cardiac function differenti iate between high and low output States and make informed decisions regarding medications mechanical support and other interventions 11 evaluation of patients for heart lung or Heart and Lung transplantation in these candidates the PAC AIDS in assessing pulmonary vascular resistance and and right ventricular function these assessments are crucial for determining the suitability of a patient for transplantation and guiding the peroperative management of transplant recipients contraindications for Pac placement one significant coagulopathy as discussed earlier coagulopathy refers to a disorder where the blood's ability to clot is impaired it can pose a significant risk during Pac placement patients with severe coagulation abnormalities such as those with very low platelet counts or impaired clotting Factor function are at a high risk of bleeding complications during or after the procedure in such cases the the potential benefits of Pac placement must be carefully weighed against the increased risk of bleeding two local trauma to the site of insertion if the site selected for Pac insertion has recently suffered local trauma it may not be suitable for catheter placement trauma at the insertion site can include bruising hematoma or damage to the blood vessels attempting to insert a Pac in such a compromised area can lead to further damage and complications three infection at the site of insertion an active infection at the intended insertion site is a contraindication for Pac placement infection can introduce pathogens directly into the bloodstream during the procedure leading to serious complications like catheter related bloodstream infections and four inability to float the PAC into the pulmonary artery successful Pac placement involves floating the catheter through the right atrium and into the pulmonary artery under fluroscopic or other guidance in some cases due to anatomical variations obstructions or other factors it may be impossible to advance the catheter into the pulmonary artery in such situations attempting to force the catheter further can lead to complications and is a contraindication overall Contra indications are important factors to consider when deciding whether to proceed with Pac placement as patient safety and potential risks must be carefully evaluated on a case-by Case basis the placement of a pulmonary artery catheter involves the use of specialized equipment and a carefully orchestrated procedure here is a brief explanation of the equipment used one the pulmonary artery catheter the PAC itself is a central component of the procedure it's a long flexible catheter with multiple lumens that terminate at various points along its length two the PAC introducer kit the kit is essential for creating the initial access point it must be 0.5 French to one French larger than the PAC it includes components like the introducer sheath and guide wire necessary for threading the PAC into the pulmonary artery three sterile gowns and drapes sterile gowns and drapes are used to create a sterile field around the patient's insertion site and the surrounding area to minimize the risk of infection number four ECG and pulse oxymetry monitoring continuous ECG and pulse oxymetry monitoring as well as intitle CO2 is employed to closely track the patient's heart rhythm and oxygen saturation levels throughout the procedure five transducer setup a transducer setup is essential for real-time monitoring of pressure measurements during and after the PAC placement the transducer is connected to the catheter's lumens to continuously display measurements six patient Monitor and cables the patient monitor along with the necessary cables is used to display and record data from the transducer setup allowing the healthcare team to closely monitor the patient's hemodynamics seven thermodilution Co set this set includes a thermore which is used for Thermo dilution cardiac output measurements it provides continuous readings of pulman artery temperature which is crucial for Co calculations eight antiseptic solution an appropriate antiseptic solution such as chlorohexidine is used to clean and disinfect the insertion site to minimize the risk of infection during the procedure N9 linee and atropine lie can is a local anesthetic used to numb the insertion site making the procedure more comfortable for the patient atropine should be on hand to treat arrhythmias that can occasionally occur during the PAC placement helping stabilize the patient's heart rhythm the PAC placement procedure demands careful coordination and the use of specialized equipment to ensure accurate and safe catheter insertion and hemodynamic monitoring",
        "Invasive Pressure Measurements": "invasive pressure measurements here's an expansion on common hemodynamic parameters and how they are typically obtained we will go in depth into each one of these later on in the lecture Central Venus pressure Central Venus pressure represents the pressure within the central Venus system and is often measured using a central line placed in large veins like the internal jugular or subclavian veins alternatively large bore and a cubicle lines or pulmonary artery catheters can be used for CVP measurements it reflects the right atrial pressure and provides information about the heart's ability to fill with blood stroke volume variation pulse pressure variation and pleth variability index svv and ppv are Dynamic parameters used to assess fluid responsiveness and are typically derived from an arterial line waveform they indicate how changes in stroke volume or pulse pressure are related to the patient's respiratory cycle pvi is a dynamic par parameter measured using the pleth waveform obtained from a pulse oximeter providing insights into fluid status and profusion systolic blood pressure systolic blood pressure is the highest pressure in the arterial system during ventricular contraction known as syy it can be measured directly from an arterial line are calculated when using an electronic cuff stolic pressure is the lowest pressure in the arterial system during ventricular relaxation also known as diast similar to the systolic pressure diastolic pressure can be measured directly from an arterial line or calculated using an electronic cuff mean arterial pressure mean arterial pressure represents the average pressure in the arteries throughout the cardiac cycle and can be measured directly using an arterial line or calculated when using a blood pressure cuff map is an extremely important parameter for assessing profusion pressure pulse pressure pulse pressure is a difference between the systolic blood pressure and the diastolic blood pressure and is an indicator of stroke volume providing information about the strength of each heartbeat pulmonary artery pressure these parameters are measured using a pulmonary artery catheter that is inserted into the pulmonary artery they provide insights into the pressure in the pulmonary circulation pulmonary capillary wedge pressure or pcwp pcwp is obtained through a Pac and is used to assess left ventricular preload it reflects the pressure in the left side of the heart cardiac output cardiac output is also measured using a Pac and is calculated based on the thermodilution method it represents the volume of blood ejected by the heart per unit of time pulmonary vascular resistance pulmonary vascular resistance is calculated from data obtained through a Pac and used to assess the resistance in the pulmonary circulation which is important in cases of pulmonary hypertension systemic vascular resistance systemic vascular resistance is calculated based on data obtained through a Pac and is used to assess the resistance in the systemic circulation indicating the pressure that the left ventricle must overcome to pump blood to the body stroke volume stroke volume is calculated using data obtained from a Pac and is an important component of determining cardiac output as it reflects the volume of blood ejected by the left ventricle with each heartbeat mixed Venus oxygen saturation this parameter is measured using a Pac and provides information about the balance between oxygen delivery and consumption aiding in the assessment of tissue oxygenation Central Venus oxygen saturation Central Venus oxygen saturation is measured using a central line and provides insights into overall tissue oxygenation helping to assess the balance between oxygen supply and demand total body surface area or tbsa tbsa is calculated based on a patient's height and weight and is used for determining factors like fluid resuscitation needs in burn patients as it provides an estimate of the body's surface area cardiac index the cardiac index is calculated from cardiac output obtained through a Pac and taking into account a patient's body surface area this allows for the assessment of cardiac performance relative to the patient's size aiding in the interpretation of cardiac output data lastly ejection fraction ejection fraction is measured using ultrasonography and is a vital parameter for evaluating the left ventricles pumping efficiency helping in the diagnosis and management of heart conditions it indicates the percentage of blood ejected from the left ventrical during syy these parameters help provide valuable insights into a patient's hemodynamic status and are important for guiding clinical management and critical care and peroperative settings the method of measurement may vary with some parameters obtained through invasive monitoring techniques While others can be calculated or assessed using non-invasive methods measuring arterial blood pressure using arterial line is a critical component of hemodynamic monitoring and Health Care settings one of the primary advantages of using an arterial line to measure blood pressure is the ability to provide continuous and real-time assessment of arterial or systemic pressure this continuous monitoring is crucial for patients who require close hemodynamic management such as those in critical care or undergoing complex surgical procedures the arterial line provides continuously updated values for systolic blood pressure diastolic blood pressure and mean arterial pressure these Dynamic parameters offer detailed insights into the patient's circulatory status and can help clinicians make timely and informed decisions in addition to numerical values arterial lines also generate an arterial waveform this waveform visually represents the pressure changes within the arterial system through each cardiac cycle it offers valuable information about the patient's cardiac performance such as the strength of ventricular contractions and the compliance of the arterial system continuous BP monitoring with an arterial line is particularly valuable in situations where rapid changes in BP are expected or where tight control of BP is necessary it allows providers to detect and respond to hemodynamic shifts promptly which can be critical in managing patients with severe illnesses during surgeries or in trauma care the data provided by the arterial line contributes to a more comprehensive understanding of the patient's cardiovascular status and facilitates the adjustment of interventions and treatments as needed the arterial waveform generated by an arterial catheter is a graphical representation of pressure changes in the arterial system throughout the cardiac cycle understanding its components is important for interpreting hemo Dynamic data the dtic notch is a distinctive point on the arterial waveform occurring just after the closure of the aortic valve it marks the end of syy and the beginning of diast the notch is caused by The Recoil of the aortic valve leaflets which briefly interrupt the smooth Descent of pressure in the aorta mean arterial pressure is represented on the arterial waveform as a horizontal line it reflects the average pressure within the arteries over the cardiac cycle and is a critical parameter for assessing perfusion syy corresponds to the period of the cardiac cycle where the heart contracts and ejects blood into the arterial system this phase is associated with the rise in arterial pressure and is represented as the ascending limb of the wave form diast is the phase when the heart relaxes and refills with blood the corresponding arterial pressure drop is displayed as a descending limb of the waveform diastolic pulse pressure is the difference between the diastolic blood pressure and the minimum pressure within the aorta during diast it provides specific insights into the arterial systems elasticity and resistance mean arterial pressure is a hemodynamic parameter that offers insights into the average pressure experienced by the arterial system throughout the cardiac cycle it provides a more comprehensive understanding of arterial profusion compared to individual systolic and diastolic blood pressure pressure measurements mean arterial pressure also known as map is calculated by specialized transport monitor software that quantifies the mean area under the arterial pulse pressure waveform which is obtained from an arterial line one significant advantage of map is that it is not influenced by the specific location of the arterial line placement making it a reliable and consistent parameter for evaluating a patient's hemodynamic status this uniformity is especially important in clinical settings where variations in arterial Anatomy can occur the map serves as a valuable reference point for healthcare providers when making critical treatment decisions as it helps ensure that organs and tissues receive adequate blood flow oxygen and nutrients for optimal physi ological functioning and tissue profusion individuals typically require a map within the range of 70 to 105 this range represents the target values for maintaining adequate organ profusion while avoiding the risks associated with excessively high or low blood pressure deviations from this range May necessitate intervention such as adjusting medications or fluid administration to bring the patient hemodynamics back into a safe and optimal range therefore the map plays a central role in guiding clinical management particularly in critical care and peroperative settings calculating map is not extremely difficult map equals your diastolic pressure plus a third of the systolic pressure minus the diastolic pressure pulse pressure is calculated by finding the mathematical difference between the systolic blood pressure and the diastolic blood pressure in essence pulse pressure represents the variation between the highest and lowest arterial blood pressures recorded during a cardiac cycle normal pulse pressure typically Falls within the range of 40 60 mm of mercury several factors influence pulse pressure including stroke volume and Vascular compliance an increase in stroke volume or a decrease in vascular compliance results in an elevated pulse pressure pulse pressure is a valuable parameter as it offers insights into the interaction between the heart's pumping action and the blood vessel's ability to expand and contract Additionally the fast flush feature is employed to assess the accuracy of arterial lines or transduc pressures and conduct Dynamic response tests like the square wave test or fast flush test these tests provide a means to verify the functionality and precision of hemodynamic monitoring equipment and their ability to accurately depict rapid changes in pressure Central Venus pressure is a critical hemodynamic parameter obtained through a central Venus line typically inserted into the internal jugular or subclavian vein Central Venus pressure also known as CVP provides valuable information about the pressures in the superior vnea and the right atrium reflecting the right side of the hearts hemodynamic status the waveform comprises three distinctive positive deflections each representing different phases of the cardiac cycle the a wve corresponds to atrial contraction when the right atrium contracts to push blood into the right ventricle the c-wave represents the closure of the tricuspid valve leading to a small increase in pressure during isov volumetric ventricular contraction the r-wave indicates passive atrial filling during diast when the tricuspid valve remains closed allowing blood to accumulate in the atrium the observation of the CVP waveform especially the presence or absence of these waves provides crucial insights into cardiac function for example the absence of a a waves in the CVP tracing suggests that atrial contractions are not occurring or are too rapid to be effective as seen in atrial fibrillation this can indicate impaired right atrial function making the CVP tracing a valuable tool in diagnosing arrhythmias and assessing the right heart's overall performance furthermore CVP measurements are essential in deter determining fluid responsiveness guiding fluid resuscitation in conditions like hypovolemia or evaluating right ventricular preload in patients with heart disease or pulmonary conditions when interpreting Central Venus pressure measurements it is crucial to consider the broader clinical context and integrate the value with other clinical information an elevated CVP can indicate various conditions or pathologies that affect the right side of the heart and circulatory system for instance an elevated CVP might suggest right-sided heart failure where the right ventricle is unable to effectively pump blood into pulmonary circulation leading to blood backing up into the right atrium and causing increased pressure additionally an elevated CVP could be indicative of cardiac tampeno a condition where fluid accumulates around the heart and compresses it leading to impaired cardiac filling and elevated pressures also a massive pulmonary imis which is a large blood clot lodged in the pulmonary arteries can obstruct blood flow causing the right side of the heart to pump against resistance and Elevate CVP significant pulmonary Vaso constriction often seen in conditions like acute respiratory distress syndrome also known as ARS can lead to increased pressure in the pulmonary circulation which might manifest as an elevated CVP hypervolemia or excessive fluid in the circulatory system can also result in an elevated CVP in this case the right heart is accommodated excess fluid causing the right atrial pressure to rise therefore interpreting CVP values necessitates considering the clinical history signs symptoms and other relevant hemodynamic parameters to determine the underlying cause of an elevated CVP and guide appropriate interventions and treatment normal right ventricular pressure is an essential parameter to remember when working with a pulmonary artery catheter as it provides insights into the right side of the heart's function a typical right ventricular pressure waveform consists of three components systolic pressure which Falls within the range of 20 to 30 mm of mercury diastolic pressure which which usually ranges from 0 to 5 mm of mercury and mean pressure which typically Falls between 10 to 20 mm of mercury when the PAC is situated in the right ventricle it's not uncommon to observe ventricular ectopy on the waveform this arhythmia occurs due to the proximity of the catheter to the ventricular myocardium pulmonary artery pressure reflects the health of the right ventricle and the vascular resistance within the pulmonary circuit a typical pulmonary artery pressure waveform comprises three main components systolic pressure which typically ranges from 15 to 30 millim of mercury diastolic pressure usually between 8 to 15 mm of mercury and mean pulmonary AR Ary pressure which typically Falls within the range of 10 to 20 mm of mercury the values of these parameters are important for understanding the hemodynamics of the pulmonary circulation when a critical care transport paramedic observes a sudden and sustained increase in pulmonary artery pressures it serves as a red flag prompting the immediate assessment and correction of any issues related to oxygen saturation or ventilation such elevations can signal potentially serious problems such as pulmonary embolism or acute respiratory distress syndrome conversely if pulmonary artery diastolic pressures suddenly drop the catheter's position should be re-evaluated to determine whether the pulmonary artery catheter has migrated into the right ventricle which could lead to inaccurate measurements and misinterpretations of the patient's hemodynamic status pulmonary capillary wedge pressure or pcwp is assessed through a pulmonary artery catheter and plays a central role in evaluating left ventricular preload making it a valuable indicator of left ventricular health in the past pcwp was considered the gold standard for assessing left ventricular preload the assessment of pcwp is an intermittent procedure that involves inflating a small balloon located at the distal tip of the PAC when the balloon is inflated the transducer measures a pressure equivalent to the left atrial pressure given that left natural pressure is closely linked to left ventricular indolic pressure which reflects left ventricular Health pcwp serves as a useful diagnostic tool the normal range for pcwp is typically between 4 to 12 millimeters of mercury hemodynamic wave forms often exhibit variations in their Baseline largely due to respiratory induced intrathoracic pressure and fluctuations similar to Central Venus pressure waveforms a standard pcwp tracing includes three positive deflections the a wve represents atrial contraction the c-wave signifies the closure of the mitro valve and the V wve represents passive atrial filling during diast importantly the pcwp waveform can provide insights into mitro regurgitation which is a clinically significant condition affecting the functioning of the mitro valve observing the characteristic waveform changes in the pcwp can alert Health Care Providers to the presence of mitro regurgitation facilitating timely diagnosis and intervention distinguishing in expiration points in waveform baselines is an essential aspect of assessing pulmonary capillary wedge pressure particularly in the context of respiratory mechanics in spontaneously breathing patients in expiration is identified at the highest point of the waveform Baseline while in mechanically ventilated patients it is at the lowest point of the Baseline elevated pcwp can result from a variety of causes but a common contributing factor is the inability of the left ventricle to effectively clear antig grade blood flow notably high levels of positive end expiratory pressure or Pete used in mechanical ventilation can also lead to increased pcwp pulmonary edema is a condition characterized by the accumulation of fluid in the lungs and critical care transport professionals often utilize pcwp measurements to help identify the underlying causes aiding in the diagnostic process and informing treatment decisions for patients with this condition while we have already discuss this it does bear repeating cardiac output is an important hemodynamic parameter assessed periodically by Critical Care transport paramedics this evaluation involves an active intervention by the provider typically conducted using the thermodilution method in this procedure a cold saline solution is injected through the pulmonary artery catheter and the resulting temperature changes in the blood are measured to determine the patient's cardiac output this measurement provides crucial insights into a patient's cardiovascular function and helps guide clinical decisions particularly in critically ill individuals it aids in the assessment of how effectively the heart is pumping blood through the body providing Vital Information for optimizing treatment strategies and patient care the thick principle developed by Adolf Fick in 1870 is a method used to calculate or estimate cardiac output it involves dividing the body's oxygen consumption by the difference in oxygen content between arterial and Venus Blood by comparing how much oxygen is taken up by tissues and how much is delivered to them this principle offers insights into cardiac performance that being said it's important to note that the FI principle relies on assumed values for oxygen consumption which are often derived from basil metabolic studies on healthy individuals the validity of these assumptions may be questionable in critically ill patients who might have altered metabolic needs or abnormal physiology despite its limitations the FI principle has historical and clinical significance as one of the early methods of assessing cardiac output modern techniques such as thermodilution using a pulmonary artery catheter has largely supplanted it in clinical practice due to its practicality and accuracy pulmonary vascular resistance or PVR is a crucial hemodynamic parameter that reflects the resistance encountered by the right ventricle as it pumps blood into the pulmonary circulation often referred to as the right side heart afterload PVR quantifies the resistance that the right ventricle must overcome to push blood through the pulmonary arteries and into the lungs for oxygenation an elevated PVR can be observed in various clinical conditions notably in patients with pulmonary hypertension where the pulmonary vascules resistance to blood flow is significantly increased additionally mitrov valve stenosis can lead to increased PVR as the narrowed valve obstructs blood flow and increases the work required by the right ventricle in critical care and peroperative settings monitoring PVR can provide valuable insights into the the status of the right heart and pulmonary circulation helping guide treatment decisions and assess the effectiveness of interventions in patients with cardiopulmonary diseases systemic vascular resistance or svr is a key hemodynamic parameter that quantifies the overall resistance to blood flow encountered by the left ventricle as it pumps blood into the systemic circulation often described as afterload svr reflects the resistance presented by the arteries throughout the body that the left ventricle must overcome to deliver oxygenated blood to the tissues by calculating svr clinicians gained valuable insights into the factors contributing to a patient's hemodynamic status and can better understand potential causes of shock monitoring svr helps in assessing vascular tone and systemic resistance aiding in the identification of conditions that could lead to inadequate cardiac output and circulatory failure such as sepsis anaphylaxis or cardiogenic shock by understanding and managing svr healthc care providers can optimize treatment strategies and improve patient outcomes in critical care and Parry operative settings stroke volume is a fundamental hemodynamic parameter that quantifies the volume of blood expelled from a ventricle in a single cardiac cycle reflecting the efficiency of the heart's pumping action typically a normal stroke volume Falls within the range of 60 to 100 mm per heartbeat with VAR variations based on individual factors like age body size and overall health stroke volume is influenced by several factors primarily ventricular contractility which represents the strength of the heart muscles contraction additionally stroke volume is sensitive to changes in preload the volume of blood returning to the heart and after load the resistance The ventricle encounters when injecting blood into the arterial system monitoring stroke volume is important in assessing cardiac performance and can help identify conditions such as heart failure or cardiogenic shock where the heart's ability to pump blood effectively may be compromised mixed Venus oxygen saturation or sv2 to is a valuable hemodynamic parameter that can be obtained by attaching a fiber optic oxygen saturation probe to the distal end of a pulmonary artery catheter unlike some other hemodynamic measurements sv2 is a continuous and passive measurement that doesn't require active interventions by clinicians once the catheter is in place svo2 provides insights into to the overall balance between oxygen delivery and consumption in the body it reflects the oxygen saturation of blood returning from the entire body to the right side of the heart monitoring sbo2 is particularly relevant in critical care settings as it can help assess whether the body's oxygen needs are being met or if there's a deficit in oxygen supply relative to demand when evaluating an sv2 value that falls outside the normal range the critical care transport paramedic should carefully consider the four components contributing to this parameter these components are one total hemoglobin level the amount of hemoglobin in the blood which can affect its oxygen carrying capacity two arterial oxygen saturation the proportion of hemoglobin in arterial blood that is carrying oxygen which is a reflection of how well the lungs are oxygenating the blood three cardiac output the volume of blood the heart is pumping per minute which influences the delivery of oxygen to the tissues and four oxygen consumption the rate at which oxygen is utilized by the body's tissues indicating the demand for oxygen examining each of these components helps the provider identify the underlying causes of abnormal svo2 values and helps make informed decisions regarding the patient's care in addition to S2 there is also another measurement mixed Central Venus oxygen saturation or scvo2 which can be obtained from a central Venus catheter this measurement is obtained by drawing a blood gas specimen or using a fiber optic oxymetric tip connected to a specialized monitor scvo2 provides a similar assessment of the balance between oxygen delivery and consumption but is taken from blood samples in the central V vus circulation often accessed through a central",
        "Heart Failure": "line heart failure it is important to maintain a balance between myocardial oxygen supply and demand in order to meet the metabolic requirements of the heart muscle and prevent esea a condition in which the heart muscle doesn't receive enough oxygen several factors can influence myocardial oxygen supply including coronary artery pathology or abnormalities in the coronary Anatomy which can affect the delivery of oxygen-rich blood to the heart muscle additionally diastolic pressure representing the pressure in the coronary arteries during the heart's relaxation phase is essential as it determines the force Force driving blood into the coronary vessels diastolic time which represents the duration of diast in the cardiac cycle is equally significant as it affects the time available for coronary profusion and oxygen delivery to The myocardium oxygen extraction the amount of oxygen removed from the blood as it passes to the coronary circulation is also a critical factor that can impact myocardial oxygen Supply heart failure is a cyclic and dynamic process where the heart's inability to effectively pump blood can lead to a series of physiologic and hemodynamic changes this can be triggered by various factors such as acute myocardial infarction which can result in damage to the heart muscle following injury there is a complex interplay between factors affecting the balance between myocardial oxygen supply and demand the treatment of heart failure primarily focuses on restoring normal cardiac function and reestablishing this balance if initial medical interventions are insufficient to achieve this equilibrium an intraaortic Bloom pump is often employed as a mechanical means to assist the heart and rebalance myocardial oxygen supply and demand the intra aortic Bloom pump accomplishes this by increasing cordary profusion and reducing the workload on the heart which can be particularly beneficial in managing heart failure and post Ami patients shock is a prevalent and serious condition in critical care settings often leading to significant morbid it it is primarily characterized by reduced systemic tissue profusion resulting in inadequate oxygen delivery to body tissues this reduced profusion leads to a shift towards anerobic metabolism which in turn can trigger a Cascade of events including multi-stem organ failure and ultimately death if not promptly addressed in the context of shock two critical hemo dnamic parameters play a key role in distinguishing the various types of shock cardiac output which represents the volume of blood the heart pumps per minute and systemic vascular resistance which quantifies the resistance encountered by Blood as it flows to the systemic circulation these parameters are important for assessing and categorizing the specific type of shock and guiding appropriate interventions for each patient hypovolemic shock results from a significant loss of intravascular volume which can occur due to various factors such as acute or chronic Hemorrhage excessive diuresis third space losses and other conditions leading to a depletion of the body's vascular volume in this type of shock the preload or the amount of blood entering the Heart during diast is notably reduced due to the decreased intravascular volume the reduction in preload causes a subsequent decline in stroke volume the amount of blood ejected from the heart with each beat ultimately resulting in a decreased cardiac output to preserve perfusion to vital organs tissues systemic vascular resistance increases as a compensatory mechanism is M to counteract the falling cardiac output thereby maintaining blood pressure and ensuring adequate end organ blood flow this physiological response aims to restore and preserve tissue profusion even in the presence of reducing circulating volume which is a Hallmark of hypovolemic shock cardiogenic shock is a multifaceted condition that can arise from various causes including myocardial depression due to esea myocardial infarctions cardiomyopathies postcardiac surgery stunning arhythmia mechanical abnormalities affecting the heart's pumping ability and obstructive conditions like massive pulmonary embolism tension num thorax paric cardial tanod and aortic clots this type of shock sets in motion a complex series of events driven by pump failure resulting in a marked reduction in cardiac output as a compensatory mechanism systemic vascular resistance typically increases to help uphold cardiac output which paradoxically exacerbates pump failure the heightened systemic vascular resistance elevates the preload or the amount of blood returning to the heart creating a state of relative total hyperemia the combination of reduced cardiac output elevated systemic vascular resistance and increased preload characterizes cardiogenic shock reflecting the heart's inability to maintain effective circulatory function and leading to impaired systemic tissue profusion distributive shock encompasses a range of conditions including sepsis systemic inflammatory response syndrome toxic shock syndrome anaphylaxis poisonings neurogenic factors like spinal cord injury narcotic",
        "Flight Considerations": "overdoses and various vasod diary causes in this type of shock vasod dilation is typically the key under L Issue leading to a notable reduction and systemic vascular resistance the significant Vasa dilation experienced in distributive shock drastically lowers afterload which counterintuitively results in an increase in cardiac output this rise in cardiac output is a compensatory mechanism to maintain tissue profusion despite the profound drop in systemic vascular resistance making distri distributive shock distinct in its hemodynamic presentation flight considerations altitude changes can have several effects on hemodynamic monitoring firstly monitoring oxygen saturation often assessed through pulso symmetry becomes extremely important as it helps the critical care transport paramedic respond promptly to variations in a patient's oxygenation status which is particularly important at higher altitudes where oxygen levels are reduced additionally patients may experience physiologic changes in response to altitude including a chemo receptor induced increase in tidal volume and a compensatory rise in cardiac output to help deliver oxygen more efficiently lastly it's essential to ensure that air is removed from IV bags because at higher altitudes lower atmospheric pressure can cause any air within the bags to expand potentially affecting the accuracy of fluid administration and leading to complications vigilance and oxygen monitoring understanding altitude induced physiologic iCal adjustments and proper IV management are essential when dealing with patients in high altitude environments when dealing with altitude changes and hemodynamic monitoring a few additional considerations do come into play it's advisable to use infusion pumps for medication infusion to ensure precise delivery rates especially as changes and atmospheric pressure at different altitudes can affect flow rates in gravity-driven systems furthermore the zeroing of pressure transducers is recommended when reaching cruising altitude during air travel or whenever there are changes in altitude of a th000 ft or more this zeroing process helps maintain the accuracy of pressure measurements which is critical for Effective hemodynamic monitoring in various clinical set settings particularly at high altitude environments or during air travel in conclusion hemodynamic monitoring stands as a Cornerstone in the critical care transport paramedic profession providing a vital window into the complex dynamics of cardiovascular anatomy and physiology by delving into arterial lines Central Venus lines and pulmonary artery catheters we gain valuable insights into our patients condition enabling us to make real-time life-saving decisions while in transit the invasive pressure measurements obtained through these lines offer a comprehensive picture of the patient's hemodynamic status allowing us to tailor interventions to the individual's needs with remarkable precision as we explored the intricacies of heart failure and considered flight specific factors affecting our practice we reinforced the significance of continuous monitoring and adaptation the ability to manage these patients effectively during flight or during ground transport despite environmental and physiological changes is a testament to our profession's dedication and expertise in essence hemodynamic monitoring empowers us to bridge the gap of between the patients initial presentation and their ultimate destination ensuring that our patients receive the highest level of care throughout their Journey"
    },
    {
        "Introduction to Mechanical Circulatory Support": "chapter 16 mechanical circulatory support introduction mechanical circulatory support is a broad term encompassing a range of interventions designed to enhance or substitute the heart's native cardiac output this remarkable approach to treatment is versatile and can be employed in various clinical scenarios addressing both acute and chronic conditions strategies are not one size fits all they offer the flexibility to support a single ventricle or both ventricles making it adaptable to the patient's specific needs the pumping mechanism of these systems can be either external to the body known as extracoporeal mechanical circulatory support or internal referred to as intraoral mechanical circulatory support this dichotomy in design allows for tailored approaches to Patient Care with external devices often serving as temporary life-saving measures while internal devices provide a more sustained solution such as ventricular assist devices which can significantly extend a patient's life while awaiting transplantation or as a destination therapy for those who were not transplant candidates mechanical circulatory support represents a Cutting Edge field that continues to evolve offering patients with heart failure and circulatory challenges new found Hope and the promise of improved outcomes it's important to understand that mechanical circulatory support isn't solely about enhancing cardiac output it can be further augmented with additional therapies to address various aspects of a patient's condition this can include gas exchange support which is crucial for patients with respiratory compromise temperature control for those who require precise thermal regulation or renal replacement therapy to manage kidney dysfunction by integrating these complimentary treatments healthc care providers can create a comprehensive care plan that caters to the individual needs of the patient making mechanical circulatory support a versatile tool in critical care this intervention is not confined to a specific Health Care setting being initiated in a variety of environments including the prehospital setting Community Hospitals or even specialized facilities with dedicated teams the flexibility in the application ensures that patients in diverse locations can access these life-saving interventions however regardless of the setting patient safety and Care Quality must remain Paramount during mechanical circulatory transport and management the process requires a careful balance of detailed patient assessment continuous monitoring and a high level of technical proficiency when dealing with the system to ensure that the patient's condition remains stable and well managed throughout the course of",
        "Intra-Aortic Balloon Pump": "care intra aortic balloon pump the intra aortic Bloom pump or iabp stands as one of the earliest and most well-known cardiac assist devices in the field of Cardiology its development revolutionized the approach to managing patients with heart failure and circulatory compromise iabp therapy is a well-established and widely used technique and it has played an important role in the management of various cardiac conditions particularly in cases of left ventricular failure the fundamental principle behind therapy involves the utilization of a specialized balloon which is connected to a sophisticated pump via a catheter this catheter is carefully inserted into the patient's aorta allowing the balloon to be positioned in close proximity to the heart the balloon inflates and deflates in synchrony with the cardiac cycle creating a counterpulsation effect that enhances coronary blood flow and reduces the afterload on the heart counterpulsation is a globally recognized and utilized therapy for assisting patients with left entric Failure Its application is not limited by geographical boundaries and is considered a valuable intervention in a variety of healthc care settings around the world over the years iabp units have undergone significant advancements in terms of miniaturization resulting in more Compact and transport friendly models this development has made it more feasible for some models to be easily accommodated within the confined space of a helicopter allowing for efficient transport of critically ill patients from one Health Care Facility to another the miniaturization of iabp units has enhanced the flexibility of its use and broaden its availability for patients requiring prompt and specialized cardiac support especially in situations where rapid transport is a critical component of the patient's care the critical care transport paramedic plays a pivotal role during the transport of a patient supported by an iabp as this is a complex and specialized intervention that requires careful attention and expertise several important responsibilities must be fulfilled to ensure the safety and effectiveness of iabp therapy during transport the most critical aspect of transporting a patient with an iabp is ensuring the secure positioning and immobility of the patient the catheter with the attached balloon is typically inserted into the patient's aorta and and this balloon inflates and deflates with each cardiac cycle any unnecessary movement can lead to complications including Bloon displacement kinking or other issues that might compromise the therapy the provider should use appropriate restraints secure the patient to a transport stretcher or bed and employ additional measures as needed to prevent any unintentional shifts or dislodgments of the system this also includes ensuring proper placement and securing of the console and power source the iabp is an electronic device that requires a stable and reliable power supply to operate the provider should ensure that all equipment including the console and power source is in optimal working condition throughout the transport regular checks and redundancies should be in place to address any power related issues promptly additionally there should be backup power sources available such as batteries or even generators to ensure that the iabp continues to function in case of power outages during transport due to the specialized nature of this therapy most critical care transport programs require that the provider be accompanied by by a certified perfusionist or a critical care registered nurse who possesses in-depth knowledge and experience in the management of iabp assisted patients this additional Personnel ensures that there is expertise readily available to handle any technical or clinical issues that may arise during transport these providers are equipped to address complications troubleshoot equipment and provide Immediate Care to the patient offering an added layer of safety and clinical support to optimize patient outcomes iabp therapy initiates with the insertion of a balloon catheter into the patient's vascular system the common insertion site is typically the femoral artery although other access points are possible depending on the patient's condition the balloon catheter is Advanced through the arterial system until it reaches its intended location the precise positioning of the balloon is crucial for Effective iabp function ideally the balloon tip should be situated just distal to the takeoff of the left subclavian artery this strategic placement ensures that the balloon can augment the heart's pumping action by inflating and deflating synchronously with the cardiac cycle when the balloon inflates it increases aortic pressure during diast which augments coronary artery profusion and reduces afterload easing the heart's workload during syy this synchronized inflation and defl of the balloon contribute to improved myocardial oxygen supply and demand balance making it an invaluable tool in managing patients with certain types of heart failure such as acute myocardial infarction or cardiogenic shock during the cardiac cycle the balloon is inflated with helium gas at the onset of diast this timed inflation increases diastolic pressure which in turn enhances coronary artery profusion and reduces myocardial oxygen consumption the balloon remains inflated during diasti to provide this essential support just before cyy the balloon is deflated this precise timing is crucial as it allows the heart to eject blood with reduced resistance subsequently decreasing myocardial workload and oxygen demand the synchronized deflation of the balloon during syy helps to optimize stroke volume in cardiac output contributing to the overall effectiveness of the therapy in essence the iabp serves as a mechanical adjunct to the heart's pumping action assisting it during diast in harmonizing ING with the cardiac cycle to improve cardiac performance and oxygen utilization the structure and positioning of the intra aortic Bloom pump catheter are essential aspects of its functionality in patient care the catheter itself is designed as a long narrow balloon mounted on a thin catheter older generation catheters typically featured two lumens while newer models incorporate a third fiber optic Lumen the central Lumen plays a crucial role in guiding the catheter's insertion into the femoral artery and throughout the arterial system additionally it allows for the monitoring of aortic blood pressure providing valuable information about the patient's hemodynamic status the second Lumen known as the gas Lumen is responsible for delivering helium gas from the pump console to control the inflation in deflation of the IAB balloon lastly the fiber optic Lumen contains fiber optic strands that are used to measure aortic pressure and in some Advanced models aortic oxymetry these components work together to ensure accurate balloon function and monitoring during the iabp therapy typically the catheter is introduced into the descending aorta via the fal artery which is the most common and widely accepted method of placement that being said alternative insertion routes do exist for instance in certain cases healthc care providers may choose to insert the IAB catheter through the axillary artery transthoracic placement on the other hand is a rarely utilized method and is typically reserved for critically ill patients to facilitate insertion clinicians can use a sheath or opt for a catheter specifically designed for sheathless insertion this approach may offer benefits by potentially reducing the risk of complications related to limit memia which is a condition characterized by reduced blood flow and oxygen supply to the limb the counter pulsation sequence is a fundamental aspect of intraaortic balloon pump therapy assisting the Heart during syy and diast the importance of this sequence lies in its ability to improve cardiac function and enhance coronary profusion while reducing myocardial workload here's how the counter pulsation sequence works and its significance in iabp therapy it starts with diastolic augmentation at the beginning of diast the console initiates the inflation of the balloon which is located in the descending thoracic aorta this is known as diastolic augmentation as the balloon inflates it displaces blood volume in the aorta increasing diastolic pressure this elevated diastolic pressure has several key benefits first it enhances coronary artery profusion ensuring that the heart receives an adequate supply of oxygenated blood during the critical diastolic phase when the coronary arteries fill second improved coronary perfusion leads to better oxygen delivery in The myocardium reducing the risk of esea in myocardial damage and third The increased diastolic pressure decreases afterload making it easier for the left ventricle to eject blood during syy after diastolic augmentation we have cyti with balloon deflation just before the onset of consistently the console triggers the deflation of the balloon this synchronization is crucial because the sudden deflation creates a vacuum effect in the aorta and this has several important implications the abrupt dropped in aortic pressure during syy significantly reduces the resistance against which the left ventricle has to work to open the aortic valve and eject blood with less resistance the left ventricle can eject blood more efficiently resulting in improved stroke volume and cardiac output and the decreased afterload reduces the workload in the heart leading to a reduction of myocardial oxygen consumption this resting effect on the heart can be particularly beneficial for patients with heart failure or those recovering from cardiac surgery or myocardial infarction all in all the counter pulsation sequence in iabp therapy optimizes the cardiac cycle by inflating the balloon during diast to enhance coronary profusion and deflating it just before assistly to reduce afterload and improve cardiac performance this synchronized intervention effectively interrupts the cycle of heart failure and esea allowing the heart to recover and and restoring the balance between myocardial oxygen supply and demand iabp therapy exerts specific physiologic effects that are critical for patients especially those in cardiogenic shock when an iabp is properly timed and synchronized with the cardiac cycle it significantly impacts hemodynamics these are the physiologic effects of the therapy iabp therapy has a unique impact on blood pressure when the balloon deflates it happens at the onset of syy which temporarily lowers the systolic blood pressure in contrast during diasty when the balloon inflates it raises the diastolic pressure this this Dynamic alteration in blood pressure helps optimize the workload of the heart ultimately improving cardiac function therapy is meticulously timed to the cardiac cycle the balloon deflates at the end of diast just before the next ventricular ejection begins this synchronization with the natural cardiac rhythm is crucial for its Effectiveness the sudden deflation of the balloon leads to a drop in aortic pressure this drop occurs because the space previously occupied by the balloon is suddenly empty the reduction of pressure significantly decreases the resistance that The ventricle must overcome to open the aortic valve and eject blood this in turn results in a reduction of myocardial oxygen consumption as a direct consequence of the reduced after load there is a maximized stroke volume this enhancement in stroke volume leads to an improvement in cardiac output without increasing myocardial oxygen demand in simple terms the heart can pump more blood with less effort which is an important benefit in patients with cardiac insufficiency the improvements in cardiac output coupled with the reduction in myoc cardio oxygen consumption effectively interrupt the Vicious Cycle of heart failure this intervention allows the heart to rest and recover from the initial insult or injury that initiated the cycle of cardiac decompensation by temporarily lightening the heart's workload and optimizing its function iabp therapy offers a lifeline for patients in cardiogenic shock supporting their recovery and potentially enhancing their overall outcomes blood volume augmentation or control in the context of intraaortic Bloom pump therapy is an important aspect of optimizing this mechanical circulatory support intervention the console is equipped with the the capability to regulate the volume of gas that is shuttled back and forth to the balloon with each counter pulsation cycle this volume control is a valuable feature that allows the operator to fine-tune the therapy to meet the specific needs of the patient by adjusting the balloon volume the critical care transport provider can influence the degree of support provided to the patient's heart ensuring that the therapy aligns with the patient's condition and requirements in routine clinical use or just during patient transport it is often the practice to maintain the balloon volume at its maximal or full capacity this approach is typically employed because patients who require therapy are often in a state of cardiac shock or acute cardiac compromise which necessitates significant support to augment cardiac output and coronary profusion by operating the iabp with the balloon at maximal volume the therapy provides more robust and consistent assistance to the failing heart helping to reduce myocardial oxygen consumption and improve coronary blood flow this proactive approach helps stabilize the patient hemodynamics and allows for a better chance of myocardial recovery in cases such as acute myocardial infarction or other cardiac emergencies maintaining the balloon volume at full capacity is a common practice because it ensures that the therapy provides the highest level of support to the patient's heart when it's needed most however it is essential for the critical care transport paramedic to be skilled in adjusted in the balloon volume if the patient's condition warrants a more nuanced approach thereby demonstrating the flexibility and adaptability of iabp therapy to meet individual patient requirements the timing of the balloon's inflation and deflation in an intra aortic Bloom pump is a critical aspect of the therapy proper timing ensures that the device effectively augments cardiac output and coronary profusion while minimizing the workload on the heart understanding and recognizing the timing of the iabp waveform changes and triggers is essential for health care providers especially Critical Care transport paramedics as incorrect timing can lead to adverse outcomes the console is synchronized to the patient e PCG or arterial pressure waveform allowing the balloon to inflate and deflate at specific points in the cardiac cycle the most common timing mode for iabp therapy is 1: one meaning that the balloon inflates and deflates with every heartbeat proper timing dictates that the balloon inflation should occur during diast when the left ventricle is relaxed and coronary arteries are filling with oxygenated blood this promotes optimal coronary profusion conversely balloon deflation should coincide with Cy reducing afterload and myocardial oxygen consumption during the left ventricular ejection phase correct timing aims to maximize stroke volume and cardiac output while minimizing the heart's workload incorrect timing can lead to adverse effects such as reduce coronary profusion decrease stroke volume and cardiac output an increased left ventricular afterload potentially causing harm to the patient clinicians should be vigilant in monitoring the iabp waveform and coordinating it with the patient's cardiac cycle common signs of incorrect timing include diminished arterial pressure during syy and a lack of diastolic augmentation the console is equipped with sophisticated monitoring capabilities to optimize therapy it constantly observes three key parameters one the console continuously evaluates the arterial pressure weight form to assess the timing of balloon inflation and deflation this waveform provides important information about the patient's cardiac cycle and guides the iab's actions two the patient's electrocardiogram is another critical signal monitored by the console the ECG helps the system synchronize balloon inflation and deflation with the cardiac cycle the QRS complex on the ECG is a comp reference point used for trigger selection and three the console also monitors the gas pressure within the catheter this waveform reflects the inflation and deflation of the balloon and is used to confirm that the balloon is functioning correctly and that gas is being delivered appropriately the selection of triggers for initiating balloon inflation and deflation varies by manuf ufacturer and is an important aspect of iabp operation the following trigger sources are typically available an ECG trigger is the most common and the most safest trigger Source used on iabp consoles it relies on the patient's ECG to locate each cardiac cycle and synchronized balloon action typically the r wave on the ECG is used as a reference point to trigger deflation during syy in some cases the arterial pressure waveform can be chosen as the trigger Source this option may be used when the ECG signal is less reliable or when there are irregularities in the patient's cardiac Rhythm many consoles offer a pacemaker trigger option which can can be further divided into atrial and ventricular paste rhythms this trigger is used when the patient has a pacemaker in place and can be synchronized with the pacemaker pacing signals iabp devices offer multiple modes often referred to as assist ratios or iabp frequencies these modes determine the timing of balloon inflation and deflation in relation to the patient's cardiac cycle it's essential for critical care transport paramedics to understand the selected mode and its implications for each waveform evaluation the provider should systematically assess several parameters of the iabp waveform to ensure proper timing and effectiveness this assessment includes pressure Peaks the waveform should exhibit clear well-defined pressure Peaks these Peaks correspond to the systolic and diastolic phases of the cardiac cycle slopes the slopes of the waveform both during inflation and deflation should be smooth and gradual abrupt change es in slope could indicate timing issues or problems with the device inflation and deflation points the points at which the balloon inflates and deflates during the cardiac cycle must be carefully observed proper timing is essential for achieving the desired physiological effects of the therapy when evaluating the waveform in an intraaortic balloon pump the provider must focus on several key parameters to ensure that the device is functioning optimally and is synchronized with the patient's cardiac cycle here is an expanded explanation of the parameters that should be evaluated syy and diast of each pressure waveform care assessment of each pressure waveform is important Cy represents the period of ventricular contraction and ejection of blood into the aorta while diast is the relaxation phase when the heart fills with blood the console should be timed to inflate during diast and deflate during syy diastolic augmentation assisted syy and unassisted syy these components of the waveform reflect the impact of the iabp on the cardiac cycle diastolic augmentation refers to the increase in diastolic pressure caused by balloon inflation assisted syy indicates the period of the cardiac cycle during which the balloon remains inflated unassisted Cy is the natural ejection of blood from The ventricle the point of inflation the specific point in the cardiac cycle when the balloon inflates is critical proper timing ensures that the balloon supports the Heart during diast reducing afterload and improving coronary profusion indolic dip in pressure created by balloon deflation when the balloon deflates at the end of diast there should be a noticeable dip in the aortic pressure this dip reflects the reduction in afterload as the balloon deflates making it easier for the heart to eject blood during syy slope of diastolic augmentation pressure and slope of assisted syy examining the slopes of these segments in the waveform helps assess the gradualness and smoothness of pressure changes abrupt changes in slope May indicate issues with Device timing or malfunction diastolic augmentation Peak pressure the peak pressure during dioic augmentation demonstrates the extent to which the balloon is increasing diastolic pressure to enhance coronary profusion and reduce myocardial oxygen consumption comparison of peak pressure of assisted syy with the peak pressure of unassisted syy this comparison allows the provider to determine how much assistance the iabp provides during syy ideally the assisted syy Peak pressure should be higher indicating improved stroke volume and cardiac output by evaluating these parameters in the iabp waveform the provider can ensure that the device is properly synchronized with the patient's cardiac cycle providing the intended benefits of reduced myocardial oxygen consumption enhanced cardiac output and mechanical support to the heart when needed while Advanced software algorithms play a significant role in monitoring and adjusting iabp timing automatically Critical Care transport paramedics should possess a thorough understanding of timing errors waveform characteristics and physiologic effects in order to achieve optimal patient care let's take a look at some of the most common early inflation proper timing is is essential and the IAB should ideally begin inflation at the dichroic Notch indicating the closure of the aortic valves early inflation occurring before this point can lead to potential harm by causing damage to the aortic valve emphasizing the importance of precise synchronization with the cardiac cycle late inflation on the contrary late inflation occurs when the dichroic Notch is visible on the pressure waveform signifying delayed initiation of Bloon inflation while this may cause minimal harm late inflation does not maximize the benefits of the iabp therapy highlighting the importance of achieving optimal timing to enhance cardiac performance early deflation Prem Ure deflation of the balloon before the end of diast can result in a rise in aortic pressure creating a plateau before syy this in turn requires the ventricles to overcome a higher end dioic pressure to eject blood early deflation not only negates the positive effects of the therapy but it also reduces the duration of increased pressure during diast negative L impacting coordin artery profusion and systemic circulation lastly late deflation this is perhaps the most critical timing error late deflation of the IAB can exacerbate myocardial esmia this is because the delayed removal of the balloon during diast interferes with the heart's ability to pump efficiently potentially worsening the patient's cardiac condition the insertion of an iabp is a vital therapeutic intervention with versatile applications in managing complex cardiovascular conditions primarily iabp proves highly effective in cases of refractory ventricular failure where conventional treatments have proven insufficient it serves as a Lifeline in situations of cardiogenic shock providing essential mechanical circulatory support to optimize cardiac output unstable refractory angina marked by persistent chest pain despite standard interventions finds relief through iabp therapy as it helps to alleviate myocardial esea and reduces the associated oxygen demand the role of iabp extends to scenarios of impending infarction and mechanical complications arising from acute myocardial infarction in cases of esemar related intractable ventricular rhythmia the iabp acts as a stabilizing Force contributing to the restoration of normal cardiac rhythm Beyond emergency situations the iabp is instrumental in providing cardiac support during highrisk surgical procedures such as coronary angiography and AIDS in the delicate process of weaning patients from cardiopulmonary bypass ensuring a smooth transition to Native cardiac function additionally its application in generating intraoperative pulsatile flow underscores its adaptability to various clinical settings in the realm of myocardial lemia unstable angina and impending infarction the insertion of an iabp demonstrates its prowess in maintaining optimal coronary artery profusion by alleviating myocardial lemia and reducing oxygen demand it actively contributes to the Del delicate balance between myocardial oxygen supply and demand impacting the pre-operative intraoperative and post-operative phases of patient care the reduction of left ventricular resistance Improvement of cardiac output and augmentation of coronary artery and systemic profusion pressures highlight the comprehensive cardiovascular benefits of iabp therapy this intervention emerges as a critical component in stabilizing severe left entric failure resulting from unsuccessful angioplasty showcasing its multifaceted and indispensable role in the advanced management of complex cardiac conditions while there are many benefits and indications to iabp therapy certain contraindications and insertion sight factors must be carefully considered to ensure patient safety contraindications to iabp therapy include severe aortic valvular insufficiency as the presence of this condition May exacerbate the regurgitation and compromise the effectiveness of the therapy additionally patients with abdominal or aortic aneurysms are deemed unsuitable candidates for iabp insertion due to the risk of further compromising the Integrity of the weakened area severe calcific aortic or iliac arterial disease and significant peripheral vascular disease represent additional contraindications to iabp therapy in these cases the compromised vascular conditions May impede the successful placement and function of the balloon pump posing potential risks to the patient addressing these Contra indications is important in determining the appropriateness of iabp therapy and ensuring the alternative treatment modalities are explored when considering insertion site factors it's important to note that sheathless insertion is not recommended under certain circumstances if the patient presents with a substantial amount of fatty tissue at the insertion site the efficacy of sheathless insertion may be compromised extensive scarring or fibrosis at the insertion site poses challenges to the successful implementation of sheathless insertion and may increase the risk of complications moreover if the patient has other contraindications to percutaneous insertion alternative approaches or therapies should be explored to address the cardiovascular needs of the individual while minimizing risks associated with the procedure the implementation of intraaortic Bloom pump therapy while offering critical cardiovascular support comes with potential side effects and complications that necessitate Vigilant monitoring and management by Healthcare professionals limb eskema stands out as one of the primary complications where the bloom pump May impede blood flow to the lower extremities leading to reduced profusion and the development of compartment syndrome additionally care must be taken to assess and prevent Lim ischemia during the therapy as complications May persist even after the IAB is remed removed excessive bleeding from the insertion site is another potential complication associated with iabp therapy the invasive nature of the procedure introduces a risk of bleeding and careful attention must be paid to ensure hemostasis and prevent complications arising from uncontrolled bleeding thrombos cenia characterized by decreased in platelet count can occur due to platelet destruction related to the presence of the iabp emphasizing the need for close monitoring of platelet levels during therapy immobilization of the balloon catheter balloon leak and infection are additional complications that may arise during or after the therapy ensuring proper functioning and positioning of the catheter is essential to prevent complications such as balloon immobilization and leaks which could compromise the effectiveness of the therapy Vigilant infection control measures must be implemented to minimize the risk of infections associated with the insertion site more severe complications such as aortic dissection and thrombosis underscore the importance of meticulous monitoring and prompt intervention during iabp therapy aortic dissection involves a tear in the aortic wall posing a serious threat to cardiovascular health thrombosis the formation of blood clots within the circulatory system is yet another critical complication that requires careful management patient assessment is a critical component in the management of individuals with acute myocardial infarction Complicated by cardiogenic shock particularly when considering the decision to transfer the patient to a tertiary facility for advanced evaluation and treatment cardiogenic shock develops in approximately 7 to 10% of patients admitted to a community hospital with AMI highlighting the significance of Timely incomp apprehensive patient assessment in the context of transferring a patient with cardiogenic shock the early insertion of an iabp is often considered to enhance the safety of the transport process this is because the IAB serves as a critical cardiac support device and its early implementation can contribute to stabilizing the patient's cardiovascular status during transp support providing valuable time for further evaluation and intervention at the receiving facility patient assessment in the context of iabp therapy involves addressing two fundamental questions first whether the therapy is effective for the patient and second whether any complications have resulted from the therapy to evaluate the effective Ness of iabp Therapy healthc Care professionals monitor Vital Signs including blood pressure heart rate and respiratory rate oxygenation levels are assessed to ensure adequate tissue profusion and parameters such as urine output peripheral profusion central nervous system function and overall General condition are closely observed parameters such as Vital Signs provide insights into the hemodynamic response of iabp therapy ensuring that the device is effectively supporting the patient's cardiovascular function oxygenation levels and urine output serve as indicators of tissue profusion with improvements in these parameters reflecting the positive impact of therapy on oxygen delivery to vital organs peripheral profusion and the patient's General condition offer additional valuable information about the overall response to therapy continuous and meticulous monitoring of patients undergoing iabp therapy is Paramount for ensuring optimal outcomes and promptly addressing any changes in the patient's condition providers should conduct assessments and document key parameters at least every 15 minutes or more frequently if there is a notable change in the patient's clinical status the frequent monitoring allows for real-time evaluation of the patient's response to iabp therapy and enables prompt intervention in case any complications or variations are noticeable in Vital Signs complications associated with therapy are most common L linked to two main factors firstly issues related to the insertion site of the device can arise including bleeding infection or damage to the surrounding structures close attention to the insertion site is crucial to identify and address any signs of complications promptly secondly the impairment of circulation by the balloon or in the extremity where it's inserted is also a critical consideration limb esea can occur leading to potential complications such as compartment syndrome emphasizing the need for Vigilant assessment of peripheral profusion and neurovascular status as stated earlier patients undergoing iabp therapy may require transportation to tertiary facilities for Specialized Care meaning that the provider must carefully consider various factors during the transport process these patients may be transported via ground ambulances or fixed or rotary Wing aircraft however several critical considerations come into play when utilizing these vehicles for transport firstly issues related to power supply must be addressed ground and Air transport Vehicles may have inverters capable of converting the direct current voltage from the engine to alternating current suitable for powering the iabp this ensures the seamless transition of power sources during Transportation Additionally the provider needs to be mindful of space and weight constraints within the vehicle as well as the loading unloading and securement of the iabp system adequate planning is essential to ensure the safe and stable transportation of the patient and the equipment transport Vehicles often incorporate systems to address power requirements such as batteries that allow for limited periods of portable operation this is important for maintaining iabp functionality during potential power fluctuations or when transitioning between power sources overall careful planning and awareness of these transport considerations contribute to the safe and effective movement of patients receiving IAB therapy emphasizing the importance of the critical care transport providers expertise in managing complex medical interventions during Critical Care",
        "Extracorporeal Membrane Oxygenation": "transport EXT Caporal membrane oxygenation extracoporeal membrane oxygenation or ECMO serves as a temporizing mechanism for extracoporeal gas exchange either with or without hemodynamic support making it a crucial intervention in critical care also referred to as extracoporeal life support or ecls emo plays a distinctive role in contrast to cardiopulmonary bypass unlike the latter emmo offers the advantage of providing more extended term support within the ICU this extended support duration is particularly beneficial in cases where prolonged respiratory or cardiac assistance is required one distinctive feature of ECMO lies in its utilization of the patient intravascular volume as the fluid reservoir a departure from the conventional use of an external Reservoir this characteristic is integral to eo's ability to capture Approximately 80% of the circulating blood volume facilitating effective gas exchange and oxygenation the Reliance on the patient's intravascular volume enhances the hemodynamic stability during EO contributing to its utility in managing in severe respiratory and cardiac failure the ecos system's capability to sustain gas exchange and provides circulatory support positions it as a vital tool in the comprehensive care of critically ill patients emphasizing its role as an advanced life support modality in the critical care setting it's important to note that ECMO is not Curative in nature rather it serves as a bridge to recovery by providing vital respiratory and circulatory support to patients with severe and potentially reversible cardiac or respiratory compromise this makes ECMO a valuable intervention in cases where conventional therapeutic approaches may be insufficient to sustain life as of now emo stands as the only available therapy capable of functionally replacing both the heart and lungs albeit there are some imperfections this distinction underscores the unique role of emo in advanced life support as it can maintain oxygenation and remove carbon dioxide from the blood essentially performing The Essential functions of the heart and lungs the imperfections in the replacement function highlight the ongoing advancements and challenges in the field in emphasizing the need for continuous research and Innovation to optimize Emo's efficacy in supporting critically ill patients with severe cardiac and respiratory failure EO support has varying canulation sites and circuit configurations each tailored to the specific needs of the patient in the intended type of support venovenous EO Mo or vvmo is one such configuration where blood is withdrawn from the Venus circulation undergos gas exchange in the ECMO circuit and is then returned as oxygenated and decarbox blood to the Venus system VV egmo operates in series allowing the native lungs to contribute to gas exchange without direct circulatory support this configuration is often employed in cases where the primary concern is respiratory failure on the other hand Veno arterial ECMO or VA ECMO involves draining blood from the Venus circulation facilitating gas exchange in the ECMO unit then returning the oxygenated blood directly to the arterial system VA EO functions in parallel to the native heart and lungs providing both respiratory support and circulatory assistance another configuration known as Veno venoarterial ECMO or venoarterial Venus ECMO just VAV ECMO for short colloquially known as triple canulation supports both respiratory and cardiac function this involves three canulation sites and ensures a balance between oxygenation and circulatory support although it does add complexity to the EO circuit each of these configurations showcases the adaptability of ECMO in managing diverse clinical scenarios addressing both respiratory and cardiac compromise with tailored support strategies the ECMO fundamental components include vascular canulas circuit tubing a pump heater cooler unit and an oxygenator vascular canulas serve as access and return points for blood allowing it to be withdrawn from the patient directed through the ECMO circuit and returned after undergoing oxygenation and carbon dioxide removal circuit tubing facilitates the seamless flow of blood through the system while the pump ensures the necessary propulsion of blood circulation within the ECMO unit the heater cooler unit regulates blood temperatures optimizing conditions for Effective gas exchange lastly the oxygenator is a critical component responsible for facilitating the exchange of oxygen and carbon dioxide ECMO circuits also incorporate additional monitoring and safety features such as pressure and blood flow monitors bubble detectors to identify potential complications and continuous arterial and Venus oxyhemoglobin saturation monitors to assess the effectiveness of gas exchange circuit access sites are strategically placed to allow healthc care providers access to the system for interventions or adjustments an emergency arterial venus Bridge may also be included providing an alternative route for blood circulation in case of complications or malfunction the intricacies of these components highlight the sophisticated engineering of ECMO circuits emphasizing the importance of their precise functioning in delivering optimal extracoporeal life support circuit impatient Management in context of ECMO involves a comprehensive and thorough approach to ensure the optimal functioning of the circuit and the well-being of the patient monitoring a patient on ECMO initiates with a standard ICU assessment with special attention directed towards the ECMO device special considerations include anti-coagulation which is a critical aspect of ECMO management patients on ECMO receive systemic anti coagulation to prevent thromboembolism and maintain circuit patency monitoring anti-coagulation status is imperative with intervals ranging from hourly to every 6 hours depending on coagulation studies however the healthcare team must be vigilant regarding the increased risk of uncontrolled bleeding associated with anti-coagulation therapy circuit assessment is equal equally vital involving a systemic evaluation of all components connections and securing points fibrin disposition and thrombus formation commonly occur at connectors pigtails and stop coocks necessitating close scrutiny monitoring support during egmo involves assessing various pressures including Venus pressure arterial pressure oxygenator Inlet pressure and the differential of arterial and oxygenator pressure these provide valuable insights into the efficacy of EO support routine documentation is an important aspect of ECMO management with hourly notations of flow revolutions per minute circuit pressures trending of coagulation studies anti-coagulation Doses and assessments of the circuit and canulation sites blood pressure and pulse are monitored closely during ammo flows are titrated to maintain a pulse pressure of at least 10 mm of mercury aiming to mitigate increased afterload in the left ventricle this approach to circuit and patient management ensures the early identification of potential issues facilitates timely interventions and optimizes the overall effectiveness of ecotherapy in critically ill patients complications in troubleshooting demand a nuanced understanding of the specific risks associated with each mode and configuration of ECMO support individualized and thorough assessments of both the ecos circuit and the patient are important for identifying underlying issues before they lead to clinically meaningful events one significant complication is patient hypoxemia which may manifest due to various factors hemolysis characterized by elevated parameters such as hematocrit serum hemoglobin and lactate dehydrogen necessitates routine monitoring a serum hemoglobin level of 50 Mig per deciliter or greater prompts Source identification pulmonary edema and left ventricular distension can occur requiring interventions such as reducing mean arterial pressures through preload afterload reduction administering Isotopes and if necessary decompressing the left ventricle Lim esmia another potential complication demands frequent assessment of limb perfusion in cases of hypoperfusion reperfusion catheter insertion may be necessary to restore blood flow to distal tissues insufficient flow signals impaired Venus damage resolving this issue may involve decreasing revolutions per minute to stabilize flow or replacing intravascular volume recirculation characterized by low arterial oxygen saturation in the presence of elevated or Rising mixed Venus saturation can be addressed by increasing the distance between canula openings ensuring additional drainage canula or using a dual Lumen canula north south syndrome also known as Harlequin syndrome where deoxygenated blood from the left ventricle mixes with highly oxygenated blood from ECMO in the aorta leading to a mixing cloud or Watershed is another complication requiring careful management strategies emergencies and circuit disruptions require a proactive approach to ensure the timely detection and remedy of potential issues routine thorough inspections are crucial in identifying and addressing problems that may arise during ECMO support oxygenator dysfunction a potential complication necessitates careful monitoring and management this may involve evaluating gas exchange efficiency and identifying any signs of clot formation or membrane damage with the oxygenator air entrainment another concern requires immediate attention to prevent the introduction of air into the circuit which can lead to IMI and compromise oxygenation disruption within the circuit Integrity can result in blood loss and compromise the effectiveness of ECMO support monitoring for signs of blood leakage such as visual inspection for external blood loss or changes in circuit pressures is essential pump failure while uncommon poses a significant threat to ECMO efficacy timely identification of any irregularities in pump function including abnormal sounds or vibrations is critical for preventing a potential circuit disruption inadvertent DEC canulation although rare can occur and requires immediate intervention to ensure that the canul remains in the correct position for optimal support EO transport whether primary or secondary introduces a set of considerations Central for ensuring the safe and effective transfer of patients requiring this Advanced life support intervention primary transport involves the movement of the emo team to the referring facility emphasizing the need for an expedience arrival to initiate EO support promptly on the other hand secondary transport involves conveying the patient to an ECMO Center emphasizing the importance of timely stabilization before transport the ECMO team must evaluate the patient's condition ensuring stability and Readiness for transfer to mitigate potential complications during transport additionally considerations extend extend to the need for supplemental equipment and supplies including ECMO related technology and monitoring devices the vehicle's capacity to accommodate the EO team along with the necessary equipment and supplies is a critical factor in facilitating a smooth and well prepared transport process in ECMO transport scenarios careful planning timely coordination and attention to patient stability are extremely important these considerations collectively contribute to the seamless execution of ECMO related inner facility transport ultimately enhancing the quality of care and patient outcomes in the critical care transport",
        "Microaxial Catheter Pump Systems": "setting microaxial catheter pump systems the microaxial continuous flow pump exemplified by devices like the impella stands out as a temporary circulatory support mechanism crucial in managing various cardiovascular conditions this Innovative system comprises an axial flow pump integrated into a catheter with a connection to a bedside console for comprehensive Control operating on the the principle of reducing ventricular workload and providing circulatory support the microaxial pump facilitates blood Movement by drawing it through the inflow canula situated in the left ventricle and expelling it through an outflow port in the ascending aorta Critical Care transport teams functioning within referral networks for cardiogenic shock should be well prepared for inner facility patient transport report s involving the microaxial continuous flow pump system particularly the impella this device has found application in diverse clinical scenarios including cardiogenic shock low output syndrome stemi ventricular support during high-risk percutaneous coronary interventions unloading the left ventricle during VA EO and managing cardiac compensation while on VV EO support despite its versatility it's noteworthy that the impella system is not explicitly designed for transport because of this transporting patients supported by this system requires specialized considerations and expertise from the transport team to ensure the seamless continuation of circulatory support during the transport process Central to the impella system is a catheter intricately connected to an automated controller and a purge fluid infusion pump the impella controller or the AIC assumes a pivotal role in overseeing and managing various aspects of the pump's operation as well as monitoring the catheter's position within the cardiovascular system the AIC is equipped to assess and regulate critical parameters including performance level impella flow placement signal and motor current the performance level denotes the efficiency and intensity of the pump's action ensuring that it aligns with the patient specific circulatory needs impel a flow refers to the rate at which blood is drawn into the pump and propelled through the circulatory system a vital metric for gauging the support provided the placement signal allows real-time tracking of the catheter's position ensuring optimal alignment within the left ventricle for Effective circulatory assistance monitoring motor current provides insights into the power consumption and mechanical function of the pump offering a comprehensive assessment of its performance transport of patients supported by impella catheters involves specific considerations to ensure the seamless continuation of circulatory support during the transition one noteworthy Advantage is the resilience of impella catheters to changes in atmospheric pressure making them well suited for both ground and Air transport this characteristic underscores the adaptability of the system to various environmental conditions facilitating the movement of critically ill patients between Health Care Facilities prior to initiating transport the provider plays a crucial role in conducting a comprehensive assessment this assessment encompasses an evaluation of the patient's overall condition emphasizing Factor that might impact circulatory support specific attention is directed towards the assessment of catheter position insertion site and depth ensuring optimal placement within the cardiovascular system for Effective ventricular assistance Additionally the critical care transport provider evaluates the patient's position immobilization of extremities and the Integrity of all lines and tubing connected to the impella system a thorough examination of the automated impella controller the status of the battery and the infusion of purged fluid further contributes to the Preparatory measures for transport this assessment ensures that all components of the system are functioning optimally and potential issues are identified and addressed the integration of these considerations ations into the transport plan reflects the commitment to maintaining the stability and efficacy of circulatory support provided by the system throughout the entire patient transfer process the assessment of the patient involves a detailed analysis of Vital Signs hemodynamic parameters and the general clinical status particular attention is is given to any signs of hemodynamic compromise or changes in the patient's cardiovascular stability concurrently the critical care transport provider scrutinizes the impella pump evaluating its operational status and verifying the continued optimal positioning of the catheter within the cardiovascular system this involves assessing the devices performance parameters including flow placement signal motor current and other relevant metrics monitored by the automated impella controller by diligently scrutinizing both the patient and the system post transport the provider ensures the seamless continuity of circulatory support and promptly addresses any issues that may arise in the event of dislodgment or malpositioning of the micro axial catheter a prompt and systematic response is essential providers should continue the catheter and Purge solution to maintain circulatory support simultaneously decreasing the power level to P2 is recommended to mitigate the risk of further complications effective communication with the accepting facility is critical ensuring that the receiving team is informed of the situation and can prepare accordingly importantly providers should refrain from attempting to reposition the catheter during transport emphasizing the need for expert intervention upon arrival at the destination catheter motor failure poses a significant challenge to the management of microaxial catheter pump systems in response to motor failure healthc care providers are advised to administer inotropic and or vasopressor agents to stabilize the patient's hemodynamics similar to scenarios involving dislodgment attempting to reposition the catheter in the transport environment is strongly discouraged instead focus should be on supportive measures and seamless communication with the receiving facility microaxial catheter pump systems are equipped with alarm systems to alert healthc care providers to specific issues three common alarms include the suction alarm Purge alarm an air in The Purge system alarm addressing a suction alarm involves investigating the underlying cause ensuring proper preload and volume status and adjusting settings as needed the purge and Air in The Purge system alarms necessitate meticulous evaluation of the microaxial catheter pump system to identify and rectify issues affecting fluid management providers should be Adept in interpreting and responding to these alarms collaborating with Specialists when needed to optimize patient care in summary managing complications in the micro axio catheter pump system Demands a thorough understanding of the device adherence to established protocols and effective communication by following appropriate steps in the face of dislodgment motor failure and common alarms healthc care providers contribute to the safe and efficient transport of patients relying on these systems for circulatory support regular training and familiarity with these systems enhance providers preparedness in handling these complexities",
        "Implantable Left Ventricular Assist Devices": "implantable left ventricular assist devices heart transplantation Remains the definitive therapeutic option for patients grappling with inst stage heart failure representing the gold standard in Cardiac Care however the demand for donor Hearts far surpasses the available Supply creating a significant imbalance in the number of patients awaiting transplantation and The Limited number of donor Hearts accessible globally there has been a sustained reduction in the overall number of heart transplantations performed with an estimated 50,000 individuals worldwide affected by this scarcity in the United States alone the situation is exemplified by the daunting figure of approximately 4,000 people people concurrently awaiting transplantation underscoring the pressing need for alternative interventions in response to the challenges posed by the scarcity of donor Hearts left ventricular assist devices or El ads have emerged as a vital and increasingly effective therapeutic Avenue for patients awaiting heart transplantation or those who are simply ineligible for the procedure temporary Continuous Flow lvads have demonstrated notable success in providing prolonged and efficient circulatory support becoming a crucial bridge to transplantation strategy for patients with heart failure who have undergone the implantation of current generation Continuous Flow lvads the clinical landscape is notably optimistic with a 30-day mortality survival rate reaching an impressive 9 5% El vads serve a multifaceted role in the realm of advanced Cardiac Care with distinct indications that cater to the diverse needs of patients grappling with heart failure one key indication is as a bridge to recovery where the elad functions as a mechanical circulatory support mechanism in this scenario the elad is deployed to provide circulatory assistance until the native heart can regain its intrinsic pumping ability this temporary support allows for a period of rest and Recovery fostering the prospect of the heart resuming normal function without the ongoing Reliance of mechanical assistance another indication for elad use is as a bridge to transplantation in instances where heart transplantation is deemed the optimal therapeutic course the elad is employed as a bridge sustaining the patient's life and cardiovascular function until a suitable donor heart becomes available in this context the elad acts as a vital interim solution enabling patients to survive and maintain a reasonable quality of life while navigating the challenging weight for a heart transplant Beyond bridging strategies lvads are also utilized as destination therapy representing a long-term solution for patients with heart failure who may not meet the criteria for heart transplantation in cases where transplantation is not a feasible option either due to Patient specific factors or other contraindications elad serve as a destination therapy providing ongoing mechanical circulatory support to enhance overall cardiac function and improve the patient's quality of life over an extended period these nuanced indications highlight the versatility of lvads in addressing the diverse clinical scenarios encountered in the management of heart failure stratifying heart failure is Paramount for tailoring precise therapeutic interventions engaging disease severity two widely adopted classification systems the American heart association's heart failure stages and the New York heart association's functional classification system serve as comprehensive Frameworks for categorizing heart failure patients based on different criteria the New York heart association's functional classification system is a subjective evaluation that assesses the extent of heart failure systems exper experienced by patients delineating stages from a to d this classification method provides a nuanced understanding of the progression of symptoms helping clinicians to delineate the severity of the disease and formulate appropriate management strategies conversely the American heart association's heart failure stages employ a more objective approach utilizing a range of diagnostic tools such as ccgs stress tests echocardiology and Radiology Imaging to Gather Comprehensive data for patient classification this method allows for a more detailed and quantifiable assessment of heart failure taking into account both clinical symptoms and objective measures of cardiac function in addition the inter agency registry for mechanically assisted circulatory support has introduced a valuable tool for stratifying patients in the context of elad implantations known as the intermax registry the registry has developed patient profile levels ranging from 1 to 7 providing an additional layer of classification to assist in the identification of Ideal candidates for elad inter ventions these profile levels offer a nuanced assessment that considers various factors including the severity of heart failure symptoms functional capacity and overall clinical status this stratification system AIDS clinicians in characterizing patients more precisely based on their unique clinical profiles facilitating the selection of candidates who are most likely to benefit from elad impl Plantation incorporation of profile levels into the stratification process enhances the decision-making process for candidacy contributing to improve patient outcomes and optimize resource utilization in the management of advanced heart failure the combined use of these classification systems contributes to a holistic understanding of heart failure enabling Health Care Providers to stratify patients based on both subjective and objective parameters this dual approach facilitates a more comprehensive evaluation of the disease supporting the development of tailored treatment plans and interventions that align with the specific needs and severity of each patient the evolution of the elad across multiple Generations reflects significant strides in mechanical circulatory support technology the advancements seen from the initial to the third generation have contributed to enhanced clinical outcomes and expanded applicability notably the progressive reduction in the size of the elad devices has been a pivotal achievement allowing for more minimally invasive implantation techniques and improving patient Comfort secondly improvements in the performance and durability of the lvads Mark another notable Milestone enhanced mechanical reliability and extended durability are important factors in the long-term success of elad therapy reducing the need for device Replacements and mitigating potential complications associated with device malfunction moreover the evolving technology has led to Advanced clinical applicability broadening the spectrum of patients who can benefit from LV add support the refinement of device algorithms optimization of hemo compatibility features and increased understanding of patient selection criteria have collectively contributed to the expanded use of lvads in diverse clinical scenarios including bridge to recovery bridge to transplantation and destination therapy the transition from first generation to Second Generation elv ads was considered a significant advancement in mechanical circulatory support technology the first generation also recognized as a volume displacement pump employed pump Chambers with one-way valves to regulate inflow and outflow replicating an augmented pulsatile flow similar to Native heart function while this design represented a significant step forward in addressing heart failure it did come with inherent limitations these limitations encompassed an elevated risk of bleeding cerebrovascular accidents both embolic and hemorragic infectious complications and a notable noise Factor during operation recognizing these challenges researchers and Engineers turned their focus towards developing the second generation transitioning from pulsatile flow to Continuous Flow technology in the second generation El vads were characterized by positive displacement pumps which brought about notable benefits these included a reduction in device size improved patient Comfort extended operating time and a quieter operation compared to its predecessor the shift to Continuous Flow technology not only addressed some of the limitations but also opened up possibilities for application in smaller patients however it is important to acknowledge that the second generation elad came with its own set of limitations including a slightly diminished ability to prevent Strokes concerns about pump thrombosis GI bleeding and potential challenges in achieving optimal ventricular unloading despite these considerations second generation lvads represented a significant Leap Forward in the refinement of mechanical circulatory support devices the evolution of lvads reached a pivotal point with the Advent of the third generation device showcasing significant achievements in design and functionality the third generation characterized by Continuous Flow technology and the centrifugal design aimed to further refine cardiac support while addressing specific challenges associated with the second generation counterparts one of the notable improvements in the third generation elad was the mitigation of non- pulsi effects that had been observed in the second generation models these effects included complications such as GI bleeding aortic in efficiency and pump thrombosis the centrifugal design of the third generation elad played a role in achieving a more physiologically effective and hemo compatible Continuous Flow mechanism by incorporating these refinements the third generation elad sought to enhance patient outcomes by reducing Adverse Events and optimizing the devices ability to provide sustained and effective circulatory support the the ongoing progress in elad technology particularly with the development of third generation devices underscores the commitment to advancing mechanical circulatory support as a viable therapeutic option for patients with Advanced heart failure the integration of el vads into the community has become increasingly prevalent with over 24,000 patients in the United States alone relying on these Advanced Mechanical circulatory support systems patients equipped with lvads are typically well-versed in the intricacies of their devices understanding that their functioning and the essential maintenance involved in ensuring Optimal Performance for emergency medical service providers possessing a comprehensive understanding of lvads is extremely important this includes the ability to troubleshoot the device discern which emergency interventions are are permissible and knowing how to promptly contact elad support staff recognize the growing significance in Community Health Care there is a pressing need for standardized and universally applicable elad Management training systems for EMS and critical care transport services such training programs ensure that healthc Care Professionals are equipped with the knowledge and skills required to navigate the unique challenges posed by Elvis patients during emergency situations as El vads continue to be a vital component of heart failure management fostering widespread Proficiency in their management ensures the seamless integration of this life-saving technology into routine emergency medical care considerations for placement involve an assessment of various factors to ensure Optimum outcomes for candidates as discussed earlier risk stratification plays a pivotal role with the valuations based on the New York Heart Association and inmax classifications allowing for a comprehensive understanding of the patient's heart failure severity and overall clinical status age aortic valver regurgitation right ventricular function infection bleeding disorders and the presence of irreversible hepatic or renal failure are all critical factors in the decision-making process additionally metastatic cancer a history of cerebral vascular accidents with neurological deficits and psychosocial status with adequate support are carefully evaluated to gauge the patients overall suitability for implantation geriatric patients often presenting with multi-organ dysfunction and comorbidities require especially thorough scrutiny during the candidate selection process assessing social support and evaluating the level of Frailty become crucial considerations in determining the appropriateness of elad placement for this demographic to mitigate the risk of pump thrombosis anti-coagulation therapy is typically initiated commonly involving the youth of warin in specific cases aspirin may be added to the anti-coagulation regimen to further optimize the balance between preventing thrombotic events and minimizing bleeding risks for lbad recipients Adverse Events associated with elad constitute a complex spectrum of complications demanding Vigilant attention and immediate intervention from Critical Care transport providers bleeding a prevalent adverse event often necessitating hospitalization the GI tract stands out as a frequent source of bleeding consideration a prophylactic use of anti-coagulants and antiplatelet agents may be warranted to mitigate bleeding risks infections among the most prevent complications associated with lvads infections are commonly localized to the drive line with potential extension to the pump and pocket predictors of infection include an elevated body mass index and advanced age prevention strategies involve the use of anchors for Drive Line immobilization and binders as recommended by elad implantation programs es schic and hemorrhagic stroke hypertension emerges as a significant risk factor for stroke maintaining a Target mean arterial pressure range of 70 to 80 is crucial in preventing Strokes mechanisms contributing to Strokes include embolic sources such as thrombus formation meticulous management of anti-coagulation during bleeding episodes is Paramount cardiac arrhythmias atrial INF ventricular arrhythmias are common in elad recipients treatment options Encompass anti-coagulation rate control beta blockers calcium channel blockers implantable cardioverter defibrillator therapy and anti-ar rythmic drugs some Tachi arhythmia may be tolerated well by patients thrombosis this is a potentially life-threatening complication that demands urgent attention signs of inadequate circulation May signal thrombosis consultation with the elad center is critical before transferring the patient right side heart failure right ventricular failure is a relatively common occurrence occurring about 5 to 13% of the time in elad patients symptoms include typical heart failure symptoms and fluid overload management focuses on right ventricular preload right ventricular after load right ventricular contractility and Rhythm adjustments in pump speed mechanical circulatory support or ECMO may be necessary device malfunction this extends Beyond pump failure encompassing malfunctions in the components malfunction can lead to heart failure symptoms cardiogenic shock and potential mortality recognition necessitates a comprehensive understanding of pump controller battery and percutaneous lead functions mental health living with an elad entails constant monitoring and significant lifestyle adjustments depression and anxiety may vary throughout the patient's care TR trory underscoring the importance of consistent psychological support respiratory failure this is a common occurrence either before or after elad implantation elad recipients experiencing respiratory failure are at an increased risk of renal failure early recognition of adverse offense related to respiratory failure is imperative to prevent a Cascade of complications shock this is defined as a map below 60 mm of mercury typically secondary to hypohemia Critical Care transport providers should anticipate in elad flows and be prepared for potential suction events hypertension this is defined as a map of greater than 110 millim of Mercury maintaining a goal map of 70 to 80 millim of mercury is recommended to prevent Adverse Events such as stroke pump thrombosis and aortic insufficiency ventricular recovery a pivotal goal in treating inst stage heart failure with elad mechanisms of recovery vary based on cardiac pathology patient specific factors and overall recovery duration ation outcomes from bridging to recovery treatment approaches demonstrate promising safety and long-term survival inflow canula Mal positioning ideally positioned along a line from the Apex to the center of the mitro valve Mal positioning may involve deviations towards Superior inferior septal or lateral walls the type of pump used influences the incident of malpositioning with axial pumps associated with a higher number of instances compared to smaller centrifugal flow pumps designed for direct intracardial placement the displayed pump flow represents a calculated value directly linked to the set revolutions per minute and power a rise in power results in a corresponding increase in the calculated flow the device flow demonstrates a direct proportionality to the revolutions per minute and an inverse relationship to the disparity between the inflow and outflow canulas the mathematical representation would be device flow equals Rotator speed over pump inflow minus pump outflow the intricacies of pump flow Dynamics are essential in understanding the performance of the left ventricular assist device the displayed pump flow a computed parameter serves as a direct indicator of the interactions between the devices rotational speed and the power it consumes notably elevations and power directly translate to heightened calculated flow highlighting the interdependence of these variables a more detailed examination reveals that device flow is intricately linked to the revolutions per minute and is inversely correlated to differential pressures between the inflow and outflow canulas the mathematical representation capturing this relationship emphasizes the importance of both speed and pressure differentials and determining the resultant flow the pump revolutions per minute setting stands as a pivotal parameter in regulating the function of the left ventricular assist device primarily this setting serves as the determinant of the pump flow a critical aspect of the device's performance the responsibility of configuring this setting typically lies with either the cardiac surgeon or the attending physician who meticulously calibrates it to a line with the dynamic requirements of the patient adjustments to the revolutions per minute setting are made in response to changing flow needs reflecting the adaptability of the elad to the varying hemodynamic conditions of the individual the output generated by the elad is intricately linked to preload afterload and the pump speed it is worth noting that unlike the heart's natural response to loading conditions the pump speed remains fixed underscoring a distinctive characteristic of elad operation this fixed pump speed ensures a consistent and controlled flow independent of the heart's loading conditions contributing to the device's reliability and predictability in providing circulatory support pump power stands out as a critical parameter providing insights into the devices operational Dynamics defined as the measurement of the current necessary to sustain the pump's Revolution per minute at a designated speed pump power is a direct indicator of the energy required to maintain optimal functionality an elevation imp pump power is a signal that warrants attention as it often signifies the formation of a thr us within the pump thrombus formation poses a serious concern as it can impede the smooth operation of the device potentially compromising its ability to provide effective circulatory support therefore an increase in pump power prompts a Vigilant response from healthc care providers to investigate and address potential thrombotic complications promptly conversely decreases in pump power power more commonly result from a low battery as the power source diminishes the device may experience reduced efficiency reflecting in lower pump power readings monitoring and addressing power related issues are crucial components of elad management ensuring the devices sustained and reliable performance in supporting the circulatory needs of patients with heart failure the pulsatility index or Pi in the context of lvads is a vital hemodynamic parameter that provides crucial insights into the Dynamics of blood flow through the pump this metric serves as a quantitative measure of the magnitude of flow puls generated by the device essentially it reflects the degree of pulsatile behavior in blood flow circulation facilitated by the elad under normal physiological conditions the pi is subject to fluctuations based on changes in preload and contractility an increase in preload and enhanced contractility is mirrored by an elevation in the pulsatility index this rise signifies a more pronounced pulsatile flow characteristic of a heart that is adequately filled with blood and Contracting effectively on the other hand the pulsatility index experiences a decrease when both preload and after load diminish conditions such as an obstruction in the circulatory pathway can contribute to decreased preload and increased after load which again results in a reduction in the pi monitoring the pi is critical for assessing the hemodynamic status of patients with lvads it provides valuable information about the device's interaction with the cardiovascular system and AIDS clinicians in optimizing settings to achieve an appropriate balance between pulsatile and continuous flow the pi therefore serves as a key parameter in the comprehensive evaluation and fine-tuning of elad therapy to meet the specific hemodynamic needs of individual patients effective management of lvads involve a comprehensive understanding of potential abnormal conditions and the ability to troubleshoot them promptly two critical issues that may arise are suction events and cable failure or disconnection suction events represent a significant concern in elad management often associated with lowf flow situations these events can occur for various reasons including arhythmia and hypovolemia during suction events the elad pump May draw blood at an excessive rate leading to a decline in left ventricular filling and potential complications addressing suction events promptly is important to prevent adverse outcomes and this involves identifying and rectifying the underlying causes such as managing arrhythmias or addressing hypohemia through appropriate fluid resuscitation the intricate nature of elad systems involves multiple specific connections and points of attachment making cable failure or disconnection a potential issue the cables play a vital role in transmitting power and control signals between the external components and the internal components a failure at any point in the cabling system can disrupt the communication and power supply to the elad jeopardizing its functionality Critical Care transport providers must be Adept in identifying cable related issues promptly this may involve inspecting cable Integrity ensuring secure connections and troubleshooting any faults or disconnections to maintain the continuous and reliable operation of the elad in both scenarios a systematic and proactive approach to troubleshooting is important this includes thorough assessments prompt identification of causitive factors and decisive interventions to restore optimal function and prevent complications associated with these abnormal conditions the battery alarm is a pivotal component of elad monitoring signaling a decrease in the power source's capacity or potential potential issues with the battery elvs typically rely on external power sources and a declining battery can compromise the device's functionality upon activation of the battery alarm Critical Care transport providers must promptly address the situation by addressing the battery status ensuring proper connections and preparing for a potential switch to Alternative power sources or a fresh battery Timely intervention is necessary to prevent interruptions to elad support and maintain patient safety during transport cable disconnect symbols are visual indicators that alert Health Care Providers to potential disruptions in the communication or power transmission between various components of the elad system these symbols may appear in response to Cable failures disconnections or other issues affecting the Integrity of the system when cable disconnect symbols are illuminated Critical Care transport providers must conduct a thorough examination of the elad's cabling infrastructure this involves inspecting connections identifying cable faults and addressing any issues that would compromise the proper functioning of the elad ensuring secure and reliable cable connections is essential for maintaining continuous elad support and preventing Adverse Events associated with system malfunctions in conclusion the comprehensive understanding of mechanical circulatory support is undeniably Paramount for critical care transport professionals as we've delved into the intricacies of intra aortic Ploom pumps extracoporeal membrane oxygenation microaxial catheter pump systems and left ventricular system ass devices you should see that these Advanced interventions are integral components in the Continuum of critical care Mastery of these mechanical circulatory support Technologies empowers providers to navigate complex clinical scenarios ensuring the safe and effective transport of patients with compromised cardiac function the information in this lecture not only enhances the technical proficiency of critical care transp professionals but also fortifies their capacity to make informed split-second decisions in high stakes situations whether managing the delicate nuances of balloon inflation and deflation in iabps orchestrating the intricacies of ECMO circuitry addressing complications in microaxial catheter pump systems or optimizing patient outcomes with Lads this expertise UR ures a holistic approach to Patient Care during transport in the dynamic field of critical care where every moment is critical the Mastery of mechanical circulatory support emerges as an indispensable asset allowing transport professionals to serve as catalysts for positive patient outcomes in the realm of cardiovascular emergencies"
    },
    {
        "Introduction": "chapter 14 electrophysiology pacemakers and defibrillators intr reduction Critical Care transport professionals are at the Forefront of providing care to patients with cardiac arrhythmias and their expertise in this field is Paramount their role goes beyond the immediate patient care extending to the interpretation in Vigilant monitoring of 12 lead electrocardiograms understanding the electrophysiological basis for ECG changes and their implications on the patient's condition is crucial providers also need to be well-versed in temporary and implanted pacemakers and defibrillators ensuring these life-saving devices are functioning optimally during transport transport safety is of utmost importance and providers must be equipped to troubleshoot any issues that may arise with these cardiac devices in route ensuring that their patients receive the highest standard of care in the critical care transport setting cardiac monitoring is a fundamental component of patient care involving a comprehensive assessment of the patient's electrical Rhythm through three or more leads additionally when necessary the serial evaluation of 12 lead ECGs is conducted to gain deeper insights into the patient's cardiac status traditionally cardiac arrhythmias have been managed with pharmacological interventions which may sometimes result in unwelcome side effects and in certain instances ineffectiveness despite proper prescription and compliance however the evolving landscape of pacing technology has ushered in a new era in the treatment of arrhythmias This Modern approach allows for the electrical treatment of various arrhythmias often with minimal to no patient awareness at the time of therapy delivery offering a promising alternative that can significantly improve the patient's quality of life while ensuring optimal Cardiac Care the management and treatment of advanced heart failure and cardiac arrhythmias have seen a remarkable expansion of therapeutic options significantly improving patient outcomes this broader spectrum of interventions encompasses various Cutting Edge Technologies such as implanted pacemakers that can provide life-saving pacing support to maintain proper heart rhythms or temporary pacemakers which can be deployed in both transvenous and transcutaneous forms to swiftly address Rhythm abnormalities additionally wearing defibrillators offer portable continuous monitoring and defibrillation capacity for high-risk patients while implantable cardio over verter defibrillators have become an essential tool in delivering timely and effective defibrillation for individuals at risk of sudden Cardiac Arrest due to ventricular teoc cardia or fibrillation this extensive range of therapeutic options has significantly improved the quality of care and quality of life for patients with Advanced heart failure and those experiencing cardiac arrhythmias underscoring the transformative impact of these Innovations in modern cardiac",
        "Cardiac Anatomy and Physiology": "medicine cardiac anatomy and physiology the heart as a vital muscular organ Demands a continuous and abundant supply of oxygen and nutrients to maintain its Relentless pumping action this essential life support is facilitated through a complex network of coronary arteries that deliver oxygenated blood directly to the heart muscle emerging from the aorta just above the aortic valve these coronary arteries serve as the principal conduits for this vital nourishment in a remarkable display of redundancy and adaptability the arterioles within the coronary circulation exhibit a capacity for anastomosis which enable the formation of collateral circulation channels in instances where blockages or restrictions occur in the primary Cor ordinary arteries this built-in resilience ensures that the myocardial cells have access to life- sustaining resources even when facing potential obstacles and underscores the remarkable design of the cardiovascular system to meet the needs of the heart the heart's rhythmic ldub Cadence represents more than just a beat it provides valuable auditory insight into the heart's function these sounds convey the harmonious operation of the cardiac valves serving as an acoustic indicator of proper cardiac function there are two primary normal heart sounds known as S1 and S2 S1 often referred to as the Lu marks the closure of the atrioventricular valves initiating ventricular contraction on the other hand S2 or the dub signifies the moment when the semi lunar valve shut denoting the end of ventricular ejection additionally there are two abnormal heart sounds S3 and S4 which when present can offer diagnostic Clues to underlying cardiac conditions these sounds combined with clinical assessments Aid healthc Care Professionals and understanding and managing various heart Related Disorders highlighting the importance of listening carefully to the hearts Symphony for Clues to its overall health and performance let's take a listen to the heart sounds we'll start with S1  S2 now let's take a listen to the S3 sound S3 will occur right after S2 lastly let's take a listen to S4 S4 will occur immediately before S1 S3 and S4 often referred to as the Kentucky and Tennessee gallops respectively provide important auditory cues during cardiac examinations S3 the Kentucky Gallop occurs at the end of the rapid ventricular filling phase at the start of diast typically taking place on 120 to 170 milliseconds after S2 the presence of S3 is of particular significance in older adults where it may serve as a marker of heart failure this sound introduces an extra dub to the heartbeat rhythm resulting in a distinctive dub Lu dub Cadence S4 the Tennessee Gallop coincides with atrial contraction at the conclusion of ventricular diast appearing just before S1 its presence adding another love to the sequence contributes to a l dub dub Rhythm recognizing and interpreting these unique heart sounds plays a crucial role in diagnosing and managing cardiac conditions further underscoring their clinical significance in a processing heart health the cardiac cycle a fundamental component of heart function encompasses a full sequence of events within the heart's chambers it involves two distinct phases diast the relaxation phase and syy the contraction phase during diast which typically spans around 520 milliseconds the left Atri serves as a reservoir for blood receiving and collecting it from various parts of the body in this phase Approximately 80% of the ventricular filling occurs as the atrium facilitates the initial passive filling of the left ventricle this phase of relaxation is crucial as it allows the heart to replenish its Chambers with oxygenated blood preparing it for the upcoming contraction during diast where it will efficiently pump the blood to meet the body's demands understanding and monitoring these phases are vital in assessing cardiac health and function during the cardiac cycle the atrial contraction serves as a crucial function known as the atrial kick this occurs just before ventricular contraction begins when the Atria contract their contents which may include the remaining 20% of blood are forcefully squeezed into the corresponding ventricles this additional boost in blood volume during the atrial kick ensures that the ventricles are maximally filled optimizing the hearts efficiency in pumping blood to the body as ventricular syy or ventricular contraction commences the atrio ventricular valves such as the mitol and tricuspid valves promptly snap shut to prevent the backflow of blood into the Atria simultaneously the force generated by the Contracting ventricles propels the blood through the semi lunar valves into the pulmonary artery and aorta ensuring the directional flow of blood and effectively facilitating the ejection of blood from the heart to supply the entire circulatory system during syy the heart undergo a series of coordinated actions as the right ventricle contracts it forces blood through the pulmonic valve and into the pulmonary arteries which will carry oxygen poor blood to the lungs for oxygenation simultaneously the left ventricle contracts pushing oxygen-rich blood through the aortic valve and into the aorta initiating its journey to supply oxygen and nutrients to the entire body these contractions and valve movements are highly synchronized and efficient typically completing the systolic phase in approximately 280 milliseconds this rapid and coordinated activity ensures that blood is efficiently ejected from the heart's chambers facilitating the delivery of oxygen and nutrients to the body's tissues and organs while maintaining a unidirectional flow of blood the human heart functions as two separate pumps intricately connected the right side serves as a low press pump collecting oxygen poor Venus blood from the vena and the coronary sinus in the right atrium and propelling it into the right ventricle the right ventricle then pumps this blood into the pulmonary artery leading to the lungs where it undergos oxygenation on the other hand the left side of the heart functions as a high press pump it receives oxygenated blood from the pulmonary veins in the left atrium and this chamber effectively propels the oxygen-rich blood into the left ventricle from there the left ventricle powerful contractions Drive the blood out of the heart against the considerable resistance of the systemic arteries ensuring that oxygen and nutrients are efficiently distributed to the body's tissues and organs this division of labor in the heart's two sides enables it to perform effectively in its role as a vital circulatory organ the autonomic nervous system plays a crucial role in regulating arterial walls primarily through the function of Barrow receptors these specialized receptors are strategically located with within the walls of blood vessels and are finely tuned to detect changes in blood pressure when Barrow receptors sense an increase in blood pressure they initiate a response by stimulating the parasympathetic nervous system this simulation leads to a reduction in heart rate and a decrease in the force of myocardial contractions thereby working to lower the blood pressure conversely if be receptors sense a decrease in blood pressure they activate the sympathetic nervous system which results in an increased heart rate and stronger myocardial contractions additionally blood pressure isn't solely dependent on cardiac output and fluid volume within the circulatory system it is also heavily influenced by the degree of constriction or dilation in the arterial walls these mechanisms collectively help maintain the body's blood pressure within a normal and stable range chemo receptors serve as essential sensors for the body's chemical environment responding to variations and factors such as partial pressure of oxygen pH and partial pressure of carbon dioxide their responses are closely linked to the autonomic nervous systems activity thereby influencing heart rate and myocardial contractility furthermore Cho receptors play a role in regulating minute ventilation by releasing dopamine and communicating with the respiratory centers and the brain stem when chemo receptors detect conditions like hypoxia acidosis or hypercarbia they stimulate the sympathetic nervous system leading to increased heart rate and and stronger contractility actions intended to enhance oxygen delivery to the tissues in contrast hyperoxia alkalosis or hypocarbia prompt sympathetic nervous system stimulation which results in a reduced heart rate and decreased contractility to maintain a balanced physiological State these finely tuned responses help ensure that the body's oxygen and carbon dioxide levels remain within the optimal range to support overall homeostasis the heart's pumping function is essential to maintaining blood circulation throughout the body cardiac output quantifies the volume of blood ejected by either ventricle and the left and right ventricles typically exhibit similar capacities due to their similar interior sizes for an average adult a normal cardiac output Falls within the range of 4 to six lers per minute stroke volume characterizes the amount of blood discharged by either ventricle during a single heartbeat or contraction ordinarily stroke volume ranges from 60 to 100 milliliters but the heart retains substantial Reserve capacity enabling it to flexibly augment stroke volume volume by a minimum of 50% this ability to adjust stroke volume allows the heart to efficiently adapt to varying physiological demands and maintain vital blood circulation in response to the body's changing needs heart rate measures the number of cardiac contractions commonly referred to as heartbeats taking place within a minute which corresponds to the the pulse rate typically the normal heart rate range for adults spans from 60 to 100 beats per minute cardiac output representing the volume of blood ejected by either ventricle in one minute can be calculated by multiplying the stroke volume the volume of blood expelled during a single Heartbeat by the heart rate in situations where the body's oxygen demand escalates significantly the heart must respond by increasing its output this can be achieved by enhancing either the stroke volume or the heart rate or a combination of both factors the heart's ability to dynamically adjust these components enables it to meet the heightened oxygen requirements efficiently during periods of increased demand the Frank Starling mechanism plays a vital role in the the regulation of cardiac output and the heart's ability to adapt to varying demands this mechanism states that when the cardiac muscle fibers are stretched they contract more forcefully this principle holds that if there's an augmented volume of blood returning from the systemic veins to the right side of the heart or from the pulmonary veins to the left side the muscle surrounding the cardiac Chambers will stretch to accommodate the increased blood volume as the cardiac muscle stretches more the force of its contraction becomes greater leading to a more complete emptying of the heart's chambers consequently the stroke volume increases since cardiac output is calculated by multiplying stroke volume by heart rate any increase in stroke volume with a constant heart rate leads to an overall increase in cardiac output therefore the Frank Starling mechanism can be activated in response to heightened oxygen demands causing the body to return more blood to the heart which increases preload and consequently boosts cardiac output in situations involving a diseased heart this mechanism may help achieve a normal resting cardiac output by enlarging the heart a process that compensates for the heart's diminished pumping efficiency and reduced cardiac function contractility or inotropic state refers to the heart's ability to adjust strength of contraction without altering the muscle stretch this property is pivotal to maintaining cardiac output and meeting the body's demands for oxygen and nutrients medications can impact contractility either positively or negatively the ejection fraction a measure of the percentage of blood ejected from the ventricles during each heartbeat is a useful indicator of overall myocardial function enhanced contractility leads to a greater proportion of ventricular blood being ejected thereby increasing stroke volume and subsequently cardiac output the nervous system regulates contractility on a beatto beat basis with heightened contractility signaled when the body demands increased cardiac output when the heart needs to increase cardiac output with a constant stroke volume it can achieve this by elevating heart rate a process known as a positive chronotropic effect unlike the Frank Starling mechanism which is an intrinsic property of heart muscle and remains unaffected by the nervous system contractility and heart rate changes are under Direct Control of the nervous system allowing the heart to adapt to varying physiological demands the heart's electrical conduction system plays a crucial role in ensuring the rhythmic and coordinated contraction of its muscle tissue this system exhibits automaticity allowing it to independently generate electrical impulses even without external nervous system stimulation composed of specialized conduction tissue it rapidly propagates these impulses throughout the heart's muscle muscular tissue guiding the sequence of contractions for critical care transport professionals comprehending the intricacies of this electrical conduction system is essential as they frequently record these impulses on the ECG understanding the relationship between the activities of the conduction system and the 12 lead ECG interpretation is vital as it helps clarify the intricate process of impulses traveling in various directions within the heart this knowledge is fundamental in understanding how alterations in the heart structure or function can affect the propagation of these electrical signals facilitating effective assessment and management of cardiac conditions the primary pacemaker of the heart known as the sinoatrial node holds a pivotal role in the initiation of electrical impulses that orchestrate the cardiac cycle fed by the right coronary artery the essay note relies on a consistent blood supply for its proper functioning however when the RCA becomes obstructed typically due to an MI the SA node faces the risk of esema in such cases the sa nodes conduction cells May succumb to es schic damage leading to a cessation of electrical discharge the sa nodes electrical signals not only serve as the fastest pacemaker in the heart but also act as the instigators of a coordinate Rhythm these impulses propagate through intraatrial Pathways sometimes referred to as atrion noal Pathways this intricate Network encompasses structures like the anterior or Bachman bundle the middle bundle and the posterior internodal system which is responsible for transmitting the electrical stimuli across the atrial walls causing depolarization of atrial tissue as they Traverse in most individuals around 85 to 90% the blood supply to the SA node is routed through the branch of the RCA while the remaining 10 to 15% it derives from a branch of the left circum flux artery underscoring the variability in this critical cardiac structure's vascularization the atrioventricular node serves a vital role in cardiac conduction by slowing down the electrical impulses progression this deliberate delay allows the Atria sufficient time to complete their contraction ensuring effective emptying into the ventricles however when the atrial rate becomes excessively rapid as in certain arrhythmias not all atrial impulses can navigate the AV Junction ordinarily these impulses proceed through the AV node enter the bundle of hiss and then propagate swiftly to the right and left bundle branches situated on either side of the intraventricular septum from there they fan out into the extensive network of preni fibers which comprises numerous fibral dispersed through the ventricular muscle this orchestrated sequence takes approximately 80 milliseconds for the electrical imp BS to Traverse the ventricles ensuring a coordinated and efficient ventricular contraction the influence of various factors on the velocity of conduction through the cardiac conduction system is described as the dromotropic effect as the electrical impulses travel through the heart they encounter cardiac cells that actively participate in the depolarization process through their inherent characteristics of automaticity and conductivity depolarization is the pivotal process that sets the stage for muscle fibers to contract within the cardiac cells an electrolyte solution envelops them while chemical pumps inside the cell meticulously manage the ion concentrations thereby creating an electric gradient across the cell membrane in its resting state a myocardial cell maintains a negative charge around negative 90 molts concerning the cell's exterior however when stimulated these cells undergo a change in permeability opening the specialized channels that allow for an influx of sodium ions this influx results in the an interior of the cell becoming more positively charged additionally calcium ions also enter the cell via a different set of specialized channels further contributing to the depolarization process that initiates myocardial contraction depolarization is a remarkable process that initiates cardiac muscle contraction it commences at a single point within the myocardia cell and propagates as a wave aptly termed the wave of depolarization extending until the entire cell undergos depolarization the entry of calcium ions which are essential for muscle contraction accompanies this depolarization including mechanical contraction within the cardiac cells importantly the magnitude of this wave of depolarization correlates with the mass of the cardiac muscle involved as individual cells undergo depolarization they each generate a small electrical vector and the collective sum of these vectors creates the electrical axis an important parameter in electrocardiography this intricate process leads to Mechanical contraction as the cells depolarize driving blood through the coronary arteries during diast to facilitate cardiac function and ensuring the pumping of blood from the base to the apex of the heart effectively propelling it through both the pulmonary and systemic circulatory systems repolarization is the phase that follows depolarization and it begins with the closure of sodium and calcium channels ceasing the influx of these ions into the cell simult ously the potassium channels open facilitating the rapid efux of pottassium ions from the cell this outflow of potassium ions restores the inside of the cell to its negative charge to reestablish the proper distribution of electrolytes sodium ions are actively pumped out of the cell and potassium ions are actively transported back into it this process ensures the cardiac cell returns to its resting or polarized State and is prepared for another cycle of electrical and mechanical activity the heart's electrical conduction system plays a crucial role in maintaining a coordinated and rhythmic heartbeat it consists of specialized cardiac cells that generate electrical impulses to initiate and regulate the heart's contractions the primary pacemaker of the heart is the SA node which is located in the right atrium near the opening of the superior vnea the SA node generates electrical impulses at a rate of 60 to 100 times per minute under normal conditions set in the pace for the heart's contractions this natural firing rate ensures that the heart beats in an appropriate Rhythm to meet the body's oxygen and nutrients demands if the SA node becomes damaged or fails to function correctly other components of the cardiac conduction system can act as secondary pacemakers these secondary pacemakers are typically located farther down the conduction pathway and have intrinsic firing rates that are slower than the SA node the atrio ventricular Junction can spontaneously fire at a rate of 40 to 60 times per minute and the pereni system can fire at a rate of 20 to 40 times per minute these secondary pacemakers serve as backup systems to initiate electrical impulses when the SA node is compromised measuring and interpreting the electrical conduction activity of the heart often through an electrocardiogram is crucial for diagnosing arrhythmias in assessing the heart's health and function understanding the electrical events within the heart is essential for Health Care Professionals particularly those involved in critical care transport as it helps them recognize and manage arrhythmias and other cardiac issues in their patients the measurement of the heart's electrical conduction activity often achieved through an ECG is a fundamental tool in diagnosing and monitoring cardiac health when observing an ECG the electrical events within the heart are displayed as a series of waves and complexes among these components the p-wave signifies the initial depolarization of the Atria that being said it's important to note that after the p-wave there is a brief pause known as the PR interval this pause occurs because the electrical conduction is momentarily slowed as it passes through the AV Junction this delay allows times for the ventricles to fill with blood following the atrial contraction the PR interval on an ECG provides valuable information about the conduction time and the coordination between the Atria and ventricles aiding Health Care Professionals in identifying any abnormalities or rhythmia as in the heart's electrical activity in the context of ECGs the QRS complex plays a significant role as it represents the electrical impulses that Traverse through the right and left bundle branches and the peni fibers indicating the depolarization of the ventricles the subsequent component the t-wave signifies the repolarization of both the Atria and the ventricles although the atrial repolarization wave is rather small and hidden within the QRS complex the larger ventricular t-wave follows it the ST segment on the ECG appears between the conclusion of the QRS complex and the commencement of the t-wave this ST segment represents the phase of inactivity during which the ventricles are maintaining contraction which has a particular clinical relevance Additionally the presence of a uwave following the t-wave although not entirely understood in its significance can provide valuable insights into certain cardiac conditions furthermore any alteration in the structure or function of cardiac cells results in changes in the size and shape or morphologic features of the ECG complexes making ECG interpretation a crucial tool in assessing cardiac health and diagnosing arrhythmias or cardiac",
        "Cardiac Monitoring: 12-Lead ECG": "abnormalities cardiac monitoring the 12 lead ECG modern cardiac monitors and defibrillators are sophisticated multi-parameter devices that provide a comprehensive Suite of functions for monitoring and managing patients in various clinical settings these devices offer continuous three-lead ECG monitoring which is crucial for tracking the heart's electrical activity in real time furthermore they are equipped with the capability for 12 lead ECG enabling more in-depth assessments of cardiac health the inclusion of semi-automatic and manual defibrillation features allows for rapid response to life-threatening arrhythmias these devices can also offer external pacing when necessary as well as capnography and pulse Lo symmetry for monitoring ventilation and oxygenation additional functionalities such as blood pressure monitoring entitle carbon dioxide measurements and even invasive pressure monitoring provide a more comprehensive view of a patient's cardiovascular status allowing Health Care Providers to make well-informed decisions and deliver effective care these multi-parameter devices are essential Tools in critical care emergency medicine and cardiac settings before initiating monitoring a thorough assessment of the patient's cardiac status is essential this assessment should Encompass a comprehensive analysis of the cardiac Rhythm and when appropriate a 12 lead ECG by evaluating the patient's cardiac Rhythm healthcare providers can identify any arrhythmias irregularities or abnormalities in the heart's electrical activity additionally a 12 lead ECG offers a more detailed examination of the heart's conduction system which can reveal critical information about esea infarction or other cardiac conditions this initial assessment is a crucial step in determining the patient's Baseline cardiac health and guides subsequent monitoring and treatment strategies ensuring the most appropriate care for the individual's specific cardiac needs lead placement is a critical aspect of acquiring accurate and consistent ECG readings but it can vary depending on the equipment and techniques used different machines and manufacturers may have their own proprietary lead sets and configurations which highlights the importance of standardization for precise 12 lead ECG interpretation the gold standard in ECG interpretation involves the ability to perform serial evaluations for comparison ensuring consistent lead placements for accurate assessments this text adheres to standard lead placements with electrodes serving as sensing devices connecting directly to the skin and Lead leads designating specific positions for the electrodes which can be limb leads or precordial leads by maintaining a standardized approach to lead placement healthc care providers can ensure the reliability and consistency of ECG data facilitating accurate diagnosis and monitoring of cardiac conditions proper preparation of the skin and electrodes is essential for obtaining accurate ECG readings to ensure a reliable connection the skin should be cleaned dried and lightly abraded with a gauze pad to remove oils and promote electrode adherence in cases of excessive chest hair safe clipping with a razor may be necessary patients with profuse sweating may require the application of topical compounds like benzoin to enhance electrode adherence furthermore the choice of conduction medium for the skin electrode is crucial typically a gel is used but it can dry out when exposed to air therefore it's important to replace electrodes daily to prevent drying and maintain optimal conduction additionally keeping electrodes in Pacer def fibrillator pads sealed in their packaging before use can help preserve the conductive medium's Effectiveness until it's applied to the patient skin these preparation steps ensure that the ECG monitoring equipment functions effectively delivering accurate cardiac data for patient assessment and diagnosis the placement of electrodes is crucial for obtaining a comprehensive view of the patient's electrical activity the six limb leads are situated in the frontal plane offering insights into the heart's electrical conduction in the vertical Dimension these limb leads are particularly useful for assessing the heart's conduction in the head to toe Direction in contrast the six precordial leads are positioned in the horizontal plane providing a view of the heart's electrical activity along the transverse axis the combination of these limb and precordial leads allows for a multi-dimensional assessment of the heart's electrical rhythms and provides valuable information for diagnosing cardiac conditions making them fundamental Tools in cardiology and Critical Care Medicine each lead whether limb or precordial is meticulously positioned to provide a specific view of the heart emphasizing the importance of consistent placement for each recording the limb leads are generated using four electrodes on the body yet they produce six distinct readings on the ECG by measuring the electrical activity from different angles this Arrangement allows for a comprehensive three-dimensional perspective of the heart's electrical rhythms by ensuring that the leads are correctly placed each time time healthc Care Professionals can obtain reliable ECG data that aids in diagnosing and monitoring cardiac conditions making an essential component of Cardiac Care and assessment one major excuse that is often heard from 911 providers is that they did not have enough time on scene or in the transport unit to place electrodes correctly on the patient in the critical care field while time is of the essence providers often have the opportunity to take the appropriate amount of care when placing the patient on the ECG monitor ensuring an accurate and clear reading obtaining a reliable 12 lead ECG during the critical care transport requires several considerations the provider should ensure that the monitoring system and Lead configuration in use at the the initial facility match those that will be employed during the entire transport process consistency in lead placement and equipment is crucial for accurate and comparable ECG recordings it is a common practice to record a baseline 12 lead before departure and then repeat it again at regular intervals especially if there are any noted changes in the patients condition or ECG readings additionally another strip should be obtained upon arrival at the receiving facility to provide comprehensive data for health care providers helping in the assessment and management of cardiac issues during Critical Care transport this systematic approach to ECG recording ensures that any alterations in the patient's cardiac status are promptly detected and addressed when obtaining a 12 lead ECG the patient should remain as still as possible however the patient's clinical condition May influence their positioning during transport necessitating adjustments to accommodate their comfort and safety before obtaining the ECG it's crucial to standardize or calibrate your equipment properly this Cali celebration ensures the ECG recordings are precise and reliable which is essential for interpreting cardiac activity accurately and making informed clinical decisions while providing Critical Care during transport interpreting a 12 lead in a transport setting can be challenging due to the critical nature of time and the constraints of a moving vehicle complex tools like calipers rulers axis wheels and straight edges are challenging to use in these conditions to effectively interpret a 12 Le during transport providers must be familiar with the typical appearance of ECG complexes in normal patterns before attempting to analyze the strip understanding what a typical complex from each lead should look like is essential for instance in the limb leads the p-wave is typically upright in leads one 2 AVL and avf while it may be basic in lead three and purely negative deflected in lead AVR in the precordial leads the p-wave is typically upright in leads V5 and V6 while lead V1 is basic and leads V2 and V4 exhibit variable patterns this Baseline knowledge is essential for accurate ECG interpretation under time sensitive and challenging circumstances during transport a noticeable change in the morphology of the p-wave on an ECG can indicate an atopic atrial Focus which is an abnormal pacemaker Lo located outside the sinoatrial node during ECG interpretation the rules for measuring the PR interval should be consistently applied as they remain unchanged from standard cardiac monitoring the PR interval signifies the time taken for atrial depolarization to transition to ventricular depolarization including the conduction delay at the atrio ventricular Junction typically the PR interval lasts from 120 to 200 milliseconds the QRS complex on the ECG reflects ventricular depolarization the interventricular septum is the first part of the ventricles to undergo depolarization and although it may not always be clearly seen on the ECG its presence can manifest as a small qwave in leads 1 AVL V5 and V6 furthermore the t-wave is usually recorded as a positive deflection in the same leads that display positive r-wave contributing to the overall ECG interpretation and assessing of the patient's cardiac status consistency in interpretation is Paramount for Reliable and reproducible results this approach ensures that healthc Care Professionals can quickly and accurately read ECGs a skill that definitely improves with experience even Specialists can have varying interpretations emphasizing the importance of sound methods thorough documentation and consideration of all all patient information continuous monitoring of ECG rhythms is essential for timely intervention in Rhythm and arhythmia interpretation assessing 10 key elements is critical including assessing the rhythm's rate regularity and the presence and consistency of p waves and QRS complexes ensuring their Association width grouping and identifying any dropped beats this structured approach enhances the accuracy of ECG analysis consistency in the method of ECG analysis is Paramount to achieving accurate and dependable interpretations by repeatedly using a standardized approach Healthcare professionals can ensure that their assessments are reliable reproducible and consistent across different readings this uniformity is crucial in the field of healthcare where precise And Timely clinical decisions are vital when the same method is employed each time it facilitates clear communication between healthc care providers ensuring that everyone interprets ECG findings in a uniform manner this reduces the potential for miscommunication and",
        "Axis Determination": "errors access determination the heart is an intricate organ composed of individual cells Each of which possesses the remarkable ability to generate its own electrical impulse these impulses are not only unique to each cell but also vary in intensity and direction to describe these complex electrical signals and their movements the term Vector is employed in this context a vector represents an electrical impulse carrying information about its strength and the direction it is traveling in within the heart's tissue an essential Concept in understanding the heart's electrical activity is the axis the axis is essentially the orientation or direction of the wave of depolarization as it transverses the heart's structures this concept is crucial because it provides insights into the overall functioning of the heart changes or variations in the axis can be indicative of an underlying cardiac condition and can be identified through the analysis of an ECG therefore the axis serves as a key reference point for health care providers when assessing the patients's cardiac health and diagnosing potential issues related to the heart's electrical system the mean electrical axis represents the sum of all electrical impulses generated by cardiac cells and the direction in which these impulses flow as they depolarize the heart's tissue as these electrical impulses travel through the heart they follow a specific path in a healthy heart this path typically progresses in a downward and leftward direction this characteristic direction is a result of the sequence of depolarization starting at the Atria specifically the right Atria moving through the atrio ventricular node and then spreading throughout the ventricles with the left ventricle being the larger of the two the mean electrical axis effectively summarizes this direction by providing a representation of the overall electrical flow in the Heart during a cardiac cycle when there is a change in the patient's normal electrical axis it indicates that a shift has occurred in either the structure or the function of the heart these changes can be due to various factors such as heart disease conduction abnormalities myocardial infarctions or other cardiac conditions alterations in the mean electrical axis often serve as a critical clue to health care providers that there may be an underlying issue with the heart's electrical system this understanding can be invaluable for diagnosing and managing cardiac conditions making it an essential component of the ECG interpretation skill especially when assessing patients with known or suspected heart problems by closely evaluating the mean electrical axis healthc Care Professionals gain insights into the heart's electrical health and can better tailor their care and treatment plans to the specific needs of the patient the hex axial Circle employs a circular diagram and is crucial for representing the frontal plane created using the limb leads 1 2 3 AVR AVL and avf in a standardized manner this circle is divided into 12 equal segments each corresponding to a specific electrical axis providing a systematic way to analyze the direction of electrical activity within the heart in this system it's important to note that the mean electrical axis is a key concept representing the overall direction of electrical impulses during the cardiac cycle to isolate and accurately determine this axis two specific leads are required for assessment the hex axial circle is further divided into four quadrants progressing from 0\u00b0 to positive 90\u00b0 positive 90\u00b0 to 180\u00b0 180\u00b0 to negative 90\u00b0 and 90\u00b0 back to 0\u00b0 the these quadrants are instrumental in categorizing the direction of electrical vectors produced during depolarization when a wave of depolarization is oriented towards a particular quadrant it offers valuable insights into the overall orientation of the mean electrical axis this axis is primarily determined by the sum of all vectors generated during ventricular depolarization this cumulative Vector represents the mean QRS Vector a collective depiction of the electrical activity in the heart and it tends to follow a direction that is both downward and to the patient's left in essence the mean QRS vector and consequently the mean electrical axis serves as a crucial diagnostic tool for assessing cardiac health and ident identifying any deviations from the norm the determination of the mean QRS Vector indicative of the cardiac electrical axis begins with the analysis of lead one in lead one the positive electrode is positioned at 0 Dees which forms the reference point for assessing the direction of electrical impulses in electrocardiographic terms electrical impulses moving toward the positive electrode result in an upright or positive deflection on the ECG while impulses moving away from the positive electrode create a negative deflection therefore a positively deflected QRS complex in lead one signifies that the wave of depolarization is traveling towards lead one indicating a normal axis range however a negatively deflected QRS complex in Lead 1 implies a deviation in the electrical axis specifically when lead one exhibits a negative deflection the axis is shifted towards the right denoting a right Axis deviation or R A the second lead avf provides additional insight into the axis determination as it has the positive electrode situated at positive 90\u00b0 or electrically to the right an upward moving wave of depolarization that heads toward the positive electrode in lead avf yields a positive deflection of the QRS complex on the ECG consequently if both leads one and avf depict positively deflected QRS complexes it signifies a mean electrical axis that is directed downward in avf and towards the patient left in lead one within the normal axis range conversely when the QRS complex is positive in lead one but negative in lead avf this reveals an upward and leftward shift of the axis identifying a left axis deviation or lad notably if lead one is negatively deflected and Lead avf is also negatively deflected it indicates an extreme right Axis deviation which Falls within the range of 90\u00b0 to 180 \u00b0 this is also relatively rare extreme rad can be associated with conditions such as ventricular tacac cardia atypical myocardial infarctions hyperemia and occasionally right ventricular hypertrophy any alteration in the electrical axis during patient transport should be considered a critical sign prompting the provider to investigate and identify the underlying cause of the deviation once an abnormal cardiac axis is identified it serves as a valuable clinical clue that prompts healthc care providers to conduct a more comprehensive assessment abnormal axes often correlate with specific cardiac conditions or anatomical changes by scrutinizing additional ECG features and considering the patient clinical presentation healthc Care Professionals can unveil Associated abnormalities that offer insights into the patient's cardiac health this in-depth evaluation can uncover critical information that guides intervention strategies including pharmacological or electrical therapies particularly in emergency situations in the context of critical care transport where rapid and efficient decision- making is vital identifying a change in the electrical axis is extremely important focusing on the change itself rather than quantifying the precise degree of axis deviation allows for more expeditious assessment of the patient's cardiac status this approach aligns with the urg of the transport environment where time constraints May limit the ability to perform detailed ECG measurements recognizing an access alteration promptly directs healthc care providers toward the appropriate interventions and management strategies ensuring that the patient receives timely and potentially life-saving care during transit to the receiving facility the hex axial Circle allows for a comprehensive analysis of the heart's electrical vectors but it's important to acknowledge that some overlap may occur between adjacent quadrants which necessitates careful interpretation the normal range for the electrical axis encompasses a relatively broad span from -20\u00b0 to positive 100\u00b0 within this range there's a 10\u00b0 o overlap between positive 90 and positive 100 in the right quadrant which is not clinically significant and Falls within the normal Spectrum when the mean electrical axis Falls within either of the two right quadrants it suggests a right Axis deviation which can be associated with specific cardiac conditions conversely the the evaluation of a left axis deviation should take into account the normal range that extends to -20\u00b0 however it's crucial to recognize that there is a narrow range from -21\u00b0 to -29\u00b0 which is deemed the physiologic left axis this range is neither inherently normal nor inherently pathologic but rather represents a transitional Zone interpretation in this range requires clinical judgment and consideration of other ECG findings and patient information to determine the significance of the left axis deviation and its potential implications for the patient's cardiac health in the context of mean electrical access deviations the left AIS deviation is a critical parameter to evaluate the true pathologic region associated with L is situated in the left quadrant and spans from -30\u00b0 to 90\u00b0 when the mean electrical axis Falls within this specific range it's indicative of a genuine pathologic L the left axis deviation when substantiated by lead 2 showing negative deflection solidifies the diagnosis of a true pathologic L this not only underscores the presence of the deviation but it also provides additional diagnostic Clarity by aligning the findings in lead 2 with the established pathologic range of the left axis deviation in utilizing the mean electrical axis determination system it's essential to locate the QRS complex exhibiting the lowest amplitude and the most isoelectric behavior in one of the limb leads once this reference point is identified the next step is to identify the corresponding perpendicular lead for instance if the the limb lead with the most isoelectric QRS complex is lead 2 which is situated at positive 60\u00b0 the matching perpendicular lead would be lead AVL lead AVL encompasses the angular range between positive 150\u00b0 and -30\u00b0 making it the corresponding perpendicular lead to lead two following the identification of the perpendicular lead the next crucial assessment is whether the QRS complex in the perpendicular lead exhibits positive or negative deflection if it shows a positive deflection this signifies that the mean electrical axis is directed at positive 150\u00b0 conversely if the QRS complex displays a negative deflection in the perpendicular lead the mean electrical axis is NE 30\u00b0 this method rooted in Vector cardiography principles allows for a precise determination of the mean electrical axis providing valuable diagnostic information for cardiac evaluation and ensuring accurate clinical interpretation in various healthc care settings causes of access deviations in electrocardiography can be multifactorial and often require A thorough clinical assessment to ensure comprehensive cardiac monitoring during Critical Care transport key considerations should be taken into account providers are encouraged to secure a baseline ECG utilizing the the designated cardiac monitor for transport this ECG should then undergo a comprehensive assessment with meticulous attention to detail regarding any abnormalities present including the mean electrical axis of particular importance is the detection of an axis that deviates beyond the normal range or significantly differs from the patient's pre-existing Baseline such axis deviations can have important clinical implications serving as vital indicators of underlying cardiac pathology upon identifying an access deviation providers must conduct a thorough analysis of the ECG to check for any corresponding changes that may offer valuable insights into the root cause of said deviation AIS deviations in ECGs can often be attributed to various cardiac and non-cardiac factors each necessitating a thorough assessment to identify their etiology commonly cardiac causes for Access deviation include esea and infarction which result in alterations in the electrical conduction system thereby directing the axis away from the affected cardiac regions one notable cardiac condition that can induce axxis deviation is the left anterior Superior faasle of the left bundle branch block leading to a left anterior Hemi block and consequent deviation of the axis in the context of an inferior wall myocardial infarction when the wave of depolarization is obstructed it may be rerouted upwards into the left thus causing a left a AIS deviation left ventricular hypertrophy associated with the enlargement of the left ventricle has the capacity to influence the electrical axis shifting it towards the enlarged muscle mass and resulting in L atopic beats and rhythms originating from different areas within the heart may also contribute to axis deviation as they redirect the wave of Deep polarization in either right or left directions thereby affecting the axis within the impacted region conversely right Axis deviation can be brought about by a range of factors such as congenital Dex cardia left posterior hemiblock occurring due to a conduction defect in the left interior fasle of the left bundle branch or an enlarged right ventricle furthermore there are non-cardiac factors to consider when evaluating axis shifts conditions that displace the heart from its typical downward and leftward position can lead to changes in axis deviation factors such as body habitus can impact the axis with tall thin individuals experiencing a vertical shift moving the heart more downward and away from the left resulting in a right Axis deviation children typically exhibit a normal axis pointing towards the right due to their larger right ventricles in comparison to adults COPD can lead to right ventricular hypertrophy consequently causing a right Axis deviation mechanical shifts are another consideration with factors like obesity or pregnancy leading to increased intraabdominal pressure that displaces the heart into a more horizontal or left position ultimately resulting in a left axis deviation in essence recognizing the diverse array of both cardiac and non-cardiac causes on access deviations is crucial for clinicians to perform accurate ECG interpretation and offer appropriate clinical",
        "Bundle Branch Blocks and Hemiblocks": "management bundle branch blocks and Hemi blocks bundle branch blocks and Hemi blocks are significant electrical disturbances within the hearts conduction system that manifest as distinct ECG patterns each with its own characteristics and diagnostic criteria bundle branch blocks which which Encompass both left and right bundle branch blocks result from A disruption in the conduction pathway for electrical impulses within the heart a right bundle branch block specifically involves the right bundle branch and its associated faical in a right bundle branch block the electrical impulses originating in the Atria initially travel along their normal Pathways up to the blockage showing no immediate change in waveforms or intervals however when these impulses reach their point of blockage within the right bundle branch they are unable to progress and as a result they continue down the left bundle branch and its facles as they usually would to circumvent the blockage the electrical signal must travel through the right ventricle by cellto cell conduction causing a delay in the depolarization of the right ventricle this delay results in a prolonged QRS interval of 120 milliseconds or more on the ECG characteristic changes include the appearance of an r-wave known as RP Prime which is seen immediately following the initial upstroke of the r-wave this pairing of an initial r-wave with a subsequent r-wave produces a distinctive rabbit ears pattern in the QRS complex to identify the changes associated with a right bundle branch block it's essential to examine specific leads on the ECG the most suitable lead for detecting these changes is precordial lead V1 which reveals the characteristic rsr complex where an r-wave follows the initial r-wave in the QRS complex further more in lead V2 a similar rsr complex may be observed in this pattern the RVE representing the additional Vector created by the delayed electrical impulse through the right ventricle is positively deflected in V1 Additionally the delayed conduction through the right ventricle leads to a slurring of the swave in the lateral limb lead such as lead one and the left side precordial lead V6 these ECG findings collectively provide the main diagnostic criteria for identifying a right bundle branch block which include a QRS prolongation of 120 milliseconds or more a slurred swave in leads 1 and V6 and an rsr pattern in V1 with the subsequent r R wve being taller than the initial r wve one of the ECG patterns associated with a right bundle branch blockage is the QR wave this wave pattern is particularly significant when observed in lead V1 which is one of the precordial leads that represents the depolarization of the anterior septum the Pres pres of a Q wave in lead V1 concurrent with a right bundle branch block can be indicative of myocardial infarction in such cases the appearance of this Q wave signifies an area of The myocardium that has undergone infarction when this waveform appears during the transport of a critically ill patient early intervention is crucial as it may help prevent the progression of myocardial esia to infarction to ensure a comprehensive assessment it's important to examine other ECG leads especially the lateral leads one and V6 in addition to V1 when diagnosing the right bundle branch blockage the management of isolated right bundle branch blocks typically does not require any specific treatment patients who exhibit this ECG pattern should undergo periodic follow-up evaluations to monitor their heart's electrical conduction system and overall cardiac health the left bundle branch block arises from an interruption in the normal electrical conduction pathway of the left bundle branch which comprises the left anterior faasle and the left posterior fasle in a typical cardiac conduction system electrical impulses initiated in the Atria follow their standard course with no deviations in waveforms or intervals until they encounter the sight of the block at this point the electrical impulses continue unobstructed down the right bundle branch bypassing the disrupted left bundle branch with the left bundle branch blocked the wave of depolarization is compelled to take an alternate path through cell to cell transmission from the right to the left side of the chest the diagnosis of a left bundle branch is primarily contingent on distinct electrocardiogram findings characteristic ECG alterations include the prolongation of the QRS complex typically exceeding 120 milliseconds in duration the most apparent impact of the block is observed in the inferior and lateral leavs specifically leads 1 V5 and V6 where ECG complexes lack Q waves and exhibit tall monomorphic R waves this change in the r-wave is a central feature of the left bundle branch block replacing the customary sharp upward sloping pattern with a more gradual bowed Ascent the peak of the r-wave is often described as notched wide or a combination of both characteristics additionally in the right side chest leads such as V1 and V2 reciprocal changes are discerned characterized by the presence of wide deep and monomorphic S waves which counterbalance the prolonged R waves witnessed in the inferior and lateral leads these ECG findings collectively signify a notable disturbance in the usual electrical conduction pattern of the heart and provide valuable insights for the diagnosis clinical interpretation and patient management in cardiology and critical care settings in bundle branch blocks repolarization which denotes the phase of the cardiac cycle where the ventricles regain their electrical charge experiences noteworthy alterations in the context of a left bundle branch block one distinct ECG characteristic is the disordinate orientation of the t- Waves relative to the terminal deflection of the QRS complexes typically the t- waves in the left bundle branch appear deflected in the opposite direction to the terminal portion of the QRS complexes exemplifying an anomalous repolarization pattern the primary diagnostic criteria for left bundle branch blockages Encompass a prolonged QRS complex duration exceeding 120 milliseconds with lead V6 showing a notched r-wave without any qwave furthermore lead V1 typically exhibits wide and deep s-waves often accompanied by a small r-wave preceding a large swave importantly a left bundle branch block seldom occurs in an otherwise healthy heart and is usually indicative of a significant issue within the cardiac induction system or may be associated with myocardial esema stemming from coronary artery disease furthermore it's essential to recognize that a rhythm originating from a pacemaker can produce wide complexes akin to those seen in left bundle branch blocks therefore Critical Care transport providers should be vigilant in identifying pacemaker spikes concurrent with the characteristic ECG pattern of a left bundle branch block as pacemaker related interventions may be required management of patients with left bundle branch blocks is multifaceted and necessitates a thorough cardiac evaluation particularly in those who exhibit concerning symptoms like near Syncopy or syncopal episodes as they may require implementation of a pacemaker accurate documentation of ECG recordings demonstrating left bundle branch blocks in symptomatic patients is crucial and should be meticulously incorporated into the patient's permanent medical record to facilitate Diagnostic and therapeutic decision making and follow-up care him blocks which represent a specific type of intraventricular conduction defect involve a block in the electrical conduction of one of the two facles within the left bundle branch of the heart a left anterior Hemi block also referred to as a left anterior facular block results from an interruption in the electrical pathway of the anterior or Antero Superior faasle conversely a posterior hemiblock denotes a block in the electrical conduction of the posterior or posterio inferior faasle these fases play a pivotal role in transmitting electrical impulses from the bundle of hiss to various regions of the left ventricle notably when Hemi blocks are present they typically use minimal to no significant widening of the C URS complexes on the electrocardiogram this characteristic is in stark contrast to the pronounce QRS prolongation seen in complete bundle branch blocks which impact both left fices and the right bundle branch despite the relatively subtle alterations in QR restoration Hemi blocks exhibit distinct ECG patterns and represent a noteworthy aspect of in of ventricular conduction abnormalities that warrant recognition and interpretation in the clinical setting each faasle originating from the left bundle branch possesses distinct anatomical characteristics and serves particular regions of the left ventricle delineating their unique roles in the conduction system the left anterior fasle with its slim arrangement of fibers functions as a delicate conduent for electrical impulses directed towards the anterior and lateral aspects of the left ventricle in contrast the posterior faasle forms a more extensive network of fibers facilitating the conduction of electrical impulses to the inferior and posterior walls of the left ventricle this structural disparity highlights the specialized nature of each aicle in their distribution of electrical signals to specific regions of the heart him blocks tend to be more frequently associated with the left anterior fasle and there are underlying reasons for this preder given the smaller size of the left anterior faasle even a relatively limited area of es schia or infarction May hinder the smooth transition of electrical impulses along the single string strand of fibers in contrast the posterior faasle receives its blood supply from branches of both the left and right coronary arteries providing a degree of redundancy a significant impact on electrical conduction within this faasle would necessitate the simultaneous occlusion of both coronary artery supplies making such An Occurrence relatively less common the varying susceptibility of these facles to disruption in electrical conduction underscores the need for precise clinical assessment and ECG interpretation in the presence of intraventricular conduction defects such as Hemi blocks the left anterior hemiblock is characterized by a block in the electrical conduction pathway that leads to the left anterior faasle this this disruption in conduction results in distinct changes in the propagation of electrical impulses within the heart in cases of La the electrical signals to the anterior Superior portion of the left ventricle are impeded and as a consequence depolarization of this myocardial region occurs primarily via the interventricular septum and retrograde conduction from the inferior and posterior walls of the left ventricle this alternative pathway for depolarization is necessitated by the interruption in the normal conduction through the left interior faasle and leads to the Hallmark ECG features of L ah the diagnostic criteria are based on specific ECG findings that distinguish it from other intraventricular conduction def effects these criteria include a left axis deviation typically falling within the range of -30\u00b0 to 90\u00b0 furthermore L A is characterized by a QR complex or a large R wve in lead one highlighting the deviation of the axis to the left this deviation may also manifest as an RS complex in lead 3 and is likely to be observed in lead 2 and avf as well accurate recognition and interpretation of these ECG criteria are crucial for the diagnosis of LA and can provide valuable insights into the underlying conduction abnormalities affecting the left anterior faasle and the overall electrical function of the heart the left posterior Hemi block is an exceptionally rare conduction abnormality in the heart's electrical system this Rarity is primarily attributed to the unique and robust dual blood supply to the area of the left posterior faasle which makes it resilient to es schic damage the extensive network of fibers in the left posterior faasle further contributes to the infrequency of L pH diagnosis can be challenging primarily due to its scarcity but it involves distinctive ECG patterns that distinguish it from other intraventricular conduction defects in lph the blockage of electrical impulses to the inferior and posterior regions of the left ventricle results in a delayed wave of depolarization that is directed inferiorly and to the right consequently this leads to a right Axis deviation on the ECG while the electrical impulses that reach the blockage site continue to conduct unopposed depolarizing the interventricular septum and the superior anterior walls of the left ventricle this phenomenon manifests itself as a small r-wave in Lead 1 and a small qwave in lead three this particular ECG pattern is a crucial diagnostic criteria for lph the definitive criteria for diagnosing lph include a right Axis deviation ranging from positive 90\u00b0 to 180\u00b0 and the presence of an r-wave in Lead 1 and a qwave in lead three diagnosing lph is Complicated by the need to to exclude other potential causes of right AIS deviation such as right atrial enlargement and right ventricular hypertrophy therefore lph diagnosis becomes one of exclusion involving a thorough assessment of ACG findings and clinical data to rule out alternative underlying conditions certain chronic lung diseases that lead to right atrial enlargement or other causes of right Axis deviation should be considered and eliminated as differential diagnosises in cases where no evidence of right atrial enlargement or right ventricular hypertrophy is found lph becomes a likely consideration it's important to note that conditions like pulmonary embolism can obscure the diagnosis of lph adding to the complexity of the diagnostic process consequently lph is a unique and challenging entity that Demands a comprehensive evaluation particularly due to its Rarity and the necessity to differentiate it from various other conditions that can manifest with right Axis deviation bif facular blocks refer to a relatively uncommon cardiac conduction abnormality where two distinct conduction Pathways in the heart's electrical system are blocked simultaneously one common presentation of bicular block is the coexistence of a right bundle branch block along with either a left anterior Hemi block or a left posterior Hemi block when this combination particularly the right bundle branch block with LA becomes a chronic or long-standing condition in an individual it's generally classified as a staple bifascicular block block however it's essential to recognize that the onset of a new bicular Block in the presence of cardiac esea or other acute factors is certainly considered unstable these newly emerging bifascicular blocks can be indicative of more critical underlying cardiac issues and therefore require close monitoring And Timely intervention to address the potential instability making the differentiation between stable and unstable bif facular blocks a crucial factor in clinical assessment and patient management B facular blocks particularly those involving a combination of right bundle branch blocks and either a left anterior Hemi block or posterior Hemi block exhibit distinct ECG patterns a bif facular block with a right bundle branch block off often presents with characteristic features such as a slurred swave in leads 1 and V6 along with an up and down appearance of the rsr complex in lead V1 these patterns contribute to a QRS duration of 120 milliseconds or longer if the bicular block is associated with an L ah the typical presentation includes a left axis deviation and a small r large S Wave in lead three in contrast a bif facular Block featuring a right bundle branch block and an lph is generally considered unstable due to the likelihood of involvement of additional conduction Pathways within the ventricles particularly in the right bundle branch this type of block can can potentially progress into a higher degree of block leading to a typical right bundle branch pattern with a right Axis deviation and a small qwave in lead three while bif facular blocks with a right bundle branch block and an L ah are typically stable they can become unstable if acute myocardial infarction occurs in the presence of es schea or tissue death from Mi there's a risk of further damage that might affect the remaining posterior fasle leading to a complete heart block for critically ill cardiac patients who already have an existing bifascicular block involving a right bundle branch block and L ah the emergence of es schic signs or indications of an MI implies the need for an urgent pacemaker placement especially if a second or third degree a atrio ventricular block is detected however such a procedure may not be readily available in the transport setting necessitating consultation with medical control and the placement of pads for external cardiac pacing it's extremely important to inform the receiving medical facility of the patient's condition to ensure that a transvenous pacemaker setup is available without delay upon arrival tricular block is a cardiac conduction abnormality characterized by the coexistence of a bifascicular block typically involving a right bundle branch block in a block in either the left anterior faasle or the left posterior faasle along with a first-degree heart block which manifests as a prolonged PR interval this combin combination of conduction abnormalities reflects a complex disruption in the heart's electrical system and is often indicative of underlying cardiac issues tricular blocks can be the result of a disease or dysfunction within the atrio ventricular node which plays a crucial role in regulating the timing and coordination of electrical impulses in the heart alternatively it may be caused by diffuse distal conduction system damage affecting the pathways responsible for transmitting electrical signals from the Atria to the ventricles the presence of tricular block necessitates close monitoring and medical evaluation as it can carry a risk of progressing to more severe conduction disturbances or symptomatic bre cardia potentially requiring intervention such as a pacemaker in cases where the block at the atrioventricular node level progresses to a complete heart block the Escape Rhythm emerges from the bundle of hiss this Escape Rhythm typically generates heart rates in the 40s and can lead to symptoms such as fatigue near Syncopy or even complete syn episodes due to the slow heart rate in situations where there is diffuse conduction system damage beyond the AV node the Escape Rhythm May originate from facular or ventricular Pathways resulting in heart rates that are extremely low and potentially life-threatening when a tricular block is identified after a myocardial infarction it usually indicates extensive cardiac damage and these patients are at an increased risk for conduction disturbances true tricular blocks necessitate immediate intervention in the form of temporary pacing to address symtomatic bre cardia followed by the placement of a permanent pacemaker to ensure proper electrical conduction and prevent further complications management and treatment in these cases are crucial to maintain cardiac function and reduce the risk of life-threatening events associated with conduction system abnormalities selected ECG",
        "Selected ECG Findings": "findings hyperacute t-waves can be a critical ECG finding often indicating an underlying es schic condition these t- waves become tall and narrow displaying an upward slanting of the ST segment and an exaggerated t-wave enlargement that is disproportionate to the QRS complex typically localized to the area of esea and infarction hyperacute t-waves may also present with Associated depression of the J point and a prolonged QT interval their appearance is generally specific to the leads that view the region affected by es schema or infarction on the other hand ST segment elevation in ECGs can result from various Factor fa s that influence ventricular depolarization and repolarization while myocardial infarction is a well-known cause nonmi related changes such as left bundle branch block certain ventricular rhythms left ventricular hypertrophy pericarditis and early repolarization can also lead to ST segment elevation persistent St segma elevation May indicate that development of ventricular aneurysm it is crucial to differentiate between benign jpoint elevation where the t-wave remains distinct and pathological myocardial disease where the elevated jpoint fuses with the t-wave a sign that warrants careful clinical attention hypertrophy in the context of Cardiology refers to the thickening or or excessive growth of the heart muscle often in response to increased workload are various underlying conditions this physiological response to the heart's way of adapting to demands such as increased blood pressure chronic valve disease or other factors that require the heart to work harder as the heart faces a greater workload it compensates by increasing its muscle mass in the affected area the structural changes associated with hypertrophy result in a higher concentration of electrical impulses within the hypertrophied region consequently hypertrophy can influence the electrical conduction system of the heart impacting its overall function and potentially leading to ECG changes which are critical for accurate diagnosis and appropriate clinical management understanding hypertrophy and its potential implications is vital for Health Care Professionals when interpreting ECG findings and providing effective patient care left atrial enlargement is characterized by the enlargement or dilation of the left atrium a chamber responsible for receiving oxygenated blood from the lungs and pumping it to the left ventricle when the left atrium becomes enlarged it leads to a prolonged electrical conduction time through his chamber this delay in the electrical impulses propagation can be detected on the ECG as changes in the p-wave specifically the p-wave May exhibit elongation or an alteration to its shape with particular emphasis on the end or trailing side of the wave these ECG findings provide crucial diagnostic information to healthc Care Professionals suggesting the presence of left atrial enlargement understanding and recognizing these ECG characteristics are essential for identifying potential cardiac issues and guiding appropriate patient management in further clinical evaluation mitop is a distinctive feature seen on the ECG that indicates left atrial enlargement this cardiac condition often results from increased pressure or volume load on the left atrium which can be due to various causes including valvular heart disease like mitro stenosis in the context of mitop the p waves appearance on the ECG is significantly altered specifically it is characterized by a notched double humped shape often referred to as a camel hump appearance the double humped p-wave typically lasts longer than 120 milliseconds and can be observed in limb leads 1 and two of the ECG this unique pattern denoting mitro P serves as an important diagnostic clue to healthc care providers signaling left atal enlargement and potentially underlying cardiac conditions guiding further evaluation and informing clinical decisions related to Patient Care right atrial enlargement a condition indicated by alterations in the ECG is primarily driven by underlying Cardiac and Pulmonary disorders that affect the pressures within the right atrium several factors can contribute to right atrial enlargement including cardiac issues like mitro stenosis or regurgitation and Pulmonary conditions such as COPD or pulmonary IMI right atrial enlargement is often associated with the pulmonary condition known as P pulmonale one of the Hallmark ECG finding in P pulmonale is the presence of tall Peak t- waves in leads two and three characterized by an amplitude of 2.5 millim or greater the distinctive ECG pattern reflects the enlarged right atrium's imp impact on the electrical activity of the heart making it an important diagnostic marker for clinicians in electrocardiography the characteristics of p waves are crucial for identifying atrial enlargement and related conditions peaked p waves while indicative of atrial enlargement must meet a specific Criterion to be associated with right atrial enlargement requiring a height of 2.5 mm or more additionally basic p waves observed in lead V1 are a common ECG finding that suggests non-specific intraatrial conduction delays these basic PWS can often be linked to atrial enlargement although they may not reach the magnitude required to be classified as mitro P or p pinol when evaluating biphasic p waves distinctive patterns can be indicative of different types of atal enlargement for example if the leading half of the p-wave is taller and wider in lead V1 than in V6 right atrial enlargement is likely conversely if the trailing half of the p-wave is wider and deeper in V1 compared to the leading upright half left atrial enlargement is more probable particularly when the trailing end of the p-wave exceeds one small block on the ECG measuring 1 millimeter in height by 40 milliseconds in duration left atrial enlargement is the most likely diagnosis by atrial enlargement the concurrent enlargement of both Atria is a notable electrocardiographic finding that can provide critical insights into a patient's cardiac health this condition manifests in various ways on the ECG in the inferior leads one key indicator is a notched p-wave that endures for more than 120 milliseconds additionally a tall imp peaked p-wave with an amplitude of 2.5 m or more is often observed in lead V1 a basic p-wave may be present meeting the criteria indicative of either right or left atrial enlargement this combination of findings the notched p-wave in the inferior leads the tall and peaked p-wave and the basic p-wave in lead V1 collectively signifies the presence of biatrial enlargement identifying this enlargement through these ECG characteristics is essential for healthc care providers as it may hint at underlying conditions that require further assessment and management in electrocardiography a strain pattern represents a distinct set of changes in the ST segment and t-wave and it is particularly associated with suboc cardial esia subendocardial esia typically occurs when the inner layers of the heart muscle experience a reduced blood supply when hypertrophy an increase in the size and mass of the heart's muscle is not complicated by es schema diagnosing esic changes can be challenging making the strain pattern an important diagnostic feature the most prominent strain pattern is observed in the ECG lead that exhibits the tallest and deepest QRS complex this pattern manifests as an abnormal curvature or deviation in the ST segment and t-wave often appearing as either an elevation or depression in the ST segment followed by t-wave abnormalities The Strain pattern is a crucial indicator of underlying cardiac conditions particularly when dealing with hypertrophy patients as AIDS in the timely detection of subendocardial esea which may require further evaluation and intervention the presence of a strain pattern in the context of left ventricular hypertrophy becomes apparent through specific ECG findings in right precordial leads such as V1 to V3 this pattern is manifested as ST segment elevation characterized by a concave appearance of the upward slope the ST segment elevation as a reflection of the increased electrical voltage generated by the hypertrophy left ventricle which is more pronounced in these particular leads in addition the t-wave in V1 to V3 typically displays an upright and asymmetric configuration which indicates the altered repolarization patterns associated with LVH conversely in the precordial leads V5 and V6 a different aspect of the strain pattern is observed here the ECG shows downward sloping t- segment depression along with inverted asymmetric t-waves these ECG changes are indicative of the electrical adaptions that occur as the heart's left ventricular muscle wall thickens and and becomes hypertrophied recognizing these strain patterns and LVH is essential for clinicians as they provide valuable insights into the structural and electrical alterations in the heart aiding in the diagnosis and management of LVH and Associated cardiovascular conditions the presence of a strain pattern in right ventricular hypertrophy is a distinct ECG manifestation reflective of the electrical and structural changes occurring in the right ventricle these ECG findings are vital for diagnosing rvh and understanding its implications The Strain pattern in rvh is typically characterized by several key features firstly due to the rightward and interior shift of the mean electrical axis it results in a right AIS deviation meaning that the general direction of the mean electrical axis of the heart is oriented towards the right in the right precordial leads such as V1 and V2 you may observe an increased r-wave amplitude Additionally the ST segment in these leads often displays a downward sloping and depressed appearance which can be accompanied by inverted and asymmetric t-waves in some cases the t-wave may also be basic with the leading half negatively deflected and the trailing half positive these ECG findings are crucial for identifying rvh and recognizing the associated changes in electrical conduction and ventricular morphology assisting in clinical assessment and treatment decisions distinguishing between the strain pattern and ST segment and t-wave changes associated with es schea and infarction is a critical aspect of ECG interpretation since it can have significant implications for patient management and outcomes in the context of esema and infarction the ST segment elevations or depressions are typically flat lacking the characteristic sloping appearance often seen in the strain pattern furthermore the t-waves in esia tend to be symmetric in contrast to the asymmetric t-waves observed in the strain pattern ECGs the J point which marks the junction between the termination of the QRS complex and the beginning of the ST segment is usually sharper or more clearly defined in es schic or infared ECGs these differences are essential because ST segment elevation in aeia can signify aute coronary syndrome and may warrant intervention to prevent myocardial damage and life-threatening complications whereas The Strain pattern although indicative of ventricular hypertrophy is not an acute emergency hence the accurate interpretation of these ECG findings is crucial for timely and appropriate clinical decision-making pre-exit ation syndromes like wolf Parkinson White syndrome represent unique electrophysiological anomalies within the heart's conduction system wpw syndrome manifests when additional electrical pathway known as the bundle of Kent forms and provides an alternate route for electrical impulses to bypass the Atri ventricular node and directly access the ventricles importantly this accessory pathway does not possess the same intrinsic properties as the AV node which can conduct electrical signals at a controlled and steady Pace as a result individuals with wpw syndrome are at risk of experiencing extremely rapid heart rates a condition referred to as supraventricular tacac cardia this may lead to severe hemodynamic instability these accessory Pathways can be found on either the right side connecting the right atrium to the right ventricle or the left side linking the left atrium to the left ventricle and their presence can significantly impact the heart's electrical conduction potentially leading to life-threatening arrhythmias the understanding and management of wpw syndrome are crucial to prevent these rapid heart rhythms and their adverse consequences wpw is characterized by specific diagnostic criteria that reflect its unique electrophysiological properties this syndrome is identified by several key ECG findings one PR interval shortening the PR interval which represents the time it takes for electrical signals to travel from the Atria to the ventricles is notably shortened to less than 20 milliseconds two QRS complex widening the QRS complex representing ventricular depolarization is widened to more than 100 milliseconds importantly this widening is not a result of a delay in ventricular activation as seen in bundle branch blocks but rather due to premature activation from the accessory pathway and C the Del Delta wave the Hallmark of wpw is the presence of a Delta wave in the QRS complex which manifests as a characteristic slurred upstroke this Delta wave reflects the premature activation of the ventricles through the accessory pathway while wpw may not cause clinical issues in many individuals it predisposes some to potentially life-threatening arrhythmias such as SVT and aib management strategies are geared towards addressing these tacki arrhythmias treatment for unstable wpw May necessitate electrical cardio version for stable patients with orthodromic atrioventricular reactant tacac cardia the first line treatment involves vagal Maneuvers followed by IV adinis and IV calcium channel blockers cases of uncertainty or where the diagnosis simply isn't clear staple patients with suspected avrt may be treated with IV propanamide followed by cardiov version if necessary ultimately the definitive treatment for wpw syndrome is accessory pathway oblas a procedure that disrupts the normal electrical pathway and eliminates the risk of these dangerous arrhythmias accessory pathway Aion is typically performed under the guidance of a cardiologist and is highly effective in managing wpw syndrome pericarditis is a medical condition characterized by inflammation of the pericardium the doubled layer membrane that envelops the heart and plays a crucial role in protecting and lubricating the heart as it beats this inflammation can be provoked by various factors and underlying disorders common causes of pericarditis include infections usually viral or bacterial in origin that directly affect the pericardium in the context of myocardial infarction pericarditis can develop as a complication often stemming from the release of inflammatory mediators in response to tissue damage during the attack autoimmune disorders like lupus or rheumatoid arthritis can lead to pericarditis when the body's immune system mistakenly targets the pericardium traumatic injuries to the chest such as from a car accident or a fall can also cause inflammation in the paric cardium additionally certain cancers that have metastasized to the pericardium and specific medications like some anti-seizure or anticho drugs have been linked to pericarditis the condition can present with a range of symptoms including chest pain and management involves addressing the underlying cause while providing relief from the discomfort and complications associated with pericardial inflammation in cases of pericarditis ECG findings often involve ST segment elevation and t-wave changes which can extend across multiple leads importantly t-wave inversion typically occurs after the ST segment returns to Baseline unlike the early t-wave inversion seen in an acute MI unlike Mi pericarditis usually does not lead to the development of Q waves additionally patients with pericarditis might present with low voltage across all ECG Fields due to the presence of pericardial affusion a common occurrence in pericarditis cases this affusion can lead to a phenomenon known as electrical alternans where the heart can rotate or shift slightly within the pericardial Sac resulting in variations in the amplitude of each ECG complex another Finding associated with pericarditis include PR segment depression notched J points and in the AVR lead reciprocal ST depression and PR segment elevation recognizing these characteristic ECG features is vital for distinguishing pericarditis from other cardiac conditions especially myocardial infarction and guiding the appropriate treatment Long QT syndrome is a congenital cardiac disorder char characterized by a prolonged QT interval observed on the ECG this condition is associated with an increased risk of developing ventricular tacki arrhythmias including a specific type known as torsades to points which can lead to Syncopy or even sudden cardiac death managing Long QT syndrome presents a challenge for critical care transport paramedics because the QT interval duration varies with the heart rate a faster heart rate results in a shorter QT interval while a slower heart rate leads to a longer QT interval during patient transport if the corrected QT interval exceeds 500 milliseconds and the patient's Rhythm hasn't deteriorated into a ventricular tachar rhythmia it may warrant preventative medical intervention this intervention involves addressing electrolyte imbalance B es administering beta blockers like mol and being prepared to manage a potential development of ventricular tach arhythmia long-term management typically revolves around the use of beta blockers in cases where patients do not respond to medication more advanced treatments such as pacemaker implantation an implantable cardio defibrillator or a procedure called Left surfo thoracic tectomy may be necessary to reduce the risk of life-threatening arrhythmias and sudden cardiac death ventricular and wide complex tacac cardia represents a cardiac Rhythm characterized by heart rate exceeding 100 beats per minute and is specifically defined as a QRS duration of 120 milliseconds or more this type of tardia typically origin Ates in the ventricles rather than the Atria which is why the QRS complex appears wide on electrocardiogram ventricular teoc cardia can be further classified into monomorphic or polymorphic each having distinct characteristics monomorphic ventricular Tac cardia displays a consistent QRS morphology with each beat which suggests a single focus of origin within the ventricles on the other hand polymorphic ventricular Tac cardia features varying QRS morphologies indicating multiple folky of origin both forms of wide complex tacac cardia are associated with increased risk of hemodynamic instability and deterioration into life-threatening arrhythmias rapid recognition and prompt intervention are crucial for managing these conditions and preventing adverse out outcomes the evaluation of wide complex teoc cardia involves considering various major categories for a precise diagnosis ventricular teac cardia is the most common cause and stems from the ventricles typically presenting with a wide QRS complex and a significant risk of hemodynamic instability additionally Supra ventricular Tac cardia with a barent conduction can sometimes mimic ventricular Tac cardia leading to wide complex Tac cardia on the ECG pre-excited Tac cardias which are often linked to Wolf Parkinson White syndrome result from abnormal electrical Pathways bypassing the AV node occasionally leading to wide complex tacac cardia electrographic artifact stemming from technical issues or artifact on the ECG may also resemble true arrhythmias patients with pacemakers may experience ventricular past rhythms which can manifest as wide complex teoc cardia on the ECG to make an accurate diagnosis healthc care providers must particularly scrutinize the ECG considering key criteria such as identifying AV dis Association detecting Fusion beats assessing the QRS complex width noting QRS duration and observing electrical coordinates across the precordium to support a ventricular teoc cardia diagnosis in the management of wide complex tacac cardia several critical considerations are essential synchronized cardiov verion is the initial therapy of choice and should be promptly administered for patients with uncertain causes of wide complex tacac cardia who are hemodynamically stable vagal Maneuvers can be both Diagnostic and therapeutic in cases where the iology remains unclear a trial of a Denison may be valuable as it can terminate certain supr ventricular teoc cardias that being said caution is warranted when using drugs like calcium channel blockers and beta blockers which can lead to hemodynamic deterioration if the wide complex tacac cardia is in fact stable ventricular tardia in cases unresponsive to initial therapies some experts proceed with elective cardioversion While others may consider propanamide as a reasonable alternative Lane is a useful choice for ventricular Tech tardia of es schic origin but it will not terminate SVT following the termination of wide complex tardia preventative treatments are initiated to maintain a stable Rhythm for critical care providers interventions are primarily limited to anti- rythmic drugs usually continuing the medication that successfully terminated the wide complex tardia further in Hospital treatments May Encompass the use of an implantable cardioverter defibrillator and catheter oblas procedures in the event of wide complex tacac cardia during transport rapid evaluation is crucial and treatment should commence immediately for hemodynamically unstable patients it is managed as if it were ventricular teoc cardia until proven otherwise with synchronized cardiov version being being the initial choice in cases of polymorphic or pulseless ventricular tacac cardia the condition should be treated as ventricular fibrillation and immediate defibrillation is indicated if the situation is witnessed during transport the patient should already be connected to a cardiac Monitor and have a patent IV line in place with the critical care paramedic prepared to provide cardiopulmonary resuscitation if necessary hyperkalemia is a condition characterized by elevated levels of potassium in the bloodstream this medical State poses a significant threat as it can potentially lead to Fatality and impede the effectiveness of certain drugs employed in resuscitation efforts hyperemia is notorious for its capacity to induce changes in the appearance of various ECG waveforms making it capable of causing a wide array of arrhythmias diagnostic criteria for hyperkalemia Encompass t-wave abnormalities often appearing tall and peaked intraventricular conduction delays p-wave abnormalities marked by missing a reduced amplitude ST segment alterations resembling an injury pattern cardiac arrhythmias primarily manifesting as braic cardias and sometimes a sinos sodial ECG pattern in a transport setting it's crucial to provide prompt supportive treatment with the establishment of IV access and continuous cardiac monitoring if the patient exhibits hypotension or significant QRS widening treatment typically involves administering intravenous calcium insulin along with 50% dextrose and Albuterol for cases involving deox and toxicity related cardiac arrhythmias magnesium sulfate can be administered complemented by other medical interventions such as feros amide and binding resins to lower potassium levels hypokalemia refers to a reduction in the concentration of pot potassium in the bloodstream unlike hyperemia hypokalemia does not typically induce dramatic changes in the ECG nor does it usually provoke arrhythmias by itself the diagnostic criteria for hypokalemia involve observations such as ST segment depression slightly diminished t-wave amplitudes minimal prolongation of the QRS interval and sometimes a small uwave that follows the t-wave in a transport setting managing hypokalemia involves discontinuing the use of diuretics addressing conditions like diarrhea and vomiting that may lead to potassium loss and employing H2 blockers to minimize potassium loss the replacement of loss pottassium is carried out by measuring the extent of loss and estimating the appropriate amount out for replacement thereby helping to restore potassium levels to the normal range hypercalcemia characterized by elevated levels of calcium in the bloodstream is most commonly attributed to malignancy or primary hyper parathyroidism making these two causes the first to be investigated other potential causes for high calcium levels are less less frequent and are generally considered only after the primary culprits are ruled out the ECG changes associated with hypercalcemia are generally subtle including shortening of the ST segment which consequently shortens the QT interval potential prolongation of the PR interval lengthening of the QRS complex flattening or inversion of the t-waves and the development varying degrees of heart block treatment for hypercalcemia involves multifaceted approaches including supporting the ABCs and increasing hydration often utilizing a loop diuretic to enhance calcium excretion and prevent hydration therapy overload hypocalcemia characterized by decreased levels of calcium in the bloodstream can lead to to specific eccg changes primarily a prolongation of the ST segment which consequently results in the lengthening of the QTC interval during in facility transfer the management of hypocalcemia mainly consists of supportive measures such as IV fluids and oxygen to stabilize the patient's Vital Signs continuous monitoring of both Vital Signs and the ECG is crucial to L identify and address any cardiac manifestations in some cases an infusion of calcium gluconate may be administered over a period of 5 to 10 minutes to restore normal calcium levels and correct the associated ECG changes additionally if the QTC interval is prolonged magnesium supplementation may be considered to prevent the development of torsades to points a life-threatening ventricular Tech acardia dexin a digitalis preparation is a medication with a specific focus on altering the function of the heart it's important to note that dexin toxicity is associated with relatively High mortality rates as a cardiac glycoside dexin exerts its effects by inducing positive inotropic and negative chronotropic activities within the heart its primary clinical applications include the treatment of chronic heart failure and the control of ventricular rate in atrial Tachi arrhythmias such as atrial fibrillation the positive inotropic effect of dexin arises from its inhibition of the sodium potassium adenosine triphosphate pump leading to an increase in intracellular calcium and sodium levels while reducing intracellular potassium concentration this in turn enhances myocardial muscle contraction when maintained within therapeutic concentrations between 1 and two nanog per millimeter dexin serves to improve cardiac performance decrease electrical conduction between the sinoatrial and atrio ventricular nodes reduce automaticity an increased diastolic resting membrane potential the therapeutic window for dexin is narrow and its serum levels are influenced by various factors with drug interactions being one of the most common causes of dexin toxicity in cases of suspected dexin toxicity it is crucial to evaluate potassium and calcium levels as well hypokalemia can develop leading to increased ined automaticity while hyperkalemia can exacerbate dexin induced conduction delays hypercalcemia can further augment ventricular automaticity and the effects of dexin at toxic levels the excessive elevation of intracellular calcium ions increase the resting potential of cardiac cells making them more prone to arrhythmias clinical manifestations of acute dexin intoxic ation often include gastrointestinal symptoms such as nausea vomiting and abdominal pain and neurological symptoms such as lethargy confusion and weakness in the context of dexin toxicity several ECG changes are commonly observed reflecting its effects on cardiac conduction and automaticity these changes May Encompass junctional atrioventricular or ventricular atopic beats as well as first-degree AV block and a slowed ventricular response in atrial fibrillation additionally dexin toxicity can result in an accelerated AV or junctional Rhythm however more severe arrhythmias are also possible including severe braic cardia high deegree heart blocks and malignant ventricular rhythms such as ventricular teoc cardia or ventricular fibrillation these ECG findings serve as crucial indicators of potential dexin toxicity and emphasize the importance of prompt recognition and intervention particularly when managing patients during inner facility transfers or Critical Care situations in patients already known to be taking dexin any arhythmia particularly when accompanied by other clinical findings should raise suspicions of dexin toxicity as a potential underlying cause importantly any accelerated Rhythm coupled with conduction delays should significantly heighten the suspicion of deox and toxicity one diagnostic clue that can be assessed before or during transport is the patient's potassium level which holds some prognostic value in the context of other developing clinical findings potassium level exceeding 5.5 mil equivalence per liter compared to the normal serum potassium level of 3.5 to 5 mil equivalents per liter in a patient with dexin toxicity and normal renal function is associated with a higher mortality rate when dexin toxicity is suspected during transport the first priority is to manage the patients's air we breathing and circulation and then stabilize the patient's hemodynamics management measures may include the administration of activated charcoal to clear the GI tract of recently ingested dexin and atropine to address specific symptoms in severe cases of dexin toxicity the standard of care involves the administration of dejin specific antibodies typically as Fab fragments or dexin immune Fab also known as digibind which bind to and neutralize the toxic effects of dexin additionally treatment strategies Encompass the use of insulin and glucose to manage any hyper calmia associated with dexin toxicity it is crucial to note that if Fab fragments are used sodium polystyrene sulphinate is not recommended for the treatment of hyperemia as it may lead to an overcorrection of serum potassium levels which in and of itself poses its own set of",
        "Cardiac Disease": "challenges cardiac disease coronary artery disease or CAD stands as the most prevalent form of heart disease and remains a leading cause of death among adults in the United States the fundamental mechanism behind CAD is aerosis characterized by the gradual buildup of fatty material within the inner walls of arteries over over time these fatty deposits enlarge into masses of atheroma which undergo calcification turning into Harden plaque this plaque will ultimately narrow the arterial Lumen limiting blood flow to the heart muscle in some cases a fixed blood clot called a thrombus May further obstruct the artery Additionally the precipitation of C calcium from the bloodstream into the arterial walls may lead to arteriosclerosis significantly diminishing the artery elasticity risk factors for developing atherosclerosis and CAD are multifaceted and include hypertension smoking diabetes elevated serum cholesterol levels sedentary lifestyle obesity a family history of heart disease or stroke and male gender early recognition and effective management of these risk factors are critical in addressing CAD reducing its prevalence and ultimately lowering the associated mortality rates peripheral vascular disorders often linked to atherosclerosis play a significant role in medical emergencies particularly when they lead to complications these disorders can manifest as arterial brewes abnormal sounds indicative of turbulent blood flow heard over the kateed arteries with the stethoscope this may also result in claudication an excruciating calf muscle pain that is triggered by the narrowing of arteries in that region and often causing a very pain painful limp furthermore it can be associated with fitis which entails inflammation swelling and discomfort along the veins potentially culminating in the formation of blood clots known as thrombo fitis one particular concern is the risk of these thrombi dislodging and transforming into imali which can travel to the heart potentially causing a light threatening condition known as pulmonary embolism the recognition of these peripheral vascular disorders and their underlying atherosclerosis is crucial for prompt intervention preventing the development of life-threatening complications several risk factors contribute to the development of peripheral vascular disorders Advanced age is a primary factor as aging is often associated with the accumulation of arterial plaque and a decline in vascular Health the use of oral contraceptives particularly in women over 35 years of age or those who smoke can increase the risk due to hormonal influences smoking itself is a major risk factor as it not only directly damages blood vessels but also promotes atherosclerosis recent surgery especially Orthopedic or vascular procedures can temporarily affect blood flow and increase the risk recreational IV drug use introduces foreign substances into the bloodstream which may lead to clot formation or vessel damage trauma whether from accidents or medical procedures can cause vascular injury and extended immobilization can result in reduced blood flow in increasing the chances of clot formation peripheral vascular occlusion can manifest in various ways with patients commonly experiencing pain swelling and warmth in the affected extremity due to compromise blood flow and tissue oxygenation flushing and tenderness are also frequent indicators reflecting the body's response to vasc compromise when peripheral occlusion is suspected prompt action is crucial IV heppard Administration starting with a bolus followed by an infusion helps prevent further clot formation and facilitate clot breakdown if ultrasound or Doppler Imaging equipment is available during transport continuous assessment of the affected limb can help monitor the effectiveness of treatment and identify any changes in the clot status to optimize blood flow and reduce the risk of complications applying warm compresses to the affected limb is a practical measure patients transported over long distances with a clot that has the potential to embolize to the lungs should receive at minimum a baseline ECG before transport and undergo frequent 12 lead ECG monitoring during the Journey ST segment depression in the limb leads and the precordial leads combined with an increased right AIS deviation May signal a pulmonary embolism necessitating immediate intervention to address this life-threatening condition the management of patients with ST segment elevation myocardial infarction or stemi is Guided by the American Heart Association and the American College of Cardiology published guidelines acute coronary syndrome also known as ACS is a term encompassing various conditions that share a common characteristic the manifestation of es schic discomfort or chest pain resulting from plaque disruption within a coronary artery while these plaques are often non-obstructive they contain a high concentration of inflammatory cells such as macrofagos which promote a series of events once the plaque is disrupted it triggers platelet activation adhesion aggregation thrombin formation and eventually the formation of a thrombus which can lead to complete occlusion of the coronary artery or one of its branches myocardial necrosis begins rapidly within as little as 15 minutes and spreads from the endocardium towards the epicardium causing damage to the heart muscle acute coronary syndrome a term used to describe clinical symptoms consistent with acute myocardial esea encompasses a spectrum of conditions including unstable angina myocardial infarction without ST segment elevation or an in stemi and and Mi with ST segment elevation patients experiencing stemi are especially concerning as they have a high probability greater than 90% of coronary thrus occlusion which necessitates urgent intervention for all patients with potential cardiac events a 12 lead ECG is an essential diagnostic tool for identifying ST segment elevation and confirming the presence of stemi prompt recognition of stemi and adherence to established guidelines are crucial to providing timely and appropriate interventions that can significantly impact patient outcomes and minimize myocardial damage the use of a 12 L ECG plays a crucial role in categorizing patients with acute coronary syndrome into two distinct groups those with ST segment elevation and those without it while many patients displaying ST segment elevation on their ECG are ultimately diagnosed with an ST segment elevation miocardial infarction patients who experience esic discomfort without ST segment elevation are often identified as having unstable angina or a non-st segment elevation MI or enemy which typically results in a non qwave Mi the differentiation is often Guided by cardiac enzymes or biomarkers which indicate evidence of cardiac injury furthermore some patients with angina or Mi May exhibit ST segment depression While others may present with no discernible changes on the ECG accurate categorization of these patients is crucial as it informs the appropriate therapeutic strategies and clinical management to optimize outcomes and mitigate cardiac damage early recognition of a stemi is absolutely critical as it enables prompt initiation of treatment or ensures the Swift Transportation of the patient to a health Care Facility where the necessary Specialized Care can be delivered recognizing the signs and symptoms such as chest and arm pain lower jaw pain shortness of breath and profuse sweating is pivotal in identifying patients with a high likelihood of having a stemi timeliness is the essence because most deaths resulting from stemi occur within the first 1 to two hours following the onset ofmt sys with ventricular fibrillation being a frequent cause to maximize the patient's chances of survival and minimize cardiac damage rapid intervention with the most appropriate reperfusion therapy should commence as soon as a diagnosis of stemi is confirmed these interventions such as percutaneous coronary intervention or thrombolytic therapy aimed to restore blood flow to The esic myocardium thereby preserving the heart muscle and minimizing potential complications performing a 12 lead ECG within the first 10 minutes of contact with a patient experiencing chest discomfort or simply displaying signs and symptoms suggestive of a stemi is an essential diagnostic step this early ECG helps rapidly identify stemi allowing for timely intervention as expeditious care is Paramount for improving outcomes if the initial ECG does not confirm stemi but there remains a high level of Suspicion based on clinical symptoms serial 12 Le ECGs should be conducted at Short intervals while maintaining continuous ST segment monitoring using specialized equipment with multi-parameter monitor monitoring capabilities for patients with inferior wall myocardial infarctions it's crucial to evaluate right side chest sads for ST segment elevation suggestive of right ventricular infarction and preemptive defibrillator plaid Pac should be considered for certain cases the classic diagnostic criteria for qmi include at least one 1 to 2 mm of ST segment elevation in a minimum of two contiguous leads it's essential to note that if there is no ST segment elevation or the ECG appears normal or simply demonstrates non-specific changes fibr linic therapy should not be administered continuous monitoring along with repeating the 12 lead ECG every 5 minutes should be maintained until serologic testing for cardiac enzymes or biomarkers is performed to exclude or confirm Mi this careful and systematic approach ensures that stemi patients receive appropriate treatment while avoiding unnecessary interventions in cases without ECG evidence of acute MI for all patients presenting with acute coronary syndrome irrespective of the presence or absence of ST segment elevation it is crucial to initiate anti-thrombin and anti-platelet therapy to inhibit further thrombus formation and reduce es schic complications patients with persistent ST segment elevation should be considered for immediate reperfusion therapy to restore blood flow to The myocardium those without ST segment elevation should receive anti-ischemic therapy and be evaluated for catheter-based interventions as needed medications like heprin and glycoprotein Inhibitors can be continued in the field to maintain anti-coagulation in cases involving marked ST segment depression in leads V1 through V4 with tall R waves in the right precordial leads and upright t- waves suggestive of a true posterior wall myocardial infarction fibr linic therapy is warranted and additional electrodes can be placed in the posterior position to form leads V7 V8 and v9 that being said primary percutaneous coronary intervention or PCI such as stinting or angioplasty may be more appropriate for patients with true pwmi the gold standard for stemi is timely arrival at a facility where the site of coordin artery occlusion can be identified and alleviated through cardiac catherization often utilizing percutaneous coronary intervention techniques like stinting or anoplasty which can significantly improve the patient outcomes by restoring blood flow to The esic myocardium the transport priorities in the context of acute coronary syndrome are multifaceted aiming to address different aspects of the patient's condition first and foremost the primary objective is to prevent further damage to the heart muscle this necessitates early diagnosis and and prompt treatment to restore coronary blood flow reducing after load and preventing the clot from getting larger are also crucial to optimizing cardiac function and minimizing the risk of worsening coronary artery occlusion simultaneously efforts are made to reduce myocardial oxygen demand typically achieved through interventions such as pain management and maintaining blood pressure within an except range maximizing oxygen delivery plays a pivotal role in supplying oxygen to The myocardium all while reducing or eliminating pain and anxiety as this is essential to ensure patient comfort and minimize stress for patients with ACS who may benefit from thrombolytic therapy it is essential to consider the administration of tissue plasmagen activators to dissolve the clot or clots and restore coronary blood flow these patients are often plac on an anti-coagulant Hein drip which requires Administration via an infusion pump providers must closely monitor patients on Hein for signs of serious bleeding while understanding that minor bleeding particularly around the mouth is common and usually not a reason to discontinue or alter the drip rates additionally patients who have received or are receiving thrombolytics may require a loading dose of an ADP inhibitor typically administered as oral medications these ADP Inhibitors have shown potential in improving percutaneous cordary intervention outcomes when administered early contributing to more favorable patient prognosis oxygen therapy another essential component should be administered to maintain an oxygen saturation of greater than 92% hyperoxia more than a 97% oxygen saturation should be avoided continuous waveform capnography is used for monitoring patients to maintain carbon dioxide levels between 35 and 45 optimizing their respiratory status in cases where long transport times are anticipated or severe coronary blockages threaten the patient's life the administration of a thrombotic agent may be indicated but strict adherence to locally determined exclusion criteria is imperative these criteria Encompass various clinical conditions including hypertension previous bleeding disorders and recent significant medical events in situations where reperfusion is achieved arrhythmias May develop as pottassium levels rapidly return to intracellular spaces While most of these arrhythmias are transient some can be serious and may require prompt intervention additionally patients receiving anti-coagulation therapy should be closely monitored for signs of bleeding and if severe bleeding occurs the Hein drip should be discontinued hypotension management with fluid suppressors may be required and transport may need to be diverted to the nearest hospital for further stabilization and treatment in critical cases angina pectoris is a clinical condition from an imbalance between the myocardium's oxygen demand and Supply which results in chest pain due to insufficient oxygen reaching the heart muscle it's crucial to differentiate between stable and unstable angina in the patient's medical history stable angina typically follows a predictable pattern where chest pain occurs after a specific level of physical exertion due to atherosclerotic lesions limiting myocardial oxygen supply during activity with many patients relying on nitroglycerin for relief in contrast unstable angina is more severe and often indicates a higher degree of coronary artery obstruction frequently resulting from plaque rupture or thrombus formation silent esea a subtler form of angina manifests without noticeable clinical symptoms but can be detected by observing ST segment elevation on an ECG this highlights the complex spectrum of anginal presentations that healthc care providers must consider during patient assessment and Care myo cardial infarction represents a critical condition in which the cardiac muscle is deprived of blood supply for a sufficient duration ultimately leading to tissue death various factors can contribute to this scenario including narrowed vessels from atherosclerosis coronary artery occlusion caused by thrombosis coronary artery spasms or a reduction in overall blood flow due to conditions like shock arrhythmias or pulmonary embolism the extent and location of an MI largely hinged on the specific coronary artery affected and the precise sight of the blockage in many cases Mis predominantly involve the left ventricle emphasizing the severe consequences of this condition which necessitate prompt recognition and intervention to mitigate potenti potential long-term damage and optimized patient outcomes inferior wall myocardial infarctions or iwmi typically result from occlusion of the right coronary artery also known as the RCA when the esic process is limited to the inner layer of cardiac muscle it's classified as a subendocardial infar however ever a more extensive infarction that permeates through the entire wall of The ventricle is known as a transal myocardial infarction a distinctive feature of Mi is the presence of a ring of a schic tissue encircling the infared area while this surrounding tissue remains viable it is deprived of oxygen rendering it electrically unstable and is often the the source of cardiac arrhythmias understanding these distinctions in mi types and the related electrical instability is vital for health care providers in diagnosing and managing patients with diverse presentations of coronary artery disease as this knowledge plays a crucial role in patient care and the prevention of potentially lifethreatening complications lastly cardiac enzymes play a critical role in diagnosing and monitoring myocardial infarction ECG changes are often considered a reflection of cell damage following an MI highlighting the need for more specific indicators to confirm and assess the extent of cardiac muscle injury as myocardial cells succumb to infarction they release their internal contents into the bloodstream including proponents T and I contractile proteins specific to The myocardium making them valuable markers for detecting myocardial cell injury canat while increasing in over 90% of Mis is less specific as it is also present in skeletal muscle myoglobin an oxygen transport protein is released into the circulation in response to damage in either cardiac or skeletal muscle however it's essential to note that these markers can be found in other medical conditions necessitating their interpretation in conjunction with other clinical and laboratory findings enabling healthc care providers to make a more accurate and reliable diagnosis of myocardial infarction and tailor treatment strategies accordingly patients at risk for sudden cardiac death incompass those with a history of Prior sudden Cardiac Arrest which underscores the gravity of the condition as well as individuals with a history of previous myocardial infarction which signifies their susceptibility to life-threatening cardiac events furthermore heart failure patients in classes two to four are at an increased risk particularly if their injection fraction is below 40% reflecting reduced cardiac pumping efficiency family history of cardiac arrest is another concerning risk factor emphasizing a potential genetic predisposition individuals with a prolonged QT interval on their ECG are at a heightened risk for life-threatening arrhythmias it's crucial to recognize these risk factors because sudden cardiac death often resulting from ventricular arrhythmias can be averted with appropriate interventions timely treatment and targeted therapies making the distinction between life and death for at risk individuals in these critical scenarios death from acute MI when properly managed is indeed preventable through various interventions including rep perfusion therapy and appropriate medications highlighting the significance of early diagnosis and immediate Medical Care in mitigating the devastating consequences of myocardial infarction the heart being a muscle relies on a constant supply of oxygen inrich blood to sustain its vital functions this crucial blood supply is facilitated by two main coronary arteries and their respective branches during diast when the heart relaxes and allows for optimal profusion these coronary arteries originate at the base of the aorta just above the aortic valve the right coronary artery extends to provide the right atrium right ventricle and portions of the left atrium and left ventricle with oxygen rich blood it also gives rise to branches such as the marginal posterior interventricular and sa noal branches each with specific roles the left coronary artery on the other hand contributes to the oxygen supply of both ventricles the interventricular septum and the left atrium with its major branches including the anterior interventricular and and the left circumflex branches the left interior descending artery further serves the right and left bundle branches the intricate network of coronary arteries and their branches ensures that the heart muscles receive the oxygen and nutrients they need emphasizing the vital role of these vessels in maintaining cardiac health and function deoxygenated blood full of waste products from the myocardium's metabolic processes is efficiently returned to the Venus circulation through the coronary sinus this large vessel acts as a crucial drainage system collecting the blood used from the coronary veins throughout the Heart It ultimately empties into the right atrium where this deoxygenated blood can then be pumped into the pulmonary circulation for oxygenation in the lungs it's worth noting that there can be subtle variations in the distribution of quinary arteries from one individual to another a phenomenon known as quinary artery dominance these differences highlight the uniqueness of each person's cardiovascular system and may have clinical implications when diagnosing and treating heart conditions as the specific Anatomy can influence the development of coronary artery disease and the distribution of esic regions in cases of heart disease a reduction in blood flow to the heart can occur through chronic processes like coronary vascular disease or acutely due to incidents such as the occlusion of a coronary artery by an embolis esema injury and infarction result from an imbalance between the oxygen supply and the demand of the myocardial tissue while esia and injury are potentially reversible conditions infarction which signifies cell death is usually permanent es schia initially manifests as a more electrically negative pattern in the effect Ed tissue compared to the surrounding healthy areas causing ST segment depression and symmetric t-wave inversion the specific characteristics of t-wave inversion with its symmetric appearance in the case of myocardial esmia serve as a key diagnostic indicator to differentiate it from other conditions that may lead to asymmetric or slur t-wave inversions these e CG changes are essential in understanding the underlying pathophysiology and guiding appropriate interventions in Cardiac Care in the context of cardiac pathology injury occurs when eskema persists without intervention during this stage the affected myocardial tissue remains partially depolarized causing it to become more electrically positive compared to the surrounding healthy tissue as a result the ST segment on the ECG becomes elevated serving as a prominent diagnostic feature despite the elevation of the ST segment The t-wave Remains inverted due to a continued abnormal repolarization pathway this ECG pattern characterized by St mment elevation and t-wave inversion signifies a critical phase in which The myocardium is at high risk for progressing to infarction or cell death recognizing these ECG changes is vital for prompt clinical intervention to prevent further deterioration of the cardiac tissue when es schea and injury remain unchecked the progression leads to infarction a critical phase in which the affected myocardial tissue becomes incapable of generating or transmitting electrical impulses as a result the ECG displays a distinctive pattern where no direct wave appears representing the nonviable nature of the infared tissue instead the ECG May exhibit Q waves which are electrical impulses that have been redirected away from the damaged area these Q waves can be observed in various leads such as the left lateral and inferior leads depending on the location and extent of the infarction for Q waves to indicate pathological conditions they must meet specific criteria including being more than 13 the total height of the associate QRS complex and wider than 40 milliseconds notably an MI can occur with or without Q waves smaller infarcts may not produce pronounced Q waves as the cellto cell conduction of electrical impulses can obscure their presence but ST segment and t-wave abnormalities will still be evident due to the simultaneous presence of aeia and injur underscoring the importance of recognizing these ECG changes during the evaluation of patients with myocardial infarctions stemies are often linked to a heightened risk of heart failure and mortality primarily due to the substantial extent of myocardial tisue damage involved the occlusion of a major coronary artery and the Associated large area of infarction can significantly impair the heart's pumping ability which can lead to heart failure and in severe cases cardiac arrest in contrast in stemies exhibit a different pattern wherein the risk of long-term mortality is comparatively higher this increased risk is attributed to the development of life-threatening arrhythmias such as vric tacac cardia or ventricular fibrillation which can originate from regions surrounding the infared area these arrhythmias can disrupt the heart's electrical stability potentially leading to sudden cardiac death it is essential for healthc care providers to recognize and manage these distinct risks associated with stemies and ins stemies tailoring their approaches to address both the extent of tissue damage and the potential AR iic complications in the context of Mi specific ECG changes offer vital insights into the affected tissue when an MI occurs the electrode situated directly above the infared area records a distinct deep negative deflection which is referred to as a qwave the these Q waves signify permanent damage to The myocardium as the tissue can no longer generate or transmit electrical impulses however what is equally important are the reciprocal changes observed in ECG leads positioned 180\u00b0 from the site of the infarction as the electrical current is directed away from the infared area these leads detect an apparent increase increase in electrical force moving in the opposite direction this will manifest as tall positive R waves contrasting with the negative Q waves seen over the infared region moreover this principle applies not only to Q waves but also to ST segment and t-wave alterations providing Medics with valuable information about the location extent and progression of myocardial damage which is crucial for diagnosis and management Mis can affect various areas of the heart and localizing the specific site of infarction is crucial because it determines both the prognosis and the most appropriate therapeutic approach the area of myocardium that undergo infarction primarily depends on which coronary arteries are included and the extent of collateral blood flow in clinical practice acute Mis often involve more than one region of the heart making it challenging to pinpoint the exact location one complicating factor is the presence of Q waves resulting from old infarctions which might coexist with findings of a new MI and potentially obscure the diagnostic process when interpreting the ECG to localize the infarction during transport Critical Care transport providers should follow a systematic approach this includes reviewing an old ECG from the patient's medical records to identify pre-existing conditions acquiring a new 12 lead ECG before and during transport and making serial evaluations along the way to assess evolving patterns or complications infarctions can be broadly categorized based on their anatomic location such as anterior inferior lateral and posterior infarctions each associated with distinct ECG changes and clinical implications accurately localizing the infarction AIDS health care providers in tailoring the appropriate interventions and improving patient outcomes an acute interior myocardial infarction is characterized by the involvement of the Interior surface of the left ventricle typically caused by occlusion of the left anterior descending artery in ECG terms one of the distinctive features of an anterior Mi is a disruption of the normal pattern of r-wave progression in the precordial leads this disruption May manifest as poor r-wave progression which can be an early indicator of an anterior Mi while the presence of significant Q waves is not uncommon in the early stages of an interior Mi is a disruption of the normal pattern of r-wave progression in the precordial lead s this disruption May manifest as poor r-wave progression which can be an early indicator of an anterior Mi while the absence of significant Q waves is not uncommon in the early stages of an anterior Mi the presence of poor rway progression especially when coupled with clinical symptoms other ECG changes or cardiac biomarker elevation should raise suspicion of this type of of infarction an acute interpal myocardial infarction is frequently associated with an occlusion of the left anterior descending artery one of the major coronary arteries the the ECG leads that provide the most informative views of this specific pattern of Mi are the septo leads particularly V1 and V V2 as well as the interior leads V3 and V4 these leads allow healthc care providers to assess and diagnose the specific location of the infarction an interior sepal Mi cases the involvement of the septal area which divides the left and right ventricles can have significant clinical implications rapid recognition of this type of MI along with its precise localization is crucial for Effective And Timely intervention to minimize damage to the heart muscle and improve the patient's prognosis an acute interpal myocardial infarction with lateral wall extension often results from the occlusion of the proximal left anterior descending artery this condition is characterized by ECG changes that are visible in multiple precordial leads particularly in V5 and V6 for the lateral extension as well as leads one and AVL the involvement of the proximal lad which supplies the anterior and lateral aspects of the left ventricle leads to a more extensive area of myocardial damage in cases like this the EC G may not always display significant qway formation but rather it exhibits ST segment elevation in leads V2 through V6 which can extend into leads one and AVL additionally reciprocal changes may be found in leads 2 3 and avf highlighting the complex nature of the ECG findings in this pattern of MI accurate localization and prompt intervention are critical in such cases to mitigate heart muscle damage and improve patient outcomes an acute lateral wall myocardial infarction is characterized by the involvement of the left lateral wall of the heart this pattern of Mi can occur either in isolation or concurrently with other infarction patterns depending on the extent of coronary artery occlusion it is often the result of oclusion in the left circumflex artery one of the primary coronary vessels supplying the lateral aspects of the left ventricle ECG changes associated with an acute lateral wall Mi are typically observed in the lateral leads including one AVL V5 and V6 where you may see ST segment elevation indicative of acute es schic injury additionally reciprocal changes May manifest in the inferior leads specifically two 3 and avf reflecting the complex electrical conduction patterns within the heart and the subsequent ECG findings that help clinicians pinpoint the affected region of The myocardium early recognition intervention and reperfusion therapy are crucial in improving patient outcomes when facing an acute lateral wall Mi an acute inferior wall myocardial infarction is characterized by the involvement of the diaphragmatic surface of the heart this type of MI is most commonly attributed to occlusion of the right coronary artery in approximately 90% of the cases although it can also result from occlusion if the descending branch of the RCA or the left circumflex artery in around 10% of patients ECG changes associated with an acute inferior wall Mii are typically observed in the inferior leads including leads two 3 and avf where you may see ST segment elevation indicative of acute es schic injury as blood supply to the inferior part of the heart is compromised it can lead to distinct changes on the ECG helping clinicians identify the affected region and providing valuable information for prompt and appropriate clinical intervention to mitigate further myocardial damage and improve Pro patient outcomes early recognition diagnosis and treatment are vital in the management of acute inferior wall Mi the characteristic ECG changes of an acute inferior wall myocardial infarction or iwmi are primarily evident in the inferior leads speciic specifically leads 2 3 and avf where ST segment elevation is commonly observed reflecting es schic injury in the diaphragmatic region of the heart these changes are often accompanied by reciprocal changes where ST segment depression can be seen in leads one and AVL indicating reciprocal esic effects in the opposite wall of the heart unless the infarction extends to involve the high lateral wall which then can mask these reciprocal changes an iwmi may also coexist with patterns of infarction affecting the lateral wall posterior wall or even a right ventricular infarction while Q waves are often a Hallmark of myocardial infarctions and tend to persist for a patient's lifetime in many cases they may not necessarily be a consistent feature in inferior inunctions making ECG interpretation an invaluable tool in identifying the location and extent of the infarction and guiding clinical management early recognition of these ECG patterns and prompt intervention is critical in optimizing patient care and improving outcomes in cases of acute iwmi an acute inferolateral myocardial infarction is characterized by specific ECG changes that are indicative of a schic injury in both the inferior and lateral walls of the heart these changes can be observed in a combination of leads primarily in the inferior leads to 3 and avf where ST segment elevation typically occurs reflecting the involvement of the inferior aspect of the heart however the lateral leads including one AVL V5 and V6 also display ST segment abnormalities in cases of inferior lateral Mi suggesting that the es schic injury extends into the lateral wall furthermore if the infar exceeds anteriorly ST segment changes may also be seen in leads V2 through V4 the presence of classic s segment and t-wave changes in the lateral precordial leads V5 and V6 is often an indicator of anterior extension in cases of the inferior lateral MI an acute apical myocardial infarction is an extension of an inferior lateral Mi and encompasses a sizable region of the inferior part of the heart with further extension anteriorly and laterally typically occurring in patients with right coronary artery dominance it results in a wide range of ECG changes that are not localized to a specific territory these ECG changes can be observed in various leads including the inferior leads 2 3 and avf the lateral leaves one and AVL and precordial leads V2 through V6 due to the diffuse and extensive nature of these ECG changes an acute apical Mi May sometimes be mistaken for pericarditis the acute right ventricular myocardial infarction or rvi is strongly associated with inferior wall myocardial infarctions and occurs in a substantial percentage of cases approximately 30 to 50% this type of Mi typically results from an occlusion of the right coronary artery which can potentially affect both the right ventricle and the inferior wall of the left ventricle simultaneously due to the anatomical distribution of the RCA diagnosis of rvi includes specific criteria which may include the presence of an iwmi ST segment elevation greater in lead three than in lead 2 ST segment elevation in V1 that could extend through V5 or V6 and ST segment depression in V2 unless of course the ST segment elevation extends through V5 or V6 when diagnosing an acute right ventricular myocardial infarction specific ECG criteria play a crucial role in accurate identification along with other established criteria the presence of ST segment depression in lead V2 not exceeding half the ST segment elevation observed in avf and 1 mm or more of ST segment elevation in right side leads v4r through v6r further enhances diagnostic Precision in cases where the criteria for rvi are met in the Standard 12 Le ECG it's prudent to consider the additional right side chest leads v4r to v6r to provide a comprehensive assessment the identification of ST segment elevation in v4r becomes a significant factor in completing the diagnostic criteria for rvi diagnosing an acute posterior wall myocardial infarction poses a unique challenge as it results from an inclusion of the right coronary artery and it lacks specific leads to examine the posterior surface of the heart in the Standard 12 Le ECG to identify this type of infarction healthc care providers rely on recognizing reciprocal changes in leads V1 and V2 such as ST segment depression upright t- waves and Tall R waves the presence of an r-wave with greater amp amplitude in the corresponding swave in these leads becomes highly suggestive of a posterior wall mi in cases where there is reciprocal evidence of this type of Mi it's crucial for the critical care transport professional to maintain a high index of Suspicion and consider recording the posterior leads V7 V8 and v9 for a comprehensive assessment cardiomyopathy is a broad term encompassing a range of heart diseases characterized by structural and functional abnormalities in The myocardium leading to a thin flabby dilated or enlarged heart muscle this condition represents a significant risk factor for heart failure acute myocardial infarction and potentially fatal outcomes patients with cardiomyopathy often present with a spectrum of symptoms including shortness of breath chest pains palpitations or Syncopy all of which can be attributed to the compromised cardiac function associated with this condition the progressive nature of cardiomyopathy underscores the need for early diagnosis appropriate management and ongoing monitoring to mitigate its impact and enhance the patient overall prognosis and quality of life life heart failure previously known as congestive heart failure is a condition characterized by a diminished ability of the heart to pump blood forcefully and efficiently enough to empty its Chambers leading to the accumulation of blood in the systemic Andor pulmonary circulatory systems while it was historically believed that congestion and fluid overload where the primary culprits responsible for the characteristic dipsia and edema observed in heart failure more recent research has revealed that a substantial portion of heart failure patients potentially up to half actually experience intravascular volume depletion this shift in understanding has significantly altered the approach to treatment with a reduced emphasis on diuretics as the initial therapy for patients presenting with dipsia and abnormal lung sounds heart failure can be caused by a variety of factors including structural abnormalities of the heart walls meaning dilated or hypertrophic malfunctioning heart valves such as the mitro tricuspid aortic and pulmonic valves damage resulting from myocardial infarctions and conduction abnormalities all of which can impair the heart's ability to function effectively and contribute to the development of heart failure the onset of heart failure is frequently precipitated by a significant myocardial infarction that affects one or more walls of the left ventricle causing damage to the cardiac muscle such damage can result in conduction pathway disruptions notably atrio ventricular blocks often necessitating the implantation of a pacemaker to restore electrical conduction additionally in the vicinity of a major infarction a distinct problem emerges characterized by the formation of new nerve fibers with an elevated density leading to a condition known as hyperinnervation this heightened inovation can contribute to the development of life-threatening arrhythmias such as ventricular attack cardia and ventricular fibrillation in cases where the infarction involves a septum the synchronization between the two ventricles is disrupted further exacerbating the electrical and functional abnormalities that can contribute to heart failure left-sided heart failure is primarily attributed to the detrimental impact on the left ventricle a condition often initiated by acute myocardial infarctions the intense often sudden loss of blood supply to a region of the Heart during an MI results in the death of myocardial cells and the impairment of left ventricular function additionally in cases of chronic hypertension the left ventricle is compelled to work persistently against increased afterload due to the constriction of the peripheral arteries which elevates systemic resistance this prolong strain can lead to a thickening of the left ventricular wall also known as left ventricular hypertrophy and an eventual reduction in its contractility these dual mechanisms can substantially contribute to left-sided heart failure leading to symptoms such as pulmonary congestion reduced cardiac output and systemic congestion perox maximal nocturnal dipsia is a distressing condition characterized by sudden and severe shortness of breath that awakens the individual from sleep it is frequently associated with left-sided heart failure or the decompensation of chronic obstructive pulmonary disease in context of left entric failure resulting from chronic overload typically due to long-term conditions like hypertension patients often recount a history of of experiencing pnd over a period of one or two weeks this gradual onset of pnd is indicative of heart failure symptoms that worsen as the heart struggles to maintain sufficient cardiac output against the elevated systemic resistance imposed by chronic conditions leading to pulmonary congestion and an accumulation of fluid in the lungs that intensifies during the night and culminates in the distressing symptom signs and symptoms of left-sided heart failure can be particularly alarming and distressing patients May exhibit extreme restlessness and agitation often accompanied by confusion as their body struggles to cope with the reduced cardiac output and the diminished ability of the left ventricle to efficiently pump blood severe dipsia and Rapid breathing are common due to pulmonary congestion resulting from fluid accumulation in the lungs Tac cardia may be present as the heart attempts to compensate for its reduced function elevated blood pressure can also occur especially if hypertension is a contributing factor upon oscilation crackles or rails in the lungs and possibly wheezing may be heard and patients May produce frothy pink tin sputum which is characteristic of pulmonary edema to help differentiate between Bronco constriction and respiratory distress caused by pulmonary edema capnography waveform analysis can be used as a valuable tool aiding health care providers in making an accurate and timely diagnosis and optimizing the management of these critical patients the management of left-sided heart failure is a crucial aspect of prehospital and critical care focusing on several key treatment priorities first and foremost the primary goals are to decrease pulmonary congestion reduce after load normalize myocardial oxygenation and decrease the myocardial oxygen demands to achieve these goals the approach may include various interventions one non-invasive ventilation if the patient is conscious incapable of maintaining their Airway applying non-invasive ventilation such as continuous positive airway pressure or bi Lev positive airway pressure can help alleviate respiratory distress and improve oxygenation two indot tral intubation in cases where the patient's level of Consciousness prevents them from managing their Airway interracial Innovation is indicated after successful intubation positive end expiratory pressure is applied using a transport ventilator and secretions are managed through intrical suctioning continuous waveform capnography is essential for monitoring ventilation three blood pressure management once Airway and ventilation are stabilized blood pressure management is critical diuretics may be considered to address significant fluid overload and promote increased urine output four hypertension management hypertension should be managed with intravenous anti-hypertensive medications and IV nitroglycerin may be employed to alleviate cardiac chest pain five hypotension manag management hypotension should be approached cautiously with volume repletion and pressors using a pressure that also provides inotropic support is often more beneficial than administering a pure pressor agent alone dopamine epinephrine and norepinephrine are commonly chosen initially number six diuretics for fluid overload if fluid overload is suspected intravenous diuretics such as Lasix or bumex can be considered to help reduce excessive fluid volume seven cardiac monitoring for all patients with heart failure or pulmonary edema it is imperative to obtain a 12 Le ECG and continuously monitor the patient for arhythmia and lastly number eight Mi management if if there is evidence of an evolving or acute myocardial infarction the therapies discussed previously for acute coronary syndrome will also be necessary during transport this may include interventions like fibrin therapy and antiplatelet therapy remember effective management of left-sided heart failure requires a multifaceted approach addressing respiratory distress hemodynamic stability fluid balance and potential comorbidities such as Mi right-sided heart failure typically arises as a consequence of left-sided heart failure though it can be triggered by other factors such as pulmonary embolism or longstanding COPD particularly chronic bronchitis in cases of right-sided heart failure there's an inability of the right ventricle to effectively pump blood forward causing a backup of blood in systemic veins this leads to an increase in pressure Within These veins resulting in their distension which can be observed for instance on the external jugular veins the heightened systemic Venus pressure forces serum out of the veins and into surrounding tissues causing edema interestingly the development of right-sided heart failure can have a somewhat paradoxical effect on left-sided heart failure while it exacerbates the overall heart failure condition it can also act as a compensatory mechanism limiting the amount of blood return to the lungs right-sided heart failure when considered by itself is generally not a life-threatening emergency treatment for right-sided heart failure primarily focuses while making the patient comfortable often achieve through positioning the patient in a semi position to alleviate discomfort and promote better lung expansion it's important to recognize that addressing the underlying cause such as left-sided heart failure or pulmonary embolism remains crucial in managing right-sided heart failure effectively the treatment of acute pulmonary edema primarily relies on non-invasive ventilation including CPAP BiPAP and high flow nasal canulas also known as HFN C's especially for patients capable of maintaining their own Airway non-invasive ventilation is considered a crucial intervention as it offers several benefits in managing this condition by improving Alvar ventilation in gas exchange non-invasive ventilation helps alleviate the respiratory distress associated with pulmonary edema it decreases the work of breathing reducing the excessive respiratory effort required to expel fluids from the lungs additionally it has the capacity to decrease both pre-load and after load which ultimately lessens the strin on the heart moreover it enhances lung compliance making it easy for the lungs to expand during inhalation and increases functional residual capacity improving overall lung function by addressing these key aspects non-invasive ventilation serves as a Cornerstone in the management of acute pulmonary edema facilitating improved oxygenation and symptom relief intubation should be considered as a last resort for patients experiencing acute respiratory distress due to conditions like asthma COPD or pulmonary edema non-invasive ventilation is the preferred initial approach in such cases offering several advantages non-invasive ventilation not only leads to fewer complications but also enhances patient Comfort making it a valuable tool in manag ing respiratory distress in the context of critical care transport it's important to have ventilators equipped with the capability to provide both CPAP and BiPAP as these are essential in administering non-invasive ventilation effectively while currently available high flow nasal canula units are not designed for transport they can be employed if an adequate gas supply is accessible Additionally the development of Transport specific units are underway which will further enhance the options available for Respiratory support during Critical Care transport reducing the necessity for intubation in these patient populations cardiac",
        "Cardiac Electrophysiology": "electrophysiology electrophysiology is a crucial field within Cardiology that plays a pivotal role in the evaluation and management of cardiac Rhythm disturbances while routine ECG monitoring is a fundamental tool in Cardiac Care more complex Rhythm disturbances often necessitate the expertise of an electrophysiologist these Specialists equipped with similar facilities and equipment to those found in cardiac catherization Labs conduct thorough evaluations and detailed mapping to pinpoint the origin of various cardiac Rhythm disturbances their work extends to addressing a wide range of conditions including ventricular and supraventricular Tachi ormas picardias AV blocks and Syncopy in a hospital setting electrophysiologists May perform electrophysiology studies which involve stimulating and recording electrical activity from multiple catheters at different cardiac sites these studies are instrumental in determining the location of heart blocks the origin of tardia and responses to specific medications or devices additionally electrophysiologists can perform catheter obl procedures which employ various energy sources such as radio frequency cryamy microwaves and lasers to eliminate or isolate sources of Rhythm disturbances during the transport of patients requiring electr physiology studies or procedures the critical care transport professionals role is to anticipate and address any rhythm disturbances that prompted the referral for patients with suspected arrhythmias devices such as HTR monitors and implantable loop recorders may be employed to provide continuous ECG monitoring patients with arhythmia have a range of therapeutic options including catheter oblas pharmacologic treatment and the implantation of devices like pacemakers and implantable cardioverter defibrillators as primary inhospital arhythmia management strategies these therapeutic approaches aim to restore normal cardiac Rhythm control symptoms and reduce the risk of life-threatening arrhythmias catheter Aion performed by electrophysiologists involves isolating or eliminating specific sources of Rhythm disturbances using various oblas techniques pharmacologic treatment often includes medications designed to regulate heart rate and Rhythm implantable devices such as pacemakers icds and cardiac re synchron therapy devices are utilized to manage bre cardias teoc cardias and heart failure in patients with complex arrhythmias these devices can provide pacing support cardiov verion or defibrillation as needed and are often used in conjunction with electrophysiology studies to tailor treatment to the patient's specific arhythmic condition Cath blasion is an Innovative and effective technique for managing a variety of cardiac arrhythmias by precisely targeting and isolating specific areas in the heart responsible for these Rhythm disturbances this therapeutic approach has demonstrated remarkable success in addressing conditions such as wolf Parkinson White syndrome and other supr ventricular teoc cardias including atrial flutter atrial tacac cardia AV node reentrant teoc cardia and some ventricular teac cardias various oblia methods such as radio frequency catheter Aion microwave catheter Aion cryothermy oblas laser catheter Aion and even surgical Aion have shown high efficiency in disrupting abnormal electrical Pathways or folky that give rise to arrhythmias advanced ments in mapping techniques have expanded the range of arhythmia eligible for oblas making it a transformative approach in the long-term management of patients with recurrent svts the procedure is often conducted on an outpatient basis and offers a high success rate ranging from 90 to 98% frequently resulting in a long-term cure and low incidence of complications this this means that for many patients with SVT catheter Aion can eliminate the need for prolonged medical therapy sparing them from potential drug induced adverse effects and enhancing their overall quality of life cathop plasan can be particularly beneficial for patients who may struggle with medication compliance or are simply hesitant to commit to long-term drug therapy making it a valuable option for those those seeking an effective and enduring solution for their arrhythmias in certain cases medications may still be employed to interfere with electrical conduction or impulse formation at specific sites in the heart such as the at of ventricular node accessory pathways are focal teoc cardia sources providing a multifaceted approach to arhythmia management left atrial appendage liation occlusion or excision has emerged as a valuable strategy in reducing the risk of thrombo emotic events particularly in patients who cannot undergo long-term anti-coagulation therapy this preventative measure is particularly relevant to individuals with Atri fibrillation a condition in which the left atrium is considered the primary source of thrombo emilii laa closure or excision can be performed during cardiac Bypass or valve surgery ensuring that patients with pre-existing cardiac conditions also receive protection against potential clot formation additionally minimally invasive percutaneous approaches have been developed with devices like the Watchmen which can be inserted into the laa through a trans con sepal approach these methods allow for a targeted intervention in the left atrium significantly reducing the risk of clot formation and subsequent embolic events especially when conventional anti-coagulation may not be an option due to contraindications or patient preferences implanted pacemakers play a crucial role in managing heart conditions characterized by impaired impulse generation or conduction these conditions can manifest as intermittent irregular or inadequately paced cardiac rhythms and in some cases a complete absence of intrinsic impulses blocks can occur at various points in the cardiac conduction system from the SA node to the distal conduction Pathways contemporary pacemakers are sophistic at devices designed to address these issues effectively they provide reliable and consistent cardiac depolarization ensuring that the heart beats in a coordinated manner by consistently monitoring the patients intrinsic cardiac activity pacemakers also prevent unnecessary pacing which helps conserve battery life moreover these devices are capable of synchronizing the depolarization of the right and left heart chambers optimizing overall cardiac function pacemakers can adapt the heart rate to match the body's metabolic or physical demands promoting efficient cardiac performance additionally they can store valuable information about cardiac events and physiologic changes aiding in the diagnosis and management of heart conditions in summary implanted paac fers offer comprehensive support to individuals with heart rhythm disorders enhancing their quality of life and reducing the risks associated with brto cardia and other conduction abnormalities implantable cardiio defibrillators have emerged as essential devices in the prevention of sudden cardiac death particularly among patients with heart failure and those with a history of resuscitation from Sudden cardiac death when it comes to managing life-threatening Tachi arrhythmias ICD therapy has demonstrated significant advantages over anti-arrhythmic drugs offering a highly effective and reliable solution Studies have indicated that icds can achieve success rates of up to 99% in terminating these dangerous arrhythmias what sets icds apart is there dual functionality as they not only serve as advanced defibrillators but also have pacing capabilities this dual role allows them to both terminate life-threatening arrhythmias and provide essential pacing support when necessary ensuring comprehensive management for patients at risk of sudden cardiac death patients at risk of sudden or rhythmogenic cardiac death are often prescribed a wearable cardiio defibrillator or wcd this Innovative device provides an important temporary solution for patients who have a transient need for protection against life-threatening ventricular arrhythmias the wcd is typically worn externally like a vest and continuously monitors the patient's heart rhythm in the event of a detected dangerous arhythmia the wcd can provide rapid defibrillation to restore normal heart rhythm thus preventing sudden cardiac death it serves as a bridge to other long-term Solutions such as implantable cardi defibrillators or other Interventional therapies offering a valuable safety net During the period when the patient's risk of life-threatening arrhythmias is at its highest wearable cardio defibrillators have proven effective in protecting individuals at risk providing them and their health care providers with peace of mind while planning the most appropriate long-term management strategy the history of pacemakers is marked by significant advancements in cardiac Rhythm management the earliest implantable pacemakers developed in 1960 were asynchronous devices which delivered pacing stimuli without regard to the hearts intrinsic electric activity this initial technology was improved in the late 1960s with the introduction of single chamber demand pacemakers which sensed the heart's own electrical signals and delivered pacing only when necessary a major Milestone occurred in 1979 with the introduction of the first dual chamber pacemaker this dual chamber design allowed for more physiological pacing by separately monitoring and stimulating both the Atria and the ventricles offering a significant Improvement in cardiac Rhythm management and enhancing the patient quality of life the introduction of the first single chamber rate respon of pacemaker in 1985 marked a significant advancement in pacemaker technology these Innovative devices were designed to adapt to the patient metabolic demands by adjusting the pacing rate in response to physical activity effectively mimicking the heart's natural rate response over the years this concept has evolved and dual chamber pacemakers now incorporate rate responsive pacing allowing them to provide a more physiologically appropriate response to the body's changing needs today these Advanced pacemakers offer a higher level of customization and adaptability promoting better synchronization of the heart's electrical activity with the individual's physiological requirements pacemakers are essential medical devices indicated for a range of cardiac Rhythm disturbances these indications Encompass various conditions such as sinus node dysfunction with documented symptomatic bradicardia including the presence of frequent sinus pauses that result in symptoms additionally pacemakers are recommended for patients with symptomatic chronotropic incompetence signifying their inability to add adequately increase or lower heart rate in response to physiological demands they are also indicated for those with symptomatic sinus spric cardia induced by necessary drug therapy as well as individuals experiencing reflex Syncopy in cases involving third degree and advanced second degree atrioventricular blocks associated with symptomatic bardia causes atal fibrillation or after catheter oblas of the AV node pacemaker implantation may be necessary furthermore cardiac resynchronization therapy is a vital function in pacemakers benefiting specific patients with heart failure other indications include hypersensitive kateed sinus syndrome and overdrive or anti-attack ofar cardia pacing for atrial or ventricular teoc cardias these pacemaker indications illustrate their versatile and critical role in managing a spectrum of cardiac arhythmia and disorders ultimately improving patient well-being and reducing the risk of adverse cardiovascular events understanding the fundamental electrical principles of cardiac pacing is vital in the management of patients with various arrhythmias a pacing impulse encompasses several key parameters including current voltage and impedance current denotes the flow of electrons through an electrical circuit over time typically measured in ampers voltage often termed amplitude in pacing systems represents the force propelling current flow and its quantity ified in volts reflecting the strength or intensity of a pacing pulse impedance measured in ohms signifies the overall resistance to current along the pacing circuit impedance encompasses all factors that hinder current flow within the conduction pathway notably the primary sources of resistance in a pacing circuit include the lead conductor the electrode and the concentration of electrically charged ions at the electrode tissue interface known as polarization it is important to highlight that while electrode existence enhances pacing efficiency lead conductor resistance and polarization don't positively impact pacing performance furthermore ohms law represented as IAL V / R articulates the relationship between current voltage and resistance if voltage halves the current flow decreases similarly and doubling impedance reduces Flow by half voltage and impedance are pivotal in determining battery longevity lastly a jewel measures energy and energy can be computed as the product of volts current and time which is a crucial consideration when assessing the devic's performance and capabilities cardiac pacing leads are vital components of pacemaker systems with approximately 95% of leads being endocardial or transvenous leads that are carefully threaded through veins typically the subclavian or calic to reach the right atrium or ventricle lead placement involves the use of an introducer which is a hollow tube and a stylet which is a stiff wire to facilitate precise positioning within the heart these leads may come in two main configurations unipolar or bipolar unipolar leads consist of a single conductor wire connected to a solitary electrode in this Arrangement the cathode is in direct contact with The myocardium while the implantable pulse generator housing serves as the anode conversely bipolar leads incorporate two conductor wires ensuring that both the anode and cathode have direct contact with the heart in this design the anode representing the ring electrode situated approximately 2 to 3 cm above the cathode is connected via a separate lead to the ipg on understanding the nuances of lead configurations is essential for the management of patients with implanted pacemakers and ensuring the Optimal Performance of these life-saving devices in a cardiac pacing system electrodes play a fundamental role in the transition of electrical impulses to the heart the cathode an electrode in direct contact with cardiac tissue takes on a negative charge when electrical current flows through it allowing it to initiate the depolarization of The myocardium this crucial interaction leads to the contraction of cardiac muscle and ensures the heart continues to beat efficiently conversely the anode which serves as the electrode receiving the electrical impulse after depolarization of the heart tissue carries a positive charge when current is passing through it this carefully or orchestrated interplay between the cathode and the anode with their opposing charges is integral to the functioning of pacemakers as it governs the electrical stimulation of the heart and maintains proper cardiac rhythm in patients who rely on these devices for life sustaining support in the realm of cardiac pacing systems the choice between single chamber and dual chamber config configurations is a pivotal decision a single chamber pacing system as the name suggests employs a single lead which can be positioned either in the right atrium or the right ventricle this simpler setup is typically used when the primary objective is to address specific heart rhythm issues or conduction abnormalities within one of these Chambers in contrast a dual chamber pacing system utilizes two leads with one placed in the right atrium and the other in the right ventricle this more intricate Arrangement allows for a more physiologically natural coordination of atrial and ventricular contractions closely mimicking the heart's intrinsic electrical activity dual chamber systems are often chosen when more sophisticated pacing is required to optimize cardiac function particularly in cases of heart block atrioventricular conduction issues or tacki arhythmia that involve both Atria and ventricles the selection between single and dual chamber systems depends on the specific clinical needs and conditions of the patient reflecting the complexity and adaptability of modern pacemaker technology the nbg code consisting of five letters serves as a standardized classification system to succinctly describe the key features of cardiac pacemakers each letter in the code holds specific significance the first letter designates the chamber within the heart where pacing is initiated the second letter pinpoints the chamber where the pacemaker senses intrinsic electrical activity the third letter characterizes the device's response to sensing such as inhibiting or triggering further pacing the fourth letter denotes the pacemaker programmability and rate modulation capabilities reflecting its capacity for external adjustments lastly the fifth letter delineates the devices anti-tack arhythmia functions illustrating its capability to manage and intervene in Tachi arhythmic events this standardized coding system plays a crucial role in the clear communication of of essential pacemaker features enabling healthc Care Professionals to accurately interpret and manage these life-enhancing devices transcutaneous pacemakers or tcps serve as a crucial emergency intervention tool for patients experiencing severe Brady arhythmia in this approach multi-function TCP pads are strategically affixed to the patient's chest wall in the anterior posterior positions the TCP delivers an electrical pacing impulse through the skin and thoracic cavity directly to the heart effectively initiating or maintaining a stable heart rate while this is most commonly employed as an initial emergency Pacer to rapidly restore adequate heart rate and profusion it is typically considered a temporary measure the objective is to bridge the gap until a more definitive transvenous pacing wire can be placed allowing for longer term management the transcutaneous pacing remains a valuable tool in emergency settings ensuring prompt and efficient pacing in critical situations especially when alternative pacing modalities are either unavailable or ineffective thereby improving patient outcomes implantable pacemakers represent a wellestablished method for managing cardiac Rhythm disturbances these devices are composed of a battery operated pulse generator connected to one or more pacing or sensing leads typically a cardiologist or thoracic surgeon inserts these leads into the appropriate myocardial wall location the pulse generator module is then surgically implanted within the body usually sit situated within a subcutaneous pocket created between the pectoral muscle and the cutaneous layer of the skin these implantable pacemakers can feature a variety of lead configurations offering a degree of customization based on the specific clinical needs of the patient depending on the patient's condition these pacemakers can operate either on demand pacing the heart only when necessary or they can be programmed to provide continuous pacing modern pacemakers often incorporate both atrial and ventricular lead configurations and can serve as combined devices that integrate defibrillation capabilities as well however these devices are not without their challenges the most common sources of failure are battery depletion and issues related to lead wires such as Detachment or fractures less frequently issues arise due to pulse generator circuitry malfunction or dislodgement from the myocardial wall necessitating careful long-term monitoring and when necessary device replacement trans thoracic or epicardial pacemakers represent an invasive form of pacing that is typically reserved for specialized clinical situations the these procedures are performed exclusively by either cardiologists or cardiac surgeons and involve the placement of pacing electrodes directly into the heart through the thoracic cavity while this approach offers precise control and is sometimes used during open heart surgeries such as coronary artery bypass grafting or valve replacement procedures it is not a commonly encountered pacing modality for most healthc care providers this would include Critical Care transport Personnel cctp teams may only encounter patients with these types of pacemakers when called upon to transport individuals who have recently undergone cardiac surgery or more likely are being transferred from one Health Care Facility to another for Specialized Care trans Venus or external pacemakers serve as a temporary solution to address pacing issues until a more permanent solution can be implemented or until a permanent pacemaker is implanted they are generally considered more reliable than transcutaneous pacing because they establish direct myocardial contact requiring considerably less energy to achieve capture these devices provide tighter control and more sophisticated settings through an external pulse generator for transport professionals is is crucial to familiarize themselves with the specific type of transvenous wire and temporary pacemakers used by local hospitals and receive a tutorial on troubleshooting these devices during patient packaging several important steps must be taken including confirming the actual settings on the temporary pacemaker ensuring electrical and mechanical capture and securing transvenous or epicardial pacing wires to prevent an advertent dislodgment over sensing is a common issue during transport as various forms of energy interference can affect pacemakers in demand mode decreasing the pacemaker sensitivity is an appropriate action to resolve interference and ensure necessary pacing remains unaffected Critical Care transport professionals should have a clear understanding of these devices to provide safe and affected patient care during transport leadless pacemakers represent a significant advancement in cardiac pacing technology as they are self-contained devices that integrate both the pulse generator and pacing sensing leads into a single unit which is implanted directly into the right ventricle this innovation has made these devices approximately 90% smaller compared to traditional pacemakers one of the key advantages is their minimally invasive implantation process conducted through a trans catheter approach via a femoral vein which eliminates the need for surgical Pockets or traditional leads these leadless pacemakers primarily offer single chamber ventricular pacing and are compatible with MRI scans enhancing diagnostic capabilities additionally they have an impressive battery life ranging from 5 to 15 years reducing the frequency of battery Replacements and the associated invasive procedure making them an attractive option for many patients pacemaker troubleshooting involves addressing various issues that may affect the proper functioning of these life-saving devices the primary areas of failure and common troubleshooting concerns are as follows one battery failure the pacemaker battery has a limited lifespan typically around 5 to 15 years depending on the device when the battery is depleted the pacemaker may stop working in such cases patients usually require replacement of the entire device two problems at the the lead Electro tissue interface issues at the electrode tissue interface can include elevated impedance which may prevent the efficient transfer of electrical signals between the pacemaker and the Heart troubleshooting involves checking lead placement ensuring proper connection and assessing for dislodgement Scar Tissue buildup is the number one reason for this interference three coiling or damage to the lead generator interface damage or coiling of the lead wires where they connect to the pulse generator can hinder electrical conduction inspecting the lead connections and addressing any physical damage as necessary four insulation failure of the lead wires insulation issues on lead wires can cause electrical short circuits this problem can be identified through impedance measurements and requires lead replacement five dislodgment of the lead at the implantation site this is very rare but leads can dislodge from their original implantation site affecting pacing detecting lead dislodgment through chest x-rays or device Diagnostics is essential and repositioning or lead replacement may be required six pacemaker programming errors in pacemaker programming can lead to suboptimal pacing or a lack of synchronization with the patient's intrinsic heart rhythm reprogramming should be reviewed and adjusted if necessary seven pacemaker pocket stimulation stimulation of surrounding tissues within the pacemaker pocket can lead lead to discomfort and interference with Device function repositioning the device or modifying the pacing settings can address this issue eight diaphragmatic stimulation diaphragmatic stimulation may occur if the pacing output is set too high causing the contraction of the diaphragm adjusting the pacing thresholds can help resolve this problem nine electromatic interference external sources of electromagnetic interference such as cell phones and personal electronic devices can and do disrupt pacemaker function minimizing exposure to these devices and maintaining a safe distance can mitigate interference in addressing these troubleshooting concerns healthc Care Professionals need to work closely with Device manufacturers anday pacemaker clinics to ensure the effective and safe operation of pacemakers and patients regular checks and remote monitoring can help detect and prevent issues before they become critical during transport it is crucial for critical care transport providers to be vigilant about recognizing the signs of pacemaker failure this is because timely intervention can be life-saving the following steps are recommended to identify and address these issues cardiac monitor indications the most apparent sign of pacemaker failure is failure to capture which means that the pacing stimulus is not resulting in an effective beat the ECG on the monitor will show pacing spikes without corresponding QRS complexes if this is observed immediate attention is required required correlation of pulse and ECG confirm that the patient's pulse aligns with the pacing presentation of the ECG lack of Correspondence between the pulse rate and the Pacer's output on the ECG monitor indicates a potential pacemaker failure assess patient for signs of decompensation conduct a thorough clinical assessment of the patient for signs and symptoms of poor profusion which can vary and include Syncopy dizziness palpitations braic cardia heart blocks hypotension teoc cardia and extracardiac stimulation sometimes indicated by hiccups or other muscle contractions that coincide with the piing stimuli identify ify external interference before assuming a pacemaker issue check for external sources of interference such as cell phones or personal electronic devices electromagnetic interference can disrupt pacemaker function and may be resolved by removing or distancing from these devices lastly patient specific treatment if quick fixes or addressing external interference do not resolve the issue the treatment should be tailored to the patient symptoms the approach may include adjusting pacing settings managing symptoms or initiating external pacing if necessary the exact interventions will simply depend on the clinical context and the nature of the pacemaker failure continuous monitoring and Vigilant assessment of the patient's clinical status are vital during trans transport the provider should be well prepared to respond to Pacemaker issues properly and appropriately coordinating with the receiving facility and healthc care providers as needed to ensure patient safety and effective Cardiac Care pacemakers significantly impact the ECG based on the type of system used single chamber pacemaker systems which imp a single lead are commonly used when only ventricular pacing is required however they do not offer atrioventricular synchrony pacing in the ventricular Pacer mode can result in the loss of Av synchrony leading to a condition known as pacemaker syndrome this syndrome manifests as various symptoms due to hemodynamic disturbances resulting in non-physiological iCal timing of atrial and ventricular contractions on the other hand dual chamber pacemaker systems utilize two leads one placed in the atrium and one in The ventricle this configuration ensures AV synchrony and allows for ventricular depolarization even in the absence of natural AV conduction this mode of pacing is referred to as h synchronous pacing atrial tracking or AV sequential pacing dual chamber systems enable more physiological cardiac Rhythm management by coordinating the timing of atrial and ventricular contractions atrioventricular pacing often referred to as cardiac resynchronization therapy represents a crucial treatment option for patients with heart failure aimed at enhancing both their quality of life and overall survival this therapy utilizes a modified cardiac pacemaker or implantable cardioverter defibrillator or ICD to resynchronize the heart's chambers the primary goal is to synchronize the ejection of the right and left ventricles which leads to more efficient cardiac output to achieve this synchronization pacing leads are strategically positioned in both ventricles and their coordination is meticulously optimized in a typical biventricular implant one lead is placed in the Atria and a lead in each ventricle facilitating a harmonious and coordinated contraction sequence that improves the heart's pumping capability and subsequently alleviates Ates symptoms and enhances the patient's well-being implantable cardioverter defibrillators are sophisticated devices designed for the primary purpose of monitoring and if necessary correcting life-threatening tacki arrhythmias these devices consist of several essential components including a housing and variable number of pacing and high voltage leads with the leads typically being placed in the abdominal or pectoral region the leads play a critical role in sensing cardiac rhythms and delivering Therapies in most cases one or two transvenous leads are used for pacing and shocking entering the Venus system through the subclavian or calic vein to reach their destination in the right ventricle or the superior vena the core function of an ICD involves continuously monitoring the ventricular rate and when it detects Tachi arhythmia based on this parameter initiates an appropriate therapy that being said this Reliance on ventricular rate alone can lead to some potential issues as atrial arhythmia and electromagnetic interference May sometimes trigger inappropriate shocks icds are programmed to deliver a predefined number of shocks typically four or five for each episode of an arhythmia this serves to restore normal heart rhythm and prevent sudden cardiac death when troubleshooting an implanted cardioverter defibrillator after it has delivered therapy to a patient thorough information gathering is of Paramount importance to determine the appropriateness of the therapy and ensure the patient well-being in such situations it is essential to gather data about the patient experience and the specific circumstances patients who have previously received shocks from their icds may have developed a familiarity with the symptoms of ventricular arrhythmias enabling them to differentiate between appropriate and inappropriate therapies key factors to consider during this process include the number of times the patient was shocked recent medical procedures any changes in the patient's medical condition or medication adherence the patient's activity at the time of the shock and their proximity to water or an electrical source when identifying a problem with an implanted cardioverter defibrillator there are are several important steps to consider first the ICD can be temporarily disabled using a magnet to prevent further discharges manufacturers of icds typically provide specialized magnets often in a donut shape which should be placed directly over the icd's pulse generator however it's crucial to note that before employing the magnet multifunction pads must be positioned on the patient and connected to the monitor to ensure continuous monitoring and assessment in the event of cardiac arrest external defibrillation can still be delivered but it's essential to avoid placing the defib paddles or pads directly over the ICD to prevent potential damage to the device furthermore providers can perform cardiopul Ary resuscitation on a patient with an ICD without endangering themselves or the patient or the implanted device for patients experiencing atrial tacac cardia icds offer effective treatment options an internal cardioversion or anti-tac cardia pacing through an atrial ICD has proven to be the preferred mode of inter prevention there are three primary methods to activate an atrial tacac cardia ICD the first approach involves a patient activated mode where patients are equipped with a small handheld remote that enables them to initiate therapy when they sense the onset of an arhythmia alternatively patients can directly activate the device ensuring that appropriate therapy is ad administered when needed in the third mode the pacemaker or ICD can be programmed to automatically detect and deliver therapy upon identifying the arhythmia offering a seamless and responsive treatment approach for patients with atrial teoc cardia wearable cardi verter defibrillators or wcds have become a valuable short-term treatment option since 2001 primarily for patients at high risk of sudden cardiac death suitable candidates for these devices include individuals who have recently experienced a myocardial infarction have a low ejection fraction are dealing with new onset arrhythmias or have survived a recent or suspected sudden cardiac death episode in certain cases cases wcds may also be appropriate for patients awaiting the resolution of an infectious process following the removal of an infected implantable cardioverter defibrillator one example of this technology available in the United States is the Z life vest comprising a lightweight monitor worn around the waist or from a shoulder strap and an electrode belt with a chest garment the device can detect lethal rhythmia and delivers electrical energy to the patient following voice and vibratory warnings that allow the patient to abort the shock if they are awake and alert patients are typically advised to wear wcds continuously except during bathing or showering as the greatest risk arises when the device is not being worn this Tech technology offers a crucial means of safeguarding high-risk patients from life-threatening arrhythmias while they await more definitive treatment options the introduction of subcutaneous implantable cardioverter defibrillators or sicds in the United States in 2015 marked a significant advancement in the field of cardiac device technology these devices utilize a lowprofile ICD referred to as a can which is surgically implanted into the subcutaneous tissue near the fifth and sixth ribs along the mid axillary line unlike traditional icds the S ICD operates without the need for any Venus leads or wires eliminating the associated risks of lead related complications and infections this Innovative technology represents a valuable alternative for patients who require protection from life-threatening arrhythmias while minimizing the potential complications associated with transvenous lead placement enhancing safety and the overall management of patients at risk of sudden cardiac death the sicd will provide ventricular pacing after a life-saving shock is delivered this pacing function can be crucial in preventing bra cardia or arrhythmias that could occur as a consequence of the shock however the sicd is typically not recommended for patients with symptomatic bardia or arhythmia that can be effectively managed with antioc cardia pacing this is because it primarily serves as a device for sudden cardiac death prevention and is best suited for patients at risk of life-threatening ventricular arrhythmias patients with Broc cardia or other arrhythmias that require pacing therapy are often better served by traditional pacemakers or implantable devices specifically designed for rhythmia management in conclusion Critical Care transport professionals play a crucial role in the evaluation care and safe transport of patients with cardiac arrhythmias the Knowledge and Skills discussed during this lecture are fundamental in providing highquality care for these patients understanding the interpretation and monitoring of 12 Le ECGs recognizing the underlying electrophysiology and its implications being proficient in handling temporary and implanted cardiac devices and ensuring patient safety during transport are all vital components of your practice moreover our discussion highlighted how cardiac monitoring and critical care transport should Encompass a broad view of the heart's electrical Rhythm and in specific cases the importance of Serial 12 lead ECG evaluations traditionally the management of cardiac rhythmia often relied on pharmacological interventions which could be associated with side effects and limitations in efficacy however advancements in pacing technology have revolutionized the treatment landscape allowing for electrical therapies with minimal patient awareness this progress provides a more effective and patient-friendly approach to addressing arhythmia as and heart failure the expanded therapeutic options including implanted pacemakers temporary pacing techniques wearable defibrillators and implantable cardioverter defibrillators offer a wide array of solutions to enhance patient care your commitment to staying informed and skilled in these areas is pivotal in ensuring that patients with cardiac arrhythmias receive the best possible care during their journey to recovery"
    },
    {
        "Introduction": "In This Chapter Looking at the basic structure and functions of the cardiovascular system Assessing cardiovascular findings and identifying acute coronary syndrome Taking care of potential cardiovascular problems More Americans experience cardiovascular-related medical conditions and emergencies than any other disease. That\u2019s the reason why the national EMT examination makes this condition a section unto itself. It has become clear that emergency medical services (EMS) can make a big difference in the big daddy of cardiovascular disease, the acute myocardial infarction (AMI). Early detection of an AMI, along with safe, rapid transport to a receiving facility of heart attack victims quickly reduces the likelihood of death and promotes a better life long after the event is over. If AMI is the big daddy, then cardiac arrest is the big momma. Sudden cardiac arrest used to be almost always fatal. However, with early, high-quality CPR and rapid use of automated external defibrillators, EMTs are part of the chain of survival that can reduce the patient\u2019s chance of dying. There are many other causes of chest pain that this chapter explores. Many have signs and symptoms of an AMI. It\u2019s not absolutely critical that you can tell the difference all the time; what matters most is making sure that you give each patient the benefit of the doubt as you perform your assessment. In this chapter, you get the basics on the cardiovascular system, discover normal and irregular cardiovascular findings, and figure out how to handle a number of cardiovascular problems.",
        "Checking Out the Cardiovascular System": "The cardiovascular system is broken down into three broad areas: the heart, the vasculature, and the blood. They interact closely to be able to create enough pressure in the system to produce perfusion (more commonly known as circulation). Surveying major structures The heart is the sophisticated pump that powers the cardiovascular system (see Figure 10-1). Its four chambers can be divided in two ways: Top and bottom, or the atria and ventricles, respectively Right and left, or pulmonary and peripheral circulation, respectively Illustration by Kathryn Born, MA Figure 10-1: The heart\u2019s chambers. One-way valves separate the atria from the ventricles, and pulmonary circulation from peripheral circulation. This structure has the effect of forcing blood to move in one direction only, starting with blood entering the heart from the right atrium and exiting to the body through the left ventricle. Blood is fluid that\u2019s comprised primarily of plasma, which contains mostly water along with various salts, minerals, and proteins. Red blood cells (erythrocytes) carry most of the oxygen you need to live. White blood cells (leukocytes) fight off infection and are part of your immune system (which I describe in Chapter 11). Platelets begin the coagulation, or clotting, process when a tear in the vasculature is detected. Carbon dioxide, nutrients such as glucose, and waste such as urea are carried in the plasma. You\u2019ve probably heard the phrase, \u201cBlood is thicker than water.\u201d Well, besides having to do with the relatives you\u2019re born with, it is indeed true that blood has a consistency, or viscosity, that\u2019s slightly heavier than water. The cardiovascular system relies on this viscosity to help create pressure within the vasculature. The vasculature is the combination of pipes that the heart pumps blood into, creating pressure. The arterial side of the vasculature carries blood away from the heart, either to the lungs via the pulmonary artery to pick up oxygen or to the rest of the body via the aorta to deliver oxygen to the body in the peripheral circulation. Arteries are made of smooth muscle and have the ability to stretch and snap back to their original shape, which helps tremendously with the flow of blood. They can also constrict and dilate, depending on the demands of the tissue for oxygen and nutrients. Arteries divide into smaller vessels called arterioles, which divide again numerous times and finally terminate in capillary beds within the tissues. Gas exchange occurs at the capillary beds. In Chapter 9, you find out how that happens in the lungs; the process is the same everywhere else. Diffusion of CO 2 and oxygen occurs based on the concentration of each gas between the capillary and the tissue cells. The heart itself has its own vasculature. Coronary arteries branch off right where the aorta exits the left ventricle, and they supply the heart tissue, or myocardium. Helping to return blood back to the heart is the venous system. Blood leaves the venous side of the capillary beds, collecting in venules. They, in turn, collect into veins. The veins are much more rigid than the arteries, which helps to maintain blood pressure as blood returns to the heart. Inside the veins are one-way valves that again force blood to travel in one direction. All together, these vessels create a closed system of pipes that, with the heart acting as a pump, creates a pressure within itself (see Figure 10-2). You measure that pressure with a blood pressure cuff. By measuring the patient\u2019s blood pressure early in your assessment, you can get a sense of how well the system is working. Illustration by Kathryn Born, MA Figure 10-2: The perfusion triangle. The heart, blood and vasculature make up a perfusion triangle, where all three parts interact with each other to create circulation. In reality, you measure perfusion by assessing the patient\u2019s blood pressure.",
        "Understanding blood pressure": "One way of talking about blood pressure is with this formula: Blood pressure (BP) = Cardiac output (CO) \u00d7 systemic vascular resistance (SVR) (the size of the vasculature) Before you panic, rest assured \u2014 you won\u2019t be calculating BP this way! However, the formula quickly illustrates what really counts in maintaining blood pressure. Cardiac output is the amount of blood that is sent out of the left ventricle in 1 minute. It, too, has a formula: Cardiac output (CO) = Heart rate (HR) \u00d7 stroke volume (SV) (the amount of blood squeezed out per contraction) Again, don\u2019t panic \u2014 no math is needed here either. But put both formulas together and this is what you get: BP = (HR \u00d7 SV) \u00d7 SVR What does all this mean? The human body controls its blood pressure through essentially one of three ways: by adjusting heart rate, stroke volume, or systemic vascular resistance. In fact, blood pressure is usually controlled via a combination of the three. Here\u2019s an example: A patient is having an AMI that\u2019s targeting the heart\u2019s electrical system (see the later section \u201cDistinguishing acute coronary syndrome from everything else\u201d for details). The result is that the heart rate slows down. If everything were to stay the same, blood pressure would drop. But it doesn\u2019t: The body constricts its arterial beds in the skin and other parts of the body so that SVR increases. The result is that the patient turns pale, the skin cools, and blood pressure remains near normal. So, if the primary function of the cardiovascular system is to maintain perfusion throughout the body, it makes sense that keeping a handle on moment-to-moment changes in blood pressure controls the system. Baroreceptors in the carotid arteries do exactly that. As the receptors sense a drop in BP, they send signals to the brain that, in turn, sends signals to the body to do such things as increase heart rate, increase the strength of ventricular contractions, constrict appropriate arteries, and even decrease the amount of water being filtered by the kidneys so that more fluid stays within the bloodstream. The process is really more complicated, but in a nutshell, that\u2019s how the body keeps its perfusion within a very narrow band of pressure.",
        "Knowing the Cardiovascular Issues to Look for When You Assess Patients": "So what are the cardiovascular system findings you should look for when assessing the patient? The following sections start with the normal findings, move to irregular findings, and wrap up with acute coronary syndrome. Recognizing normal cardiovascular findings You can use yourself as a \u201cnormal\u201d picture when it comes to cardiovascular findings. Your normal resting pulse should be strong, regular, and pumping at about 60\u2013100 beats per minute while at rest. You should be able to easily find this pulse by checking your radial artery on the thumb side of your wrist. While you\u2019re feeling the pulse, get a sense of how the skin looks and feels. Unless something is happening to you that I can\u2019t see right now, I\u2019d guess that your skin has a normal color; has a normal, warm temperature; and is dry. That\u2019s because your skin, an organ of the body, is being adequately perfused. Now, skin can be cooler to the touch when it\u2019s cool outside or a little sweaty when you\u2019ve just finished a workout (or you\u2019re panicking about your national exam), but it should return to its normal look and feel within a matter of minutes. Your blood pressure should be roughly around 120 mm Hg or less systolic and about 80 mm Hg or less diastolic when measured at the distal bicep region of the arm. Many people have blood pressures that are higher than normal (hypertension) but live with that pressure. On the other hand, athletes and other fit folks often live with much lower BP. In general, having a lower-than-normal BP is much better than having high BP. Tightly connected to the cardiovascular system is the respiratory system; what happens in one is often reflected in the other. Under normal conditions, the patient\u2019s respiratory rate should be about 12 to 20 breaths per minute without any major effort. When things start to go wrong with the cardiac system, the respiratory system tries to compensate for the issue. Flip to Chapter 9 for more information about the respiratory system.",
        "Noting when cardiovascular findings aren\u2019t normal": "Problems can arise within the cardiovascular system itself, and problems found elsewhere in the body can cause the cardiovascular system to compensate for the issue, sometimes responding so severely that it injures itself. (You find a list of common issues later in this chapter.) When the body senses that perfusion is or may be compromised, several things happen. Heart rate increases, and the skin turns cool, pale, and clammy. Breathing speeds up too, trying to add more oxygen to the bloodstream and take out excess carbon dioxide. Combine all of these changes and the blood pressure remains as close to normal as possible, even higher than normal sometimes. If the problem isn\u2019t repaired, at some point the cardiovascular system can no longer compensate and begins to fail. Blood pressure falls. The heart slows. The brain, suffering from worsening hypoxia, loses its ability to maintain an alert state; the patient moves from being anxious to being confused and finds it harder to stay awake. As the condition worsens further, the patient becomes unconscious and unresponsive to a painful stimulus.",
        "Distinguishing acute coronary syndrome from everything else": "The heart is especially sensitive to changes in perfusion. Because of its importance, the heart has a well-developed system of coronary arteries that feed the myocardial muscle. These arteries are fairly small and become easily blocked with a rupture of plaque (a layer of fat and minerals that embeds within the inner layers of an artery) or emboli (small particles of plaque) that float in from other parts of the body and lodge within the coronary artery itself. If either of these happens, the patient may experience a partial or complete loss of blood flow distal to the blockage. This occurrence marks the beginning of an acute myocardial infarction (AMI), or death of cardiac tissue. As the cardiac tissue becomes ischemic (starved of oxygen and becoming more acidic), it sends signals back to the brain. In turn, the brain interprets these signals as the sensation of pressure, burning, tightness, sharpness, or aching. The patient may also feel nauseous, faint, lightheaded, or dizzy. Additionally, because of the close relationship of the lungs and heart, the patient can experience shortness of breath. Because of the way the nerves make their way through the body, the brain may sense related or radiating pain or discomfort to the arms, jaw, or other places in the body. Sometimes coronary blood flow isn\u2019t blocked by plaque or emboli. The patient may have atherosclerosis, or narrowing of the arteries that decreases blood flow to the myocardial tissue. Sometimes the arteries themselves can experience a spasm. In these situations the condition known as angina may occur. These patients have a lot of the same signs and symptoms as those with myocardial infarction. Usually someone with angina can relieve the symptoms by resting or self-administering nitroglycerin, which dilates the arteries and increases blood flow. Angina and AMI are part of a spectrum of conditions known as acute coronary syndrome, or ACS. Recognizing these signs as early as possible is critical. Because determining the difference between angina and AMI often isn\u2019t possible, your safest bet is to assume the worst and treat the patient quickly. Part of that treatment is to transport as quickly and safely as possible to the nearest hospital that\u2019s capable of rapidly restoring coronary blood flow, either through angioplasty or fibrinolytic therapy.",
        "Acting on Potential Cardiovascular Problems": "Like the respiratory system (covered in Chapter 9), the cardiovascular system can be affected both directly and by conditions outside of it. In the following sections, you discover problems with the heart, vasculature, and blood, and you find out how to handle a cardiac arrest. Pump problems In order to work effectively, the heart has to have good blood flow to its muscle via its coronary arteries and an intact electrical system that controls the rate, strength, and timing of the contractions between the atria and ventricles. Table 10-1 outlines the most common heart conditions.",
        "Pipe problems": "The body\u2019s vasculature can develop leaks that cause fluid to leave the system quickly. On occasion, part of the vasculature can weaken, potentially causing massive failure. Table 10-2 notes common vasculature conditions.",
        "Fluid problems": "If there isn\u2019t enough blood inside the vasculature for the heart to pump, perfusion is affected. Table 10-3 notes common conditions related to blood volume.",
        "Managing a cardiac arrest": "A heart that beats so weakly that it doesn\u2019t create a pulse or doesn't contract at all causes the condition known as cardiac arrest. Because there is no blood flow, skin becomes cold and cyanotic (blue), and the patient becomes unresponsive to all stimuli. If cardiac arrest continues for more than a few minutes, enough brain cells die to cause permanent death. Research in the past decade has shown that effective chest compressions are the foundation of successful resuscitation. In other words, during a \u201cworking code\u201d everything that is done revolves around the nonstop, high-quality chest compressions. Keep these points in mind: After checking to see whether the patient is unconscious, spend no more than 10 seconds to confirm there is no carotid pulse and breathing is absent or inadequate (gasping). Begin CPR with compressions, not ventilations. Immediately begin pushing on the chest, while others are assembling other equipment and preparing to ventilate. For adults, administer compressions at a rate of at least 100 per minute, with at least 2 inches of depth, and a full recoil of the chest during release. For pediatric patients, compress the chest at least one-third to one-half the depth of the chest. For adults, space ventilations so two breaths are provided after every 30 compressions. Deliver just enough to make the chest visibly rise. For two-person CPR on a pediatric patient, space ventilations so two breaths are provided after every 15 compressions. Rescuers should switch roles every 2 minutes or 5 cycles of compressions and ventilations, to keep compressions accurate and effective. Apply AED pads as soon as possible. As soon as the pads are applied, everyone stops and the AED is activated. Follow the prompts and make sure everyone stands clear of the patient. After the AED has analyzed, continue compressions while the AED is charging for defibrillation. When the AED is charged, stop compressions, clear the patient, and deliver the shock. Immediately afterward (or if the AED tells you that no shock is indicated), immediately begin CPR again. Do not pause to check for a pulse. At the end of the next 2-minute interval, look for signs of effective breathing and check for a pulse. If they are absent, immediately resume CPR. If the AED indicates a shock is needed, continue compressions while the AED charges and then clear the patient and deliver the shock. During two-person CPR on a child or infant, the ratio of compressions to ventilations is 15:2. This ratio allows more ventilations to be delivered to the patient."
    },
    {
        "Introduction": "Emergency medical services physicians often use the same approach in the field and the hospital to provide patient care, even though the goals in each area differ. The care of patients with dysrhythmias before hospital arrival focuses on treating all life-threatening or imminently life-threatening rhythm changes within minutes. In the emergency department (ED) and in the hospital, the same need exists but more time is available to identify other non-lethal rhythms and deliver definitive long-term treatment.\n\nThis chapter discusses a pragmatic method of providing medical oversight for non-arrest dysrhythmias. The most important field observations and actions will be highlighted to help simplify the approach when giving direct medical oversight, creating written protocols, or providing direct patient care. We offer a \u201clow-tech\u201d approach to the problems, emphasizing simple tools including a brief history, physical examination, and standard 3- or 12-lead field ECG. Similarly, we focus on interventions that are effective and easily provided in the out-of-hospital setting. In general, the approach offered is consistent with the 2010 American Heart Association (AHA) Advanced Cardiac Life Support (ACLS) guidelines, although we highlight areas where simplified or alternative approaches exist.",
        "Evaluation": "Three basic sources of information are available during the assessment of field dysrhythmias: patient history, physical examination, and the ECG. Rarely will any one of these suffice in guiding treatment. Rather, all three considered together guide care. Four steps can be used to manage patients with dysrhythmias in the field. Treatment decisions often can be made before completing all steps, allowing an economy of effort.",
        "Step 1: identify symptoms and how they relate to the rhythm": "Two groups of patients present with dysrhythmias: asymptomatic patients with incidental rhythm changes and patients with symptomatic rhythm changes. Incidental dysrhythmias may relate to the symptoms, but are the result and not the cause of another problem, and they do not worsen the immediate outcome. Patients with incidental dysrhythmias or who are asymptomatic rarely require field rhythm-directed treatment. Those with incidental dysrhythmias typically require treatment of any underlying acute condition (e.g. analgesia for pain or fluids for hypovolemia).\n\nA 67-year-old male patient with a history of \u201cextra heart beats\u201d transported for an isolated ankle injury displays a sinus tachycardia (from pain) and occasional premature ventricular complexes, but no other symptoms or abnormalities on physical examination. He requires splinting and analgesia, not antidysrhythmics. This should not be confused with dysrhythmias with symptoms, such as tachycardia or bradycardia associated with chest pain, weakness, breathing difficulties, or syncope.",
        "Step 2: identify stable and unstable patients": "Because asymptomatic or incidental dysrhythmias usually require no direct treatment, the prehospital focus shifts to those dysrhythmias associated with symptoms. These patients are classified based on the severity of symptoms as either stable or unstable. Although many patients have symptoms attributable to the change from a \u201cnormal\u201d rhythm, most tolerate these well and are stable. However, unstable patients are likely to suffer harm or deteriorate. Providers and EMS physicians must identify these unstable patients and rapidly intervene.\n\nUnstable patients have signs and symptoms of inadequate end-organ perfusion due to the rhythm disturbance. A few brief historical questions and physical examination steps must be rapidly completed to identify these patients early in their evaluation.\n\nHypotension \u2013 often arbitrarily defined as a systolic blood pressure below 90 mmHg, though any departure of more than 15% from a known baseline may be functional hypotension.\n\nCardiac dysfunction \u2013 seen as chest pain, shortness of breath, or rales (signifying inadequate myocardial perfusion or function).\n\nAltered consciousness \u2013 from mild agitation or somnolence to obtundation or coma (signifying central nervous system [CNS] hypoperfusion).\n\nDelayed capillary refill and lowered skin temperature can indicate poor perfusion; the subjective nature of these observations and multiple other potential causes limit their use in the field.\n\nAssessing instability is usually a continuum, not an \u201call-or-nothing\u201d phenomenon. Either a single severe sign or symptom or multiple mild findings is diagnostic of an unstable rhythm. A single mildly abnormal finding suggests \u201cborderline\u201d stability. The blood pressure is the simplest method of assessing circulatory adequacy, but it alone may be insufficient in accurately classifying patients. A patient with a systolic blood pressure of 60 mmHg is always unstable. Another patient with a blood pressure of 90 mmHg systolic, rales, and a depressed sensorium is also unstable. If awake and with no rales, chest pain, or other symptoms, the patient with a systolic blood pressure of 90 mmHg occupies a borderline position due to the singular mild finding. Similarly, agitation suggests mild CNS hypoperfusion and borderline stability, whereas coma is associated with more profound derangement and instability.\n\nIn the absence of clear evidence of instability, each patient can receive a more complete evaluation, although the total prehospital time interval should not be prolonged. Unstable patients need rapid therapy, usually with electrical interventions such as external countershock or pacing. Symptomatic but stable or borderline unstable patients can be initially treated with pharmacological agents, with electrical devices nearby in case of deterioration. The more extreme the sign or symptom of instability (e.g. coma versus mild anxiety), the more intensive the initial treatment should be.",
        "Step 3: classify the electrocardiogram findings": "After assessing stability, the field providers need to categorize the ECG. Using a traditional approach of separating dysrhythmias into dozens of categories is tempting. In the field evaluation, a simpler scheme should be used based on the assessment of stability and three ECG features: QRS complex rate, regularity, and duration.\n\nElectrocardiogram interpretation is performed in two ways: by medical oversight physicians receiving transmitted tracings, or independently by the field personnel. Transmitted tracings are occasionally hampered by technical problems which can obscure salient features. Field providers can learn the basics of ECG interpretation to identify common and lethal rhythms. However, some errors are common. For example, misclassification of QRS duration and rate occurs in up to 20\u201330% of tachycardias. Protocols and medical oversight decisions must assume that the potential for misclassification exists and attempt to minimize attendant adverse outcomes. The strategies outlined herein apply to both field and transmitted interpretation. In all steps, ECG interpretation must be done from a printed strip and not \u201cguessed\u201d from the monitor screen.",
        "Rate": "Initially, the rate should be classified as fast (>120/minute), slow (<60/minute), or normal/near normal (60\u2013120/minute) based on the frequency of QRS complexes over 6 seconds multiplied by 10. After the estimation of rate, sinus P-waves should be sought in those patients with normal or fast rates. Sinus P-waves always precede the QRS complexes and have a consistent appearance and relationship (i.e. distance) to the QRS complexes.\n\nAs a simple rule, all unstable patients with non-sinus fast rhythms (no discernible P-waves and QRS rate >120/ minute) deserve immediate synchronized countershock with 100J. Often, lower energy levels can convert specific rhythms, such as supraventricular tachycardia (SVT) or atrial flutter, but little benefit is gained by attempting to make fine distinctions in these unstable patients. Although changes in heart rate that fall into the normal range can cause symptoms, these are usually of little importance in the field management.\n\nBiphasic waveform defibrillators are increasingly common among EMS services. In general, lower energy biphasic waveform shocks are equally or more effective than monophasic shocks. However, no outcome benefit to biphasic waveforms has yet been demonstrated. In addition, the ideal energy for first-shock biphasic waveform defibrillation is uncertain. The defibrillator manufacturer\u2019s recommended energy levels for cardioversion and defibrillation should be used.\n\nPatients with slow dysrhythmias only require classification of their stability. All other details (e.g. P-wave characteristics, type I or II second-degree block, junctional versus ventricular escape) add little value in prehospital management. Slow stable dysrhythmias need no intervention besides continued monitoring for deterioration. Slow unstable dysrhythmias require external pacing (preferred) or atropine (0.5\u20131 mg IV in adults, repeated up to 2\u20133 mg total). Transcutaneous pacing is best started as early as possible to maximize the potential for mechanical or clinical capture and restoration of perfusion. Also, do not delay pacing in unstable patients to administer atropine. Conversely, concerns of clinical deterioration after atropine are unwarranted when the correct dose is given to those with symptomatic bradycardia, though there may be no response.\n\nInternal, implanted pacemakers should prevent bradycardias, but they may malfunction. When a patient has pacer spikes on the ECG and is still bradycardic, the pacemaker is not working properly and the patient should be treated in the same fashion previously described with atropine or external pacing. The pacer pads should be kept 10 cm or more away from the internal pacemaker pouch. Trying to evaluate the pacemaker in the field is impossible and should await hospital evaluation.\n\nBradycardias resulting from beta-blocker or calcium channel blocker overdoses may be refractory to atropine. In these cases, glucagon (1\u20133mg IV) may improve the heart rate. Again, drug administration should not delay transcutaneous pacing. Previously, isoproterenol was a second-line therapy for atropine-resistant bradycardias. With the availability of external pacemakers in the field and the poor clinical effectiveness of isoproterenol, this treatment is not currently recommended. In adults, a pressor medication (e.g. dopamine) infusion and a fluid bolus should be administered if transcutaneous pacing has normalized the heart rate but hypotension persists.",
        "Regularity and duration": "In contrast to bradycardia, if the ventricular rate is fast, the regularity and duration of the QRS complexes should be assessed. Regularity is divided into two categories: mostly or completely regular, and chaotic (i.e. \u201cirregularly irregular\u201d without any pattern). Chaotic rhythms are usually due to atrial fibrillation, irrespective of the appearance of the baseline or QRS duration. Other less common causes include multifocal atrial tachycardia and frequent extrasystoles (i.e. atrial, ventricular, or junctional).\n\nTo simplify the process of measuring duration and assessing regularity, EMS personnel should run an ECG strip. From this, they or the medical oversight physician can measure in \u201csmall boxes\u201d how wide the QRS duration is and look for irregularity. Each small box represents 0.04 seconds at normal paper speed. Having providers seek out \u201cHow many small boxes wide is the QRS complex?\u201d will limit mathematic or conversion errors. Similarly, evaluating printed strips also helps detect irregularity, which may be difficult to appreciate on a monitor screen if the ventricular rate is greater than 150/minute. In these cases, close tracking on a 6-second ECG strip may help detect chaos and identify atrial fibrillation.\n\nThose rhythms with a QRS duration of less than three small boxes (0.12seconds) are narrow-complex dysrhythmias. Conversely, any rhythm with a QRS duration of greater than three small boxes is a wide-complex dysrhythmia. Nearly all narrow complex rhythms originate from atrial or nodal (i.e. supraventricular) sources. Wide complex rhythms can originate from a ventricular or a supraventricular source. In the latter situation, some abnormality in ventricular conduction is responsible for the prolonged QRS duration. In the field, attempts to separate the myriad causes of wide-complex tachydysrhythmias (WCTs) rarely alter therapy and are unnecessary. Treatment should be based on the clinical stability of the patient, basic history, and the simple ECG characteristics previously defined.",
        "Unstable tachydysrhythmias": "Aside from sinus tachycardia, all unstable patients with a WCT or a narrow-complex tachydysrhythmia (NCT) deserve countershock(s), irrespective of the exact source, ventricular or supraventricular. The QRS duration will help dictate care after countershock, but does not fundamentally drive the initial care in unstable patients with a tachydysrhythmia.\n\nThe initial energy level used to treat tachycardias is based on the QRS pattern. If the QRS pattern is regular or nearly regular in any unstable patient with a tachydysrhythmia and a palpable pulse, synchronized cardioversion with 100J should be used, followed by step-wise energy increases to 200J with a biphasic device or 360J with a monophasic device, if necessary. Some rhythms may require less energy, but attempts to carefully titrate this life-saving therapy in unstable patients is of little practical benefit. Synchronized countershock is recommended to avoid post-countershock ventricular fibrillation (VF). However, sensing problems often make reliable identification of the QRS complex needed for synchronization impossible. We recommend an unsynchronized shock promptly if any sensing problem occurs. Any patient without pulses and/or an irregular tachydysrhythmia should be immediately given a high-energy unsynchronized countershock.\n\nPatients with internal pacemakers or automatic implantable cardioverter defibrillators (AICDs) are still at risk of cardiac dysrhythmias. Although meant to cardiovert dysrhythmias, AICDs do not always convert these rhythms, and sometimes these devices deliver shocks inappropriately. If a patient has an unstable tachydysrhythmia and the AICD is not firing or is ineffective, externally cardiovert as previously recommended, with pads in the anterior-posterior configuration and 10cm away from the internal device pouch. Postconversion care with medical therapy will be unaffected.\n\nIf an AICD is repeatedly firing absent a ventricular dysrhythmia (wide complexes), a magnet over the device may inactivate the shock mechanism, simplifying patient care and improving patient comfort. However, given the rarity of this event, the EMS director should weigh deployment of magnets and training for all providers versus likely benefits. Prompt transfer to the ED is wise in many settings.\n\nIf countershock fails in an unstable patient with a WCT, give either amiodarone (5mg/kg) or lidocaine (1\u20132mg/kg) as a bolus and repeat the countershock. The ALIVE trial and recent AHA guidelines recommend amiodarone as the first-line agent in unstable and especially pulseless WCT. Lidocaine is still the easiest to deliver quickly, but is considered a second-line agent due to variable success in terminating ventricular tachycardia (VT).\n\nIf the QRS complexes are chaotic, the most common diagnosis is atrial fibrillation. When chaos and a QRS duration of more than three small boxes appear together, atrial fibrillation with altered conduction is the diagnosis. All unstable fast chaotic rhythms should be cardioverted with 50\u2013100J unsynchronized initially, and titrated up as needed. No post-countershock medications are needed.\n\nOne practical point: if regularity versus irregularity cannot be established during assessment of a patient with an unstable WCT or NCT, 100J is an appropriate starting energy level for countershock. Similarly, if simplicity of treatment protocols is sought, 100J is reasonable for all unstable non-sinus tachycardias, because the extra energy delivered to the rapid atrial fibrillation patient is unlikely to cause harm or worsen discomfort compared to 50J.",
        "Step 4: focus actions to evaluate stable but symptomatic and borderline patients": "Up to this point, little specific history and only a few basic physical examination and ECG reading skills have been required. This is intentional, so as not to \u201cclutter\u201d the field evaluation of those who need it the most (i.e. the unstable patient) or do not need it at all (i.e. the asymptomatic patient). The remaining patients are those with symptoms, albeit none clearly identifying instability. Here, a few questions and actions can help to deliver the appropriate prehospital care.",
        "History": "The field teams should focus on cardiac-related previous problems in stable patients. For example, a patient who presents with new-onset WCT with a history of previous myocardial infarction is much more likely to have ventricular tachycardia than a supraventricular rhythm with abnormal conduction. Similarly, one with a history of a previous dysrhythmia who presents with similar symptoms again is likely to have recurrence rather than a new dysrhythmia. Neither of these clinical rules is infallible, but this information can help guide therapy. Other points are also helpful. For instance, a patient with a history of poorly controlled hypertension presenting with a lowered but \u201cnormal\u201d blood pressure suggests a dramatic change, prompting more intensive treatment.\n\nHistory can influence the dosing of field agents. Subjects with liver or heart failure, and those aged 65 years and older, should receive lower lidocaine infusions or follow-up boluses. Those patients with renal failure are at risk for hyperkalemia and rhythm changes. The current medications can provide a clue to any previous conditions or guide field drug therapy. A patient treated with digoxin or a beta-blocker plus warfarin for palpitations may have atrial fibrillation. Finally, although rare, a brief search for drug allergies or intolerances (\u201cHas any heart drug been bad for you?\u201d) may help avoid a complication. The key is to take a focused history, looking for information regarding heart disease and other specific conditions.",
        "Physical examination": "In addition to a search for signs of instability, some manipulations can help when assessing and managing tachycardias. Specifically, actions that alter atrioventricular node conduction (\u201cvagal maneuvers\u201d) can help terminate or uncover a specific dysrhythmia. In a patient less than 50 years old, carotid body massage can be attempted. This procedure is often restricted or prohibited in the field because of poorly documented concerns about embolization. The Valsalva action can be used with massage in young patients or as the sole maneuver in those over 50 years old. Other maneuvers, including ocular and rectal massage, ice packs or cold-water dunking, and rapid inflation of pneumatic antishock garments, are not recommended.",
        "Stable narrow-complex tachydysrhythmias": "In patients who are symptomatic but stable or who have one borderline symptom of instability (e.g. dizzy or anxious with a low blood pressure), certain actions are indicated. Patients with a regular NCT between 120 and 140 per minute are likely to have a sinus tachycardia and require no antidysrhythmic treatment. Stable patients with a regular NCT at a rate of 140 per minute or greater should have vagal stimulating maneuvers performed to terminate the rhythm. Sometimes, this maneuver uncovers sinus P-waves, clarifying the sinus or atrial etiology. When P-waves are seen, treatment is directed at the cause, not the rhythm.\n\nThose with minor symptoms (e.g. isolated subjective dizziness or palpitations) do not require field treatment beyond vagal maneuvers. For those with more prominent symptoms during a regular NCT at 140 per minute or greater, give adenosine (6\u201312mg as a rapid IV bolus followed with a flush). The smaller initial dose (6mg) is effective about 60% of the time, and it should be repeated within 2 minutes at the higher dose if no effect is seen. If adenosine causes slowing followed by a return to tachycardia, repeat or larger doses will not help. The cause is a non-reentrant source, often an atrial rhythm, possibly atrial tachycardia, fibrillation, or flutter.\n\nAdenosine is effective in 85\u201390% of patients with regular NCT. The drug has a duration of effect of 20 seconds or less, and recurrence of an NCT may occur in 10\u201358% of cases. It is common for patients to complain of transient chest pain, flushing, or dyspnea during adenosine treatment. Some patients may experience bradycardia or asystole after adenosine. Usually, this lasts only seconds, but it may require temporary external pacing if prolonged. Contrary to popular belief, adenosine can occasionally terminate VT, although the majority of such patients are unaffected.\n\nVerapamil (2.5\u20135mg IV initially followed by 5\u201310mg in 15 minutes if unsuccessful) and diltiazem (0.15mg/kg initially, followed by 0.20\u20130.25mg/kg in 15 minutes if unsuccessful) will terminate 85\u201390% of regular NCT. However, both can cause hypotension and congestive heart failure, though diltiazem is alleged to have slightly lower rates of this in equipotent doses. Because of these disadvantages, many prefer to use adenosine in the field. Whenever giving adenosine, verapamil, or diltiazem in the field, it must be absolutely clear that the QRS duration is less than three small boxes (0.12 seconds). This will help avoid the hemodynamic collapse that can occur with these drugs in VT or atrial fibrillation with an accessory pathway. Most patients tolerate the transient effects of adenosine, often \u201cfooling\u201d providers into thinking no harm is possible if given in error. The potential harm is real, albeit much less frequent than with calcium channel blockers. If hypotension occurs after IV verapamil or diltiazem in the absence of bradycardia, treatment with saline infusions, IV calcium salts (5\u201310mL of a 10% calcium chloride solution) or catecholamines (i.e. dopamine or epinephrine) should be given.\n\nMany WCTs are erroneously classified in the field as narrow (up to 20% of cases). Therefore, many medical oversight physicians prefer adenosine to treat all regular and symptomatic NCT, avoiding the risks associated with giving a calcium channel blocker to a patient with WCT. For those patients with chaotic NCT, atrial fibrillation is the likely rhythm. If mildly symptomatic and stable, no field treatment is required. An example is an elderly patient with an irregular NCT at a rate of 130/minute complaining of weakness. Although rapid atrial fibrillation may contribute to the symptoms, no field treatment is needed in the absence of other clear signs or symptoms of decompensation. Those with instability deserve immediate countershock with 50\u2013100J. If transport is prolonged and the patient has either borderline symptoms or a rate of 140\u2013180/minute, metoprolol (5\u201310mg intravenously) or diltiazem (0.15\u20130.25mg/kg intravenously) will control the ventricular rate in 85\u201390% cases of rapid atrial fibrillation.\n\nOne pitfall in the treatment of stable NCT must be highlighted. When the ventricular rate is greater than 220/minute, the risk of decompensation rises and the ability to detect irregularity is limited. Therefore, all adults with a very fast regular NCT (heart rate >220/minute) should be either cardioverted with 100J or treated with adenosine and prepared for cardioversion. If the rate rises to greater than 250/minute, cardioversion is the best choice given the risk of deterioration. Irregular NCT greater than 220/minute deserves countershock promptly as previously noted (50\u2013100J).",
        "Stable wide-complex tachydysrhythmias": "Wide-complex tachydysrhythmias can be due to VT or a SVT with abnormal conduction. Until proven otherwise, field providers should assume any new WCT is due to VT. Hospital data suggest that about two-thirds of patients with new WCT have VT. With a history of previous myocardial infarction, the frequency of VT increases to 90%. Although it is possible to assemble evidence to detect supraventricular rhythms from a detailed examination and 12-lead ECG, these data are not easily obtainable in the field. Thus, actions in managing WCT should either treat or cause no harm in VT.\n\nAll unstable patients with WCT should be cardioverted with 100J, with escalating energy doses if needed. When stable or borderline, a few simple measures can help stratify patients. It is always an option to observe this group, intervening only if conditions worsen.\n\nIf P-waves precede each QRS complex during a stable WCT with a rate of 140/minute or less, a supraventricular source is likely, especially sinus or atrial tachycardia, although VT is a remote possibility. Treatment focuses on correcting any potential causes (e.g. pain, hypovolemia, or hypoxemia) and observation. Irregular QRS complexes suggest atrial fibrillation or multifocal atrial tachycardia. Neither requires field rhythm-directed therapy in stable patients, although other actions (e.g. oxygen, bronchodilators) may be needed.\n\nWhen no clear P-QRS relationship exists, differentiating between SVT and VT is difficult during a WCT. The following key features help decide a clinical course of action.\n\n- A patient with new-onset WCT and a history of previous myocardial infarction or VT very likely will have VT.\n\n- VT will often not slow during vagal maneuvers. Therefore, slowing of a WCT during these efforts suggests SVT. However, the absence of change does not diagnose VT.\n\n- Most VT does not respond to adenosine, whereas SVT usually slows or terminates. Conversely, lidocaine has little effect on most SVT and will terminate 75\u201385% of VT.\n\n- VT is usually regular and rarely seen at a rate of greater than 220/minute. Any chaotic WCT should be considered atrial fibrillation with abnormal conduction. When a chaotic WCT at a rate of greater than 220/minute occurs, atrial fibrillation from Wolff-Parkinson-White syndrome is present. This rhythm is prone to deterioration.\n\nFrom these clinical observations, the following scheme can be used in approaching the stable or borderline (one minor sign or symptom of instability alone) patient with a WCT.\n\n- All stable patients with regular WCT at a rate of 120\u2013220/ minute should receive vagal maneuvers. Those who slow but then elevate again should receive adenosine (6\u201312mg IV). If no slowing with vagal maneuvers occurs, one of three paths should be taken.\n\n- Young (age <50years) previously healthy patients with stable (or borderline) regular WCT that slows with vagal maneuvers should receive adenosine. If this fails or there is no response to vagal maneuvers, or if the patient has had prior VT or prior MI, assume VT and give amiodarone (5mg/kg IV over 5 minutes) or possibly lidocaine (1.0\u20131.5mg/kg IV up to 3mg/kg). The AHA has emphasized the role of amiodarone over lidocaine despite limited direct comparisons. If lidocaine converts the rhythm, repeat boluses at 5\u201310 minutes of 0.5mg/kg should be given during transport to prevent recurrence. Continuous infusions after lidocaine loading are generally impractical in the field unless prolonged transport times are likely and infusion pumps are available.\n\n- Because of the risk of deterioration, any patient with WCT at a rate of greater than 220/minute deserves countershock with 100J, irrespective of symptoms.\n\n- Patients with a chaotic WCT usually have atrial fibrillation with altered conduction. If stable with a heart rate of less than 200/minute, they deserve close observation and expeditious transport. If the rate elevates to 220/minute or higher, immediate countershock with 100J is indicated.\n\nOther agents are available but have a limited role in the field. Procainamide (50\u2013100mg IV every 1\u20132 minutes up to a maximum of 15\u201318 mg/kg or until side-effects occur) treats both VT and SVT but is difficult to give in the field.",
        "Controversies": "Rhythm strip versus monitor interpretation\n\nBesides clearly abnormal rhythms (e.g. obvious VT or severe bradycardia), ECG interpretation should be taken from a tracing and not from the monitor screen. It is tempting to avoid printing strips, but misclassifications may result from a \u201cscreen look.\u201d Strips are valuable in the ED evaluation, documenting conditions before and after field treatment, which helps unravel the causes in certain dysrhythmias. At least two leads should be sampled.\n\nSynchronization and sedation during countershock\n\nWhen possible, delivering a countershock synchronized with the intrinsic QRS complexes is preferred. Synchronization helps avoid depolarization during the vulnerable phases of repolarization, theoretically decreasing the risk of post-countershock VF. During most dysrhythmias, the defibrillator unit senses the underlying QRS pattern and delivers the shock at the appropriate time. When the rhythm is extremely fast or irregular or the QRS complexes are markedly abnormal (i.e. very wide or small), sensing is difficult. In these cases, an unsynchronized countershock is appropriate. Electrophysiological data do not support the notion that this will increase the likelihood of VF. If post-countershock VF occurs, repeat countershock is usually successful in restoring an organized rhythm.\n\nThe usual controversy surrounding field countershock is the awake unstable patient. Medical oversight must clearly communicate the need for this unpleasant but life-saving intervention for appropriate patients. Sedation with a benzodiazepine before countershock may improve patient comfort. However, countershock should not be delayed in unstable patients while awaiting clinical sedation.\n\nProphylactic lidocaine for premature ventricular contractions\n\nIn the past, lidocaine was given for all patients with suspected acute coronary ischemia and any evidence of ventricular ectopy. Research clearly details that most patients do not benefit from this medication and some may be harmed.\n\nIf the premature ventricular contractions (PVCs) are asymptomatic or trivial, there is no proven benefit from treatment. PVCs associated with more pronounced symptoms should receive an antidysrhythmic, usually lidocaine. Although oft-cited lists of ominous ECG \u201cwarning\u201d signs exist (e.g. multi-form, >6/minute, couplets, R-on-T, or runs of PVCs), treatment of these and other asymptomatic PVCs does not confer any benefit. Do not use prophylactic lidocaine for all patients with chest pain. Lidocaine may reduce the risk of VF but will increase the risk of asystole.\n\nPediatric dysrhythmias\n\nWhen evaluating pediatric tachycardias, a crucial difference compared with adults must be stressed. Children under the age of 5 years can sustain a sinus tachycardia at much higher rates (up to 225/minute) in response to physiological stresses. Therefore, a search for hypovolemia, hypercarbia, and hypoxemia is mandatory in stable children with NCT before drug therapy is used. A volume challenge with 10\u201320 mL/kg of saline IV is useful before other therapies. Although some guidelines make a distinction between energy levels when performing synchronized versus unsynchronized countershock, the use of this distinction is dubious. To keep treatments simple but effective, unstable children deserve countershock with 2J/kg. Antidysrhythmic principles are otherwise similar to those outlined previously, with agents given in the appropriate weight-based doses. Pediatric non-cardiac arrest bradycardias are also usually secondary to another cause, often respiratory distress or hypoxia. When symptomatic, these rhythms are treated primarily with epinephrine and airway maneuvers and rarely need transcutaneous pacing or atropine (0.02 mg/kg/dose).\n\nTorsades de pointes\n\nThis rare dysrhythmia classically presents with paroxysms of syncope and polymorphic \u201ctwisting\u201d of the QRS complexes. Torsades de pointes (TdP) in adults is usually \u201cpause dependent,\u201d flourishing when intrinsic heart rate drops below 80\u2013100/minute. A variety of antidysrhythmics (essentially all aside from lidocaine and calcium channel or beta-adrenergic blocking agents), antihistamines, antimicrobials, and psychoactive drugs, along with metabolic disorders, can precipitate TdP. Field treatment consists of countershock when unstable and transcutaneous pacing or isoproterenol (titrated to a heart rate >120/minute). Magnesium sulfate, 2 g as a rapid IV bolus, is also suggested for those who fail countershock.\n\nA more practical problem is mistaking VT or VF for TdP. VT or VF often display some changes in QRS complex appearance. Field providers may mistake these variations for the classic, but rare, QRS twisting. If recurrent polymorphic VT occurs in a patient with one or more of the aforementioned risks, treatment should be started. Otherwise, orders and protocols should focus on the treatment of common VT.\n\nRhythm disturbances in renal failure patients\n\nThis group often falls prey to metabolic derangements that alter rhythms, in addition to having high rates of underlying heart disease. Hyperkalemia is a common complication of renal failure that can cause a bradycardia or a wide complex rhythm, although the latter is usually not above a rate of 100\u2013120/minute and often much slower. Treatment should include IV calcium (10 mL of 10% of CaCl\u2082), sodium bicarbonate (1\u20132 ampules intravenously), nebulized albuterol, and insulin plus glucose. The last three interventions rapidly (but temporarily) shift potassium into the cells and should be part of protocols for any renal failure patient with new-onset symptomatic bradycardia or a wide-complex rhythm. Because of the risk of hypoglycemia, insulin and glucose infusions in the field are best done under medical oversight supervision rather than by protocol.\n\nLidocaine can cause asystole in the presence of hyperkalemia. The role of other agents, including amiodarone, is unknown in the rare event of hyperkalemia and new-onset WCT. If a rhythm-specific intervention is needed in unstable patients with suspected hyperkalemia, electricity (pacing for slow, countershock for fast rates) is a safe choice.",
        "Protocols": "When developing protocols, focus on the simple data and steps. For example, both the bradycardia and tachycardia protocols should start with a division between \u201cstable/no symptoms\u201d and \u201csymptomatic and unstable or borderline.\u201d Those in the \u201cstable/ no symptoms\u201d category should be observed, expeditiously transported, and monitored, with precautionary IV insertion and oxygen. As a corollary, unstable patients with bradycardia or tachycardia should receive prompt electrical therapy (pacing or countershock), airway support, monitoring, and IV insertion occurring either in tandem with or after electrical therapy. Remind the providers to save rhythm strips and to give sedation if possible, but not to withhold life-saving treatment trying to \u201cget a good strip\u201d or titrating sedation. Unless the signs of instability are subtle, medical oversight contact should follow the initial treatment of unstable patients.\n\nFor patients who are symptomatic without signs of instability, EMS personnel should assess a rhythm strip first. In the tachycardia protocols, three questions should be asked: rate, QRS duration in small boxes, and regularity. Narrow-complex tachycardias that are regular deserve either vagal maneuvers (carotid massage and/or Valsalva) or adenosine. Those patients with irregular narrow-complex rhythms deserve calcium channel blocker therapy if symptomatic but stable. Patients with wide-complex regular rhythms who are stable or borderline should receive lidocaine or amiodarone, and countershock if these medications fail or deterioration occurs. Finally, those with irregular WCTs should be transported without therapy unless unstable, in which case, they should be treated with countershock.",
        "Conclusion": "Prehospital dysrhythmia evaluation must be tailored to the time restraints, physical limitations, and outcome needs that are specific to the field setting. Decision trees should be simple and effective, focusing on treating patients, and not rhythms per se. Protocols must identify and treat all unstable patients. Those without symptoms or with trivial symptoms do not require rhythm-directed therapies. For symptomatic but stable patients, a few key steps should be taken to help manage each case."
    },
    {
        "Introduction": "The original motivations for the development of EMS were to improve the care of patients suffering from major trauma and out-of-hospital cardiac arrest (OHCA). Physicians and resuscitation researchers often focus on patient-level perspectives of cardiac arrest care (e.g. specific drug agents or treatment algorithms). However, the most important factors determining OHCA survival involve the systems of community care. The recognition that sudden cardiac arrest (SCA) survival depended on the time intervals from collapse to initiation of cardiopulmonary resuscitation (CPR) and to defibrillation spurred extensive EMS and public safety efforts to achieve faster response and earlier defibrillation. These efforts included the use of fire fighters and police officers as first responders, training EMTs to perform defibrillation, and strategic deployment of ALS units (systems status management). However, there were (and remain) inherent logistical limits to first responder speed. The development of the automated external defibrillator (AED) led to the concept of public access defibrillation (PAD). The AED highlighted the critical importance of immediate bystander action in the management of cardiac arrest. Every EMS medical director, manager, and provider must recognize the importance of this principle. EMS responders and hospital staff have less impact on OHCA survival than bystander CPR and AED use. OHCA survival when bystander CPR and AED are used may be as high as 33\u201350%. Optimal OHCA survival depends on a comprehensive community-based approach that includes collecting essential OHCA outcome data as part of a continuous quality improvement program to improve care. In 2004 only 13 of the 50 largest cities in the US collected meaningful OHCA outcomes. Today 45 of these communities collect OHCA outcome data. Programs like CARES and the Pan Asian Resuscitation Outcomes Study (PAROS) provide communities with the necessary tools to collect OHCA data in an ongoing efficient manner, allowing for benchmarking and gauging effectiveness in a real-world environment. In King County, Washington, the Resuscitation Academy was created to help communities develop local quality assurance programs through a 3-day fellowship program designed specifically for EMS providers, administrators, and medical directors. Implementation of this community systems-based approach is as important a role for EMS agencies as is training and preparing for their own direct patient care. This chapter provides an overview of the system-level considerations in cardiac arrest resuscitation and care. The other components of clinical cardiac arrest care are discussed in Volume 1, Chapter 12.",
        "Epidemiology of cardiac arrest": "The annual incidence of SCA in the United States is estimated at between 166,000 and 450,000 cases. The reported incidence varies with the source of the data and definitions used. Precise epidemiological information is limited because the Centers for Disease Control and Prevention (CDC) does not consider OHCA a reportable disease. Many cardiac arrests are due to ventricular fibrillation (VF) or ventricular tachycardia, but the proportion in a shockable rhythm on EMS arrival varies with the time from collapse to initial assessment. Studies based on hospitalized patients report a shockable rhythm in about 75% of cases, whereas EMS studies report figures ranging from 24% to 60%. EMS data suggest that the rate of out-of-hospital VF/ventricular tachycardia (VT) may be decreasing, but the overall incidence of OHCA is not. However, studies with rhythms recorded by on-site defibrillators continue to identify VF/VT as the most common initial rhythm. VF/VT was the presenting rhythm in 61% of arrests in the Casino trial and 59% of the patients in the PAD trial. The average survival to hospital discharge after OHCA is estimated to be between 5% and 10% but reported OHCA survival rates also vary widely. There are likely several reasons for this, including differing denominators, varying definitions of survival, and possibly true regional differences. In the Resuscitation Outcomes Consortium composed of nine communities in North America, a five-fold difference in survival was found between sites. Survival rates are highest in patients in whom the collapse is witnessed and the presenting rhythm is shockable. CARES data in 2012 revealed a 37% survival rate for this subset of patients, which increased to 50% with use of an on-site defibrillator. Survival is lowest for unwitnessed and asystolic arrests.",
        "Elements of a community cardiac arrest care system": "The key elements of a community cardiac arrest care system include the following. Early recognition and calling for help. 9-1-1 dispatching and provision of bystander CPR instructions. Bystander CPR. PAD. First responder BLS care, including defibrillation. ALS care. Postarrest care. Participation in an OHCA registry and local quality improvement program. Emergency medical services directly provide only two elements of this chain. Thus, community-oriented approaches are essential in facilitating improved cardiac arrest survival. EMS medical directors and agencies cannot successfully care for victims of OHCA in isolation. They must work with the community to optimize all elements of care and should serve leadership roles in this effort.",
        "Bystander cardiopulmonary resuscitation": "Bystander CPR refers to CPR performed by someone who was already present at or passing by the location of the patient. This contrasts with CPR performed by dispatched emergency responders. Bystanders have the earliest opportunity to provide CPR to the cardiac arrest victim. Multiple studies have demonstrated the survival benefit of bystander CPR as well as the increase in mortality with delays in CPR delivery. EMS medical directors and agencies should monitor and optimize the rate of bystander CPR in their communities. Prior efforts have included community education about OHCA and the importance of CPR, increasing access to training, and teaching CPR in schools to develop a culture of bystander assistance. When callers do not know CPR, the dispatcher should provide real-time instructions over the phone. Most current EMD protocols detail specific CPR instructions. Growing evidence suggests that properly performed chest compressions are more important than ventilations. Most emergency dispatch protocols now favor providing instructions only for chest compressions. The AHA recommends that bystanders not trained in CPR and those trained but not confident or willing to perform ventilations should perform chest compression-only CPR until a defibrillator is ready for use (Class IIa). Unrecognized fatigue is common after just 1-2 minutes, so bystanders providing chest compressions should switch frequently.",
        "Public access defibrillation": "The most important cardiac arrest interventions for patients in VF or VT are early chest compressions and defibrillation. Although 70-80% of VF can be successfully converted to a perfusing rhythm if shocked within 3 minutes of VF onset, this success rate deteriorates rapidly with each additional minute. Survival decreases 7-10% for each minute that passes before defibrillation. Automated external defibrillators provide lay bystanders with the ability to deliver rescue shocks. These devices were first used clinically in 1979 to recognize and deliver rescue shocks for VF and rapid VT. AEDs are automated and simple to use with visual and audible instructions for operating the defibrillator and initiating CPR. They are relatively inexpensive and extremely safe; modern AEDs do not allow delivery of inappropriate shocks. Most are equipped with memory modules that can record the entire resuscitation event, including continuous ECG and audio recording. Defibrillators with CPR feedback use accelerometers embedded within chest defibrillation pads to measure depth and rate of compression, or use variations in chest impedance to reflect chest wall movements. These devices are able to give verbal as well as visual prompts to cue the rescuer to speed up, slow down, or increase the depth of compressions or ventilations. Such devices have been shown to improve the quality of CPR for out-of-hospital as well as in-hospital cardiac arrest. A variety of AED models are now available, ranging in sophistication and ruggedness. Some models are designed for minimally trained lay bystanders, and are available for consumer purchase without physician prescription. There is strong scientific evidence confirming the efficacy of early first responder, bystander, and public access defibrillation. A trial which trained security personnel in casinos to recognize OHCA, start CPR, and use on-site AEDs achieved 53% survival from VF, and among patients shocked within 3 minutes survival was 74%. AEDs have also been successfully used on aircraft and in the airport. In the multicenter PAD trial, 993 high-risk locations were randomized to deploy or not deploy on-site AEDs. A response plan with identification and training of on-site responders was implemented at all sites. Survival was double at AED sites compared to non-AED sites. Other reports also describe successful PAD programs. One successful real-world example is Japan, where public access defibrillators have rapidly become more available since 2004. The cumulative number of public access defibrillators (excluding medical facilities and EMS institutions) increased from 9,906 in 2005 to 297,095 in 2011. From 2005 to 2007, the proportion of bystander-witnessed VF/VT arrests who received public access defibrillation increased from 1.2% (45/3841) to 6.2% (274/4402). The latest data show that over 40% of cardiac arrests in public places like train stations and sports facilities received shocks with public access defibrillators. The observation that a majority of OHCA events occur in residential settings raised interest in home deployment of AEDs. This concept was evaluated in a large, multicenter, international trial of anterior wall myocardial infarction survivors who were not candidates for implantable cardiac defibrillators. A related innovation is the wearable cardioverter-defibrillator, which combines a long-term ECG monitoring system with an AED. Locations at high risk can be identified using public health surveillance tools such as registries that collect standardized data on OHCA. Cardiac arrest locations can be analyzed using geographic information systems and spatial epidemiology methods to identify and target high-risk neighborhoods within a community. These should have emergency preparedness and response plans that include AED deployment. These areas may include airports, fitness centers, large workplaces, arenas and convention centers, and even jails. AED deployment and response plans should include registration with dispatch centers, development of a notification system to alert on-site responders, selection and training of responders, and deployment of appropriate AED and other rescue equipment. Equipment maintenance, annual response plan review, and quality improvement incident reviews are essential components of an effective PAD program. Smartphone apps are also available which can show the location of the nearest AED during an emergency. These can be integrated into local response systems. There is an important opportunity for local EMS agencies and medical directors to assist public and private sites with implementing PAD programs. Several websites and publications provide detailed suggestions for PAD program development.",
        "First responder and Basic Life Support care": "Before the advent of PAD, medical directors sought ways to shorten the delays to initial defibrillation. One solution was to equip first responders with AEDs because these individuals could often reach a cardiac arrest victim faster than an ALS ambulance. The first important report of this concept involved firefighter-first responders in King County, Washington, in 1989. Police first responders in Rochester, Minnesota, and suburban areas near Pittsburgh, Pennsylvania, also successfully used AEDs. These programs demonstrated benefit even if the first responders arrived only 2 minutes before EMS. Cardiac arrest survival was 50% in Rochester, Minnesota, after introducing a police AED program. The use of motorcycles in urban settings to reduce response time has also been described. The OPALS study specifically evaluated the effect of optimizing time to defibrillation by BLS responders, with a goal of having a defibrillator-equipped vehicle on scene within 8 minutes of 9-1-1 call receipt in 90% of calls. Increasing the proportion of responses that met the 8-minute standard from 77% to 92% improved survival to hospital discharge from 3.9% to 5.2%. A subsequent analysis found that increasing time to defibrillation was associated with decreased survival. These observations further underscored the greater importance of bystander action in facilitating additional survival. Performing high-quality, continuous chest compressions is another important role for first responders. There is increasing evidence of the role of high-quality chest compressions in improving defibrillation success. Research indicates that the quality of CPR is vitally important, especially rate, depth, and reducing prolonged interruption of chest compressions, as interruptions result in less cycle time and lower coronary perfusion pressures. Use of multiple first responders (teams of four or more) to allow for closely supervised BLS has also been advocated as \u201chigh-performance CPR.\u201d Also, use of mechanical CPR has been recommended, especially if transport with ongoing CPR is needed, for example in BLS ambulance systems.",
        "Advanced Life Support care": "Although traditionally viewed as the cornerstone of cardiac arrest care, the limited effectiveness of traditional ALS interventions in cardiac arrest is increasingly being shown. In the OPALS study, which added ALS care to previously optimized first responder defibrillation, ALS care did not further improve cardiac arrest survival. In other words, early CPR and defibrillation had greater effects on cardiac arrest survival than advanced airway management or drug administration. In the systematic and comprehensive evidence review undertaken for the production of the International Liaison Committee on Resuscitation (ILCOR) guidelines in 2010, many ALS interventions previously accepted as routine were found to be supported by little good-quality evidence. ILCOR Consensus on Science authors stated that there were no data to support the routine use of any specific approach to airway management during cardiac arrest, and elaborated on concerns that extended attempts to insert an endotracheal tube may lead to harmful interruption of chest compressions. They concluded that there was insufficient evidence to define the optimal timing of advanced airway placement during cardiac arrest, and also stated that supraglottic airway devices may be considered by health care professionals trained in their use as an alternative to bag-valve-mask ventilation during CPR. Cricoid pressure was not recommended for use in cardiac arrest, whereas waveform capnography was. A lack of evidence supporting many ALS pharmacological interventions was emphasized, including vasopressors, atropine, steroids, fibrinolytics, and fluids during cardiac arrest, with placebo-controlled trials being called for; calcium and sodium bicarbonate were not recommended. Since 2010, studies have continued to show that advanced airway management during cardiac arrest appears not to benefit patients. A prospective, population-based study in Japan involving 650,000 out-of-hospital cardiac arrest patients showed that any type of advanced airway management was independently associated with decreased odds of neurologically favorable survival compared with conventional bag-valve-mask ventilation. If dispatched, ALS personnel may play a supervisory role on scene, taking part in team leading to ensure that required interventions are made by basic-level responders. ALS providers also have advanced skills and resources that may be helpful in select scenarios (e.g. treating a tension pneumothorax or a hyperkalemia-induced cardiac arrest). Recent changes in cardiac arrest guidelines based on this evidence have simplified the management of cardiac arrest, highlighting the preeminence of BLS measures such as immediate bystander chest compressions, and the use of AEDs by bystanders whether or not previously trained, with ALS interventions being delayed until later in the course of the patient journey. Of interest is that interventions considered to be most beneficial in the postresuscitation care phase, such as the induction of therapeutic hypothermia, have increasingly been trialled in the prehospital phase of cardiac arrest. It has been shown that prehospital cooling can be carried out safely and efficaciously; however, survival benefit has not yet been convincingly demonstrated.",
        "Postresuscitation care": "Postresuscitation care and in-hospital postarrest therapies are an important factor affecting OHCA survival and subsequent functional outcome. Significant morbidity and mortality after OHCA are due to cerebral and cardiac dysfunction in what has been termed the \u201cpostcardiac arrest syndrome.\u201d Despite initial coma after OHCA, subsequent neurological recovery can be influenced by in-hospital postarrest treatments. Despite these advances, many medical centers do not provide standardized postarrest care for reasons including a sense of futility, staffing, cost, expertise, and resources. This is despite published recommendations on postarrest care including implementation and barriers to implementation and guidelines for cardiac resuscitation systems of care. Regionalized postresuscitation care has been proposed, with \u201ccardiac arrest centers\u201d equipped and staffed to provide guideline-based therapies such as targeted temperature management, 24-7 postcardiac arrest percutaneous coronary intervention, and extracorporeal membrane oxygenation (ECMO). An example of a state-wide regionalized system of postarrest care was implemented in Arizona in 2007.",
        "Role of the medical director": "Stewart commented, \u201cWithout dedicated medical leadership, the EMS system of a community flirts with mediocrity.\u201d The medical director plays a pivotal role in community systems of cardiac arrest care. It is the medical director\u2019s responsibility to ensure that all components of the system are in place. The importance of medical director involvement cannot be overemphasized. In Houston, the increase in VF survival from 0% to 21% over a 5-year period was attributed to the hiring of a full-time EMS medical director. Indeed, Williams et al. showed significant variation in EMS scope of practice with varying involvement of a medical director, and Greer et al. showed that EMS agencies with paid medical directors or agencies with medical director interaction with EMTs in the preceding 4 weeks were more likely to have prehospital cardiovascular procedures in place.",
        "Training and equipment": "Cardiac arrest resuscitation requires timely and accurate execution of interventions. Because of the multitude of simultaneous tasks, cardiac arrest resuscitation requires a carefully coordinated team effort, potentially between rescuers from different agencies. EMS personnel should regularly train for cardiac arrest situations to determine the most efficient ways to carry out protocols. When possible, such training should involve the first responders who may also respond to these incidents. Recent studies of medical emergency team training in simulation settings demonstrate the importance of teamwork and assigned roles. One systematic review described a lack of well-designed studies examining the retention of adult ALS knowledge and skills in health care providers but commented that the available evidence suggests that ALS knowledge and skills decay by 6 months to 1 year after training, with skills decaying faster than knowledge. Simulation has been shown to be superior in the development and maintenance of skills in cardiac arrest management, and another large systematic review showed that non-simulation intervention, learner satisfaction, and process skill outcomes favored simulation over non-simulation teaching, and commented that simulation-based training for resuscitation is highly effective, particularly if employing strategies such as team/group dynamics, distraction, and integrated feedback. Team training, particularly using simulation, is potentially even more important since the 2010 ILCOR and American Heart Association guideline changes to cardiac arrest processes, as cardiac arrest management involves strategies such as charging while chest compressions are continuing, which despite having been shown to be highly effective in decreasing non-CPR periods, causes anxiety among providers about injury due to defibrillation. Another recent study showed that charging during compressions was underutilized but was associated with minimal risk to patients or rescuers. Emergency medical services personnel must possess the equipment necessary to carry out cardiac arrest resuscitation. Key resuscitation equipment includes monitor-defibrillators, airway management tools, vascular access equipment, and appropriate medications. Cardiac monitors that record and provide real-time chest compression feedback are preferable, as are monitors that are able to use dynamic filtering to remove compression artifact and reveal underlying rhythms, although it must be remembered that accelerometer-based compression feedback devices overestimate chest compression depth when performed on soft surfaces. In addition to intubation equipment, airway management tools should include capnography and alternative airway devices such as the Combitube\u2122, King LT airway\u2122, or iGel\u2122. In addition to standard IV catheters, EMS crews should also carry rapid-access vascular tools such as intraosseous devices. Medical directors should provide regular training on the use of all equipment to ensure that personnel can operate them efficiently. Even in busy systems, many personnel may not perform these various skills or use specific equipment for months at a time.",
        "Optimizing system design": "Medical directors should play a key role in developing the system design for cardiac arrest care. One potential intervention is to optimize the positioning of EMS and other resources to match areas with the most cardiac arrests. Geographic mapping systems can play an important role, illustrating not only the distribution of cardiac arrest cases throughout a community but also variables such as the preferred placement of AEDs. The OPALS study reduced cardiac arrest response and defibrillation times by moving first responders closer to areas with many cardiac arrests. Some have touted the advantages of system status management, a formal system of continuously redeploying units based on current and anticipated use. Others suggest that skill dilution occurs with too many ALS personnel; these experts recommend using fewer ALS personnel in a tiered response fashion. A Scottish study reported on an initiative to more fully formalize the roles of senior EMS personnel, who are known to be able to contribute characteristics essential to high-quality resuscitation including non-technical skills such as resuscitation team leadership, communication, and clinical decision making in a second tier, expert paramedic response to OHCA.",
        "Hospital liaison": "There is growing awareness of the importance of postresuscitation care, which formally constitutes the final link in the chain of survival. Care initiated in the field may prove fruitless if not continued in the hospital. The medical director should work closely with receiving hospitals to ensure continuity in cardiac arrest care, and targeted interventions and care algorithms initiated in the field should be continued in the hospital. For example, when determining the receiving hospital facility, EMS agencies that induce hypothermia after cardiac arrest in unconscious survivors should consider if the receiving facility will continue this therapy. Studies are currently being performed which use a system-based approach in an attempt to integrate therapies which may have synergistic effects, and which are likely to show codependence in outcome. These are typified by the CHEER study, which aims to treat cardiac arrest patients with mechanical chest compressions and cool them to 33\u00b0C in the prehospital setting, place them on ECMO at the hospital, transport them to the interventional cardiac catheter laboratory for angioplasty, then maintain hypothermia for 24 hours. Davis et al. demonstrated that diverting postarrest patients past the closest available hospital to a tertiary care center did not worsen outcomes. Future work should consider if regionalization of care and transfer of these patients to specialty facilities improves outcomes as it does for victims of major trauma. Regional systems of care have improved both provider experience and patient outcomes, for those with ST-elevation myocardial infarction and with life-threatening traumatic injury. A Japanese cardiac arrest registry of 10,000 OHCA patients transported to critical cardiac care hospitals showed improved 1-month survival compared with those patients transported to hospitals without specialized cardiac facilities. Compared with historical controls, survival to hospital discharge in the Take Heart America Program, a regionalized system of cardiac arrest care in Minnesota, improved from 8.5% to 19%, driven by a dramatic improvement in survival after admission to intensive care from 24% to 51%. This program is based on optimization of prehospital care including EMS and community training, while establishing transport and treatment protocols with three dedicated cardiac arrest centers providing therapeutic hypothermia, interventional coronary artery evaluation and treatment, and electrophysiological evaluation. However, a similar relationship between survival or neurological outcome and presence of a coronary catheterization laboratory or the volume of patients received was not seen in an analysis from CARES data.",
        "Quality improvement program": "A prerequisite for improving cardiac arrest resuscitation quality is the collection of performance and quality data. Medical directors should implement quality inspection and assurance programs to ensure the delivery of high-quality cardiac arrest care. Commonly collected cardiac arrest quality data include treatment time intervals such as call to dispatch, dispatch to scene arrival, arrival to patient side, and call to first defibrillation. Another important measure is CPR performance. Monitors now permit the medical director to evaluate the depth, rate, and interruptions of chest compressions delivered throughout the entire episode.\n\nThe Utstein style for reporting of cardiac arrest data attempts to provide some common denominators for comparing resuscitation rates among various systems [128]. EMS services should adopt standardized data collection methods that allow for uniform reporting and benchmarking capability."
    },
    {
        "Introduction": "Although detailed algorithms and consensus guidelines exist for management of cardiac arrest, often referred to as Basic Life Support (BLS) and Advanced Cardiac Life Support (ACLS), there are unique practical and scientific considerations that may affect the execution of resuscitation efforts in the out-of-hospital setting. EMS medical directors and field personnel including EMS physicians must be aware of these factors when developing protocols for prehospital resuscitation. They must also understand the scientific basis for and the controversies surrounding recommended resuscitation actions.\n\nThis chapter reviews scientific and practical considerations for carrying out BLS and ACLS in the prehospital setting. For specific treatment algorithms, the reader is referred to the American Heart Association (AHA) Emergency Cardiac Care (ECC) guidelines.",
        "Specific interventions - Chest compressions": "Chest compressions are essential in cardiac arrest resuscitation. Paradis demonstrated that only chest compressions generate coronary perfusion pressure (CPP) and that a CPP of at least 20 mmHg is important for achieving return of spontaneous circulation (ROSC). Multiple studies highlight the role of early chest compressions in survival from cardiac arrest.\n\nThe most recent BLS and ACLS guidelines emphasize the delivery of continuous chest compressions with as few interruptions as possible. Kern et al. demonstrated that several consecutive chest compressions are necessary to generate adequate CPP. CPP drops off immediately when chest compressions are discontinued. The proportion of resuscitation time without chest compressions, termed hands-off time or no-flow fraction, is inversely associated with cardiac arrest survival. Compression depth, rate, and full recoil are also critical characteristics for effectiveness.\n\nPrior work highlighted the often substandard CPR performed by prehospital and in-hospital providers. In a series of prehospital cardiac arrests in Europe, Wik et al. showed that chest compressions were delivered on average only half of the time while the patient was in arrest and that most compressions were too shallow. Abella et al. found similar observations in an in-hospital series.\n\nDelivering chest compressions during cardiac arrest resuscitation poses practical challenges. The treating EMS team must provide continuous chest compressions with as few interruptions as possible and must ensure high-quality chest compressions with adequate depth, rate, and recoil. To achieve these chest compression goals, additional rescuers should be dispatched to provide assistance at cardiac arrests. Team members providing chest compressions should rotate frequently, ideally every 1\u20132 minutes.\n\nSeveral cardiac monitors use a compression paddle or other technology to measure the depth and rate of chest compressions. These monitors are able to provide real-time audio and/or visual feedback, indicating to the rescuer whether or not to increase the depth or rate of compressions. Preliminary data suggest improved clinical chest compression performance through the use of feedback systems.\n\nVarious mechanical devices for automating chest compressions are now available. The Thumper (Michigan Instruments, Grand Rapids, MI) has been used for approximately 40 years and provides chest compressions using a pneumatic piston. The Autopulse Resuscitation System (Zoll Corporation, Chelmsford, MA) facilitates chest compressions using a circumferential load-distributing band. The Lund University Cardiopulmonary Assist Device (LUCAS) (Lund, Sweden) provides active compression and decompression through a pneumatic piston attached to a suction cup on the chest. Use of mechanical compression devices is fairly widespread in Europe and is growing in the United States.\n\nThe scientific data evaluating the effectiveness of these devices remain inconclusive. One urban EMS agency evaluated the Autopulse in a before/after fashion and found increases in both ROSC and survival. However, a larger, multicenter, randomized controlled trial demonstrated worsened outcomes with the intervention. The authors attributed this observation to potential delays in CPR required to place and activate the device. The LUCAS device was effective in a small study of 100 patients, but its benefit was only noted in those who received it within 15 minutes from the ambulance call. Additional innovations and trials are sure to follow. It is important to note that each device requires time to place on the patient, during which no compressions occur. Any protocol that incorporates the use of mechanical devices must stress the importance of continuing manual compressions as much as possible until the device starts; some experts suggest withholding use of mechanical devices during the initial resuscitation effort.",
        "Specific interventions - Defibrillation": "Defibrillation of ventricular fibrillation or ventricular tachycardia (VF/VT) is the most effective intervention for resuscitation from cardiac arrest. Ideally, automated external defibrillators (AEDs) are present at the site of the arrest for use by willing trained or untrained bystanders, perhaps at the prompting of the 9-1-1 call-taker. All medical first responders and BLS providers, including all BLS ambulances, should be equipped with AEDs. Most ALS personnel deliver shocks by manually operating a cardiac monitor-defibrillator after determining the patient has a shockable rhythm. Although many devices are configured with both hand-held paddles and cables for \u201chands-off\u201d self-adhesive pads, use of the pads is believed to be safer, particularly in the uncontrolled field setting.\n\nAn important technical consideration is the type of electrical waveform delivered by the defibrillator. Older defibrillators use monophasic electrical current. In this mode, the device delivers electrical current in a single direction only. To compensate for increased impedance (electrical resistance), older protocols specified escalating energy levels for each successive rescue shock. Now that shocks are given one at a time, each shock should be at maximum energy output, typically 360 J. Although most current defibrillators are biphasic, some EMS systems may still use monophasic defibrillators.\n\nIn a biphasic defibrillator, electrical current flows first in one direction, then in the opposite direction. This modality theoretically purges excess electrical charge from the heart. Biphasic defibrillators measure the impedance across the chest and adjust the voltage and/or duration of current appropriately. Different models also alter the pattern of delivered current, most often using a rectilinear or truncated exponential waveform. Compared with monophasic defibrillators, biphasic defibrillators demonstrate higher rescue shock success at lower energy levels and have been associated with increased rates of ROSC. Energy levels for biphasic defibrillators should be based on manufacturer recommendations because each model has different waveform and delivery characteristics that affect shock efficacy. Although some manufacturers endorse non-escalating low-energy shocks (150 J), recent data suggest that higher energy biphasic shocks may increase rescue shock success without impairing cardiac function.\n\nAnother consideration is the interface between BLS and ALS defibrillation equipment. Some AEDs can be converted to manual mode by ALS personnel. This feature is an important logistical consideration because switching from the BLS AED to the ALS defibrillator may incur delays. Some brands use the same defibrillation pads on BLS and ALS models, allowing providers to simply unplug the connector from one device and plug into the other. The EMS physician should be aware that the AED \u201canalyze and shock\u201d algorithm may add 49\u201359 seconds of hands-off time. This is an important consideration when ALS rescuers care for a patient with an AED attached. One method of minimizing hands-off time is to continue chest compressions until just before defibrillation. Recent data have suggested that continuing chest compressions during defibrillation may be feasible. Others have demonstrated that standard examination gloves may be insufficient protection from electrical shock during external defibrillation. Balancing safety and minimizing hands-off time remains an active area of research.\n\nA current scientific controversy is whether initial defibrillation should precede or follow an initial course of chest compressions. Prior AHA ECC algorithms specified rescue shocks first for VF, regardless of arrest duration. However, several factors support performing initial chest compressions before rescue shocks, including the prolonged duration of most out-of-hospital arrests before treatment is initiated, which leads to the depletion of myocardial high-energy phosphates, cellular damage resulting from accumulated free radicals, and the development of severe acidosis. Theoretically, a period of chest compressions may perfuse the heart and reduce the severity of these anomalies, better preparing the heart for defibrillation. However, a recent randomized clinical trial between chest compressions before rhythm analysis and immediate rhythm analysis showed no difference in the rate of good neurological outcome between groups (19.4% in early analysis versus 18.5% in chest compressions before analysis cohorts). Two clinical studies have demonstrated improved outcomes in prolonged (>4 minutes) VF arrests when chest compressions were delivered before defibrillation. Current ACLS guidelines recommend immediate defibrillation in witnessed arrests but delivering chest compressions for about 2 minutes before rhythm analysis in unwitnessed arrests.",
        "Specific interventions - Airway management": "For many years airway management received emphasis in cardiac arrest care, and ALS rescuers placed high priority on endotracheal intubation (ETI) of cardiac arrest patients. However, the results of several studies question the wisdom of intubation during out-of-hospital cardiac arrest resuscitation. Some of the adverse events noted were tube misplacement, tube dislodgment, multiple laryngoscopy efforts, and failed ETI efforts. Aufrderheide et al. found that inadvertent hyperventilation often occurs after ETI, raising intrathoracic pressure and compromising CPP. Perhaps most important is the frequent and often prolonged interruption of chest compressions.\n\nThe application of these findings to EMS practice poses important challenges. Although bag-valve-mask ventilation is theoretically adequate for resuscitation, the technique is difficult to execute in the prehospital setting, in which providers may need to deliver ventilations with the patient situated on the floor, in the back of a moving ambulance, or on a moving stretcher. Most EMS agencies still perform ETI for cardiac arrest, but many try to limit the number and duration of ETI attempts. Capnography should be used to verify endotracheal tube placement. Although dependent on the quality of chest compressions, capnography waveforms in low-flow states are still useful for ensuring endotracheal tube position.\n\nAnother emerging approach to cardiac arrest airway management is to use supraglottic airways (such as the King LT*) instead of ETI. These devices are inserted blindly into the airway without the need for direct laryngoscopy, and can typically be placed very quickly without pausing compressions. Several EMS agencies have chosen this approach, reasoning that they cannot perform traditional ETI without compromising chest compressions. Retrospective studies have conflicting results. In a review of out-of-hospital cardiac arrests in Japan between 2005 and 2008, there was no difference in the rate of good neurological outcome in patients receiving endotracheal intubation rather than supraglottic airways (odds ratio (OR) 0.71; 95% confidence interval (CI) 0.39, 1.30). A subanalysis of the ROC PRIMED trial demonstrated a higher rate of survival with good functional status in patients receiving endotracheal intubation rather than supraglottic airway placement (OR 1.40; 95% CI 1.04, 1.89) during the resuscitation.",
        "Specific interventions - Ventilation": "Another important consideration is the role of ventilation during chest compressions. Recent data question the need for ventilation with bystander CPR in patients with short-duration VF. The theoretical bases for this approach include:\n\n\u2022 the distractions posed by multiple interventions\n\u2022 the subsequent reduction in number of chest compressions\n\u2022 the adverse effect of hyperventilation on CPP\n\u2022 bystander reluctance to perform mouth-to-mouth ventilation.\n\nAlthough \u201cno ventilation\u201d has practical value for bystander care, it is not clear how or if these principles should be applied to EMS care. There is some evidence that prearrival instruction for compression-only CPR by dispatchers results in delivery of earlier and more chest compressions, but not an increase in survival. Some EMS systems have adopted protocols making active ventilation optional during the initial resuscitation, instead placing an oral airway and oxygen mask until sufficient rescuers are on scene. This allows the first-arriving crew to focus on compressions and defibrillation.\n\nConsiderable scientific data have highlighted the importance of controlled ventilation during resuscitation. Aufrderheide et al. demonstrated in cardiac arrests that hyperventilation increases intrathoracic pressure, resulting in decreased preload and CPP. They also showed that inadvertent hyperventilation occurs frequently during resuscitation efforts, despite specific training to avoid this phenomenon. Ventilation during cardiac arrest should consist of tidal volumes of 500\u2013600 mL at a respiratory rate of 8\u201310 breaths/min.\n\nThe impedance threshold device (ITD) is a ventilation adjunct that may be attached to either a face mask or an endotracheal tube and contains a one-way valve that permits exhalation during the downstroke of chest compression but prevents passive inhalation during the upstroke of chest compression. As a result, the ITD generates increased negative intrathoracic pressure during chest recoil, increasing cardiac preload and CPP. While preclinical and small trial data were favorable, a large randomized trial of the ITD versus sham device yielded similar rates of survival with good neurological outcome between groups (ITD 5.8% versus sham device 6.0%; p=0.71).",
        "Specific interventions - Medications": "Although numerous medications may be used during treatment of cardiac arrest, the primary agents are vasopressors (e.g. epinephrine and vasopressin) and antiarrhythmics (e.g. lidocaine and amiodarone). ACLS algorithms provide specific guidelines for the use and doses of these agents.\n\nNo drug has demonstrated improved outcomes following cardiac arrest in humans. The continued use of these drugs is based on tradition, theory, and animal research, and the selection of specific agents in each class is largely a matter of individual choice. EMS physicians must be aware that the only medications evaluated by randomized clinical trials are epinephrine, amiodarone, vasopressin, and magnesium. Current ACLS guidelines downplay the use of these medications in favor of quality CPR performance.\n\nVasopressors serve two intended purposes in cardiac arrest: vasoconstriction, and exerting positive inotropy and chronotropy. Alpha-agonists increase peripheral resistance, shunting blood flow to the brain and heart. Beta-agonists increase inotropy and chronotropy. In the clinical context, these agents should help to sustain coronary and cerebral perfusion before restoration of pulses. AHA guidelines suggest administering 1 mg of IV epinephrine every 3\u20135 minutes and provide an option to substitute one dose with 40 units of vasopressin.\n\nCompelling animal data indicate increased ROSC with the early delivery of epinephrine or vasopressin. Although several small clinical series have reported increases in ROSC and survival to admission for patients treated with vasopressin, a randomized trial comparing vasopressin with epinephrine versus epinephrine alone did not demonstrate additional benefit from vasopressin use. Two randomized controlled trials have shown no improvement in survival to discharge, but have shown increased rates of ROSC.\n\nWith the use of vasopressors, there is a trade-off between increased coronary perfusion and reduced cerebral perfusion (possibly via increased cerebral vasoconstriction). A once-popular ACLS approach was the use of high-dose epinephrine (5\u20137 mg IV). Although clinical trials using high-dose epinephrine demonstrated increased rates of ROSC, this did not translate into survival to discharge.\n\nAntiarrhythmics are commonly used in cases of VT/VF cardiac arrest and may increase the likelihood of conversion to a perfusing rhythm. Lidocaine and amiodarone are currently recommended antiarrhythmics for shock-refractory VF; both have Class IIb recommendations (conflicting evidence). One randomized controlled trial of amiodarone demonstrated an increase in ROSC, but not improved survival to hospital discharge. An important point for use in critical situations, especially with limited resources such as the out-of-hospital setting, is that amiodarone is logistically more difficult to administer than lidocaine, requiring the medication to be dispensed from glass vials. ACLS guidelines indicate that amiodarone has a stronger supporting evidence base than lidocaine, as there have been no studies evaluating lidocaine. EMS physicians may choose between an IV bolus of 300 mg of amiodarone or 1\u20131.5 mg/kg of lidocaine for patients suffering pulseless VT/VF. A randomized, controlled trial evaluating amiodarone, lidocaine, and placebo is currently enrolling and might help to clarify this issue.\n\nEpidemiological studies suggest that pulseless electrical activity (PEA) and asystole are increasingly common in out-of-hospital cardiac arrests. Atropine is a vagolytic and reverses cholinergic-mediated decreases in heart rate, blood pressure (BP), and vascular resistance. Although traditionally it has been used in PEA or asystolic cardiac arrest, the limited available research does not suggest any benefit, and this drug is no longer recommended for routine use. Epinephrine should be administered, and potentially treatable causes (the 5 Hs and 5 Ts of ACLS) considered.\n\nAn additional drug worth comment is sodium bicarbonate. For years, sodium bicarbonate was administered routinely during cardiac arrest to reverse the metabolic acidosis of cardiac arrest, and hopefully increase the effectiveness of vasopressors and antiarrhythmics. In formal trials, this drug did not improve survival [74]. Sodium bicarbonate may be reasonable in scenarios of suspected hyperkalemic arrest (such as individuals with known renal failure) and in prolonged resuscitations with adequate ventilation. Calcium (chloride or gluconate), however, is the most effective medication in cases of severe hyperkalemia affecting cardiac conduction.",
        "Specific interventions - Additional therapies": "Cardiac arrest represents the ultimate scenario of cardiovascular collapse. Consequently, cardiopulmonary bypass or extracorporeal life support (ECLS) may represent one potential solution. In tightly defined populations, ECLS combined with early angiography and hypothermia therapy has yielded good neurological outcomes in a significant proportion of patients. In a study which used ECLS only after standard therapy failed, the rate of good neurological outcome was small. Optimal selection of patients for this therapy will require early mobilization of resources given the association between prolonged arrest and poor neurological outcomes.",
        "Principles of management - Resuscitation protocols": "Cardiac arrest care interventions are time-critical. Thus, protocols should allow EMS personnel to initiate resuscitation immediately. Non-physician providers should provide initial cardiac arrest care using standing orders, as there is inadequate time to consult with the direct medical oversight physician for detailed guidance. The protocols should detail interventions for the various ECG rhythms likely to be encountered: VF, VT, PEA, and asystole. Protocols should provide convenient reference to medication dosages, mixtures, and administration rates. Other practical information should also be included, such as criteria for termination of resuscitation. Many systems use current AHA ACLS algorithms as the basis for cardiac arrest protocols.\n\nEmergency medical services personnel should be encouraged to contact the direct medical oversight physician for additional direction after initial successful or unsuccessful resuscitative efforts, as well as for unusual or complicated situations. Due to the time-sensitive nature of cardiac arrest and the often chaotic resuscitation scene, radio or phone interactions with the EMS personnel must be short, directed, and relevant. The physician must understand that detailed medical history or preceding symptoms are usually not known and are largely (although not entirely) irrelevant to the acute resuscitation phase of the patient\u2019s care. EMS personnel may seek medical oversight physician direction for more complex interventions and situations, such as initiating a dopamine infusion or external pacing. Direct medical oversight physicians must be prepared to provide adequate direction for these less common situations.",
        "Principles of management - High-performance CPR: the pit crew approach": "Based on the emerging concepts described above, an appreciation has developed for the importance of doing CPR in a very high-quality and precise manner and for providing the other components of resuscitation in a more timely and more measured way. Achieving these goals requires a team of providers working together in a carefully choreographed approach. Some have suggested that personnel at a cardiac arrest scene should function like a racing pit crew, each very skilled, with a specific task or tasks, and working in a synchronized manner.\n\nThis concept also emphasizes and includes practice sessions on high-quality performance: assuring continuous chest compressions with proper depth, rate, and recoil, changing compressors (quickly) every 100\u2013200 compressions, and integrating defibrillation such as charging the defibrillator with 20 or so compressions left in the cycle so the operator can quickly assess the rhythm and push to shock as soon as the compressor is off the chest. The first two responders should position themselves on each side of the chest, and while one (EMS1) starts compressions, the other (EMS2) applies the defibrillation pads and turns on the monitor. As EMS1 finishes the first round of compressions, the rhythm is analyzed. If a shockable rhythm is found, EMS2 can defibrillate and then begin chest compressions. Meanwhile, EMS1 is relieved of compressing (for 1 minute), and he or she should insert an oral airway and place an O\u2082 mask (or ventilate with a bag-valve-mask). When EMS2 is relieved for his or her minute break, he or she looks for IV or IO access and administers epinephrine (or vasopressin, based on system protocol as established by the medical director). The rhythm should be checked every 200 compressions or every 2 minutes. As more personnel arrive, attention can be paid to ventilation and placement of an advanced airway (endotracheal intubation or supraglottic airway). Finally the team leader should reassess all ongoing therapies, monitor function, and consider potentially treatable specific conditions.\n\nCare during this initial 10\u201320 minutes of resuscitation should all occur at the location where the patient was found, or an area as close as possible. Efforts to \u201cpackage the patient\u201d or to begin to transfer the patient to the ambulance compromise all resuscitation efforts, not just the quality of chest compressions. Moving the patient to the ambulance or transporting immediately, except for some very rare situations, is not beneficial.",
        "Withholding resuscitation": "In the past, EMS personnel initiated resuscitative efforts regardless of the family\u2019s or patient\u2019s wishes or a written do not resuscitate (DNR) order. This practice was fueled by the belief that EMS personnel could follow only the orders of an EMS medical oversight physician, not those of an independent physician, such as the patient\u2019s own primary care physician or oncologist. Also, EMS personnel feared medicolegal repercussions if they did not initiate resuscitation. Fortunately, current practices take a more progressive approach, recognizing the importance of patient autonomy, the futility of initiating or pursuing resuscitation in select cases, and the unwarranted risks of futile resuscitation.\n\nThe primary EMS situations involving non-initiation of resuscitation efforts include the following.\n\n\u2022 The patient has a DNR order and should not receive resuscitative efforts.\n\u2022 The patient has clear signs of irreversible death (such as rigor mortis) and should not receive resuscitative efforts.\n\nEmergency medical services agencies should have protocols and policies reflecting these situations. Personnel should receive education in the ethical principle of patient autonomy and the local regulations regarding patient directives. In each situation, consultation with the direct medical oversight physician is appropriate.",
        "Do not resuscitate status": "Do not resuscitate is a specific physician order. This differs from living wills or advance directives that merely outline the patient\u2019s general wishes regarding life-sustaining interventions. The most common EMS scenarios involving cardiac arrest patients with DNR orders include nursing home or assisted living facilities. Patients with known terminal conditions may also have DNR orders but may live in private residences or hospice facilities.\n\nBystanders or caregivers may summon 9-1-1 despite the presence of a DNR order. This may occur because of lack of knowledge of the patient\u2019s status, uncertainty about the patient\u2019s condition, panic, or simply the caregiver\u2019s wish to have an independent person confirm death. EMS personnel should not be surprised by these situations. Prompt consultation with the direct medical oversight physician may be appropriate in these situations.\n\nA recent initiative, Physician Orders for Life-Sustaining Treatment (POLST), is an effort to provide a uniform DNR order sheet transcending prehospital, hospital, and long-term care settings. A number of states are enacting legislation for this program. The specific operational details must be implemented prospectively to avoid confusion and misunderstanding at the patient\u2019s side.",
        "Dead on arrival": "Non-initiation of resuscitation may be appropriate in certain situations when lividity, rigor mortis, decomposition, and other signs of obvious death are present. Protocols should specify when EMS personnel should and should not initiate resuscitation. These guidelines should address special circumstances, such as hypothermia and trauma, in addition to medical arrests. Consultation with the direct medical oversight physician is prudent in unclear situations.\n\nProtocols should also detail specific tasks that EMS personnel must carry out after non-initiation of resuscitation, including notification of police, the coroner, or the medical examiner. EMS providers should also receive training in providing emotional support to family and bystanders.",
        "Termination of resuscitation": "Traditionally, in many areas EMS crews transported all cardiac arrest victims to the hospital, continuing resuscitative efforts en route. However, there is growing awareness that cardiac arrest patients who are not responding to initial treatment will likely not receive additional benefit from transport to the hospital. Therefore, many EMS agencies now have protocols for terminating resuscitation efforts in the field.\n\nSeveral studies have evaluated the prediction of futility by BLS providers. The Verbeek/Morrison rule indicates termination of resuscitation in patients with an unwitnessed arrest after three periods of CPR, three AED analyses without shock recommendation, and no ROSC.\n\nPatients who receive appropriate initial ACLS (including airway management and IV access) and who remain in asystole or PEA for greater than 20\u201330 minutes of resuscitative efforts without return of pulses are unlikely to be resuscitated. ACLS guidelines support cessation of efforts in these patients without transport to the hospital. Consultation with the direct medical oversight physician may be appropriate in these cases. Non-transport after termination of efforts applies only to patients with sustained pulselessness from suspected cardiac etiologies. This approach does not apply to patients with drug overdoses, hypothermic arrest, or other special situations.\n\nThe decision to terminate resuscitation or transport to the hospital involves important social and ethical concerns. Although some express concern that cessation of resuscitative efforts at the scene may be poorly accepted, two studies suggest that non-transport is well accepted and often preferred if proper counseling and explanation are given to bystanders and family members. Nonetheless, there may be circumstances in which transport to the hospital may be prudent (e.g. cardiac arrests occurring in public locations, unexpected death in the very young, and situations with extremely distraught or unaccepting family members). Paramedics are often uncomfortable terminating resuscitation in children. Direct medical oversight physician input may prove helpful in these situations.\n\nAs resuscitation strategies and postarrest care continue to improve, the accepted criteria for termination of resuscitation will have to be reevaluated.",
        "Postarrest care": "A common misconception is that the resuscitation ends after restoration of pulses. In fact, the body is in an extremely tenuous state in the immediate postarrest period. Without proper support, cardiac arrest may recur. In essence, the restoration of pulses represents the beginning of postarrest care.\n\nThe goals of postarrest care are to maintain hemodynamic stability, preserve the brain, and correct metabolic derangements. The salient elements of postarrest care include:\n\n\u2022 vasopressor titration\n\u2022 therapeutic hypothermia\n\u2022 appropriate cardiac catheterization\n\u2022 sedation\n\u2022 glucose and electrolyte management.\n\nThe most important EMS consideration is vasopressor support after ROSC. Animal models of cardiac arrest predictably develop cardiovascular collapse shortly after ROSC. This hemodynamic instability may result from myocardial stunning as well as the waning effect of epinephrine. These patients frequently require vasopressor support. Because of the likely need for vasopressor support, it is reasonable to prepare a dopamine, norepinephrine, or epinephrine infusion immediately after achieving ROSC. Rescuers need to anticipate cardiovascular collapse. If they wait for collapse to occur, the patient will deteriorate before rescue therapy can be initiated.\n\nCoronary artery disease is common in this population, and is independent of the primary arrest rhythm. Early coronary angiography is strongly supported in guideline statements and has been associated with improved outcomes following ROSC. Consequently, 12-lead ECG analysis is indicated in the patient successfully resuscitated from cardiac arrest. Patients with a history consistent with acute coronary syndrome or obvious ECG changes should be transported to a percutaneous coronary intervention center and receive prompt coronary angiography.\n\nThe induction of mild hypothermia for brain preservation has demonstrated significant improvement in neurological outcome in comatose patients following cardiac arrest. Hypothermia is believed to decrease cerebral metabolism, reduce free radical production, and impose direct protective effects on neural and cardiac tissue.\n\nIn the Hypothermia After Cardiac Arrest (HACA) study, comatose survivors of VF/VT cardiac arrest were randomized to a goal temperature of 32\u201334\u00b0C for 24 hours or normal care and normothermia. The investigators noted that 55% of patients receiving hypothermia enjoyed a good outcome (defined as a Cerebral Performance Category 1 [Good Recovery] or 2 [Moderate Disability]) compared with 39% of normothermic patients. In the Bernard study, patients were randomized to a goal temperature of 33\u00b0C for 12 hours or normal care and normothermia. Further, 49% of the hypothermic patients enjoyed a good outcome (defined as discharge home or to acute rehabilitation), compared with 26% of the normothermic patients.\n\nControlling temperature between 32\u201336\u00b0C results in similar outcomes in the out-of-hospital VF/VT population.\n\nEarly prehospital induction of hypothermia is empirically appealing and supported by animal studies. Kim et al. have demonstrated that induction of hypothermia during the prehospital phase is feasible. The Bernard trial initiated cooling in the ambulance while en route to the hospital. Perhaps the most compelling reason for starting hypothermia in the field is that hospital personnel often fail to initiate the therapy. Initiation of hypothermia by EMS personnel may remind or compel hospital caregivers to continue this intervention.\n\nInduction of hypothermia is relatively simple, does not require specialized techniques, and can be initiated in the prehospital setting. Kim et al. noted that rapid infusion of 1\u20132 L of cold (4\u00b0C) saline resulted in a 1\u00b0 drop in patient temperature in the first 30 minutes. Bernard et al. used surface cooling with skin exposure and ice packs, an approach that is slower but complementary. Moore et al. demonstrated that healthy volunteers could achieve a 1\u00b0 temperature drop with infusion of 30 mL/kg of cold saline during a 30-minute infusion. The initial temperature in many postarrest patients is approximately 35\u201335.5\u00b0C. Therefore, practitioners may potentially reach the target temperature with only a 1\u00b0 reduction in body temperature. In the largest randomized controlled trial to date, prehospital cooling was not associated with a higher rate of good neurological outcome than the hospital-initiated group (risk ratio 0.90; 95% CI 0.70, 1.17). In addition, recent data demonstrate that rapid infusion of saline in the prehospital arena is associated with pulmonary edema. To date, intraarrest hypothermia has not yielded additional survival benefit. Nasogastric, bladder, and endovascular cooling are other viable options in the hospital, but they are impractical in the prehospital setting.\n\nMost importantly, the receiving medical facility must continue hypothermia therapy for it to be effective. The EMS physician should ensure that a patient cooled in the prehospital arena is transported to a facility that can continue this therapy. Although the ultimate target temperature is 32\u201334\u00b0C, this goal may require several hours with concomitant sedation and pharmacological paralysis.\n\nThe other elements of postarrest care do not need to be initiated in the field. However, the postarrest patient is critically ill and frequently requires the care of multiple specialists who may not be available at all hospital facilities. The management of the postarrest patient is a low-frequency, resource-intensive event requiring regimented, multidisciplinary strategies to optimize outcome. One retrospective study has demonstrated that the risk of rearrest during prolonged air medical transport is low, but critical events such as hypotension or hypoxemia were encountered in 23% of patients. Because many hospitals cannot provide these services at all hours, some systems have regionalized the care of postarrest patients. EMS medical directors should consider developing policy regarding the proper destination for postarrest patients in their systems.",
        "Conclusion": "Successful resuscitation of patients from out-of-hospital cardiac arrest requires a comprehensive system of care. Prehospital care providers face many practical and logistical challenges in this setting, but intense, expert resuscitation efforts can improve the bleak rate of survival from this condition. Prompt initiation and continuous performance of high-quality chest compressions, timely defibrillation, avoidance of hyperventilation, and appropriate postarrest care are the keys to successful outcomes."
    },
    {
        "Introduction": "Shock is a life-threatening physiological state characterized by decreased tissue perfusion and end-organ tissue dysfunction, and is a significant predictor for complications including death. The presence of shock must be recognized and therapeutic interventions must be started early to prevent progression. Unfortunately, the identification and treatment of shock in the out-of-hospital setting are fraught with many difficulties and potential pitfalls. Patient assessment is often limited by the challenging out-of-hospital environment and lack of diagnostic and therapeutic options. The tools available for the diagnosis and treatment of shock in the field are limited. Even when shock is properly identified, the most appropriate out-of-hospital management is often unknown or the subject of great debate.\n\nIn the out-of hospital setting, the identification of shock relies primarily on the recognition of signs and symptoms, including tachycardia, poor skin perfusion, and altered mental status. Note that hypotension, arbitrarily defined at a systolic blood pressure of less than 90 mmHg, is not an adequate definition of shock and may not adequately reflect the onset of tissue hypoperfusion. Unfortunately, the early stages of compensated shock, with only subtle alterations in physical findings, are easily overlooked or misinterpreted by out-of-hospital care providers. Physiological changes associated with age, pregnancy, or treatment for medical conditions, such as beta-blockers for hypertension, may also mask or alter the body's compensatory responses. As a result, the patient with severe shock may present with near-normal vital signs.",
        "Pathophysiology": "Shock is a complex physiological process defined as the widespread reduction in tissue perfusion leading to cellular and organ dysfunction and death. In the early stages of shock, a series of complex compensatory mechanisms act to preserve critical organ perfusion. In general, the following relationships drive this process.\n\nBlood pressure = Cardiac output \u00d7 Peripheral vascular resistance\nCardiac output = Heart rate \u00d7 Stroke volume\n\nAny condition that lowers cardiac output and/or peripheral vascular resistance may decrease blood pressure. Alterations of heart rate (very low or very high) can lower cardiac output and hence blood pressure secondary to decreased cardiac filling. Also, decreasing stroke volume may lower cardiac output with a possible reduction in perfusion, as well. Stroke volume may be reduced by lower circulating blood volume (e.g. hemorrhage or dehydration), by damage to the heart (e.g. myocardial infarction or myocarditis), or by conditions obstructing blood flow through the thorax (e.g. tension pneumothorax, cardiac tamponade, or extensive pulmonary embolism).\n\nTo aid in the evaluation and treatment of shock, it is often useful for the physician and EMS personnel to categorize the etiology of the shock condition. Most EMS providers are familiar with the 'pump-fluid-pipes' model of the cardiovascular system, with the pump representing the heart, pipes representing the vascular system, and fluid representing the blood. Thus, categorizing shock into four categories may help prehospital providers and EMS physicians organize their assessments and approaches. Accurate physical assessment is vital for the EMS provider to determine the etiology of the shock state.",
        "Evaluation": "The diagnosis of shock depends on a combination of key historical features and physical findings in the proper clinical setting. For example, tachycardia and hypotension in an elderly patient with fever, cough, and dyspnea may represent pneumonia with septic shock. Hemorrhagic shock should be suspected in a middle-aged man with epigastric pain, hematemesis, melena.\n\nEmergency medical services providers should look for the signs and symptoms of system-wide reduction in tissue perfusion, such as tachycardia, tachypnea, mental status changes, and cool, clammy skin. When available, adjunctive technologies can provide improved recognition and assessment of shock by demonstrating reductions in expired CO\u2082, hypovolemia, obstruction, or poor contractility on ultrasound, and elevated serum lactate levels.\n\nVital signs that fall outside of expected ranges must be correlated with the overall clinical presentation. Vital signs have a broad range of normal values and must be interpreted in the context of the individual patient. A petite 45 kg, 16-year-old female with lower abdominal pain with a reported blood pressure of 88 mmHg systolic by palpation may have a ruptured ectopic pregnancy, or may just be at her baseline blood pressure. An elderly patient with significant epistaxis may be hypertensive due to catecholamine release and vasoconstriction despite being relatively volume depleted. Consideration should be given to patient age, comorbid conditions, and medications that may affect the interpretation of vital signs.\n\nIn the noisy field environment, providers often measure blood pressure by palpation rather than auscultation. Blood pressure by palpation provides only an estimate of systolic pressure. Without an auscultated diastolic pressure, the pulse pressure (difference between systolic and diastolic pressure) cannot be calculated. A pulse pressure less than 30 mmHg or 25% of the SBP may provide an early clue to the presence of hypovolemic or obstructive shock. Conversely, a wide pulse pressure may be indicative of distributive shock. Dividing the pulse rate by the systolic pressure typically produces a ratio of approximately 0.5 to 0.8, which is called the \u201cshock index.\u201d When that ratio exceeds 1.0, then a shock state may be present.\n\nPreviously healthy victims of acute hypovolemic shock may maintain relatively normal vital signs with up to 25% blood volume loss. Sympathetic nervous system stimulation with vasoconstriction and increased cardiac contractility may result in a normal blood pressure in the face of decreasing intravascular volume, especially in the pediatric population. In some patients with intraabdominal bleeding (e.g. ruptured abdominal aneurysm, ectopic pregnancy), the pulse may be relatively bradycardic despite significant blood loss.\n\nEmergency medical services personnel may equate \u201cnormal\u201d vital signs with normal cardiovascular status. The field team may be lulled into a false sense of security initially if the early signs of shock are overlooked, only to be caught off guard when the patient\u2019s condition dramatically worsens during transport. Following trends in the vital signs may also help identify shock before patients reach abnormal vital sign triggers. Early recognition and aggressive treatment of shock may prevent progression to the later stages of shock that can result in the death of potentially salvageable patients.\n\nPrehospital hypotension may predict in-hospital morbidity and mortality in both trauma and medical patients. Jones et al. noted a 30% higher mortality rate for medical patients with prehospital hypotension. Other studies have shown similar findings in trauma patients with prehospital hypotension, even with subsequent normotension in the emergency department. Therefore, hospital providers should consider any episode of prehospital hypotension as evidence of significant shock and the presence of a critical illness.\n\nDespite their questionable value, orthostatic vital signs are often evaluated in the emergency department, and occasionally in the field. A positive orthostatic vital sign test for pulse rate would result in a pulse increase of 30 beats per minute after 1 minute of standing. Symptoms of lightheadedness or dizziness are considered a positive test. Occasionally, orthostatic vital signs are performed serendipitously by the patient who refuses treatment while lying down, then stands up to leave the scene, and suffers a syncopal episode. This demonstration of orthostatic hypotension is often helpful in convincing the patient to allow treatment and transport. However, rescuers should not equate absence of orthostatic response with euvoolemia.\n\nCapillary refill, an easy test to perform in the field setting, is not a useful test for mild-to-moderate hypovolemia. Moreover, environmental considerations, such as cold temperatures and adverse lighting conditions, also affect the accuracy of this technique for shock assessment. On-scene estimates of blood loss by EMS providers may influence therapeutic interventions, including fluid administration. However, studies suggest that providers are not accurate at estimating spilled blood volumes.\n\nHypoxia is a common manifestation of shock states. Patients in various stages of exsanguination may not have sufficient blood volume to adequately perfuse the body with oxygen. Unfortunately, pulse oximetry alone cannot detect the adequacy of oxygen delivery. Pulse oximetry may fail to detect a pulse when blood flow is reduced. Like pulse oximetry, capnography may also serve as an important tool in the evaluation and treatment of shock in the prehospital setting. Capnography is the measurement of the exhalation of carbon dioxide from the lungs. Exhaled end-tidal carbon dioxide (EtCO\u2082) levels vary inversely with minute ventilation, providing feedback regarding the effect of changes in ventilatory parameters. Additionally, changes in EtCO\u2082 are virtually immediate when the airway is obstructed or the endotracheal tube becomes dislodged. EtCO\u2082 concentration may be influenced by factors other than ventilation. For example, EtCO\u2082 levels are reduced when pulmonary perfusion decreases in shock, cardiac arrest, and pulmonary embolism. EtCO\u2082 is most useful as an indicator of perfusion when minute ventilation is held constant (e.g. when mechanical ventilation is applied). Under these conditions, changes in EtCO\u2082 levels reliably indicate changes in pulmonary perfusion. In any patient suffering from a potential shock state, diminished EtCO\u2082 should be a warning of the critical nature of the patient\u2019s problem.",
        "Future technologies in the assessment of shock": "Use of portable ultrasound in the field can facilitate the recognition of immediately life-threatening causes of shock including intraabdominal hemorrhage, cardiac tamponade, or an abdominal aortic aneurysm. Many EMS agencies, primarily air medical services, have deployed ultrasound for field evaluations, including the focused assessment by sonography in trauma (FAST) examination. Ultimately, the EMS medical director must determine if the cost and time of acquiring equipment, training, and performing the skills translates into improved patient outcomes. The use of field ultrasound has the potential to worsen patient outcome if the procedure delays the time to definitive care, does not influence patient destination or care, or interferes with basic skills (e.g., airway maintenance).\n\nThere is growing interest in the use of biomarkers that can be used to identify, monitor, and predict the outcome in shock. Point-of-care testing devices make measurement of biomarkers in the field an attractive option. Elevation of the serum lactate may reflect anaerobic tissue metabolism in acute sepsis and shock. In the emergency department, elevated lactate in the setting of infection indicates septic shock and the need for early sepsis therapy. Elevated point-of-care venous lactate is associated with increased mortality risk and the need for resuscitative care in trauma patients. Indeed, recent work by the RESUSCITATION OUTCOMES CONSORTIUM in prehospital trauma research indicates that lactate levels may rise before blood pressure drops, and that an elevated lactate level in the setting of trauma may be a useful predictor of a patient that will require aggressive resuscitation. Serial lactate measurements may indicate the progress of ongoing resuscitation.\n\nIn summary, although technology may offer future value, the current evaluation of the potential shock victim in the out-of-hospital setting is challenging due both to limited assessment capability in this environment as well as fewer diagnostic tools. Both the provider and the medical oversight physician must be cautioned on placing too much emphasis on a single set of vital signs or a limited assessment.",
        "Shock interventions": "All treatment approaches to shock must include the following basic principles.\n\n1. Perform the initial assessment.\n2. Deal with issues identified in the initial assessment such as airway, breathing, and circulation issues, including active external bleeding.\n3. Determine need for early definitive care.\n   - Hemorrhage control and volume resuscitation\n   - Needle thoracostomy\n   - Electrical therapy for dysrhythmia\n   - Invasive airway management\n4. Maintain adequate oxygen saturation (SaO\u2082 > 94%).\n5. Ensure adequate ventilation without hyperventilating.\n6. Monitor vital signs, ECG, oxygen saturation, capnography, and lactate (if available).\n7. Prevent additional injury or exacerbation of existing medical conditions.\n8. Protect the patient from the environment.\n9. Determine the etiology of the shock state, and treat accordingly.\n10. Notify and transport to an appropriate facility.\n\nOften the etiology of the patient's shock state and the initial management options are clear from the history. For example, the out-of-hospital treatment of a young, previously healthy college student with hypotension secondary to severe vomiting and diarrhea includes IV fluids. The treatment of cardiogenic shock in an unresponsive elderly patient with ventricular tachycardia (VT) requires prompt cardioversion. Occasionally, the primary problem may be strongly suspected but not readily diagnosable or treatable in the field (e.g. pulmonary embolism). Less frequent, but most difficult to manage, is the patient in shock without an obvious cause. With the understanding of the limited treatment options in the out-of-hospital setting (primarily fluids, inotropic agents, and vasopressors), field treatment may be individualized for the four categories of shock: hypovolemic, distributive, obstructive, and cardiogenic.",
        "Hypovolemic shock": "\n\nHypovolemic shock is the result of significant loss of intravascular volume resulting in hypotension. The many etiologies of hypovolemic shock include external fluid loss and shifting of fluids from the vascular system to a non-vascular body compartment. The treatment of hypotension and shock caused by hypovolemia is relatively straightforward. External bleeding should be controlled. Fluid replacement via vascular access is the mainstay of treatment. Unfortunately, the ideal fluid for the resuscitation of hypovolemic shock and the amount of fluids that should be provided remains controversial.",
        "Distributive shock": "\n\nDistributive shock, characterized by a decrease in systemic vascular resistance, is associated with abnormal distribution of microvascular blood flow. Causes of distributive shock include sepsis, anaphylaxis, medication overdose, and acute neurological injury. The treatment of distributive shock involves the combination of vasoactive medications, which constrict the dilated vasculature, and fluids, which fill the expanded vascular tree. Commonly used vasoactive medications in the out-of-hospital setting for distributive shock include epinephrine, norepinephrine, and dopamine. Although epinephrine is easily administered via several routes (e.g. intramuscular, intravenous bolus or infusion), the drug has significant side-effects. Norepinephrine infusions are associated with a lower incidence of cardiac dysrhythmias than either dopamine or epinephrine. In addition, recent studies of cardiogenic shock suggest increased mortality associated with dopamine. However, continuous infusions may be difficult to maintain without special infusion pumps.",
        "Obstructive shock": "\n\nObstructive causes of shock are often difficult to diagnose and treat. If possible, the obstruction should be resolved, such as by decompression of a tension pneumothorax. However, when the primary problem cannot be treated successfully in the field (e.g. massive pulmonary embolus or cardiac tamponade), intravenous fluids may be helpful in increasing preload and temporarily improving the condition.",
        "Cardiogenic shock": "\n\nCauses of cardiogenic shock include arrhythmias, valvular heart disease, cardiotoxic agents, and myocardial infarction. As a result, cardiogenic shock requires individualized treatment. Cardiogenic shock from severe dysrhythmias should be treated with appropriate electrical or pharmacological therapy. \u201cPump failure\u201d is often difficult to diagnosis and to treat without invasive monitoring. Adult patients without obvious pulmonary edema may benefit from fluid challenges of approximately 200\u2013300 mL of crystalloid. An improvement in the patient\u2019s condition suggests that enhancing preload would be beneficial. A worsening of the patient\u2019s condition with a modest fluid challenge, or the presence of obvious pulmonary edema on initial evaluation, suggests that fluid therapy would not be helpful. In such settings, treatment with inotropic agents or pressors, such as dobutamine or norepinephrine, would be more appropriate. Intravenous infusions are often difficult to manage in the field without an infusion pump and must be monitored closely.\n\nThe causes of cardiogenic shock also can include beta-blocker and calcium channel blocker toxicity. These agents block sympathomimetic receptors, impairing the body's normal compensatory responses. These patients present with profound bradycardia and shock, often refractory to sympathomimetic treatment and fluid challenges due to the receptor blockade. Alternative therapies may include IV glucagon or calcium, which facilitates heart rate stimulation and vasoconstriction through alternative cellular receptors, and which many EMS agencies carry for the treatment of hypoglycemia.",
        "Shock of unclear etiology": "In a few disconcerting situations, the primary etiology for the patient's shock state may be difficult to determine. The primary treatment decision is whether or not to give fluids. In hypovolemic, distributive, and obstructive shock, fluids are an appropriate initial treatment for hypotension, given the important caveats mentioned above regarding that in the setting of uncontrolled hemorrhage, indiscriminate administration of large volumes of IV fluids may not improve patient outcome. Some cases of cardiogenic shock will respond to fluids. However, fluids should not be given to patients in cardiogenic shock with pulmonary edema. Fluids are also not appropriate when cardiogenic shock has been precipitated by a treatable arrhythmia. Response to fluid challenges (where appropriate) should dictate whether additional fluid challenges should be given or whether a trial of a sympathomimetic agent should be used.\n\nOccasionally, shock will be refractory to initial attempts at resuscitation. This may reflect the need for definitive care in the hospital (e.g., thoracotomy, laparotomy). If, after vigorous field treatment, the patient remains hypotensive, other etiologies for the hypotension must be considered, including adrenal suppression, hypothyroidism, or toxidromes. In some cases patients with profound acidosis will not respond to vasopressors or inotropes, as their receptors are pH dependent. Administration of sodium bicarbonate at 1 mEq/kg may improve perfusion by buffering acidosis and increasing vasopressor activity. Use of vasopressin to supplement other vasopressors may also improve perfusion as it increases systemic vascular resistance even during acidosis. In cases of refractory shock or adrenal suppression, administration of steroids may also be of benefit. Hydrocortisone is ideal for this purpose, as patients may benefit from both mineralocorticoid and glucocorticoid properties. Methylprednisolone is far more widely available in the prehospital environment and may have some limited utility in refractory shock. Patients exposed to potent cellular toxins such as cyanide or hydrogen sulfide may also present with refractory shock, prompting therapy with agent-specific antidotes.",
        "Shock in the pediatric population": "The recognition and management of shock in the pediatric population follow the same general principles as in adults, with a few notable exceptions. Children in shock more commonly present with a low cardiac output and a relatively high systemic vascular resistance (SVR). This has been described as as opposed to the low-SVR state or frequently seen in adults. Children presenting in distributive shock usually require more aggressive fluid resuscitation with volumes of 60 cc/kg or more. If children fail to respond to the initial fluid resuscitation, epinephrine is preferred as the first-line vasopressor in order to counter the relatively low cardiac output seen in pediatric shock. Additional support for patients with low SVR and wide pulse pressure may be provided with norepinephrine or vasopressin. Dobutamine may provide inotropic and chronotropic support in patients with very low cardiac output and improve delivery of oxygen to tissues.\n\nFollowing initial treatment with fluids and vasoactive agents, pediatric patients may also benefit from adjunctive therapies for shock. Early airway management should be considered, as children may use up to 40% of their cardiac output to support the work of breathing. Ketamine is the preferred induction agent as it preserves cardiac output and will not result in the hypotension or adrenal suppression potentially seen with other induction agents. Hydrocortisone should be administered to children with adrenal insufficiency. Transport to an appropriate facility with pediatric critical care should be an important consideration.",
        "Shock Interventions - Fluids": "The treatment of shock must be customized to the individual EMS agency and geographic location. In the urban setting with short transport times, the victim of a penetrating cardiac wound probably benefits most from hemorrhage control, airway maintenance, and rapid transport to the hospital. IV or IO access could be attempted en route if it will not delay delivery to definitive care. On the other hand, with longer transport times in the rural setting, a similar patient might benefit from carefully titrated crystalloid volume infusion during the transport. Fluid delivery could be initiated while the patient is en route to the hospital, thereby prolonging neither scene time nor time until definitive care. In the patient who presents a difficult IV access problem, IO infusions may be attempted. Placing the IO needle in the humeral head may result in faster infusion rates than the proximal tibia.\n\nThe ideal fluid for use in the field would be small in volume, portable, non-allergenic, inexpensive, and would not interfere with clotting factors. Unfortunately, this ideal fluid has yet to be discovered. Isotonic crystalloids are currently the fluid of choice for out-of-hospital resuscitation in the United States. They are inexpensive and widely available but may contribute to dilutional coagulopathy, hyperchloremic acidosis, and hypothermia when given in large volumes.\n\nWhole blood would arguably provide the greatest benefit as a resuscitation fluid in the setting of hemorrhagic shock but is impractical due to issues of cost storage and availability. Use of blood products in the out-of-hospital environment is limited to a few air medical services which carry O-negative blood for administration to victims of hemorrhagic shock. Prehospital administration of plasma and factor concentrates is being investigated. Several centers have studied hypertonic saline, colloids, and artificial blood substitutes as alternatives to isotonic saline. Problems with these alternative fluids include high cost; increased risks including allergic reactions, kidney injury, coagulopathy, and hypernatremia; and lack of demonstrated benefit versus isotonic crystalloids. As a result, none of the alternative fluids has gained widespread acceptance.\n\nThe optimal volume of fluids to administer in the out-of-hospital setting is not known, especially in the trauma victim with uncontrolled hemorrhage. Older trauma algorithms indicate the administration of 2 liters IV fluid for all major trauma victims. Evidence suggests, however, that attempts at normalization of blood pressure with a large volume of fluids in the patient with uncontrolled hemorrhagic shock may be deleterious to patient outcome. Complications may include acidosis, dislodgment of blood clots, and dilution of clotting factors. In such a patient, it appears that the best course is to give sufficient crystalloid to maintain a peripheral pulse, pending the delivery of the patient to the appropriate facility.\n\nAdministration of IV fluids is a gold standard treatment that has a long tradition in the care of critically ill patients. The route of IV administration depends on many factors, including the severity of the patient's illness and the available cannulation sites. Extremity veins provide the typical routes of venous access. External jugular veins are also useful sites in many patients. Few EMS systems use central venous access.\n\nThe IO route for vascular access has been used for generations. This was a common form of vascular access during World War II, though it became a less popular route in the postwar era with the rising use of IV cannulation. IO access has become so important as a method of vascular access that it is supported by a position statement from the National Association of EMS Physicians. In patients in extremis or cases in which peripheral access is not immediately available, IO access may be preferred. Various devices are available, and EMS medical directors must work with their systems to determine the most appropriate device for use by their providers.\n\nControlling external hemorrhage is essential for maintaining vascular volume. Direct pressure is usually sufficient to control external bleeding. Military and civilian experience suggests that tourniquets should be used early and liberally. An assortment of topical hemostatic materials to be placed directly on the bleeding wound also exists. The hemostatic dressing must be applied in conjunction with direct pressure to be effective. Pelvic binders may compress bleeding pelvic vessels while reducing the internal volume available for hemorrhage into the pelvis.\n\nTranexamic acid (TXA) is a lysine derivative which blocks fibrinolysis. It has long been used to control hemorrhage during surgery. In a randomized controlled study, TXA demonstrated an ability to reduce mortality from traumatic hemorrhage if administered within 3 hours of the time of injury. Some prehospital systems are beginning to use TXA to treat hemorrhagic shock. Evidence for its benefit is found in its early administration, with late administration of TXA being associated with worsening outcomes.",
        "Shock Interventions - Ventilation": "The patient in shock may require assisted ventilation. Venous return requires a relative negative pressure in the right atrium to ensure return of blood to the heart. Assisted ventilation using any of the typical techniques, such as bag-mask ventilation, endotracheal intubation, or supraglottic devices, results in an increase in airway pressure, raising intrathoracic pressure. Patients in shock from any cause are extremely sensitive to increases in intrathoracic pressure. Studies in a swine hemorrhagic shock model showed that even modest increases in the rate of positive pressure ventilation significantly reduce brain blood flow and oxygenation. EMS personnel must carefully control the rate of assisted positive pressure ventilation in the shock patient, as overventilation is very common. Generally speaking, a one-handed squeeze on the ventilation bag at a rate of approximately once every 8 seconds is reasonable for an adult, producing a minute ventilation of about 5 L/min. Minute ventilation should be adjusted to ensure an EtCO\u2082 between 35 and 45 cmH\u2082O.",
        "Shock Interventions - Vasopressor agents": "Administration of vasoactive medications may be required to reverse systemic hypoperfusion from distributive or cardiogenic shock. These agents increase cardiac inotropy, chronotropy, and/or vasoconstriction. Although a wide variety of vasoactive agents is available in the hospital, the drugs carried by prehospital services are limited by local, regional, or state-wide protocols or regulations. In general, most services carry epinephrine and dopamine. Dobutamine, norepinephrine, and vasopressin may also be included in the drug armamentarium of some services.\n\nThe choice of vasopressor depends on the suspected underlying pathological process and the patient\u2019s response to therapy. Unfortunately, in the out-of-hospital setting, the etiology of the shock state is often unclear, and close monitoring of vital signs is difficult. The administration of vasoactive agents in the field is fraught with many other potential pitfalls such as the difficulty of calculating weight-based drug dosages. Rescuers should use calculators or templates or seek direct medical oversight, where an experienced clinician in a more controlled setting can perform important calculations. When available, particularly during interfacility or air medical transport, portable IV infusion pumps should be used to ensure accurate and precise medication administration.",
        "Shock Interventions - Other drug agents": "Other agents used for shock resuscitation include corticosteroids, antibiotics, colloids, inotropic agents, recombinant human activated protein C, and dextran. The role of these agents in out-of-hospital shock management remains undefined. It would be reasonable to administer steroids to shock victims with known adrenal insufficiency or chronic steroid use and refractory hypotension.",
        "Controversies - Shock science": "The lack of definitive studies on the treatment of shock in the out-of-hospital setting leaves the EMS medical director without clear guidelines for treating these patients. As a result, considerable controversy exists with respect to many areas of the treatment of shock (especially traumatic shock) in the out-of-hospital setting.\n\nThe benefit of an out-of-hospital procedure must be weighed against potential risks. A major pitfall associated with shock treatment is that resuscitative interventions may delay definitive care. For victims of myocardial infarction, for example, Pantridge and Geddes demonstrated that some aspects of definitive care, such as defibrillation and arrhythmia management, can and should be delivered in the field. However, for trauma victims with uncontrolled internal hemorrhage, definitive care can only be provided in the hospital. Any field procedure that significantly delays delivery of definitive care must have proven value. For example, pneumatic anti-shock garments (PASG) were implemented in clinical EMS practice without supporting evidence, and then a formal assessment revealed that PASG actually worsened patient outcome in certain circumstances, particularly thoracic injury.",
        "Treatment of hemorrhagic shock": "Hemorrhage is a common cause of shock in the trauma victim. Field clinical trials have suggested that volume resuscitation before controlling hemorrhage may be detrimental. Possible mechanisms for worse outcomes include dislodgement of clot, dilution of clotting factors, decreased oxygen-carrying capacity of the blood, hyperchloremic metabolic acidosis, and exacerbation of bleeding from injured vessels in the thorax or abdomen.\n\nStudies in Houston and San Diego suggest that mortality following traumatic hemorrhage is not influenced by prehospital administration of fluid. Survival to hospital discharge rates were not significantly different for patients receiving fluids versus patients not receiving fluids in the field. Both studies were performed in systems with relatively short scene and transport times.\n\nAs discussed above, currently field providers in most clinical settings are taught to administer only enough IV or IO fluid replacement to restore a peripheral pulse or to reach a systolic blood pressure of 80\u201390 mmHg. However, the optimum target blood pressure for these patients remains undefined. Trauma victims with isolated head injuries who receive excess fluids may develop worsened cerebral swelling. In addition, excess fluids may precipitate congestive heart failure in susceptible individuals or lead to impaired immune response following severe injury.\n\nConversely, the benefit of limited volume resuscitation has been derived from military and urban data with a predominance of penetrating injuries and young, healthy patients. This population may be more tolerant of hypovolemic resuscitation and benefit from relative hypotension while reducing the risk of clot dislodgment. However, patients with blunt injury and limited organ reserve due to comorbid illness or age may be intolerant of hypotensive resuscitation. A multicenter trial evaluating limited crystalloid resuscitation versus standard aggressive resuscitation coordinated by the Resuscitation Outcomes Consortium (ROC) is currently under way.\n\nAttempts at establishing intravascular access in critically injured trauma victims may delay time to definitive care, especially in the urban setting. The majority of IV fluid studies have taken place in urban settings primarily with penetrating trauma victims and rapid transport times. The effectiveness of IV fluids for similar patients in the rural and wilderness settings remains undefined. The subject remains controversial, with several studies providing mixed messages.",
        "Protocol development": "A treatment protocol for treating shock in the field should address the following factors.\n\n1. Performing the initial assessment.\n2. The definitive or life-saving interventions appropriate for these patients.\n3. Access to definitive care without unnecessary prehospital delay.\n4. Resources to be used in the field.\n5. Skills of the various levels of prehospital care providers in the field.\n\nProtocols developed for the out-of-hospital treatment of shock must consider the heterogeneity of the disease state, the limited assessment and treatment options, and the environment in which the protocols will be applied. Protocols for the inner city may not be appropriate for the rural setting. The level of training and clinical experience of the providers must also be considered. Ideally, medical directors would use evidence-based medical decision making when developing treatment protocols. It is strongly recommended that the EMS medical director draw from best practices for establishing clinical protocols addressing the evaluation and treatment of shock.",
        "Conclusion": "\n\nShock must be correlated with the patient's clinical condition, age, size, and present and past medical history. Providers must identify signs of decreased tissue perfusion when assessing for the presence of shock. Treatment modalities for shock are limited in the field, but include bleeding control, fluid administration, inotropic agents, and careful control of assisted ventilation. Although the mainstay of shock treatment is IV fluids, approaches should be individualized for different clinical scenarios. The potential benefits of shock care interventions must be weighed against the potential risks of delaying definitive care."
    },
    {
        "Introduction": "While discussions continue concerning the utility of obtaining prehospital vascular access, the skill remains a standard taught to EMS providers. Methods of access include peripheral and central intravenous (IV) catheterization and intraosseous (IO) access, depending on the local scope of practice and the qualifications of prehospital personnel. The medications and fluids administered through these various routes depend on local EMS protocol and the practices of the EMS medical director. Those specifics are beyond the scope of this chapter, but are discussed elsewhere in this text.",
        "Benefits": "Similar to its benefit in the emergency department (ED) or any other acute care setting, vascular access provides an avenue for medical intervention by the EMS provider. Early prehospital initiation of treatment for cardiac arrest, cardiac arrhythmia, and sepsis has been shown to be beneficial for patients. For the more stable yet ill or distressed patient, the initiation of an IV or IO for symptomatic treatment of nausea, pain, or dehydration can help the continuum of care that will likely progress in the ED. Treatment of potentially reversible conditions like hypoglycemia and narcotic overdose in the prehospital setting can prevent deterioration of the patient\u2019s condition and potentially negate the need for transport. Vascular access also facilitates advanced care such as rapid sequence intubation and the administration of vasopressors and thrombolytics.",
        "Risks": "Obtaining vascular access involves inherent risks to the provider, including blood exposure and needlestick injury. Whether it is attempted at the scene or in transit, the prehospital environment is often characterized by poor lighting, limited space, or movement in the rear of an ambulance. This offers less than ideal conditions in which to handle lancets, IV and IO needles, and other sharps. A combative and/or confused patient can add to the difficulty. Transmission of HIV, hepatitis B, and hepatitis C remains a constant threat to the EMS provider, with the risks of infection following needlestick injury estimated at 0.3%, 6\u201330%, and 1.8%, respectively. Consistent use of universal precautions is imperative to reduce the likelihood of occupational exposures. Potential risks to the patient include bleeding, damage to adjacent structures, infection, and thrombosis and will be discussed later. Establishing an IV is often part of EMS protocols. In many cases, protocols allow for EMS provider assessment and judgment regarding whether or not an IV is necessary. One study revealed that while over 50% of the patients who arrived at an ED via EMS had IVs in place, almost 80% of those IVs were not used in the prehospital setting. The tendency to err on the side of caution to avoid punitive measures from perceived undertreatment seemed to contribute to the discrepancy. Another study similarly found that protocols seemed to drive the decision to start an IV as opposed to an actual need for administration of medicines or fluids. Medical oversight is indicated to continually evaluate the appropriateness of \u201cprecautionary\u201d IVs in the contexts of potential risks and costs to the system and to patients. Several studies in the trauma setting have unveiled a lack of significant benefit regarding prehospital vascular access. The classic EMS mantra of \u201ctwo large-bore IVs\u201d for trauma patients has been muted by concern for increased on-scene times and delay of transport to definitive medical care. Nevertheless, two studies have shown high success rates when IVs were attempted in transit without delaying transport. However, a literature review by the Eastern Association for the Surgery of Trauma resulted in a set of practice management guidelines that found no demonstrable benefit from prehospital IV placement or IV fluid administration for either penetrating or blunt injury patients. Recent research in the field of trauma resuscitation suggests that routine administration of IV fluids may have no benefit and in fact can be harmful in the prehospital setting. Another study endorsed \u201cscoop and run\u201d transport for EMS as it found that each prehospital procedure before ED thoracotomy led to a reduction in the odds of survival.",
        "Peripheral IV access - History": "Early records document the use of feather quills and animal bladders for intravenous therapies with animal-to-human transfusions. These were later replaced by hollow steel needles with rubber tubing leading to glass bottles. The evolution to over-the-needle plastic catheters has been focused on operator safety and patient comfort. Flow rate through the catheter is based on Poiseuille\u2019s law, dealing with pressure and resistance. The pertinent determinants of the equation include the radius of the catheter and the catheter length. Flow is directly proportional to the radius to the 4th power (r\u2074), and inversely proportional to catheter length. As such, a large-gauge, short IV catheter can profoundly improve the potential flow rate over a smaller gauge, longer catheter. Typical locations for peripheral IV access include the antecubital fossa, veins in the forearm and dorsum of the hand and foot, external jugular vein, and scalp veins.",
        "Peripheral IV access - Technique": "1. Preparation When the decision to pursue vascular access is made, the preparation for the procedure is just as imperative as the skill itself. Temptations for speed in the prehospital setting, assumptions regarding the patient\u2019s health, or other neglectful behavior deviating from the practice of universal precautions can result in occupational exposure. When possible, wash hands prior to putting on gloves. Prepare the equipment. You will need an IV start kit (if available) or you can assemble your own (tourniquet, alcohol wipe or other cleaner, tape or a commercially available adhesive device). Select an IV needle with catheter, saline lock, saline flush, and/or IV fluids. Check the IV catheter for integrity. Prepare the patient for the procedure. When appropriate, discuss with the patient the reason for the procedure along with risks and benefits. Unless a true emergency exists or the patient is not able to make his/her own decisions, verbal consent should be obtained. 2. Site selection Position the patient\u2019s extremity to help straighten the desired vein. Apply the tourniquet proximal to the targeted area. When possible, look distally first to allow additional proximal attempts on the same extremity, if necessary. Once the tourniquet is applied, you can have the patient pump his/her fist open and closed several times to help the vasculature become engorged. Feel for a soft, spongy, non-pulsatile vessel. 3. Clean the site Use an alcohol pad, betadine, chlorhexadine, or a similar antiseptic product to clean the proposed IV site. Allow the area to dry. 4. Insertion of the IV Hold the skin taut with one hand while inserting the needle with your dominant hand. Approach the vessel as shallow as possible (less than 30\u00b0 angle to the skin) with the bevel of the needle facing up or away from the patient. Once you feel a \u201cpop\u201d and/or see a flash of blood in the reservoir of the IV needle, advance the needle slightly further and slowly slide the catheter over the needle, cannulating the vessel with the plastic catheter while not moving the needle itself. 5. Removing the needle Hold firm pressure over the tip of the cannulated plastic catheter while you withdraw the needle from the hub of the catheter. If applicable, push the button to retract the needle to its safe position and move the needle to a safe area. The needle needs to be disposed of in a sharps container as soon as the IV is secured. 6. Securing the IV Attach the saline lock and flush the lock with saline or attach IV fluid tubing directly to the hub of the catheter. Secure the catheter hub with tape or a commercial securing device. Check for signs of infiltration (i.e. localized swelling, inability to flush catheter, pain). External jugular vein access has a similar technique. The needle is inserted in a caudad direction, but no tourniquet is used. Instead, the index finger of the non-dominant hand can be used to apply gentle pressure to the external jugular vein just above the clavicle to facilitate venous engorgement. Care should be taken to avoid placing a needle puncture too low in the neck (i.e. at or immediately above the clavicle) to avoid lung injury. Blind attempts when the external jugular vein is not readily apparent are not advised due to potential for serious injury to surrounding structures. Contraindications to intravenous access relate mainly to site selection. Sites with burns, cellulitis, trauma, and other conditions that compromise the integrity of the overlying skin should be avoided. Extremities on the side of a recent mastectomy or lymphatic chain removal, those that contain known thromboses, and those that contain permanent modifications for dialysis access should be used only when all other options have been exhausted. Special consideration must be given to patients with known bleeding disorders and those who are taking medications that may alter coagulation, as ensuring ease of compressibility becomes an important factor to limit excessive bleeding from cannulation attempts. Maintenance of vascular access in the prehospital setting may often prove difficult as perspiration, mud, dirt, and water reduce the effectiveness of tape and adhesive dressings used to secure the catheter. Combative or confused patients can also intentionally or unintentionally dislodge their IV access during transport and may require additional verbal instruction and reminders along with extra padding/support to maintain the line. Gauze wraps, elastic bandages, and arm boards are just a few examples of adjuncts used to protect and optimally position venous access.",
        "Intraosseous access": "Intraosseous devices function to access the intramedullary vessels found in the bone marrow of spongy bone that lead to the central circulation of the body. The IO needle, embedded in the bony structure, is protected by the non-collapsible periosteum, solving any problems with patency that may be encountered with IVs during vasoconstriction and low-flow states found in sepsis and cardiac arrest. Intraosseous access is currently attainable with manual, impact-driven, and powered drill methods. The gauge and length of some of the commercially available products will vary for the adult and pediatric patient. The commonly available EZ-IO\u2122 uses a 15mm long needle for children under 39kg while 25 mm and 45 mm lengths are available for patients 40kg or greater; all are 15 gauge. The sites of insertion vary by manufacturer recommendations but locations may include the proximal tibia, distal tibia, proximal humerus, and sternum. Contraindications to IO access are generally site specific and include infection of the overlying skin, fracture at or above the IO site, vascular compromise, and previous surgery or significant deformity of the bone. Previous sternotomy, suspected sternal fracture, and CPR with chest compressions exclude use of sternal IO access. Potential complications include osteomyelitis, fat emboli, fracture, growth plate injury, compartment syndrome, infection, and extravasation resulting in local tissue injury and swelling. Drinker and Lund in the 1920s were the first to use IO vascular access in the sternum of animal models, demonstrating that the fluid given did indeed reach intravascular circulation. Josefson followed in 1934, reporting the first IO use in humans. Soon after, in the 1940s, the first use of the IO was documented in the pediatric population. While its use with military personnel during World War II was advocated when IV access was delayed or difficult, the development of the over-the-needle PVC IV catheter by Massa in the 1950s temporarily curtailed use of the IO. The reemergence of the IO in the 1980s in the Pediatric Advanced Life Support and Advanced Pediatric Life Support courses supported its use after failed IV attempts. More recent guidelines from the American Heart Association advocate for the use of IOs as first-line access in pediatric emergencies and as first alternative in adult cardiac arrest, including in out-of-hospital settings. Several recent studies have shown the success of obtaining vascular access through IOs after failed or difficult attempts at IV access. IO vascular access has demonstrated high first-attempt success rates and overall success rates of 90% and greater in adults and children. The advantages of the commercially available battery-powered driver used in the study included its short learning curve, ability to easily penetrate thick cortical bone given its power source, and rapid drug delivery into the systemic circulation. IO access has been proven to be as quick and effective as IV access. In patients with inaccessible peripheral veins, IO access is faster and more successful than central IV lines. Most medications given through the peripheral IV can be given through an IO, with bioequivalence proven between the two routes. IO has been shown to have clinically comparable times to peak drug concentration compared to central IV access. Wilderness, tactical, disaster, and other specialty EMS groups may encounter situations requiring early consideration of the use of the IO for vascular access. Austere conditions, limited access to an entrapped patient, or cumbersome gear and clothing of both patient and provider can obstruct efforts to initiate peripheral IV access. One study showed significantly shorter times to IO access compared to IV access in providers wearing chemical, biological, radiological, and nuclear (CBRN) protective equipment. IO access is recommended during any resuscitation when IV access is not readily attainable.",
        "Technique (IO)": "1. Preparation Wash hands, don the appropriate personal protective equipment (PPE), and prepare the equipment. 2. Identify the landmarks and site \u2022 Humeral head \u2013 keep the arm adducted with the palm pronated. Palpate the proximal humerus and locate the greater tuberosity, which will be the site of insertion. \u2022 Proximal tibia \u2013 identify the tibial tuberosity. The site of insertion should be two finger breadths below and just medial to this landmark. \u2022 Distal tibia \u2013 abduct and externally rotate the hip. Palpate the flat portion of bone just proximal to the medial malleolus. 3. Clean the site Cleanse the targeted area with alcohol prep, betadine, chlorhexadine, or other antiseptic. Allow the site to dry. 4. Insert the IO Insert the IO needle into the skin overlying the desired location until bone is reached. Insert the needle through the cortex into the marrow either manually or per device-specific instructions. The needle should be relatively stable and freestanding in the bone if inserted appropriately. 5. Assess IO patency Remove the trocar and dispose of it in a sharps container. Attach a syringe or IO-specific tubing and assess for patency of the IO. Monitor the extremity for extravasation. Attach IV fluids if indicated; use a pressure bag or manually push fluids via syringe to achieve desired infusion rates. 6. Secure the IO Stabilize the IO in place with gauze and tape or a commercially available device. In a non-urgent setting, lidocaine or other anesthetic drugs may be injected into the area of the proposed IO and infused with the fluids to reduce pain and discomfort.",
        "Central intravenous access": "Prehospital central venous access is a procedure sometimes performed by advanced-level paramedics, nurses, and EMS physicians. Usually in the form of a large 8.5 French single-lumen catheter, the route provides rapid access to the central venous circulation and a route for rapid fluid resuscitation. Central venous access may be the preferable option when attempts at peripheral and IO lines have failed and/or are contraindicated, but its use in the prehospital arena is sparsely reported. Central venous line placement by air medical transport teams has been reported. Similarly, one report documented the performance of 115 prehospital central lines placed by field response EMS physicians over a 3-year period. Critical care teams are often responsible for maintenance of these lines during interfacility transport, so familiarity with this form of vascular access is important. The internal jugular (IJ), subclavian, and femoral veins are options for central venous access. Traumatic injuries above the diaphragm often dictate a femoral location. Attempts at access in the IJ and subclavian veins have a risk of pneumothorax, which should be considered if the patient acutely decompensates during the procedure. Placement of a central line, especially in the upper body, often causes an interruption of CPR efforts. Risks of bleeding from venous or inadvertent arterial puncture, infection, thrombosis, and nerve damage also exist. The prehospital environment makes it nearly impossible to preserve sterile technique. Given that these lines are performed as \u201ccode\u201d lines under emergency, semi-sterile (similar to a peripheral IV line) conditions, it should be expected that the line would be removed and another one placed if the patient survives to the ED.",
        "Special considerations - Accessing dialysis catheters and indwelling catheters": "In the prehospital setting, dialysis catheters, infusion ports, and other long-term artificial structures should not be considered as first-line options for gaining vascular access. The health of these difficult access patients often depends on frequent IV access and medication administration; improper utilization of these routes may result in serious consequences. Alternative forms of vascular access or medication routes should be considered. In the case that the EMS provider must access these types of catheters, special attention must be paid to sterile technique and the specific proper method for accessing each individualized access point. System medical directors may provide training and protocols for specific patient populations that may include accessing such devices earlier in the treatment algorithm.",
        "Pediatric considerations": "The pain and anxiety in the pediatric patient associated with vascular access is often a difficult matter to address in the prehospital setting. The need for rapid vascular access in a critically ill child along with varying transport times does not typically allow for some of the pharmacological options for relieving the pain of IV insertion that are available in the ED and hospital setting. Various commercially available creams, gels, and patches often require from several minutes up to an hour of application time for effectiveness. Local infiltration of lidocaine with either a small-gauge needle or needle-free system such as the J-Tip provides quicker anesthetic delivery but requires a second, often psychologically traumatizing needle puncture or startling noise due to pressurized CO\u2082. Often, if the child is stable enough to consider the use of these pain-reducing interventions, vascular access can be deferred until arrival to the hospital. Medical oversight and training for pediatric patient care should focus on helping the EMS provider distinguish the stable transport from the critically ill patient who would benefit from early vascular access. Additionally, attempts at IV access in young children are infrequent and often difficult. Training may be needed to improve technical skills and confidence to increase success.",
        "The future: ultrasound-guided IV access": "In ED care, ultrasound technology has become a useful tool to improve the success of IV access. Previously, patients who could not be cannulated by more traditional methods were often subject to more invasive procedures such as cut-downs or central lines, posing an increased level of risk. The growing widespread availability of ultrasound technology augments the ability of providers to obtain IV access in a less invasive fashion. While detailed instruction is beyond the scope of this text, ultrasound techniques can be used in a static fashion to identify the location of a suitable vein when one cannot be seen or palpated. The vein is then accessed by the usual techniques. Alternatively, a dynamic approach is often used, wherein the provider uses ultrasound to visualize the needle tip and subsequently the catheter entering the vein, confirming placement. The materials and methods are largely similar to standard peripheral access techniques, with the exception of the need for an ultrasound machine, gel, and longer length catheters for accessing deeper veins. Multiple studies have been performed analyzing the efficacy, speed, patency, and complications of ultrasound IV access. Across several inpatient and ED environments, ultrasound-guided peripheral access shows trends towards being a comparable or preferable modality with regard to risk of failure, number of attempts, and procedure time. There is clear demonstration of reduction of central line use when ultrasound is available to facilitate peripheral IV placement. Success of ultrasound peripheral IV attempts was non-inferior to the external jugular approach in those who failed traditional attempts. With regard to prehospital use of this technology, there are limited data and several barriers to implementation. Ultrasound machines remain expensive, and despite advances in miniaturization, most devices require a non-trivial amount of physical space. Hand-held ultrasound devices have been produced in recent years and may allow for feasibility studies of EMS-initiated ultrasound-facilitated IV access. As other applications for ultrasound are studied and implemented for prehospital use, the ability to gain vascular access may be an added benefit of the technology, even if not purchased for that primary purpose. As several other modalities are equivalent to if not faster than ultrasound-guided peripheral IV placement, this technology may find a greater stronghold in systems permissive of longer on-scene times or for long-distance/critical care transport.",
        "Conclusion": "Vascular access is commonly pursued as part of prehospital emergency care. In some cases it is to facilitate administration of needed medications or resuscitative fluids. In other cases IVs are placed as a precaution in case such measures are eventually needed. Many IVs are not used prior to arrival at an ED. It is important for EMS clinicians to possess the necessary skills and equipment to initiate vascular access under myriad conditions. Further, this is an area that is appropriate for monitoring and evaluating from a quality improvement perspective, including both decision-making and technical skill domains."
    },
    {
        "Introduction": "In the United States, someone experiences a myocardial infarction every 26 seconds, and alarmingly the disease claims one life each minute. Acute myocardial infarction (AMI) accounts for almost five times as many deaths in the United States as are attributed to unintentional injuries, which has major implications for EMS systems. About half of those who suffer acute myocardial infarctions are transported to the hospital by EMS, and many more patients call EMS for help because they are experiencing chest pain. The prehospital management of chest pain has improved with better clinical examination, earlier administration of effective medications, and the broad use of 12-lead ECGs to detect acute coronary syndromes (ACS) and myocardial infarction more accurately before arrival in the emergency department (ED). Because more rapid reperfusion during acute myocardial infarction improves heart function and patient survival, EMS and health care systems have focused on developing strategies to identify chest pain patients with myocardial infarction quickly and to provide effective treatment while transporting them directly to definitive care. The goals of management for patients with chest pain include rapid identification of patients with ACS, relief of their symptoms, and transport to an appropriate hospital. This chapter will cover the assessment and treatment of patients with a chief complaint of chest pain and will focus on the scientific basis for prehospital medical care of those patients. It will also review common conditions that can cause chest pain.",
        "General approach": "When evaluating a patient with a complaint of chest pain, EMS professionals should begin by assessing the patient's stability and then obtain a basic clinical history and examination. Early in the assessment, an EMS provider should apply a cardiac monitor to rapidly identify dysrhythmias, perform a diagnostic 12-lead ECG, and administer specific treatment depending on the results of the initial evaluation. Because only a small minority of the patients with chest pain actually have ACS, maintaining vigilance in this assessment and diagnostic routine can be difficult. Complete accuracy in the diagnosis of chest pain is not always possible in any setting, not even in the hospital. The prehospital provider should not expect to diagnose a patient with a complaint of chest pain definitively. A careful history can lead the provider to a correct \u201ccategory\u201d of diagnosis much of the time. As a general approach, the patient should be treated as if he or she has the most likely serious illness consistent with the signs and symptoms. Discomfort due to cardiac ischemia is usually, but not always, substernal and may radiate to the shoulder, either arm, both arms, upper abdomen, back, or jaw. Other symptoms such as nausea and diaphoresis are commonly present but do not predict the presence or absence of ACS accurately. Cardiac disease is most often seen beginning in middle-aged men and older women. However, even younger adults under the age of 40 with no cardiac risk factors and a normal ECG have a 1\u20132% risk of ACS. Taking a focused history using the \u201cPQRST method\u201d can be helpful. There are many causes of chest pain and their incidence changes depending on the characteristics of the population being studied. Patients calling on EMS are more likely to have acute myocardial infarction or other serious causes of chest pain than are patients in the general emergency department (ED) population. Although the majority of this chapter focuses on the management of an ACS, other causes of chest pain are present more commonly.",
        "Role of emergency medical dispatch": "Prehospital care of the patient with a complaint of chest pain begins at emergency medical dispatch. Identification of patients suspected to have ACS allows an EMS system to send advanced-level providers to the patient. Many EMS systems with both basic and advanced-level ambulances use a trained emergency medical call taker who asks the caller a series of questions to determine the nature of the emergency and the likelihood that advanced-level care will be needed. A retrospective cohort study from England took a rigorous approach to determining the accuracy of one set of dispatcher questions in identifying patients with ACS. About 8% of calls at the \u201c9-9-9\u201d center were classified as \u201cchest pain.\u201d Subsequent chart review at the hospital identified all patients with the ultimate diagnosis of ACS and found that this represented only 0.6% of all 9-9-9 patients. About 80% of the ACS patients were classified correctly as chest pain at the dispatch level. Another 7% were classified in a variety of other categories that still received a paramedic level response (e.g. severe respiratory distress). Sensitivity of the dispatch system for detecting ACS was 71% and specificity was 93%. However, a great deal of overtriage occurred, and the positive predictive value of the dispatch system for detecting ACS was only 6%. Additional refinement of the dispatch question sequence to reduce overtriage seems possible. The emergency dispatch question sequence for stroke performs much better, with a positive predictive value of 42% and a similar sensitivity to ACS at 83%. The American Heart Association (AHA) and American College of Cardiology (ACC) recommend that emergency medical dispatchers prompt patients with non-traumatic chest pain to take aspirin if they have no contraindications while awaiting EMS arrival. This recommendation is based on extrapolation from data showing that patients who take aspirin before hospital arrival are less likely to die and that the practice is likely quite safe.",
        "The 12-lead electrocardiogram": "The 12-lead ECG remains the quickest method of detecting myocardial ischemia or infarction. Although ECGs have been used to diagnose ACS since 1932, the technology has now advanced to the point that a prehospital ECG can be done quickly and accurately and can be sent wirelessly to the receiving hospital at a relatively low cost. Additional benefit can be gained by having the prehospital ECG become the first of a series of ECGs, increasing the sensitivity of diagnosis of coronary syndromes. Performing a prehospital ECG on a patient exhibiting signs and symptoms of ACS is a Class I AHA/ACC recommendation. This recommendation is based on evidence demonstrating that, despite at most slightly increased time spent on scene for patients receiving ECGs, the time to definitive treatment for ST-elevation myocardial infarction (STEMI) with fibrinolysis or percutaneous coronary intervention (PCI) is shortened overall, with a significant reduction in mortality.",
        "Prehospital electrocardiogram: interpretation": "With the ease of obtaining a prehospital 12-lead ECG comes the need for its accurate interpretation. Precise interpretations can influence decisions to transport patients to more appropriate but more distant facilities, as well as immediate management strategies on hospital arrival. A 12-lead ECG is required to diagnose STEMI and can often provide evidence that ACS is present. Currently three methods of out-of-hospital ECG interpretation exist: computer algorithms integrated into the ECG machine, direct interpretation by paramedics, or wireless transmission of the ECG to a physician for interpretation. One, two, or all three can be used in a given EMS system. All prehospital 12-lead ECG machines contain computer programs that will interpret the ECG, and the machines can be configured to print the interpretation on the ECG. If this technology is sufficiently sensitive and specific for STEMI, the EMS professionals would theoretically not require education in interpretation, which would allow EMS systems to use advanced- and basic-level providers to acquire 12-lead ECGs. Additional benefits of using the computer\u2019s interpretation include avoidance of the technical issues and cost of establishing base stations dedicated to receiving incoming ECGs, as well as the provision of consistent interpretation that does not depend on the variable skills and experience of EMS providers. Many prehospital 12-lead ECG systems use computerized interpretation systems which have high specificity, but the computer interpretation alone can miss up to 20% of true STEMI events. Despite the high specificity, many emergency physicians and cardiologists do not place enough trust in the computer interpretation alone to routinely activate the cardiac catheterization PCI team that can provide rapid reperfusion treatment for a STEMI patient. EMS provider interpretation is another option. More extensive training is required, and interpretation accuracy can be affected by both experience and interest in the subject matter. Although several studies have shown that trained paramedics can accurately interpret the presence of STEMI, experience also plays an important role. Having a paramedic identify and report \u201ctombstones\u201d on the 12-lead is a powerful motivator for action by experienced physicians.\n\n The third method of interpretation is by transmission of the acquired ECG to a base station for interpretation by a physician. This method has generally been used as the gold standard when comparing other methods of interpretation, and its accuracy has been shown to be slightly better than other methods. It relies both on the availability of the interpreting physician and on an infrastructure that allows reliable transmission of the ECG. In one observational cohort study, positive predictive value of prehospital 12-lead ECGs was improved by transmitting them to emergency physicians compared with interpretation solely by paramedics. In some cases automated systems have been developed that allow simultaneous transmission of the 12-lead ECG to the receiving ED and to an invasive cardiologist on call. These systems have the potential to decrease treatment times further because both the ED staff and the PCI team are activated early. The AHA guidelines state that the ECG may be transmitted for remote interpretation by a physician or screened for STEMI by properly trained paramedics, with or without the assistance of computer interpretation. Advance notification should be provided to the receiving hospital for patients identified as having STEMI. Implementation of 12-lead ECG diagnostic programs with concurrent medically directed quality assurance is recommended. No diagnostic test is perfect, and the 12-lead ECG is no exception. There are a number of conditions other than acute myocardial infarction that can cause ST-segment elevation, such as left bundle branch block and hyperkalemia. Some of the differences between STEMI and the mimics of acute ST-segment elevation are subtle and missed easily.",
        "Oxygen": "Despite its historical use, the evidence review leading up to the 2010 AHA guidelines did not find sufficient evidence to recommend the routine use of oxygen therapy in patients with uncomplicated AMI or ACS who have no signs of hypoxemia or heart failure. The guidelines do, however, recommend oxygen administration if the patient is dyspneic, or has an arterial oxyhemoglobin saturation <94%, signs of heart failure, or shock.",
        "Medications": "Several medications are important for EMS management of the patient with chest pain. Providing the chest pain patient with medication for relief of pain whenever safe and feasible and regardless of the etiology of the pain is fundamental. Treatment of pain reduces anxiety in addition to relieving the patient's discomfort. For ACS patients, treatment of pain can reduce catecholamine levels and thus improve the balance between oxygen demand and supply for ischemic cardiac muscle.",
        "Aspirin": "Aspirin is inexpensive, readily available, and has been shown to benefit patients having myocardial infarction or other ACS. The ISIS-2 study established that the absolute benefit of aspirin administration for myocardial infarction patients results in 26 fewer deaths per 1,000 patients treated, with the maximum benefit occurring in the first 4 hours. Prehospital administration of aspirin is safe and may improve outcome, and should be given as soon as possible to patients with suspected ACS unless contraindicated. Varying doses of aspirin have been proposed, but for ACS the most widely used dose is four 81 mg baby aspirin tablets. These tablets are well tolerated, easy to swallow, and more rapidly absorbed than other preparations. Rectal preparations (300 mg) should be considered in patients unable to swallow. Acceptable contraindications to aspirin administration include definitive aspirin allergy or a history of active gastrointestinal bleeding.",
        "Nitroglycerin": "Nitroglycerin is a time-honored treatment to relieve chest pain due to angina by decreasing myocardial oxygen demand and increasing collateral blood flow to ischemic areas of the heart. Somewhat surprisingly, nitroglycerin is not effective at reducing STEMI patient mortality, nor is the response, or lack thereof, to nitroglycerin administration an accurate diagnostic test to determine whether cardiac ischemia is the underlying cause of a patient's chest pain. For example, because it relaxes smooth muscle, nitroglycerin may also relieve pain in patients with esophageal spasm. Nitroglycerin can be administered as sublingual tablets or an oral spray. The usual dose of either method of delivery is 0.4 mg. Although up to three doses can be given at an interval of 5 minutes between doses, current AHA/ACC recommendations for self-administered patient use of nitroglycerin is for them to call EMS if chest pain is not improved 5 minutes after only a single dose of nitroglycerin to avoid a 15\u201320-minute delay before activating the EMS system among STEMI patients. Nitroglycerin should be avoided in several groups of patients with chest pain. Patients who have used phosphodiesterase inhibitors and then take nitrates can have profound, refractory hypotension. Nitrates generally should be avoided for 24 hours following sildenafil or vardenafil use, and for 48 hours following tadalafil use. Patients with right ventricular infarction are dependent on right ventricular filling pressure to maintain cardiac output and a normal systolic blood pressure. If the patient has a systolic blood pressure below 100 mmHg or a heart rate below 60 beats per minute, nitroglycerin should be avoided until a 12-lead ECG, including right-sided leads, documents the absence of a right ventricular infarction. Nitroglycerin should also be avoided in patients who already have systolic blood pressures <90 mmHg or heart rates <50 or >100 beats per minute.",
        "Morphine sulfate": "A large retrospective case series of hospitalized patients with non-ST segment elevation ACS found that patients who received morphine had a higher mortality than those who did not. It is unclear whether this was a causal effect or simply indicated that those who required morphine may have had more severe disease. The AHA/ACC treatment guidelines for patients with unstable angina or non-ST-elevation MI (NSTEMI) reduce the strength of recommendation for morphine from Class I to Class IIa for patients with NSTEMI. The 2013 AHA/ACC STEMI guidelines give morphine a Class I recommendation in STEMI patients because those patients are going to have reperfusion therapy. The recommended dose of morphine in the patient with chest pain is 2\u20134 mg intravenously with increments of 2\u20138 mg intravenously repeated at 5\u201315-minute intervals when pain is not adequately controlled with nitroglycerin.",
        "Beta-blockers": "Older guidelines recommended IV beta-blocker (typically metoprolol) administration early in the course of acute myocardial infarction because of data suggesting reduced rates of reinfarction and recurrent ischemia when patients received both fibrinolitics and IV beta-blockers. A large placebo-controlled randomized trial showed that the effect of beta-blockers in reducing arrhythmic events is equally offset by an increase in development of cardiogenic shock, and survival is similar regardless of early administration of intravenous beta-blockers. Current AHA/ACC recommendations for administration of intravenous beta-blockers in the setting of STEMI are limited to patients who are hypertensive or have ongoing ischemia with no contraindications to their use. On balance, the guidelines suggest that the need for prehospital administration of beta-blockers to patients with STEMI is limited.",
        "Prehospital fibrinolysis": "Since fibrinolitics were introduced to emergency cardiac care in the mid-1980s, some have proposed initiating these drugs in the prehospital setting. Several studies published in the early 1990s showed that the strategy was feasible and that it could decrease mortality from STEMI in settings that had relatively long EMS response and/or transport time intervals. Additional studies reinforced the original findings, and a metaanalysis of pooled results from six randomized trials enrolling more than 6,000 subjects concluded that prehospital initiation of fibrinolitics decreased all-cause mortality by shortening initiation of treatment by 58 minutes. Few systems in the United States have implemented prehospital fibrinolysis, although additional research has continued to show time savings over in-hospital treatment. In Europe, particularly where there are often physician-staffed ambulances, prehospital fibrinolysis is used more frequently. A primary reason why prehospital fibrinolysis is not used regularly in the United States has been a shift in favor of primary PCI for treatment of STEMI. In a prospective observational cohort study of 26,205 consecutive patients with STEMI in Sweden, representing about 95% of the population of STEMI patients in the country, those who were treated with primary PCI had lower 30-day mortality than those treated with fibrinolytics in the hospital (4.9% versus 11.4%). Primary PCI patients also had lower mortality than those treated with prehospital fibrinolitics (4.9% versus 7.6%). Several large clinical trials have examined the strategy of transferring patients to a PCI-capable institution from a local hospital compared with administration of fibrinolytics at the local hospital. A metaanalysis of six large studies involving 3,750 patients showed that timely transfer for primary PCI strategy is superior in reducing rates of reinfarction, stroke, and the combined end-point criteria of death, reinfarction, or stroke. For situations in which transfer directly to a center capable of primary PCI is not possible in a timely fashion, a strategy of prehospital or non-PCI hospital-based fibrinolysis is reasonable. The available science suggests that the drugs can be safely administered by full-time paramedics or EMS physicians in the field. The EMS system should have a medical director with experience in STEMI management and a well-organized quality assurance program.",
        "Systems of care for ST-elevation myocardial infarction": "The EMS system plays a key role in shortening the process of caring for patients with STEMI. Patients who are transported by EMS have shorter treatment intervals than those of patients who arrive at the hospital by other means. Patients can be encouraged to use EMS appropriately. A community intervention to shorten the time interval from symptom onset to ED arrival was shown to increase the proportion of ACS patients who used EMS for transport to the ED.",
        "Prehospital notification and field cardiac catheterization laboratory activation": "A key benefit of a prehospital 12-lead ECG is notification of the receiving facility of an impending STEMI patient's arrival. Shortening door-to-balloon time by 30 minutes reduces in-hospital mortality from STEMI by about 1%. Implementation of a prehospital 12-lead ECG program with prehospital notification shortened door-to-balloon times by about 60 minutes in San Diego. In an evaluation of a large patient registry, prehospital notification with ED activation of the catheterization team before patient arrival at the hospital shortened door-to-balloon time by about 15 minutes. Occasional false-positive activation of the PCI team is a necessary byproduct of an aggressive field approach to alerting hospitals about patients with suspected STEMI. One report suggests that up to 15\u201320% of team activations may not result in any intervention. The rate of false-positive activations depends on the pretest probability of finding a STEMI. If EMS providers perform 12-lead ECGs broadly (e.g., everyone over the age of 30 with any of the following characteristics: chest pain, shortness of breath, abdominal pain, diabetes, or cardiac history), such that the prevalence of actual STEMI is between 0.5% and 5%, then the positive predictive value of a \u201cSTEMI-positive\u201d prehospital 12-lead ECG may be around 50%. Such a system would result in more false-positive than true-positive activations of the PCI team. When patients have a reasonable likelihood of STEMI based on their clinical presentations and 12-lead ECG findings, prehospital cardiac catheterization PCI team activation has consistently been shown to shorten time to definitive treatment of STEMI patients considerably. For example, Nestler et al. showed that prehospital activation of the catheterization laboratory reduced the median door-to-balloon times from 59 to 32 minutes. Cone et al. found that field activation of the catheterization laboratory was associated with 37 and 35 minute shorter door-to-balloon times than ED activation for walk-in STEMI patients or STEMI patients arriving by EMS without field activation, respectively. In addition, field activation of the catheterization laboratory was associated with better compliance with 90-minute STEMI treatment benchmarks. Finally, Horvath et al. found similar reduction in the door-to-balloon times (44 versus 57 minutes) in EMS-transported STEMI patients who had prehospital activation of the cardiac catheterization laboratory compared to those who had the laboratory activated after ED arrival. In summary, field activation of the cardiac catheterization laboratory when a prehospital ECG shows evidence of STEMI is strongly supported by published data. EMS systems should work with their PCI-capable hospitals to establish cardiac catheterization laboratory prehospital STEMI activation protocols and quality improvement monitoring.",
        "Destination protocols": "Almost 80% of the adult population of the United States lives within 60 driving minutes of a PCI-capable center. Of those patients whose closest hospital is not capable of PCI, 74% require additional transport time less than 30 minutes to reach a PCI-capable institution. Therefore, several urban communities have developed protocols to encourage EMS to transport STEMI patients directly to hospitals with 24/7 capability to perform PCI. In Ottawa, a STEMI bypass protocol for EMS was implemented in May 2005. Paramedics performed a 12-lead ECG, and if STEMI was identified in a hemodynamically stable patient, the patient was transported directly to the region\u2019s single cardiac center catheterization lab with prehospital notification of the impending arrival of the STEMI patient, often bypassing one of the four other EDs in the city. The median first door-to-balloon time was 69 minutes for patients brought to the catheterization lab directly by EMS, compared with 123 minutes for those needing interhospital transfer. In The Netherlands, prehospital identification of patients with STEMI and transport to a PCI-capable center bypassing other EDs was associated with improved left ventricular function. Some systems are directing EMS to take STEMI patients directly to the heart catheterization lab, bypassing the ED. The strategy reduces door-to-balloon time up to 60 minutes. In more rural settings without available PCI centers, coordinated programs with regional STEMI receiving centers can achieve remarkable door-to-balloon times, even when measuring from the first door (i.e., the door of the rural ED). Two reports from Minnesota show that excellent treatment times can be achieved. In the Minneapolis area, the median first door-to-balloon time was 95 minutes if the referring hospital was less than 60 miles from the PCI center and 120 minutes if the referring hospital was further away. In the Mayo Clinic STEMI system, patients were transferred from 28 regional hospitals up to 150 miles away from the PCI center. The median first door-to-balloon time for the transferred patients was 116 minutes.",
        "Air medical evacuation of ST-elevation myocardial infarction patients": "A key to a successful regional STEMI system is ready access to air medical transport. Rapid transport of the patient by highly skilled teams in medical helicopters can save significant time from the first door to balloon. Some air medical programs are working closely with referring hospitals and ground EMS systems to dispatch helicopters before arrival of a STEMI patient at a referring hospital.",
        "Expanding the role of Basic Life Support providers": "Many prearrival 9-1-1 instructions already direct callers to take aspirin if they have chest pain. Allowing BLS providers to administer aspirin, if not contraindicated, and if permitted by EMS laws and regulations, seems the next logical step. One reason stated for the lack of aspirin administration to eligible ACS patients is the inability of BLS providers to administer it based on local protocols or regulations. Basic Life Support providers can be taught to acquire and transmit 12-lead ECGs. This approach may be particularly beneficial in rural areas, with scant ALS coverage and long transport times to definitive care. Using the 12-lead ECG to triage STEMI patients to air transport from the scene may lead to improved cardiac care in rural areas and more efficient use of available resources.",
        "Other common causes of chest discomfort": "Although most of the available prehospital interventions for chest pain are focused on the identification and treatment of ischemic cardiac disease, the majority of EMS chest pain patients will have other causes for their symptoms, some of which are also immediate threats to life. A chest pain protocol should focus on treatments that may benefit the ACS/STEMI patient while considering the effects of these treatments on other causes of chest pain.",
        "Aortic dissection": "Acute aortic dissection classically causes sudden pain in the chest, sometimes radiating to the back. The dissection is caused by a tear in the intimal lining of the aorta with entry of high-pressure blood into the wall of the aorta. The dissection propagates distally and sometimes also proximally. If the dissection extends around the origin of a peripheral artery, then that vessel can be partially or completely occluded, creating a >15\u201320 mmHg difference in blood pressures between both patient arms. If the origin of a carotid or vertebral artery is occluded, then the patient may develop neurological signs suggesting a stroke. Occlusion of a spinal artery off the aorta can cause acute paralysis of both legs. Most patients with dissection have long-standing hypertension, but the problem can occur in younger patients with other conditions such as Marfan syndrome. In the majority of cases of aortic dissection, the 12-lead ECG will be abnormal, but will not show ST-segment elevation unless the origin of a coronary artery is occluded by the dissection. Without imaging capability that exists in the hospital, EMS providers may suspect, but cannot identify, aortic dissection definitively. If aortic dissection is suspected, morphine can be used for pain control but aspirin should be avoided since patients with acute aortic syndrome who receive antithrombotic agents such as aspirin or fibrinolytics are more likely to bleed.",
        "Pericarditis": "Individuals with pericarditis may present to EMS with ST-segment elevation on an ECG that looks similar to an extensive myocardial infarction. Administration of fibrinolytics in this condition may be fatal because these patients can bleed into the pericardial sac, resulting in pericardial tamponade. Aspirin administration is somewhat less concerning because antiinflammatory medications are part of the recommended treatment.",
        "Pneumothorax": "A pneumothorax may cause chest pain, shortness of breath, hypoxia, and diaphoresis. Clinical signs may point more to this diagnosis than to acute myocardial infarction. EMS systems should have a separate protocol for management of a pneumothorax. Oxygen and morphine may help the patient. Nitroglycerin should be avoided because it can cause hypotension by further decreasing venous return if the patient is developing a tension pneumothorax. If a developing tension pneumothorax is evident, needle decompression is required.",
        "Pulmonary embolism": "Pulmonary embolism is a great masquerader because its symptoms may be similar to those of other causes of chest pain and shortness of breath. Its presentation can easily be confused with myocardial infarction or anxiety. Treatment should focus on maximizing oxygenation to the patient. If pulmonary embolism is suspected, nitroglycerin should be avoided because it can cause significant hypotension. Administration of fibrinolytics may potentially benefit the patient, but it is preferable to delay administration until the patient has reached a hospital and undergone a definitive diagnostic imaging study.",
        "Esophageal perforation": "A patient with a perforated esophagus may present with chest pain. A careful and focused history and examination will often help differentiate this condition from other causes of chest pain. Nitroglycerin should be avoided because it may cause significant hypotension, and fibrinolytics are contraindicated because of the need for immediate surgery.",
        "Conclusion": "Quality prehospital care of patients with chest pain can relieve discomfort and improve outcome. EMS systems should have the capability to perform prehospital 12-lead ECGs and regional protocols should focus on delivering patients with STEMI to PCI centers promptly. Prehospital activation of the cardiac catheterization laboratory is highly effective at shortening the time to definitive reperfusion treatment and should be encouraged."
    },
    {
        "Introduction": "Each year, EMS professionals assess about 360,000 patients who are in cardiac arrest. Resuscitation is attempted for about 60% of those assessed. Over the past decade, the median survival rate to hospital discharge for all patients with attempted resuscitation has slowly risen from about 5% to about 10%, with individual systems reporting rates between 3% and 16%. Despite significant efforts devoted to improving survival from out-of-hospital cardiac arrest (OHCA) since 2000, a large gap remains between research on the disease and its effect on public health. This chapter will review some of the issues that investigators should consider when developing OHCA clinical research.",
        "Exclusion criteria": "There is wide variation in the reported incidence of EMS-treated cardiac arrest, ranging from 48 to 70 cases per 100,000 population per year. This difference has been primarily attributed to variations in case ascertainment but real differences in incidence rates likely exist among communities, such as variations in prevalence of heart disease among populations and a general decline in the incidence of ventricular fibrillation (VF) outside the hospital. Those patients obviously dead at the scene should ideally be tracked even though they have no chance of successful resuscitation, in order to verify case ascertainment approaches. These include patients with rigor mortis, decapitation, or dependent lividity on the arrival of EMS responders. However, these cases are not included in the denominator of survival statistical analyses.\n\nWhen the Utstein style was proposed, only arrests of cardiac etiology were included to maximize comparability between studies. Determination of cardiac etiology is often accomplished retrospectively through history obtained from family members, secondary survey physical examination, hospital chart review, autopsy reports, and EMS run records. Accurate determination of cardiac etiology is unlikely in some cases with only EMS records. As a result, the Resuscitation Outcomes Consortium has chosen to track all cases without obvious trauma regardless of etiology.\n\nWith the declining incidence of VF, the proportion of OHCAs that are of non-cardiac etiology appears to be increasing. That may be sufficient reason to pay more attention to the care of these complex patients. Some researchers point out that a patient who has a pulse following a shock by an automated external defibrillator (AED) used by a member of the public prior to EMS arrival and who does not receive any EMS CPR does not directly benefit from EMS cardiac arrest care; but most investigators include those patients.\n\nPatients with advance directives indicating their desires to avoid any resuscitative efforts should also be excluded from research studies. Often these patients may initially receive treatment only to have resuscitation preemptively terminated once EMS learns about the advanced directive.\n\nThe pediatric population presents additional challenges for OHCA investigator. The incidence of cardiac arrest in this population is low; data suggest that fewer than 1,000 children experience out-of-hospital VF events per year in the entire United States. Additional ethical and consent issues are raised when dealing with children younger than age 18, and accurate determination of age is not always possible during sudden cardiac arrest. The latest edition of the Utstein reporting guidelines includes a section on pediatric cardiac arrest.",
        "Consistent definitions": "Since its introduction in 1991, the Utstein style has become the gold standard for reporting data from OHCA. This system of uniform terms and definitions for resuscitation reporting, last updated in 2014, allows useful comparison of outcomes among systems of out-of-hospital care across a plethora of countries. Aspects of the Utstein style are controversial. For example, there is wide variation in classification of the etiology of cases. When hospital and autopsy information is available, investigators will discover that many patients have a diverse set of causes in addition to heart disease compared to a determination based only on the EMS records.\n\nA challenge is differentiation of cardiac arrest from simple syncope. Cardiac arrest is the sudden onset of lack of blood circulation leading to unresponsiveness. Although patients are commonly apneic on EMS arrival, an agonal respiratory pattern is often present early in the evolution of an arrest. A cardiac arrest event persists longer than several seconds and generally does not resolve spontaneously. Cases lasting only a few seconds most likely represent syncopal episodes rather than true cardiac arrest. Although rarely the patient is revived with only a brief period of cardiopulmonary resuscitation (CPR), therapy in addition to chest compressions and ventilation is typically needed to restore spontaneous circulation. From a practical point of view, the simplest approach is to include cases in which EMS provided chest compressions or a shock with a defibrillator.",
        "Population description": "The reader\u2019s ability to compare results across different studies relies upon an accurate description of the patients included in the study, such as their age, sex, geographic locale, and EMS response. Factors such as previous cardiac disease, other comorbidities, tobacco use, and family history may also be useful, although they may be more difficult to obtain. A standard approach to describing patients who were included and excluded can often be achieved by using the Consolidated Standards of Reporting Trials (CONSORT) patient flow diagram.\n\nA description of the location (e.g. home or EMS vehicle) and witness status of the arrest should be included. The description of the EMS system in which the study was conducted and the associated population density (rural, suburban, or urban) are relevant because these characteristics may affect the results of the study and will assist the reader with determining its generalizability. For example, a study of a device for supporting circulation likely will be doomed to failure if the trained responders cannot be at the patient\u2019s side until 25 minutes after the patient\u2019s collapse. Ideally, the number of potential first responders and paramedics should be reported so that the frequency of exposure of individual EMS professionals to cardiac arrest events can be estimated.",
        "Data collection and reporting": "Established in 1991 as the metaphor for describing emergency cardiovascular care, the \u201cchain of survival\u201d may assist the researcher in arriving at clinically relevant conclusions. In 2010, a fifth link was added to the chain: immediate recognition and activation of help, early CPR, rapid defibrillation, effective advanced life support, and integrated postarrest care. Many well-conducted clinical OHCA studies concentrate on one specific link in the chain in order to test the effectiveness of a particular intervention. Other investigators choose to test a \u201cbundle\u201d of interventions, affecting several links in the chain, that show promise of acting together to improve outcomes.\n\nOne of the primary challenges to implementing cardiac arrest research is the fact that the disease is exquisitely time-sensitive and time data are generated from multiple different sources. For example, the emergency medical dispatch center clock often displays a time that is different from the time on the responder\u2019s watch or on the defibrillator used in the resuscitation. Time synchronization of devices and clocks used in the EMS system allows for accuracy in the recording and reporting of relevant events. Most defibrillators currently available will synchronize their clocks automatically when ECG waveform data are downloaded from the defibrillator to a computer.\n\nAll results should be reported in terms of intervals (i.e. the difference between event times) in order to ameliorate any ambiguity regarding terminology. For example, the call receipt-to-first-shock interval represents the difference between the time the 9-1-1 call was received and the time the first defibrillation was attempted. Time points such as call receipt, EMS dispatch, defibrillator application, and shock delivery are reliably recorded electronically. Ideally, time intervals should be reported in minutes and seconds.\n\nDefibrillators can be purchased with voice recording capability, and use of voice recording significantly enhances decoding of the events during a resuscitation attempt. If voice recording is available throughout the resuscitation process, times for arrival at the scene, EMS administration of CPR, return of spontaneous circulation (ROSC), invasive procedures and medication delivery, scene departure, and emergency department arrival may all be reliably extracted.\n\nBystander accounts of collapse time and administration of CPR are important data points. Unfortunately, these reports are unlikely to be synchronized or accurately recorded. Reliable information may be obtained through witness interview via the telephone after the event is over.\n\nElectronic capture of cardiac rhythm information is relatively easy. When captured electronically, ECG information is available for in-depth digital signal analysis. Ideally, the presenting rhythm should be ascertained through blinded review of rhythm strips. Specific methods for adjudicating differences in opinion should be explicitly outlined. For example, 1 mm of amplitude deflection is commonly used as the cut-off for fine VF versus asystole.\n\nElectronic data capture also allows assessment of the quality of chest compressions and ventilations provided to the patient. Given the important effect that chest compression quality has on patient outcomes, a research design that does not collect this information is substandard. Measuring and improving chest compression quality may make the difference between a positive and negative trial because medications given but not circulated will not be effective.",
        "Outcome assessment": "Relevant outcome measures in the study of OHCA include survival, ROSC, neurological status, and quality of life. For example, the researcher may be interested in different outcomes when judging defibrillator performance as opposed to testing prehospital administration of therapeutic hypothermia.\n\nSurvival is one key endpoint in most cardiac arrest clinical studies. Alive at hospital discharge is the simplest survival data point to collect. Thirty-day, 6-month, and 1-year survival represent more rigorous endpoints because patients may be discharged to extended care facilities due to severe neurological impairment and then die within 30 days.\n\nThe use of ROSC is controversial as a patient-centered outcome. Spontaneous circulation is obviously necessary to achieve survival, but it is a less interesting outcome from the point of view of the patient compared to neurologically normal long-term survival. Nonetheless, it represents an important first step. If an intervention cannot improve ROSC, it is unlikely to improve 30-day survival. Clinically significant short-term survival may be defined as survival to 4 hours after the initial call for help.\n\nWhen evaluating outcomes, the researcher must be aware of the potential effect of the intervention being tested. For example, what constitutes \u201csuccessful\u201d defibrillation? In the truest sense of the term, defibrillation means termination of VF, whether that results in asystole or more organized electrical activity. Survival may not be an appropriate endpoint when testing a defibrillator because multiple factors in addition to defibrillator function may affect a patient\u2019s survival.\n\nAn important adjunct to survival as an endpoint is the neurological status of the patient, both short and long term. The clinical neurological examination including objective, functional, and cognitive assessments provides a useful tool for neurological evaluation. The Cerebral Performance Category is a simple standardized tool for the assessment of both cerebral and overall neurological performance. This assessment can often be made via simple chart review. However, it lacks precision. More objective scales such as the modified Rankin Scale are more sensitive but require contact with the patient.\n\nQuality-of-life evaluation is an excellent patient-centered outcome. Separating health-related issues from overall quality of life may be challenging because many confounders such as economic factors or interpersonal relationships may affect these assessments. While there have been studies assessing the quality of life among survivors of OHCA, much remains to be learned.",
        "Outcome sources": "Sources of outcome information are as widely variable as the outcomes themselves. When planning to access medical records and other data sources, researchers must clarify requirements regarding consent with respective institutional review boards. Once permissions are obtained, the researcher may access information in medical records, death registries in local communities or states, online obituaries, or the Social Security Death Index. Searching multiple sources may help ascertain all outcomes. Researchers, with such approval, may contact patients, their families, or their primary physicians directly for outcome information.",
        "Quality control": "Quality control is essential in a clinical study. Regular audits should be performed to ensure that the data collected are accurate. Sponsors of studies evaluating new drugs, biologics, and devices are required to monitor these studies.\n\nData and safety monitoring boards (DSMBs) monitor clinical trials involving interventions that entail potential risk to the participants. The primary responsibilities of the DSMB are to periodically review and evaluate the accumulated study data for participant safety, study conduct and progress, and efficacy when appropriate, and to make recommendations concerning the continuation, modification, or termination of the trial. The DSMB members consider study-specific data as well as relevant background knowledge about the disease, test agent, or patient population under study. If at any point during the study, profound benefit or detriment to patients is discovered, the DSMB will make a determination about terminating the study and reporting the data.",
        "Conclusion": "OHCA researcher has the opportunity to have an important effect on the lives of thousands of patients. Following well-established study design principles helps ensure that meaningful results are obtained and that patient outcomes are ultimately improved."
    },
    {
        "Intraaortic balloon pump": "The intraaortic balloon pump (IABP) is a mechanical device used in the stabilization of an acutely ill cardiac diseased patient. The EMS physician or critical care transport team will most commonly encounter the device during a patient transfer from a facility with limited or unavailable cardiac surgery capabilities to a tertiary care center. The role of the IABP is to provide cardiac stabilization until definitive care can be obtained. Goals of IABP therapy include decreasing cardiac afterload, augmenting diastolic perfusion pressure, and increasing coronary artery perfusion. These efforts help to improve cardiac output that can in turn improve tissue perfusion. The decrease in afterload reduces the workload on the heart, and the improved coronary artery circulation can increase oxygen supply to the myocardium. Indications for IABPs most commonly encountered by EMS physicians are acute myocardial infarction, cardiogenic shock, ventricular aneurysm, left ventricular failure, valve or papillary muscle rupture, or a combination of these factors. The patient is most commonly found in a catheterization lab, operating room, or coronary intensive care unit. The IABP catheter is placed via an incision in the lower extremity, inserted in the femoral artery, and then advanced into the thoracic aorta. The balloon should be placed 1\u20132 cm distal to the beginning of the subclavian artery, and must be above the branches of the renal arteries. If the balloon is not placed correctly, occlusion of coronary, subclavian, or renal arteries could occur. On a chest x-ray, the tip of the catheter should be visible between the second and third intercostal spaces. When inflated, the balloon should not completely occlude the aortic lumen, as this can damage the aortic wall and blood components. Most devices have different sized balloons for patients based on weight or height. It is important to ensure the appropriate balloon volume is being used. Absolute contraindications for an IABP include aortic dissection, abdominal aortic aneurysm, and aortic valve incompetence. Relative contraindications include bleeding disorders and atherosclerosis. A patient with an IABP who requires interfacility transportation must be attended to by a specially trained team. In some cases, critical care paramedics, nurses, or physicians are trained to address IABP complications. Otherwise, it is vital that the transport team include a perfusionist or biomedical engineer. Intraaortic balloon pump function is critically dependent on timing. The balloon is cycled in conjunction with the cardiac cycle. It is important to remember that the balloon is inflated during diastole and deflated just prior to systole. While the balloon is inflated, blood is pushed both back toward the heart, as well as further down the aorta. The result is increased blood flow to coronary and carotid arteries, and increased systemic perfusion. The balloon is deflated very rapidly, and this rapid loss of volume reduces the pressure in the aorta. The result is that the left ventricle does not contract as hard as it would otherwise. Cardiac workload and myocardial oxygen demands are reduced. If the timing is not correct, these advantages are lost, and further harm to the patient may occur. The IABP can use several different triggers for the inflation and deflation cycle. The most common modalities use the ECG or the arterial pressure waveform as a trigger. The IABP may also have an internal trigger in the event of cardiac arrest. Using arterial pressure as a trigger requires the patient to have an arterial catheter placed and connected to the balloon pump. Some IABP devices may have specialized fiberoptic connectors to measure arterial pressures. It is important to note that once a fiberoptic connector is placed and zeroed, it cannot be removed and connected to a different transport IABP. Another trigger modality needs to be used, such as ECG. Most devices have an \u201cautomatic\u201d trigger mode, where the pump automatically switches between trigger modes if needed. An example would be a switch between ECG and arterial pressure modes if the ECG signal is lost. Most modern pumps can also compensate for arrhythmias such as atrial fibrillation and pacing modes. With the trigger mode established, attention should focus on timing. Most patients are transported with a 1:1 frequency, where each cardiac cycle is assisted. In order to assess timing, it may be helpful to place the device in a 1:2 frequency to get a better picture of the arterial pressure waveform landmarks. For transport, the operator should ensure that the balloon is set to inflate at the dicrotic notch, and to deflate during the next isovolumetric contraction (IVC) phase. The dicrotic notch phase on the arterial pressure waveform represents aortic valve closure and diastole. Once the timing is correct, the device can be placed back into a 1:1 frequency and put in the \u201cautomatic\u201d mode if available. Potential complications include limb ischemia, compartment syndrome, aortic dissection, bleeding, thrombocytopenia and red blood cell destruction, gas embolus, infection, and cardiac decompensation from incorrect timing. Special care must be taken when transferring a patient from one brand of IABP to another to enable transport. There may be a difference in the balloon size, and an adapter may be needed to connect a \u201cBrand D\u201d catheter to a \u201cBrand A\u201d IABP. The balloon size should be noted and adjusted on the pump if necessary. On arrival to a patient\u2019s side, the transport team should examine the patient paying particular attention to the insertion site, as well as to the distal extremity. The insertion site should be examined for bleeding or protruding balloon. The catheter tubing should be examined for any blood or blood flecks. The distal extremity should be examined for ischemia. Catheter tubing should be examined for kinking. Any positive findings noted above should delay the transport until the situation can be corrected. Fresh ECG leads should be applied to the patient. The referring hospital balloon pump should not be disconnected or shut off until the transport pump is connected and tested. The transport balloon pump should be plugged into an outlet during this time and not run on battery power. The pump should also be plugged into an aircraft or ambulance power inverter during transport. Pure battery operation should be used only to transport the patient from the vehicle to his or her hospital destination.",
        "Special circumstances": "In the event of cardiac arrest, the IABP will lose all trigger modes, give a \u201ctrigger arrest\u201d alarm, and then stop counterpulsation. If left unchanged, this could result in a thrombus formation. When cardiopulmonary resuscitation (CPR) is initiated, the IABP should be switched to \u201carterial trigger.\u201d Effective CPR should allow for the IABP to function off the arterial pressures. In the event that arterial pressures are not sufficient, the IABP should be switched to an \u201cinternal trigger.\u201d This last resort trigger provides asynchronous counterpulsation and will help prevent clot formation. \u201cInternal trigger\u201d mode should be stopped if there is a return of circulation and the ECG or arterial pressure mode is restarted. \n\nIn the event of IABP failure during transport, a large Luer-Lok syringe should be attached to the quick connector to aspirate the balloon for blood. If no blood is found, use air to inflate the balloon to the volume capacity of the balloon. Then quickly aspirate the air and deflate the balloon. Repeat 4\u20135 times every 5\u201310 minutes until the pump is repaired or replaced.",
        "Ventricular assist device": "Ventricular assist devices (VAD) are surgically implanted pumps that are intended to assist one or both ventricles of the heart to pump when disease has diminished the heart\u2019s native ability to do so. They are most often placed in patients with severe congestive heart failure. Devices include left ventricular assist devices (LVAD), right ventricular assist devices (RVAD), and biventricular assist devices (BIVAD). The most commonly placed device is the LVAD. The LVAD will have a cannula placed in the apex of the left ventricle with blood flow to the pump and a cannula placed into the ascending aorta with blood flow from the pump. Thus the device assists the ventricle in moving blood through the circulatory system. Ventricular assist devices were first developed in the 1960s and the technology progressed during the 1970s and 1980s. Advances made them more portable, but the patient was still confined to the hospital. In the 1990s fully portable devices were developed that, for the first time, allowed VAD patients to be discharged from the hospital. The devices are most commonly used as a bridge to cardiac transplantation, but they also may be used as a bridge to a reversible cardiac condition, or as a permanent therapy. There are two types of VAD patients: those with non-portable VADs, who would require critical care transport with a perfusionist, and those with portable VADs who may be living at home or in an assisted living facility. It is the second group of patients who are potentially encountered by EMS. Currently, there are four generations of VADs with features that can vary based on the generation and the particular device. First-generation devices mimic the pumping action of the left ventricle via the use of diaphragms or pusher plates that cause blood to be sucked into the left ventricle and expelled into the aorta. This mechanism results in pulsatile blood flow. The patient will have a pulse and blood pressure that can be measured. The pumps are powered by electricity and can be either electromechanical or pneumatic. Electromechanical pumps use an electromagnetic pusher plate to drive the blood, whereas pneumatic devices use air pressure to move the blood. Both devices require electrical power to function. Pneumatic devices may come with a hand pump in case of device failure. Second-generation LVADs have continuous-flow rotary pumps. If the device only assists with the work of the left ventricle, the underlying function may result in a palpable pulse. If the LVAD is fully replacing the function of the ventricle, there may not be a palpable pulse. As with other technology advances, these devices offer advantages in size, ease of implantation, and durability. The number of moving parts has been reduced to one: the impeller. Second-generation LVADs are subdivided into devices with axial pumps and those with radial (centrifugal) pumps. Axial pumps use a corkscrew and the Archimedes principle against gravity. The inflow and outflow pumps are in line with the impeller, resulting in a smaller size pump. In contrast, centrifugal pumps have the inflow and outflow cannulas at right angles to the flow. Right angles allow for less suction, which can decrease the risk of the ventricle collapsing around the inflow cannula or distortion of the interventricular septum. Both can result in right ventricular failure. One study found 58% survival rates for continuous-flow devices versus 24% for pulsatile flow devices. They also have a lower rate of complications. As continuous-flow pumps are valveless, there is an increased risk of blood flow back into the aorta if the pump stops. Third-generation LVADs represent a further technology step forward. They can use continuous-flow, axial flow, or centrifugal pumps. The impeller is suspended by magnets and driven by electromagnets. This results in no contact between the impeller and the sides of the pump. Benefits include less trauma to blood components and less thrombus formation. The devices are also quieter and can last longer. Fourth-generation LVADs, currently in testing and trials, are exploring further advances in technology, including wireless monitoring and elimination of the driveline. This would remove the cabling from the pump, which must travel through the skin in order to connect to the power source. As driveline infections are a major source of LVAD complications, driveline removal could result in significantly less morbidity. The results of these advances are devices that allow the patient to leave the hospital and function either at home or in an assisted living facility. Prior to discharge, the patient and family are given extensive training on the operation and maintenance of the device, and how to troubleshoot problems and alarms. The patient is followed by a hospital team, and is given written instructions for EMS providers, which outline the device, emergency interventions, and hospital contact information.",
        "Left ventricular assist device complications": "Left ventricular assist device complications can be divided into two categories: device problems and patient problems. The most common problems consist of neurological events, bleeding, and cardiac arrhythmias. Neurological events include acute strokes and transient ischemic attacks. Thrombotic and hemorrhagic events can occur. The incidence of stroke has been reported ranging from 8% to 25%. The risk is increased for patients with stroke histories and those who have had device-related infections. The most commonly experienced forms of bleeding include epistaxis, gastrointestinal bleeding, and hematoma formation. Bleeding can result from trauma to blood components, from acquired von Willebrand disease, or from iatrogenic anticoagulation. Most patients are given anticoagulants and/or antiplatelet drugs to reduce the risk of thrombus formation. LVAD patients are also at increased risk of arrhythmias. Patients may have atrial fibrillation, often as a result of underlying disease. The LVAD will provide left ventricle support, but the loss of atrial \u201ckick\u201d may affect right ventricular function. LVAD patients may also suffer from ventricular arrhythmias. These arrhythmias may result from underlying disease, from irritation of the myocardium by the device, or from ventricular collapse or septal deviation from excessive pump function. Some patients may require an implanted cardioverter-defibrillator (ICD). Infection is the most common complication, with infection rates ranging from 18% to 59% among LVAD patients. Infection is second only to heart failure as a cause of mortality in these patients. Infections can present at the surgical site, the driveline, the pump pocket, or the pump itself in the form of endocarditis. Device-specific problems can manifest as device failure (fortunately rare) or from battery or cable connection issues. Suction events can occur when there is not enough volume in the left ventricle to support the speed of the pump. This causes the intake cannula to collapse and subsequent ventricular arrhythmias. LVADs in place for a long time can become dislodged, resulting in incomplete left ventricle emptying, right ventricular failure, and arrhythmias. LVAD placement may also result in thrombosis. The patient might then suffer symptoms ranging from dyspnea to cardiogenic shock.",
        "Prehospital encounters": "Balloon pump patients are not routinely encountered by EMS providers except during critical care interfacility transports. In contrast, a patient with a portable LVAD could be at home, have an event, and summon EMS. It is beneficial for EMS services to be aware of LVAD patients in their service area, and have device information and contact information accessible. Hospital policies may dictate that a perfusionist or pump technician be sent to the scene to evaluate the device in the event of a problem. This situation then could result in a delay in patient transport while the perfusionist is in transit. If the patient is having a medical issue not related to the device, a medical oversight decision may need to be made regarding transport. For example, a portable LVAD patient is having an acute stroke or gastrointestinal (GI) bleed, and no LVAD issues. The perfusionist can arrive in 45 minutes. The patient can be transported by helicopter to the tertiary care center in 15 minutes. The crew is not familiar with the LVAD. The medical oversight physician will need to weigh the risks of delay to care in waiting for the perfusionist versus the risk of an LVAD complication during the 15-minute flight. The LVAD patient in distress might be having an issue with the device, an exacerbation of the underlying cardiac disease, or an unrelated medical event. The initial EMS assessment should be to determine if the issue is LVAD related or not. If the event does not seem to be LVAD related, then local protocols and/or medical oversight should be consulted for further guidance. The next step would be to determine the type of LVAD involved. The patient and caregiver should have device information available. This information should include whether the patient can receive electrical therapy, and whether or not CPR can be performed. Obviously, these questions need immediate answers. Emergency medical services personnel must determine if the device provides pulsatile or continuous flow. A patient with a pulsatile flow device should have a palpable pulse and blood pressure. Pulsatile pump LVAD failure requires the use of a hand pump to continue flow. A patient with a continuous-flow device will have no detectable pulse. A functioning pump should make a humming sound on auscultation. In the event of device malfunction, the LVAD should generate a series of auditory and visual alarms. These alarms will be device and manufacturer specific. The patient, caregiver, and device literature should be used to determine alarm causes. Power alarms may be triggered by low voltage in the batteries, necessitating battery changes, or, in the case of a pulsatile device power failure, hand pumping. Low-flow pump alarms most likely result from hypovolemia, which would indicate the need for IV fluids or blood products. Other alarms may indicate cable disconnections which will require troubleshooting. Transport should not be delayed to perform these interventions. As with all patients, the initial assessment should consist of airway, breathing, and circulatory assessments. Patients with continuous-flow devices may not have reliable pulse oximetry readings due to low pulse pressures. Furthermore, a continuous-flow device will not produce a palpable pulse or a measurable blood pressure. The EMS provider will need to then use other signs to assess perfusion, such as pale skin, diaphoresis, or mental status changes. The patient should be placed on a cardiac monitor and a 12-lead ECG should be performed if possible. Patients showing signs and symptoms of another illness, such as stroke, should be assessed in the usual fashion, regardless of the assist device. LVAD patients should also be exposed to examine for cable disconnections. The driveline skin site should not be routinely examined unless absolutely necessary, due to risk of infection. Clothes should not be cut with shears as there is risk of cutting the cables with disastrous results. For the same reasons the patient should be moved carefully to prevent dislodgment. Patients with evidence of hemodynamic compromise and/or hypoperfusion should have large-bore IV access, and be volume resuscitated. Vasopressors are not generally a good initial therapy, as many problems are volume related, and vasopressors will increase afterload, which can worsen pump flow. Arrhythmias should only be treated if they are symptomatic. An LVAD patient with full left ventricle support may be able to tolerate ventricular tachycardia or fibrillation. If the arrhythmia requires treatment, the usual therapies can be used for rate control and rhythm conversion. The patient can also receive electrical therapy. Defibrillator pads should not be placed over the device. Some devices may require that the system controller cables be disconnected prior to defibrillation to prevent damage to the electronics. The patient should also be examined for the presence of an ICD, which would provide the appropriate treatment. Not have the ability to maintain perfusion of organ systems. Patient survival is not likely. Lack of compressions may also result in a thrombus formation in the pump, resulting in obstruction to pump flow and potential downstream embolic events. EMS awareness of the patient's advance directives regarding resuscitation may be important, as these patients have chronic severe disease and may wish to not be resuscitated. Ideally, device information, patient wishes and treatment plans, and contact information should be prepared prior to initial discharge from the hospital. In the event of an EMS contact with a patient who is hypoperfused and has a non-functioning pump, an attempt may be made to contact the LVAD coordinator for further recommendations. If the coordinator cannot be reached, and the patient is to be resuscitated, compressions should be started and transport initiated. The LVAD patient should be transported to the hospital that placed the device. These hospitals are usually tertiary care centers, and should be capable of managing not only LVAD complications but also other issues such as stroke or GI bleeding. If there are distance issues, air medical transport should be considered. This can shorten time and also provide critical care services. Regardless of transport mode, the LVAD patient should be transported with all device equipment, batteries, controllers, documentation, and caregivers (if possible).",
        "Implanted cardiac devices": "Emergency medical services personnel may also encounter patients in the field with implanted cardiac devices, such as pacemakers and ICDs. The approach to a patient with an implantable device who is suffering from a medical condition is to determine if the problem lies with the device or the underlying medical condition.",
        "Pacemakers": "Cardiac pacemakers are implanted devices used in patients suffering from bradyarrhythmias. If the patient's intrinsic rhythm falls below a set target, the pacemaker will provide an electrical stimulus to the myocardium. There are a variety of pacemaker manufacturers and pacing modes, depending on the needs of the patient. The device will be palpable within the patient's chest wall.",
        "Pacing modes": "Pacemakers are designated with a five-letter code; the first three letters are referred to most often. The first letter indicates the chamber paced, the second letter indicates the chamber sensed, and the third letter the response after sensing. AOO Atrial pace; no sense, no inhibitions AAI Atrial pace; atrial sense, inhibited by atrial beat VOO Ventricular pace; no sense, no inhibitions VVI Ventricular pace; ventricular sense, inhibited by ventricular beat DOO Dual chamber pace; no sense, no inhibitions DVI Dual chamber pace; ventricular sense, inhibited by ventricular beat DDD Dual chamber pace; dual chamber sense, inhibited by either chamber The EMS physician who responds to a pacemaker patient with a clinical issue first needs to determine if the device is the problem. Vital signs and cardiac monitoring are the best tools to identify the problem. The first determinant is the heart rate. If the patient is markedly bradycardic, the pacemaker should be presumed to have failed. The patient will require hemodynamic support, which may include external cardiac pacing. If external pacing is indicated, care should be taken to not cover the implanted device with the external pads. If the patient is tachycardic, the physician will need to determine if the pacer is firing inappropriately, or if there is another medical cause. The presence of pacer spikes prior to every tachycardic beat is the best indicator of a pacer issue. The next step is to determine what therapy is needed. Optimally, the patient can be transported to a facility where the implanted device can be interrogated by an electrophysiologist, preferably at the hospital where the device was implanted. If the patient's clinical condition requires more urgent intervention, a special magnet can be placed to suspend inappropriate pacing. The magnet will not turn the pacer off, rather it will trigger the device to pace at an asynchronous (fixed) rate depending on the device and manufacturer. A DDD pacemaker will pace at DOO, a VVI device will pace at VOO, and an AII device will pace at AOO. Magnet therapy is only effective when the magnet is on the skin over the pacemaker. In the event that magnet therapy is ineffective, it is theoretically possible to cut the pacer wires, but this would be difficult in the field, may permanently damage the device, and should only be performed as a last resort.",
        "Implantable cardioverter-defibrillators": "Implantable cardioverter-defibrillators are a first-line therapy for many patients at risk for sudden cardiac death. ICDs are usually implanted in the left infraclavicular region and are typically palpable. All patients with the device get an ID card that notes the manufacturer and device model. ICDs have four main functions: sensing atrial and ventricular signals, classification of those signals into programmable heart rate zones, administration of electrical therapy to terminate ventricular tachycardia or ventricular fibrillation, pacing for bradycardia and/or cardiac resynchronization therapy (equivalent to a standard pacemaker). If ventricular fibrillation or ventricular tachycardia is detected, high-energy shocks of 1\u201340 can be delivered. Although this is less energy than external defibrillation or cardioversion, the shock can be painful to the patient. The EMS physician will most likely encounter one of three possible scenarios in an ICD patient who is suffering from an ICD-related cardiac event. The first is device failure in the event of a ventricular arrhythmia. The second is an appropriately functioning device in the setting of a ventricular arrhythmia. The third possibility is the ICD delivering shocks inappropriately in the absence of a ventricular arrhythmia. The first step in all cases is assessment of mental status, vital signs, and cardiac monitoring. If the patient has an unstable ventricular arrhythmia and the ICD does not fire, it should be assumed the device is non-functional and ACLS protocols should be followed. If external defibrillation is needed, the defibrillator pads should not be placed over the implanted device. If the patient has a ventricular rhythm and the ICD is giving appropriate shocks, care should be focused on additional treatment of the arrhythmia, as well as rapid transport to the hospital. The patient may benefit from analgesia and possibly sedation in the event of multiple shocks. External electrical therapy should not be needed. In the third scenario, the ICD is giving inappropriate shocks in the absence of a ventricular arrhythmia. As with pacemaker malfunctions, ideally the device can be interrogated by an electrophysiologist at the receiving hospital. If the patient's condition requires emergency intervention to stop inappropriate shocks, a special magnet can be placed over the device. The magnet will suspend detection of ventricular fibrillation and ventricular tachycardia and should stop the shocks. The magnet will not stop the pacemaker function of the ICD, nor place the pacer in asynchronous (fixed) mode. In the event of magnet placement, cardiac monitoring is required because the ICD will no longer be able to sense nor shock arrhythmias. Magnet therapy is only effective while the magnet is secured to the skin over the device. It may also be prudent to apply external defibrillator pads during transport. As with a pacemaker, cutting the lead wires of an ICD will most likely permanently damage the device, is difficult to perform in the field, and is not recommended short of a dire last resort.",
        "Pericardiocentesis": "Pericardiocentesis may be indicated in the ACLS algorithm for pulseless electrical activity (PEA) in the event of cardiac arrest. If the PEA is the result of cardiac tamponade, pericardiocentesis may reverse the condition. The prehospital provider should use the subxiphoid approach, inserting a needle to the left of the xiphoid and aiming at the left shoulder at a shallow angle. An 18 gauge spinal needle or 3\u201d IV catheter may be used. Aspiration of blood that does not clot indicates removal from the pericardial space, as opposed to intraventricular blood. This procedure is more difficult to perform in the prehospital environment where ultrasound guidance is typically less available. It should be used as a final resort when all other therapies have failed.",
        "Conclusion": "Only critical care teams with extensive additional training should attempt to transport patients with IABPs, unless they are accompanied by a perfusionist. Such patients are not generally encountered by the EMS system except to facilitate interfacility transportation. Careful attention must be paid when transitioning a patient from one pump to another, and proper timing of inflation is crucial. Patients in the community with VADs are growing in prevalence. Preplanning for potential emergencies, including awareness by the EMS system, is an important aspect of ensuring an appropriate response when complications or unrelated medical events arise. A coordinated exchange of information between the VAD hospital team and surrounding EMS agencies is key to the safe and effective treatment and transfer of these patients. Depending on the brand and type of VAD, the patient may or may not have a palpable pulse or blood pressure. Most pump flow alarms occur because of low volume and require volume resuscitation. Vasopressors in these patients may do more harm than good. The prehospital provider may also encounter patients with implanted cardiac devices. Assessment of these patients will determine if the clinical condition is due to a device malfunction or not. While not routinely carried or used by EMS personnel, the EMS physician may want to have access to a special magnet used to turn off an ICD, or reset a pacemaker to asynchronous pacing."
    },
    {
        "Cardiac Arrest": "There are an estimated 435,000 out-of-hospital cardiac arrests each year, according to the American Heart Association\u2019s Heart Disease and Stroke update 2014. Thus it is important to review adult and pediatric advanced cardiac life support algorithms, which have changed as of the American Heart Association\u2019s 2015 update. The most recent guidelines are not a significant change from those released in 2010 in relation to basic life support (BLS) and the use of automated external defibrillators (AED); however, key changes are important to note, including employment of a \u201cpit crew\u201d approach, quality of chest compressions, use of mechanical compression devices, changes to medications utilized, and implementation of therapeutic hypothermia in return of spontaneous circulation (ROSC).",
        "CPR Quality": "It is important to monitor CPR quality.3 In the best scenarios, CPR will: \u2219Push hard and fast: compress at least 5 cm (2 inches) and between 100-120 compression/minute \u2219Allow for full relaxation between compressions (avoid leaning on the patient) \u2219Minimize interruptions in compressions, including when rotating and between defibrillation \u2219It is also important to avoid hyperventilation as this can lead to reduced cardiac output1 \u2219No advanced airway: 30:2 (adult) or 15:2 (pediatric) compression-to-ventilation ratio \u2219Advanced airway: continuous compressions and 1 breath every 6 seconds (10 breaths/minute) \u2219If advanced airway is placed remember to confirm placement: \u2219Visualizing endotracheal tube passing between vocal cords \u2219Confirm bilateral breath sounds \u2219End-tidal CO2 \u2219Waveform capnography",
        "content": "At 13:00, two paramedics responded to a call for a cardiac arrest at a local restaurant. Per the 911 dispatcher, a 66-year-old man was eating at the restaurant with his wife when he collapsed. A bystander attempted to palpate a pulse and was unsuccessful. CPR (compressions only ) was started. An AED (automated external defibrillator) had been applied to the patient\u2019s chest. A shock was advised, and the bystanders continued CPR following the shock. The employment of the pit crew, or assignment of roles to each team member, optimizes utilization of resources. For instance, the 2 most important determinants of outcome following cardiac arrest are early defibrillation and quality of CPR.1 By-stander-initiated CPR, as well as a shock delivered in <5 minutes, have been shown to significantly improve a patient\u2019s survival following cardiac arrest.1,2 Yet, historical information can play a huge role in patient outcomes:1 \u2219Did anyone witness the arrest? \u2219What time was the person last seen \u201cnormal\u201d? \u2219What time did the arrest occur, and what was the person doing at that time? \u2219Was there any intervention prior to arrival (CPR initiated, AED applied, shock delivered)? \u2219Is there any pertinent past medical history (PMH)? \u2219What medications does the patient take? \u2219Any possibility for ingestion or overdose? \u2219Determine code status. A cardiac arrest in the field should be organized similar to a cardiac arrest in the hospital (number of personnel may vary by system): 1. A recorder to keep track of the time and interventions 2. 2 people performing CPR 3. 1 person to draw up medications The paramedics arrived on scene approximately 5 minutes after ar- rest. An engine crew from the local fire department arrived simultane- ously. Two firefighters take over CPR from the bystanders and continue with high-quality chest compressions and begin bag-valve mask venti- lation. One paramedic starts recording, noting times of interventions and changes in the patient\u2019s status. The second paramedic assesses the AED, finding it to be connected to the patient correctly. He then applies a cardiac monitor. He speaks with the patient\u2019s wife and bystanders, gathering pertinent past medical history and events prior to the car- diac arrest. Prior to lunch the patient had been complaining of chest discomfort. While eating he fell over and was found by a bystander to have no palpable pulse. CPR was started, and the AED was applied. One shock was given. The patient\u2019s past medical history is significant for hypertension and hyperlipidemia. He takes Lisinopril and Lipitor and has a 20-pack year tobacco history. Be cognizant of the reversible causes.4 Some conditions to keep in mind include: \u2219Hypovolemia \u2219Hypoxia \u2219Hydrogen Ion (acidosis) \u2219Hypo/Hyperkalemia \u2219Hypothermia \u2219Tension pneumothorax \u2219Tamponade (cardiac) \u2219Toxins \u2219Thrombosis (pulmonary) \u2219Thrombosis (coronary) If return of spontaneous circulation (ROSC) is achieved: 1. Check pulses and blood pressure 2. PETCO2 typically will show an abrupt and sustained increased (usually >40 mmHg)1 3. Proceed to the ROSC pathway **AHA post arrest guidelines** 5 4. Obtain 12 lead EKG \u21a6 Prioritize transport to a STEMI/Hypothermia center The firefighters continued CPR. IV access was obtained and an ad- vanced airway was placed. At 2 minutes, pulse and rhythm checks were done. The patient was still pulseless, and ventricular fibrillation was seen on the monitor. A shock was given, followed by epinephrine 1mg. Capnography showed an ETCO2 of 22. The firefighters continued with high-quality CPR, and 2 minutes later another pulse and rhythm check was completed. The patient was found to have a pulse, and NSR was seen on the monitor. Capnography showed an ETCO2 of 55. The ASA post-arrest guidelines were intiated12 and the patient was prepared for transport to the nearest STEMI center. An EKG obtained post-arrest showed ST-segment elevation in the anterior leads. This was relayed to the accepting STEMI center and the cardiac catheterization suite was readied."
    },
    {
        "Termination of Resuscitation": "Mathew Martinez, MD Jeff Goodloe, MD, FACEP DNR laws vary by state, and appropriate documentation must be presented to EMS personnel on arrival.",
        "When to terminate resuscitation": "Obvious death No pulse AND No spontaneous respirations AND Fixed pupils AND at least one or more of the following: Rigor mortis, Decapitation, Decomposition, Dependent lividity Blunt Traumatic Cardiac ArrestNo pulse AND No spontaneous respirations AND No shockable rhythm AND No organized cardiac activity (i.e. asystole, PEA < 40 bpm) Penetrating Traumatic ArrestNo pulse AND No spontaneous respirations AND Fixed pupils AND No spontaneous movement AND No organized cardiac activity (i.e. asystole, PEA < 40 bpm) Source:  State of Oklahoma 2014 Emergency Medical Services Protocols. http:// www.oudem.org/ems-protocols/"
    },
    {
        "Introduction": "The detection and management of shock in the prehospital environment has been historically limited. While technical advances and new research have led to significant changes in recent years regarding the prehospital phase of care of these critically ill patients, there remain significant limitations on the ability to manage shock in the field. This creates a difficult balance between stabilization in the field and rapid transport to the hospital for definitive care.",
        "What is shock?": "Shock is the widespread failure of the circulatory system to supply adequate oxygen and nourishment to the tissues and organs of the body.",
        "What is perfusion?": "Perfusion is the supply of oxygen to cells and tissue with subsequent removal of wastes as a result of blood flow through the capillaries.",
        "What is hypoperfusion?": "Hypoperfusion is the inability to supply oxygen and remove wastes from the cells and tissues due to poor circulation of blood.",
        "What is SIRS?": "Systemic Inflammatory Response Syndrome (SIRS) may be due to infection, but other causes, such as burns and pancreatitis, may exist. It requires 2 of the following: \u2219Temperature < 36oC or > 38oC \u2219Pulse > 90 beats per minute \u2219Respiratory rate > 20 breaths per minute or PaCO2 < 32 mmHg \u2219WBC > 12000 or < 4000 or differential with > 10% bands",
        "Stages of shock": "Compensated or Non-progressive Low perfusion activates multiple systems to maintain and restore perfusion, resulting in: \u2219Tachycardia \u2219Vasoconstriction \u2219Renal system retaining fluid and volume \u2219Maximization of blood flow to the brain, lungs, and heart \u2219Few symptoms \u2219Aggressive management slows progression Decompensated or Progressive Failure to compensate; unable to improve and maintain perfusion. \u2219Symptoms reflect poor perfusion. \u2219Oxygen deprivation to the brain causes confusion. Irreversible Prolonged lack of perfusion results in permanent damage to organs and tissues, resulting in: \u2219Cardiac failure \u2219Renal failure \u2219Cell death Endpoint is death of the patient.",
        "What are the different types of shock?": "\u2219Hypovolemic \u2219Distributive \u2219Cardiogenic \u2219Obstructive \u2219Neurogenic",
        "HYPOVOLEMIC SHOCK": "Hypovolemic shock is the rapid reduction of blood volume, typically due to hemorrhage, that results in activation of baroreceptors. This has a positive inotropic and positive chronotropic effect. As hypovolemia progresses, catecholamines and hormones are released, resulting in vasoconstriction and tachycardia. Hemorrhage first increases pulse and cardiac contraction and then increases vasoconstriction to maintain tissue perfusion. This narrows pulse pressure. As blood loss continues, ventricular filling decreases, cardiac output falls, and there is a reduction in systolic BP. As CO2 decreases, blood flow to noncritical organs and tissues decreases, leading to the production of lactic acid. After 1/3 of total blood volume is lost, cardiovascular reflexes no longer sustain adequate filling of the arterial circuit and frank hypotension occurs. Urine output decreases and thirst is stimulated to maintain circulating volume.",
        "How is hypovolemic shock managed?": "Resuscitation strategies are to optimize tissue perfusion while avoiding complications of overaggressive volume replacement. The goal of a trauma assessment is early recognition of circulatory dysfunction prior to development of hypotension and end-organ damage. If there is a bleeding wound, apply direct pressure. If the wound is on an extremity and bleeding does not cease, elevate the extremity above the level of the heart. Apply additional dressings as needed. If bleeding continues on the arm, apply direct pressure to the brachial artery. If the wound is on a leg, apply direct pressure to the femoral artery. Application of cold packs will cause vasoconstriction. Additional management techniques include: \u2219If there as a penetrating injury, stabilize the object if it is still impaled. \u2219Maintain airway. \u2219Apply high flow oxygen and be prepared to intubate at any point. \u2219Do not give an anticoagulant, such as aspirin. \u2219If there is no concern for a spinal cord injury, place the patient in Trendelenburg position. \u2219Keep the patient warm. \u2219Administer bolus of normal saline.",
        "What is permissive hypotension?": "A combination of the patient\u2019s natural coagulation cascade, hypotension, and vessel spasm will temporarily arrest traumatic hemorrhage. Often the patient will have no apparent bleeding, but once resuscitation occurs and hypotension reverses, rapid arterial bleeding occurs. Permissive hypotension is the minimization of fluid resuscitation in the prehospital setting in patients with palpable radial pulses and normal mental status. Goal SBP is around 90. Aggressive fluid resuscitation could maintain sufficient blood flow to prolong survival until definitive hemorrhage control occurs. Contraindications to permissive hypotension include traumatic brain injury, spinal cord injury, patients who are hypertensive, patients with angina pectoris and cardiovascular disease, carotid artery stenosis, impaired renal function, and intermittent claudication stage III/IV.",
        "DISTRIBUTIVE SHOCK": "Distributive shock is peripheral vasodilation and blood flow maldistribution, commonly caused by sepsis or anaphylaxis. Septic shock is caused by infection with any microbe, although frequently no specific organism is identified. Three major issues must be addressed during resuscitation: hypovolemia, cardiovascular depress, and induction of system inflammation. Patients have relative hypovolemia as a result of increased venous capacitance, which reduces right ventricular filling. GI loss, tachypnea, sweating, decreased oral intake, and third spacing also contribute to relative hypovolemia.",
        "How is septic shock managed?": "Airway management is always priority in resuscitation of any patient. Two large bore IVs with aggressive normal saline infusion and vasoactive agents in patients refractory to fluid resuscitation should be initiated. Norepinephrine, while not commonly used by ground EMS, is the preferred agent as the patient is typically tachycardic. Blood sugars should be monitored as patients are commonly profoundly hyperglycemic. For those prehospital agencies with established protocols, early antibiotic administration should occur, with the preferred agents being vancomycin and piperacillin/tazobactam due to the broad spectrum nature. (Note: Antibiotics are not common on ground ambulances.)",
        "How is anaphylactic shock managed?": "Immediate administration of epinephrine (1:1000) 0.3 mg IM in the lateral thigh should be performed. This may be repeated in severe reactions. Diphenhydramine 50 mg IV/IM, methylprednisolone 125 mg IV, and fluid resuscitation are the mainstays of treatment. Consider albuterol 2.5 mg/3 mL nebulizer if bronchospasm persists following epinephrine. If refractory hypotension persists, dopamine 5 to 20 mcg/kg/min should be initiated if available.",
        "CARDIOGENIC SHOCK": "Cardiogenic shock results when more than 40% of the myocardium undergoes necrosis from ischemia, inflammation, toxins, or immune destruction. Similar to hemorrhagic shock, alterations in circulation and metabolism occur. There is interference with blood flow from the heart, resulting in dyspnea, tachycardia, pulmonary or peripheral edema, and cyanosis.",
        "How is cardiogenic shock managed?": "The goal of management is adequate oxygenation of the myocardium. Oxygen and continuous positive airway pressure (CPAP) therapy are used to relieve dyspnea. Furosemide may be administered if pulmonary edema is noted upon exam. However, note the furosemide may be detrimental in patients who are dehydrated secondary to infection. Preferred vasopressors for refractory hypotension include dopamine, dobutamine, and norephinephrine if available.",
        "OBSTRUCTIVE SHOCK": "Obstructive shock is an extracardiac obstruction to blood flow. This is commonly caused by a pneumothorax, pulmonary embolism, or pericardial tamponade.",
        "How is obstructive shock managed?": "The most important management is to maintain adequate oxygenation. \u2219Tension pneumothorax \u21a6 Needle decompression on affected side in second intercostal space along mid-clavicular line. \u2219Pulmonary embolism \u21a6 High flow oxygen and intubation. \u2219Pericardial tamponade \u21a6 Pericardiocentesis.",
        "NEUROGENIC SHOCK": "Neurogenic shock affects autonomic responses. Sympathetic outflow is disrupted, causing unopposed vagal tone. This results in hypotension and bradycardia with warm, dry skin. This is the ONLY type of shock where the skin remains warm and dry. The higher the injury, the more likely severe symptoms will occur. Neurogenic shock, though, is a diagnosis of exclusion.",
        "How is neurogenic shock managed?": "Airway management is of utmost importance. For hypotension, fluid resuscitation with normal saline and vasopressors for refractory hypotension should be administered. If symptomatic bradycardia occurs, administer atropine 0.5 mg IV. If atropine does not reverse bradycardia, a transcutaneous pacemaker should be placed. EMS should transfer the patient to a facility with neurological and neurosurgical services.",
        "What is spinal shock?": "Spinal shock stems from acute spinal cord injury and results in the loss of all voluntary neurologic activity and reflexes below the level of the injury. Flaccid paralysis and loss of sensation occur. Spinal shock can last months. Some sources group spinal shock and neurogenic shock together. Although spinal and neurogenic shock can occur in the same patient, they are not the same disorder. The management, though, is the same."
    },
    {
        "Key Terms": "Acute coronary syndrome (ACS): Term that describes a range of clinical conditions, including unstable angina and myocardial infarction, that are due to insufficient blood supply to the heart muscle resulting from coronary heart disease (CHD)., Acute myocardial ischemia: An episode of chest pain due to reduced blood flow to the heart muscle., Angina pectoris: Pain in the chest that comes and goes at different times; caused by a lack of oxygen reaching the heart; can be stable (occurring under exertion or stress) or unstable (occurring at rest, without reason)., Arrhythmia: Electrical disturbances in the regular rhythmic beating of the heart., Asystole: A condition where the heart has stopped generating electrical activity., Atherosclerosis: A condition in which deposits of plaque, including cholesterol (a fatty substance made by the liver and found in foods containing animal or animal products) build up on the inner walls of the arteries, causing them to harden and narrow, reducing the amount of blood that can flow through; develops gradually and can go undetected for many years., Atrial fibrillation: Irregular and fast electrical discharges from the left or right atrium of the heart that lead to an irregular heartbeat; one of the most common types of abnormal cardiac rhythm., Atrioventricular (AV) node: A cluster of cells in the center of the heart, between the atria and ventricles; serves as a relay to slow down the signal received from the sinoatrial (SA) node before it passes through to the ventricles., Automated external defibrillator (AED): A portable electronic device that analyzes the heart\u2019s electrical rhythm and, if necessary, can deliver an electrical shock to a person in cardiac arrest., Cardiac arrest: A condition in which the heart has stopped or beats too irregularly or weakly to pump blood effectively., Cardiac Chain of Survival: A set of five critical steps that, when performed in rapid succession, increase the patient\u2019s chance of surviving cardiac arrest; each link of the chain depends on, and is connected to, the other links., Cardiopulmonary resuscitation (CPR): A technique that combines chest compressions and ventilations to circulate blood containing oxygen to the brain and other vital organs for a person whose heart and normal breathing have stopped., Cardiovascular disease: A disease affecting the heart and blood vessels., Chest compressions: A technique used in CPR in which external pressure is placed on the chest to help circulate oxygen-rich blood through the arteries and to the vital organs., Cholesterol: A fatty substance made by the liver and found in foods containing animal or animal products; diets high in cholesterol contribute to the risk of heart disease., Commotio cordis: Sudden cardiac arrest from a blunt, non-penetrating blow to the chest, of which the basis is ventricular fibrillation (V-fib) triggered by chest wall impact immediately over the heart., Congestive heart failure: A chronic condition in which the heart no longer pumps blood effectively throughout the body., Coronary heart disease (CHD): A disease in which cholesterol and plaque build up on the inner walls of the arteries that supply blood to the heart; also called coronary artery disease (CAD)., Defibrillation: An electrical shock that disrupts the electrical activity of the heart long enough to allow the heart to spontaneously develop an effective rhythm on its own., Electrocardiogram (ECG or EKG): A diagnostic test that measures and records the electrical activity of the heart., Heart: A fist-sized muscular organ that pumps blood throughout the body., High-performance CPR: Providing high-quality chest compressions as part of a well-organized team response to a cardiac arrest., Hypertension: Another term for high blood pressure., Implantable cardioverter-defibrillator (ICD): A miniature version of an AED, implanted under the skin, that acts to automatically recognize and help correct abnormal heart rhythms., Myocardial infarction (MI): The death of cardiac muscle tissue due to a sudden deprivation of circulating blood; also called a heart attack., Normal sinus rhythm (NSR): The normal, regular rhythm of the heart, set by the SA node in the right atrium of the heart., Pacemaker: A device implanted under the skin, sometimes below the right collarbone, to help regulate the heartbeat in someone whose natural pacemaker (the sinoatrial node) is not functioning properly, causing the heart to skip beats or beat too fast or too slow., Return of spontaneous circulation (ROSC): A term to describe the successful resuscitation of a patient in cardiac arrest; a return of a pulse during resuscitative efforts., Risk factors: Conditions or behaviors that increase the chance that a person will develop a disease., Silent heart attack: A heart attack during which the patient has either no symptoms or very mild symptoms that the person does not associate with heart attacks; mild symptoms include indigestion or sweating., Sinoatrial (SA) node: A cluster of cells in the right atrium that generates the electrical impulses that set the pace of the heart\u2019s natural rhythm., Sudden cardiac arrest: A condition where the heart\u2019s pumping action stops abruptly, usually due to abnormal heart rhythms called arrhythmias, most commonly ventricular fibrillation (V-fib) or ventricular tachycardia (V-tach); unless an effective heart rhythm is restored, death follows within a matter of minutes., Transdermal medication patch: A patch on the skin that delivers medication; commonly contains nitroglycerin, nicotine or other medications; should be removed prior to placing defibrillation pads on the chest., Ventricular fibrillation (V-fib): A life-threatening heart rhythm in which the heart is in a state of totally disorganized electrical activity., Ventricular tachycardia (V-tach): A life-threatening heart rhythm in which there is very rapid contraction of the ventricles.",
        "INTRODUCTION": "In this chapter, you will learn how to recognize and provide care for a patient who is experiencing signs and symptoms of a heart attack or whose heart stops beating. A heart attack occurs when blood vessels supplying the heart become blocked and fail to provide the heart enough blood and oxygen necessary to function properly. The condition in which the heart stops functioning is known as cardiac arrest. It can sometimes result from a heart attack but cardiac arrest can also be caused by sudden, irregular electrical activity of the heart as well as many other causes. To provide care for a patient in cardiac arrest, you need to know how to perform cardiopulmonary resuscitation (CPR) and use an automated external defibrillator (AED). CPR can keep a patient\u2019s vital organs supplied with blood containing oxygen until more highly trained personnel arrive to provide advanced life support care. In many cases, however, CPR by itself cannot correct the underlying problem. An AED can analyze the heart\u2019s electrical rhythm and deliver a shock to help the heart to restore an effective rhythm. Sudden cardiac arrest can happen to anyone at anytime, and although not common, can occur in children and infants. As an emergency medical responder (EMR), you must assess patients quickly and be prepared to perform high-quality CPR and use an AED in cases of cardiac arrest. This chapter covers the basic principles of how to recognize cardiac emergencies and provide the appropriate care.",
        "Anatomy of the Circulatory System": "The heart is a muscular organ, which functions like a pump. About the size of the patient\u2019s fist, it lies between the lungs, in the middle of the chest, behind the lower half of the sternum (breastbone). The heart is protected by the ribs and sternum in front and by the spine in back. It has four chambers and is separated into right and left halves. The right side of the heart has two chambers known as the right atrium, which receives oxygen-depleted blood from the veins of the body, and the right ventricle, which pumps the oxygen-depleted blood to the lungs where waste products are removed and oxygen is absorbed. The now oxygen-rich blood returns to the left side of the heart, where it enters the left atrium and goes on to the left ventricle, where it is pumped to all parts of the body. One-way valves direct the flow of blood as it moves through each of the heart\u2019s four chambers. For the circulatory system to be effective, the respiratory system must also be working so that the blood can pick up oxygen in the lungs.",
        "How the Heart Functions": "Too often we take our hearts for granted. The heart is extremely reliable. The heart beats about 70 times each minute or more than 100,000 times a day. During the average lifetime, the heart will beat nearly 3 billion times. The heart moves about a gallon of blood per minute through the body. This is about 40 million gallons in an average lifetime. The heart moves blood through about 60,000 miles of blood vessels.",
        "The Heart\u2019s Electrical System": "An electrical system in the heart triggers the contraction or pumping action of the heart muscle. In a healthy heart, an electrical impulse comes from a point near the top of the heart called the sinoatrial (SA) node. The impulse travels through the atria, the upper chambers of the heart, down to the atrioventricular (AV) node, near the bottom of the right atrium. From the AV node, the impulse divides into two branches, then into the right and left ventricles. These right and left branches become a network of fibers, called Purkinje fibers, which spread electrical impulses across the heart. Under normal circumstances, these impulses reach the muscular walls of the ventricles causing the muscles to contract and force blood out of the heart to circulate throughout the body. The contraction of the left ventricle results in a pulse. The pauses between the pulse beats are the periods between contractions. As the left ventricle relaxes, or is at rest, blood refills the chamber and there is a pause between pulse beats.",
        "An electrocardiogram (ECG or EKG)": "is a diagnostic test that graphically measures and records the electrical activity and rhythm of the heart. Electrodes attached to an electrocardiograph pick up electrical impulses and transmit them to a monitor. The peaks and valleys of each wave, the size, shape and frequency, show the heart\u2019s rhythm and how the electrical system is functioning. The normal conduction of electrical impulses without any disturbances is known as normal sinus rhythm (NSR).",
        "Perfusion": "As the blood flows through the arteries, oxygen and nutrients such as glucose are delivered to cells throughout the body, and as blood flows through the veins, carbon dioxide and other wastes are taken away. This continuous process is called perfusion. The primary gases exchanged are oxygen and carbon dioxide. All cells require oxygen to function. Cells also require energy to function. Glucose, a simple sugar molecule, is the main source of energy inside the cell.",
        "CRITICAL FACTS": "Cardiovascular disease afflicts approximately 90 million Americans and is the number one killer in the United States. Common conditions caused by this disease include CHD and stroke.",
        "Pathophysiology of the Circulatory System": "Cardiovascular disease is an abnormal condition that affects the heart and blood vessels. An estimated 90 million Americans suffer from some form of the disease. It remains the number one killer in the United States and a major cause of disability. The most common conditions caused by cardiovascular disease include coronary heart disease (CHD), also known as coronary artery disease (CAD), and stroke. (See Chapter 14 for more information on stroke.) CHD occurs when the arteries that supply blood to the heart muscle become hardened and narrowed, a process called atherosclerosis. This damage occurs gradually, as cholesterol and fatty deposits called plaque build up on the inner artery walls. As this buildup worsens, the arteries become narrower, reducing the amount of blood that can flow through them and preventing the heart from getting the blood or oxygen it needs. Patients who suffer from acute myocardial ischemia (reduced blood flow to the cardiac muscle) suffer chest pain, which usually results from CHD and is referred to as acute coronary syndrome (ACS). This reduced blood and oxygen supply to the heart can cause symptoms of angina pectoris or a heart attack. A heart attack, or myocardial infarction (MI), occurs when coronary blood vessels become blocked by plaque buildup or a blood clot blocks one of the arteries supplying the heart. This may lead to an irregular heartbeat (arrhythmia) which then causes the pumping action of the heart to work less efficiently. A heart attack is one of the leading causes of cardiac arrest, which is when the heart ceases to function as a pump. As the reduction of blood flow or blockage progresses, some people experience symptoms such as chest pain, pressure or discomfort, an early warning sign that the heart is not receiving enough oxygen-rich blood. Others may suffer a heart attack or even cardiac arrest without any warning signs or symptoms. If a blockage in a coronary artery of the heart is not treated quickly, the affected heart muscle tissue will die.",
        "Pathophysiology of the Circulatory System - Pediatric Considerations": "Cardiac Pathophysiology Heart problems in children and infants are almost always secondary to airway and respiratory problems but can also be related to congenital heart conditions. When cardiac arrest occurs in children and infants, it is often caused by: \uf0a7 Airway and breathing problems. \uf0a7 Traumatic injuries or other incidents (e.g., motor-vehicle collision, drowning, electrocution or poisoning). \uf0a7 A hard blow to the chest (e.g., commotio cordis). \uf0a7 Congenital heart disease. \uf0a7 Sudden infant death syndrome (SIDS).",
        "Considerations for Older Adults - Cardiac Pathophysiology": "In older adult patients, a general decrease in pain perception may cause a different reaction to a heart attack. Older adults often suffer what is known as a \u201csilent heart attack,\u201d meaning that there is an absence of chest pain or pressure. The symptoms of a heart attack most commonly shown by older adult patients include general weakness or fatigue, aching shoulders and abdominal pain or indigestion.",
        "Angina Pectoris": "A medical term for \u201cpain in the chest,\u201d angina pectoris develops when the heart needs more oxygen than it gets, because the arteries leading to it are too narrow. Angina pectoris is normally a transient condition. When a person with angina exercises, gets excited or is emotionally upset, the heart might not get enough oxygen. This lack of oxygen can cause chest discomfort or pain. People with angina usually have medicine they can take to stop the pain. Stopping physical activity or easing the distress and taking the medicine usually end the discomfort or pain.",
        "Arrhythmias": "Arrhythmias are electrical disturbances in the regular rhythmic beating of the heart. Some people have heart arrhythmias that do not cause problems. In others, they can indicate a more serious problem that leads to heart disease, stroke or sudden cardiac death.",
        "Atrial Fibrillation": "Atrial fibrillation is one of the most common types of abnormal cardiac rhythm. When someone experiences atrial fibrillation, the two upper chambers of the heart (the atria) beat out of coordination with the two lower chambers (the ventricles). This causes an irregular and often rapid heart rate that leads to the inability to adequately deliver blood to the ventricles. Atrial fibrillation can be controlled with medication and other treatments. Although not usually life threatening, atrial fibrillation is a risk factor for stroke and heart attack.",
        "Congestive Heart Failure": "Also called heart failure, congestive heart failure is a chronic condition in which the heart no longer pumps blood effectively throughout the body. This may cause high blood pressure and a buildup of fluid throughout the body, resulting in difficulty breathing and weight gain. Fluid buildup and swelling usually occur in the face, hands, legs, ankles and feet.",
        "Hypertension": "Also known as high blood pressure, hypertension is one of the main risk factors for heart attack and stroke. A patient is considered to have hypertension when blood pressure is higher than 140/90 mmHg. The causes of hypertension are not clear; however, certain medications, sodium intake and stress can contribute to a rise in blood pressure. Secondary hypertension is caused by an underlying condition such as a kidney abnormality or tumor of the adrenal gland.",
        "Diabetes": "Diabetes can affect the nerves; therefore, people with diabetes may not experience the classic heart attack sign of chest pain and may suffer a \u201csilent heart attack.\u201d People who experience silent heart attacks may have no warning signs or they may have very mild signs. When this occurs, the diagnosis of a heart attack may have to be confirmed by special tests. (See Chapter 14 for more information on diabetes.)",
        "Women and Heart Attacks": "Although women may experience chest pain, pressure or discomfort during a heart attack, they are more likely to experience some of the other warning signs and symptoms, particularly shortness of breath; nausea or vomiting; stomach, back or jaw pain; or unexplained fatigue or malaise. When they do experience chest pain, women may have a greater tendency to have atypical chest pain: sudden, sharp but short-lived pain outside the breastbone. As a result, women often will delay telling others about their symptoms.",
        "CRITICAL FACTS 2": "A heart attack is caused by blockages from plaque buildup or blood clots, which affect the ability of the heart to pump effectively. A heart attack is one of the leading causes of cardiac arrest, which is when the heart ceases to function as a pump.",
        "Assessment of Cardiac Emergencies": "The sooner you recognize the signs and symptoms of a heart attack and act, the better chance you have to save a life. Many people will deny they are having a heart attack. Summon more advanced medical personnel if the patient shows some or all of the following signs and symptoms:\n\uf0a7\tDiscomfort, pressure or pain. The major symptom is persistent discomfort, pressure or pain in the chest that does not go away. Unfortunately, it is not always easy to distinguish heart attack pain from the pain of indigestion, muscle spasms or other conditions. This often causes people to delay getting medical care. Brief, stabbing pain or pain that gets worse when you bend or breathe deeply is not usually caused by a heart problem but may be associated with other serious medical conditions.\n\uf0a7\tThe pain associated with a heart attack can range from discomfort to an unbearable crushing sensation in the chest. The patient may describe it as pressure, squeezing, tightness, aching or heaviness in the chest. Many heart attacks start slowly, as mild discomfort, pressure or pain often felt in the center of the chest. It may spread to the shoulder, arm, neck, jaw, stomach or back. The discomfort or pain becomes constant. It is usually not relieved by resting, changing position or taking medicine. When interviewing the patient, ask open-ended questions, such as \u201cCan you describe how you feel for me?\u201d so you can hear the symptoms described in the patient\u2019s own words.\n\uf0a7\tAny chest discomfort or pain that is severe, lasts longer than a few minutes (about 3\u20135 minutes), goes away and comes back or persists even during rest requires immediate medical care. Even people who have had a previous heart attack may not recognize the signs and symptoms, because each heart attack can have entirely different signs and symptoms.\n\uf0a7\tPain that comes and goes, such as with angina pectoris. Some people with CHD may have chest pain or pressure that comes and goes and is usually treated with a medication called nitroglycerin. Nitroglycerin is prescribed in several forms including tablets, spray, paste or patches. This medication dilates blood vessels, including the coronary arteries, to help reduce the workload of the heart.\n\uf0a7\tDifficulty breathing is another sign of a heart attack. The patient may be breathing faster than normal because the body tries to get much-needed oxygen to the heart. A patient who is sitting upright and learning forward with hands on knees in the tripod position is struggling to breathe. Difficulty breathing also includes noisy breathing and shortness of breath.\n\uf0a7\tOther signs and symptoms include pale or ashen skin, especially around the face. The patient also may be damp with sweat. Some people suffering from a heart attack sweat heavily, feel dizzy or lightheaded and/or may lose consciousness. Nausea is also a sign and symptom of a heart attack.",
        "CRITICAL FACTS 3": "The key to saving the life of a patient having a heart attack is early recognition of signs and symptoms, including chest discomfort, pressure or pain that does not go away or comes and goes, and difficulty breathing.",
        "Providing Care for Cardiac Emergencies": "If you think someone is having a heart attack:\n\uf0a7\tTake immediate action and summon more advanced medical personnel.\uf0a7    Have the patient stop any activity and rest.\n\uf0a7    Loosen any tight or uncomfortable clothing.\n\uf0a7    Closely monitor the patient until more advanced medical personnel take over. Notice any changes in the patient\u2019s appearance or behavior.\n\uf0a7    Comfort the patient.\n\uf0a7    If medically appropriate and local protocols or medical direction permit, give aspirin if the patient can chew, swallow and has no known contraindications. Be sure the patient has not been told by their physician to not take aspirin.\n\uf0a7    Assist the patient with their prescribed medication and administer supplemental oxygen if the patient is hypoxic and it is available, according to local protocols.\n\uf0a7    Be prepared to perform CPR and use an AED.",
        "Aspirin Can Lessen Heart Attack Damage": "You may be able to help a conscious patient who is showing early signs of a heart attack by offering an appropriate dose of aspirin when the signs first begin. Local protocols regarding administration of medicines, such as aspirin, may vary for EMRs and should be followed. Aspirin should never take the place of more advanced medical care. If the patient is conscious and able to take medicine by mouth, ask if they:\n\uf0a7    Are allergic to aspirin.\n\uf0a7    Have a stomach ulcer or stomach disease.\n\uf0a7    Are taking any blood thinners, such as warfarin (Coumadin\u00ae).\n\uf0a7    Have been told by a physician to not take aspirin.If the patient answers no to all of these questions, administration of two to four 81-mg low-dose (162 mg to 324 mg) aspirins or one 5-grain (325-mg) adult aspirin tablet should be considered based on local protocols. Have the patient chew  the aspirin completely, which speeds up the absorption of the aspirin into the bloodstream.\nBe sure that only aspirin is given and not acetaminophen (e.g., Tylenol\u00ae) or nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (e.g., Motrin\u00ae or Advil\u00ae) and naproxen (e.g., Aleve\u00ae). Likewise, products meant for multiple symptoms/uses, such as cold, fever and headache, should not be used. Coated aspirin may be administered as long as the patient completely chews the aspirin.",
        "CARDIAC ARREST": "When the heart stops beating, or beats too ineffectively to circulate blood to the brain and other vital organs, this is called cardiac arrest. The beats or contractions of the heart become ineffective if they are weak, irregular or uncoordinated, because, at that point, the blood no longer flows through the arteries to the rest of the body.\nWhen the heart stops beating properly, the body cannot survive. Normal breathing will stop soon after, and the body\u2019s organs will no longer receive the oxygen they need to function. Without oxygen, brain damage can begin in about 4 to 6 minutes, and the damage can become irreversible after about 8 to 10 minutes.\nA person in cardiac arrest is not breathing normally and has no pulse. The heart has either stopped beating or is beating weakly and irregularly so that a pulse cannot be detected.\nCardiovascular disease is the primary cause of cardiac arrest, but not the only cause. About 610,000 people in the United States die each year from all forms of the disease. Other causes of cardiac arrest include drowning, choking, drug overdose, severe injury, brain damage and electrocution.\nCardiac arrest can happen suddenly, without any of the warning signs usually seen in a heart attack. This is known as sudden cardiac arrest or sudden cardiac death and accounts for more than 350,000 deaths annually in the United States. Sudden cardiac arrest is caused by abnormal, chaotic electrical activity of the heart (known as arrhythmias). The most common life-threatening abnormal arrhythmia is ventricular fibrillation (V-fib).",
        "Adult Cardiac Chain of Survival": "The five links in the Adult Cardiac Chain of Survival are:\n1\ufffd Recognition of a cardiac emergency and activation of the emergency response system \ufffd The sooner more advanced medical personnel are called, the sooner EMS personnel will respond and provide care to the patient \ufffd\n2\ufffd Early CPR \ufffd CPR helps supply blood containing oxygen to the brain and other vital organs to help prevent brain damage and death \ufffd\n3\ufffd Early defibrillation \ufffd An electrical shock called defibrillation may help restore an effective heart rhythm and significantly increase the patient\u2019s chance for survival \ufffd\n4\ufffd Advanced life support \ufffd Advanced medical personnel can provide the proper tools and medication needed to continue the lifesaving care \ufffd\n5\ufffd Integrated post-cardiac arrest care \ufffd Integrated care to optimize ventilation and oxygenation and treat hypotension immediately after the return of spontaneous circulation (ROSC) \ufffd",
        "Pediatric Cardiac Chain of Survival": "The five links in the Pediatric Cardiac Chain of Survival are:\n1\ufffd Prevention of arrest \ufffd\n2\ufffd Early high-quality CPR \ufffd\n3\ufffd Rapid activation of the EMS system or response team to get help on the way quickly\u2014no matter the patient\u2019s age \ufffd\n4\ufffd Pediatric advanced life support \ufffd\n5\ufffd Integrated post-cardiac arrest care \ufffd",
        "Cardiac Chain of Survival": "During the primary assessment, you learned to identify and care for life-threatening conditions. As an EMR, you must learn how to provide care for cardiac emergencies, such as heart attack and cardiac arrest. To effectively respond to cardiac emergencies, it helps to understand the importance of the Cardiac Chain of Survival . Following the links in the Cardiac Chain of Survival gives a patient in cardiac arrest the greatest chance of survival. See the Cardiac Chain of Survival sidebar for more information. For each minute CPR and defibrillation are delayed, the patient\u2019s chance for survival is reduced between 7 and 10 percent. In the adult and pediatric Cardiac Chain of Survival, each link of the chain depends on and is connected to the other links. The layperson or bystander is the first link in the cardiac chain of survival and can greatly influence the first three links, which, when performed rapidly, have demonstrated to improve outcomes. But for this five-step sequence to work and ensure the greatest chance of survival, it is very important to quickly recognize the emergency and call for help, start CPR promptly and continue until an AED is ready to use or more advanced medical personnel arrive and coordinate care. Laypersons should be informed through community outreach programs and public awareness campaigns that by taking quick action, including calling 9-1-1 or the designated emergency number, starting CPR immediately and using an AED if one is available, it is more likely a person in cardiac arrest will survive.",
        "HIGH-QUALITY CPR": "Cardiopulmonary resuscitation (CPR) circulates blood that contains oxygen to the vital organs of a patient in cardiac arrest when the heart and normal breathing have stopped. CPR includes chest compressions and ventilations as well as the use of an AED (see Skill Sheets 13-1 to 13-3). For adult patients, CPR consists of 30 chest compressions followed by 2 ventilations. To ensure optimal patient outcomes, high-quality CPR must be performed. You can ensure high-quality CPR by providing high-quality chest compressions, making sure that the: \uf0a7 Patient is on a firm, flat surface to allow for adequate compression. In a non-healthcare setting this would typically be on the floor or ground, while in a healthcare setting this may be on a stretcher or bed with a CPR board or CPR feature applied. \uf0a7 Chest is exposed to ensure proper hand placement and the ability to visualize chest recoil. \uf0a7 Hands are correctly positioned, with the heel of one hand in the center of the chest on the lower half of the sternum with the other hand on top. Most responders find that interlacing their fingers makes it easier to provide compressions while keeping the fingers off the chest. \uf0a7 Arms are as straight as possible, with the shoulders directly over the hands to promote effective compressions. Locking elbows will help maintain straight arms. \uf0a7 Compressions are given at the correct rate of at least 100 per minute to a maximum of 120 per minute, and at the proper depth of at least 2 inches, but no more than 2.4 inches for an adult to promote adequate circulation. \uf0a7 Chest must be allowed to fully recoil between each compression to allow blood to flow back into the heart following the compression.",
        "HIGH-QUALITY CPR - Science Note": "Evidence shows that a rate of chest compressions that exceeds 120 compressions per minute begins to detrimentally impact compression depth by causing responders to be less likely to compress the chest at least 2 inches for an adult. Additional evidence shows that depth of chest compressions greater than 2.4 inches leads to increased non-life-threatening injuries, such as rib fractures, in the average adult and should be avoided. These upper limits for the rate and depth of compressions exist to improve patient outcomes, but it is also critical to maintain a rate between 100 and 120 compressions per minute and a depth of at least 2 inches. Both rate and depth of compressions are best measured using a feedback device if available.",
        "CRITICAL FACTS 4": "The five links in the Adult Cardiac Chain of Survival are: recognition of a cardiac emergency and activation of the emergency response system, early CPR, early defibrillation, advanced life support and integrated post-cardiac arrest care. A patient who is unconscious, not breathing normally and has no pulse is in cardiac arrest and needs CPR. CPR is a combination of chest compressions and ventilations that circulates blood containing oxygen to the brain and other vital organs for a person whose heart and breathing have stopped.",
        "Chest Compressions": "Effective chest compressions are essential for high-quality CPR. While not fully understood, it is believed the compressions increase the level of pressure in the chest cavity, which squeezes the heart and stimulates a contraction, causing oxygenated blood to circulate through the arteries to the brain and other vital organs. Chest compressions can also increase the likelihood that a successful shock can be delivered to a patient suffering a sudden cardiac arrest, especially if more than several minutes have elapsed since the patient\u2019s collapse. The effectiveness of compressions can be reduced if \uf0a7 Compressions are too shallow. \uf0a7 Compression rate is too slow or too fast. \uf0a7 There is sub-maximum recoil (not letting the chest come all the way back up). \uf0a7 There are frequent interruptions. \uf0a7 The patient is not on a firm, flat surface.",
        "Correct Hand Position": "Keeping your hands in the correct position allows you to give the most effective compressions. The correct position for your hands is over the lower half of the sternum (breastbone) in the middle of the chest. At the lowest point of the sternum is an arrow-shaped piece of hard tissue called the xiphoid process. Avoid pressing directly on the xiphoid process, which can break off and puncture underlying organs and tissues causing potentially serious injury. To find the correct hand position, place the heel of one hand on the center of the exposed chest, along the sternum, and then place the other hand on top. Use only the heel of your hand to apply pressure on the sternum when compressing the chest. Try to keep your fingers off the chest by interlacing them or holding them upward. Applying pressure with your fingers can cause inefficient chest compressions or unnecessary injury to the chest. Positioning the hands correctly allows for the most effective compressions and decreases the chance of causing injury.",
        "Position of the Responder": "Your body position is important when giving chest compressions. Compressing the chest straight down provides the best blood flow. The correct body position is also less tiring for you. Kneel at the patient\u2019s side opposite the chest with your hands in the correct position. Keep your elbows as straight as possible, with your shoulders directly over your hands. When you press down in this position, you are pushing straight down onto the patient\u2019s sternum. Keeping your arms as straight as possible prevents you from tiring quickly. Compressing the chest requires less effort in this position. When you press down, the weight of your upper body creates the force needed to compress the chest. Push with the weight of your upper body, not with the muscles of your arms. Push straight down. Do not rock back and forth. Rocking results in less effective compressions and wastes energy. If your arms and shoulders tire quickly, you are not using the correct body position.",
        "Rate of Compression": "Give compressions at a rate of at least 100 per minute to a maximum of 120 per minute. You can help yourself maintain the right pace by counting either aloud or in your head: one (as you press down) and (as you release the pressure) two (pressing down again) and (release again) and so on. When you get to 13, you can drop the \u201cand\u201d as it may be tiring and may alter the timing of compressions. Use a feedback device if available as it may help you to maintain a steady rhythm. Count the number of compressions, then give ventilations, before starting another cycle of compressions and ventilations.",
        "Depth of Compressions": "Each time you push down, the breastbone of an adult should move at least 2 inches. The downward movement should be smooth, not jerky. Maintain a steady down-and-up rhythm and do not pause in between. If your hands slip out of position, follow the steps listed earlier to quickly reposition them. To avoid possible injury to the patient\u2019s ribs and sternum, try to limit the maximum compression depth to 2.4 inches if using a feedback device. If in doubt, always press harder to ensure you reach at least 2 inches.",
        "Recoil": "After each compression, completely release the pressure on the chest. It is not necessary to break contact with the chest; simply allow the chest to fully return to its normal position (full recoil) before you start the next compression. It is during this phase of CPR that the chambers of the heart will refill with blood, ready to be circulated throughout the body with the next compression. The heart also receives its supply of oxygenated blood during this phase, making full recoil crucial.",
        "Interruptions": "It is critical to minimize interruptions in giving chest compressions. If compressions must be interrupted, do so for no more than 10 seconds. For example, you may need to move the patient to a location where CPR can be more effectively administered. Chest compressions are more effective when the patient is on a firm, flat surface. If the patient is on a softer surface such as a bed, couch or pressure-relieving mattress, carefully position the patient face-up on the floor or a backboard. CPR may also be interrupted briefly for defibrillation, insertion of an advanced airway or when responders change positions between compressions and ventilations.",
        "Hands-Only CPR": "Hands-only CPR, or continuous chest compressions, is a simplified form of CPR that eliminates ventilations or rescue breaths. It has its roots in dispatcher-assisted cardiac emergency situations where the caller is untrained, unwilling, unsure or otherwise unable to perform full CPR (chest compressions with ventilations or rescue breaths). Providing instruction on how to give chest compressions alone is less complex than trying to explain full CPR. The main focus of hands-only CPR is on the untrained layperson or a bystander who witnesses the sudden collapse of an adult. EMRs should be aware that if they come upon a bystander giving chest compressions only, that person is performing CPR correctly. Chest compressions alone may provide effective circulation of blood containing oxygen in the first few minutes of an out-of-hospital cardiac arrest. The same quality compression techniques of full CPR apply to compression-only CPR, including hand position, compression depth, speed, full recoil and minimal interruptions. Hands-only CPR does not affect the use of an AED.",
        "Ventilations": "Artificial ventilation is a way of forcing air into the lungs of a patient who is not breathing. The oxygen in the air will be absorbed by blood flowing through the lungs and carried to tissues and the body\u2019s vital organs. Different methods of providing ventilations are covered in Chapters 10 and 12, including:\n\uf0a7 Mouth-to-mask ventilations.\n\uf0a7 Ventilations using a bag-valve-mask (BVM) resuscitator.\nIn addition, if a resuscitation mask or BVM are not available, you may need to provide mouth-to-mouth ventilations based on local protocols and your willingness to do this without a barrier device. To provide mouth-to-mouth ventilations:\n\uf0a7 Open the airway past a neutral position using the head-tilt/chin-lift maneuver.\n\uf0a7 Pinch the nose shut and make a complete seal over the patient\u2019s mouth with your mouth (for an infant, make a seal over the infant\u2019s mouth and nose with your mouth).\n\uf0a7 Give ventilations by blowing into the patient\u2019s mouth. Ventilations should be given one at a time. Take a break between breaths by breaking the seal slightly between ventilations and then taking a breath before resealing over the mouth.\nIf you are unable to make a complete seal over a patient\u2019s mouth, you may need to use mouth-to-nose ventilations:\n\uf0a7 With the head tilted back, close the mouth by pushing on the chin.\n\uf0a7 Seal your mouth around the patient\u2019s nose and breathe into the nose.\n\uf0a7 If possible, open the patient\u2019s mouth between ventilations to allow air to escape.",
        "Ventilations - Science Note": "With mouth-to-mouth ventilations, the patient receives a concentration of oxygen at approximately 16 percent compared to the oxygen concentration of ambient air at approximately 20 percent. Giving individual ventilations can help maintain this oxygen concentration level. However, if you do not break the seal and take a breath between ventilations, the second ventilation may contain an oxygen concentration of 0 percent with a high concentration of carbon dioxide (CO2).\nProviding ventilations can save a patient\u2019s life, but overventilation can be potentially harmful, especially for a patient in cardiac arrest. For example, if the ventilation is given too forcefully, or at too fast a rate, the pressure in the patient\u2019s chest will remain too high even between breaths. This stops the blood from returning to the right side of the heart, and means that less blood is available to be pumped to other vital organs and tissues as CPR continues.",
        "Compression and Breathing Cycles": "When performing CPR on an adult, child or infant, it is delivered in cycles of chest compressions followed by ventilations. Complete the compressions, then re-establish an open airway by tilting the patient\u2019s head and lifting the chin, and then provide ventilations. When you are finished giving ventilations, quickly reposition your hands on the center of the exposed chest and start another cycle of compressions and ventilations. The pause to provide 2 ventilations should take less than 10 seconds from the last compression to the first compression of the next cycle of CPR.",
        "One-Responder CPR": "When performing one-responder CPR on an adult patient, the lone responder is responsible for conducting the scene size-up and the primary assessment, and for performing all the steps of CPR including the use of the AED, if available. CPR can be exhausting, and attempts should be made to find additional resources as early as possible during the scene size-up.CRITICAL FACTSWhen giving ventilations during CPR, if the chest does not rise after the first breath, reopen the airway, make a seal and try a second breath. If the breath is not successful, move directly back to compressions and check the airway for an obstruction before attempting subsequent ventilations. If an obstruction is found, remove it and attempt ventilations. However, NEVER perform a blind finger sweep.",
        "Two-Responder CPR": "When two responders are available, Responder 1 performs the scene size-up and primary assessment, and begins the process of providing CPR, starting with chest compressions. Meanwhile, Responder 2 calls for additional resources and gets/prepares the AED, if available. Responder 1 continues to provide high-quality CPR with 30 compressions to 2 ventilations until Responder 2 is ready to assist and/or the AED is ready to analyze. When the AED is ready to analyze, Responder 1 should move to the patient\u2019s head, and Responder 2 should prepare to provide chest compressions and get into the hovering position. Responders should continue providing cycles of chest compressions and ventilations, switching positions about every 2 minutes or when the responder performing compressions begins to fatigue. Given that AEDs prompt to analyze every 2 minutes, the AED analyze period is an ideal time for responders to switch positions. Responders call for a position change by using an agreed-upon term (such as \u201cSwitch\u201d) at the start of the last compression cycle. The responder providing compressions should count out loud and raise the volume of their voice as they near the end of each cycle (\u2026 21 \u2026 22 \u2026 23 \u2026 24 \u2026 25 \u2026 26 \u2026 27 \u2026 28 \u2026 29 \u2026 30 ). The responder at the chest will move to give ventilations while the responder at the head will move to the chest to provide compressions. In a healthcare setting, often there will be more than two responders. It is the responsibility of the team leader to orchestrate movements between responders to ensure no one responder becomes fatigued and that all critical areas are addressed: compressions, ventilations and AED. For example, additional responders may be assimilated into roles of compressor or ventilator, allowing the team leader to monitor performance and ensure that high-quality CPR is maintained. Additionally, if a BVM is available, ideally it is prepared by a third responder positioned at the top of the head with one responder squeezing the bag while another responder maintains an open airway and seals the mask.",
        "Advanced Airways": "When a patient has an advanced airway such as a supraglottic airway device or an endotracheal tube, CPR must be performed a little differently. A supraglottic airway device (e.g., a laryngeal mask airway) is an advanced airway that does not enter and directly protect the trachea like an endotracheal tube, but it allows for improved ventilation. At a minimum, two responders must be present. One responder gives 1 ventilation every 6 seconds, which is about 10 ventilations per minute. At the same time, the second responder continues giving compressions at a rate of between 100 and 120 compressions per minute. There is no pause between compressions or ventilations, and responders do not use the 30 compressions to 2 ventilations ratio. This process is a continuous delivery of compressions and ventilations with no interruption.",
        "Drowning": "When a patient is removed from the water, responders should assume the nature of arrest was the result of a drowning and that the patient is hypoxic. The sequence of care for suspected drowning patients of all ages is different than the sequence of care for other cardiac arrests. Prior to starting CPR, responders should deliver 2 initial ventilations to suspected drowning patients of all ages if there is no normal breathing or only gasping and no pulse.",
        "Stopping CPR": "Once you have started providing CPR to an adult, continue with 30 compressions followed by 2 ventilations (1 cycle = 30:2) until:\n\uf0a7 You see signs of return of spontaneous circulation (ROSC) such as patient movement or normal breathing.\n\uf0a7 An AED is ready to analyze the patient\u2019s heart rhythm.\n\uf0a7 Other trained responders take over and relieve you from compression or ventilation responsibilities.\n\uf0a7 You are presented with a valid do not resuscitate (DNR) order.\n\uf0a7 You are alone and too exhausted to continue.\n\uf0a7 The scene becomes unsafe.",
        "AUTOMATED EXTERNAL DEFIBRILLATION": "Each year, more than 350,000 Americans die suddenly of cardiac arrest. CPR can help by supplying blood containing oxygen to the brain and other vital organs. In many cases, however, an AED is needed to correct an abnormal electrical problem and allow the heart to restore an effective rhythm. Sudden cardiac arrest can happen to anyone at any time, and although less common, it can occur in children and infants.",
        "AUTOMATED EXTERNAL DEFIBRILLATORS": "Automated external defibrillators (AEDs) are portable electronic devices that analyze the heart\u2019s rhythm and can deliver an electrical shock, known as defibrillation, which helps the heart to re-establish an effective rhythm.",
        "CRITICAL FACTS 5": "Once you begin CPR, do not stop. If you must, do so for no more than 10 seconds. Reasons to discontinue CPR include more advanced medical personnel taking over for you, seeing obvious signs of life, an AED being available and ready to use, or being too exhausted to continue.",
        "History of Defibrillation": "The presence of cardiac arrhythmias or disturbances of the heart\u2019s electrical system, and the ability to correct fibrillation with electrical shock, has been known since the mid-19th century. Electrical-shocking devices, or defibrillators, were first developed during the 1920s. A portable version was introduced onto mobile coronary units in Belfast, Northern Ireland, in 1966. Defibrillation by emergency medical technicians (EMTs) without the presence of a physician was first performed in Portland, Oregon, in 1969. As technology improved over the years, newer generations of more compact, simple-to-operate, semi-automatic defibrillators known as AEDs evolved allowing EMTs and EMRs, as well as trained lay responders and the general public, to provide this lifesaving technology. With these devices, a computer analyzes the heart\u2019s rhythm and advises whether a shock is needed. Typically, the responder is guided through the steps of providing defibrillation by voice instructions and visual prompts from the AED. This includes placing the electrode (defibrillation) pads on the person\u2019s chest, analyzing the heart\u2019s rhythm, delivering a shock if needed and reminders to perform CPR when appropriate. Some AEDs can be configured to deliver lower energy levels considered appropriate for children and infants. When EMRs and other responders are trained to use AEDs, they can significantly reduce the amount of time it takes to administer a first shock in a sudden cardiac arrest, researchers say. In Eugene and Springfield, Oregon, AEDs were placed on every fire truck, and all firefighters were trained to use them. Researchers saw these communities\u2019 survival rates for cardiac arrest increase by 18 percent in the first year. The vast majority of states recognize defibrillator training for EMTs, EMRs and other responders. All states and the District of Columbia have enacted AED Good Samaritan protection for lay responders. Today, AEDs are widely dispersed and can be found in areas where large groups of people gather, such as convention centers, airports, stadiums, shopping malls, large businesses, schools and industrial complexes. The most common abnormal heart rhythm that causes sudden cardiac arrest occurs when the ventricles simply quiver, or fibrillate, without any organized rhythm. This condition is called ventricular fibrillation (V-fib). In V-fib, the electrical impulses fire at random, creating chaos and preventing the heart from pumping and circulating blood. Another less common life-threatening heart rhythm, called ventricular tachycardia (V-tach), occurs when the heart beats too fast. In V-tach, an abnormal electrical impulse controls the heart, originating in the ventricles instead of in the SA node. This abnormal impulse fires so quickly that the heart\u2019s chambers do not have time to fill, and the heart is unable to pump blood effectively. With little or no blood circulating, there may be no pulse. As with V-fib, there is no breathing or pulse.",
        "AEDs": "Automated external defibrillators (AEDs) are portable electronic devices that analyze the heart\u2019s rhythm and can deliver an electrical shock, known as defibrillation, which helps the heart to re-establish an effective rhythm. They can greatly increase the likelihood of survival if the shock is administered soon enough. For every minute lifesaving care, including CPR and defibrillation, is delayed, it is estimated that survival declines between 7 and 10 percent. Different types of AEDs are available, but all are similar in operation and have some common features, such as electrode (AED or defibrillation) pads, voice prompts, visual displays and/or lighted buttons that help guide the responder through the steps of the AED operation. AEDs monitor the heart\u2019s electrical activity through two electrodes (i.e., AED pads) placed on the chest. The computer determines the need for a shock by looking at the pattern, size and frequency of EKG waves. If the EKG waves resemble a shockable rhythm, such as V-fib or V-tach, the machine readies an electrical charge. When the electrical charge disrupts the irregular heartbeat, it is called defibrillation. This allows the heart\u2019s natural electrical system to correct itself and begin to fire off electrical impulses that will cause the heart to beat effectively. Delivering an electrical shock with an AED disrupts all electrical activity long enough to allow the heart to spontaneously develop an effective rhythm on its own. If V-fib or V-tach is not corrected, all electrical activity will eventually cease, a condition called asystole. Asystole cannot be corrected by defibrillation. You cannot tell what, if any, rhythm the heart has by feeling for a pulse. CPR, started immediately and continued until defibrillation, helps maintain a low level of circulation in the body until defibrillation, and increases the likelihood that the defibrillation shock will allow the heart to correct the abnormal rhythm. Use an AED when the following conditions are present: \uf0a7 The patient is unresponsive. \uf0a7 There is no normal breathing. \uf0a7 You do not detect a pulse.",
        "CRITICAL FACTS 6": "V-fib is the most common cause of sudden cardiac arrest. In V-fib, heart ventricles quiver instead of beating properly, due to erratic electrical impulses. AEDs are portable electronic devices that analyze the heart\u2019s rhythm and can deliver an electrical shock, known as defibrillation, which helps the heart to re-establish an effective rhythm. When a cardiac arrest occurs, an AED should be used as soon as it is available and ready to use. If the AED advises that a shock is needed, follow protocols to give 1 shock followed by about 2 minutes of CPR.",
        "Using an AED": "When a cardiac arrest occurs, an AED should be used as soon as it is available and ready to use. If the AED advises that a shock is needed, follow protocols to give 1 shock followed by about 2 minutes of CPR. If CPR is in progress, chest compressions should not be interrupted until the AED is turned on, the defibrillation pads are applied and the AED is ready to analyze the heart rhythm. Chest compressions can increase the likelihood that a defibrillation shock will be successful. Always follow local protocols and medical direction when using an AED and performing CPR. Be thoroughly familiar with the manufacturer\u2019s operating instructions and maintenance guidelines for the device that you will be operating. The general steps of operating an AED include: 1. Turning on the AED and preparing it for use. Once the AED is turned on, it will guide the responder through all the steps of operation with voice and visual prompts. Some models have a power button that must be pressed or a handle that has to be pulled, while others will activate upon opening the case or lid. 2. Exposing the patient\u2019s chest and wiping the chest dry if necessary. The AED pads must be applied to the patient\u2019s bare, dry chest. If the patient\u2019s chest is moist or wet, it should be wiped with a small towel or gauze pads to ensure the best adhesion of the AED pads. 3. Attaching the AED pads to the patient\u2019s bare, dry chest. Remove the AED pads from their sealed packaging. Peel the backing off from each pad, one at a time, to expose the adhesive, conductive surface of the pad before it is applied to the patient\u2019s bare chest. Many AED pads have illustrations on them that show correct pad placement. Some AED pads are preconnected to the device, and some must be plugged into the device before rhythm analysis can begin. The pads should be appropriate to the patient. For example, pediatric AED pads must not be used on an adult patient because the lower energy levels may not be enough to defibrillate the patient, but if no pediatric pads are available, adult pads can be used on a child or infant. 4. Analyzing the heart rhythm. Most AEDs will automatically begin analysis when the pads are attached to the patient and connected to the device, while others have an \u201canalyze\u201d button that must be pushed. No one should touch or bump into the patient during the rhythm analysis as this could produce faulty readings. 5. Delivering a defibrillation shock. Once the analysis of the rhythm is complete, the AED will advise either to shock or not to shock the patient. If a shockable rhythm is detected, the AED will cycle up an electrical energy charge that will supply the shock to the patient. Some models can deliver the shock automatically, while others have a \u201cshock\u201d button that must be manually pushed to deliver the shock. No one should be in contact with the patient when the shock is delivered, because they could also receive a shock and thereby reduce the effectiveness of the defibrillation shock by absorbing some of the electrical energy. After a shock is delivered, or if no shock is advised, a period of time is programmed to allow for CPR until the next rhythm analysis begins. If the AED prompts to troubleshoot a problem such as \u201ccheck electrodes\u201d or \u201ccheck pads,\u201d check to see that the AED pads are connected properly to the device and placed on the patient\u2019s chest with good adhesion, according to the manufacturer\u2019s instructions and local protocols. Spare batteries should be available in case of a \u201clow battery\u201d warning, but shocks can still be delivered with a low battery warning on some models. After a shock is delivered or if no shock is indicated, immediately perform about 2 minutes of CPR, starting with compressions, before the AED begins analyzing the heart rhythm again. This pause is automatically programmed into the device and will be preceded by a voice prompt to resume CPR. You do not need to wait for the AED prompts to finish to begin chest compressions after a shock was delivered or a no shock advised prompt. If at any time you notice a sign of ROSC, such as normal breathing, stop CPR and monitor the patient\u2019s condition.",
        "Pacemakers and Implantable": "Cardioverter-Defibrillators Sometimes patients may have had a pacemaker implanted. These small implantable devices are sometimes located in the area below the right or left collarbone. There may be a small lump that can be felt under the skin. Other patients may have an implantable cardioverter-defibrillator (ICD), a miniature version of an AED, which acts to automatically recognize and restore abnormal heart rhythms. Sometimes, a patient\u2019s heart beats irregularly, even if the patient has a pacemaker or an ICD. If the implanted device is visible or you know that the patient has one, do not place the defibrillation pad directly over the device. This may interfere with the delivery of the shock. Adjust pad placement if necessary and continue to follow established protocols. If you are not sure, use the AED as needed. It will not harm the patient or responder. Responders should be aware that it is possible to receive a mild shock if an implantable ICD delivers a shock to the patient while CPR is performed. This risk of injury to responders is minimal, and the amount of electrical energy involved is low. Much of the electrical energy is absorbed by the patient\u2019s own body tissues. Some protocols may include temporarily deactivating the shock capability of an ICD with a donut magnet or other precautions. EMRs should be aware of and follow any special precautions associated with ICDs, but delays in delivering CPR and defibrillation shocks from an AED should not occur.",
        "AEDs Around Water": "If the patient is in freestanding water, remove the patient before defibrillation. A shock delivered in water could conduct to responders or bystanders. Once you have removed the patient from the water, be sure there are no puddles of water around you, the patient or the AED. Remove wet clothing from the chest for proper pad placement, if necessary. Dry the patient\u2019s chest and attach the AED pads. If it is raining, ensure that the patient is as dry as possible and sheltered from the rain. Wipe the patient\u2019s chest dry. Minimize delaying defibrillation when taking steps to provide for a dry environment. The electrical current of an AED is very directional between the pads. AEDs are quite safe, even in rain and snow, when all precautions and manufacturer\u2019s operating instructions are followed.",
        "Transdermal Medication Patches": "Some patients may use a transdermal medication patch. The most common of these patches is the nitroglycerin patch, used by those with a history of cardiac problems. Since nitroglycerin or other medications can be absorbed by a responder, remove the patch from the patient\u2019s chest with a gloved hand before placing the defibrillation pads on the chest. Nicotine patches used to stop smoking look similar to nitroglycerin patches. To avoid wasting time trying to identify patches, remove any patch you see on the patient\u2019s chest with a gloved hand. Never place AED electrode pads directly on top of medication patches.",
        "Hypothermia": "Some patients who have experienced hypothermia have been resuscitated successfully even after prolonged exposure. If you do not feel a pulse, begin CPR until an AED becomes available. Follow local protocols as to whether an AED should be used. If the patient is wet, dry their chest and attach the AED pads. If a shock is indicated, deliver a shock and follow the instructions of the AED. If there are no obvious signs of life, continue CPR. Continue CPR and protect the patient from further heat loss. Wet garments should be removed, if possible. The patient should not be defibrillated in water. CPR or defibrillation should not be withheld to rewarm the patient. EMRs should handle hypothermia patients gently, as shaking them could result in V-fib.",
        "Trauma": "If a patient is in cardiac arrest resulting from traumatic injuries, an AED may still be used. Defibrillation should be administered according to local protocols.",
        "Chest Hair": "Some patients have excessive chest hair that may cause difficulty with pad-to-skin contact. Since time to first shock is critical, and chest hair rarely interferes with pad adhesion, attach the pads and analyze the heart\u2019s rhythm as soon as possible. Press firmly on the pads to attach them to the patient\u2019s chest. If you get a \u201ccheck pads\u201d or similar message from the AED, remove the pads and replace with new ones. The pad adhesive may pull out some of the chest hair, which may solve the problem. If you continue to get the \u201ccheck pads\u201d message, remove the pads, shave the patient\u2019s chest and attach new pads to the patient\u2019s chest. Spare defibrillation pads and a safety razor should be included in the AED kit.",
        "Jewelry and Body Piercings": "Jewelry and body piercings do not need to be removed when using an AED. These are simply distractions that do no harm to the patient, but taking time to remove them delays delivery of the first shock. Do not delay the use of an AED to remove jewelry or body piercings. Do not place the defibrillation pad directly over metallic jewelry or body piercings. Adjust pad placement if necessary and continue to follow established protocols.",
        "AED PRECAUTIONS": "When operating an AED, follow these general precautions: \uf0a7 Do not use alcohol to wipe the patient\u2019s chest dry; alcohol is flammable. \uf0a7 Do not use pediatric AED pads on an adult, as they may not deliver enough energy for defibrillation. \uf0a7 Do not touch the patient while the AED is analyzing. Touching or moving the patient may affect the analysis. \uf0a7 Before shocking a patient with an AED, make sure that no one is touching or is in contact with the patient or the resuscitation equipment. \uf0a7 Do not touch the patient while defibrillating. You or someone else could be shocked. \uf0a7 Do not defibrillate someone when around flammable or combustible materials such as gasoline or free-flowing oxygen. \uf0a7 Do not use an AED in a moving vehicle. Movement may affect the analysis. \uf0a7 Do not use an AED on a patient who is in contact with freestanding water. Move the patient away from puddles of water or swimming pools, or out of the rain, before defibrillating. \uf0a7 Do not use an AED on a patient wearing a nitroglycerin patch or other medication patch on the chest. With a gloved hand, remove any patches from the chest before attaching the defibrillation pads.",
        "AED MAINTENANCE": "For defibrillators to function optimally, they must be maintained like any other machine. AEDs require minimal maintenance. These devices have various self-testing features. However, it is important that operators be familiar with any visual or audible prompts the AED may have to warn of malfunction or a low battery. It is important that you read the operator\u2019s manual thoroughly and check with the manufacturer to obtain all necessary information regarding maintenance. In most instances, if the machine detects any malfunction, you should contact the manufacturer. The device may need to be returned to the manufacturer for service. While AEDs require minimal maintenance, it is important to remember the following: \uf0a7 Follow the manufacturer\u2019s specific recommendations for periodic equipment checks. \uf0a7 Make sure that the batteries have enough energy for one complete rescue. (A fully charged backup battery should be readily available.) \uf0a7 Make sure that the correct defibrillation pads are in the package and are properly sealed. \uf0a7 Check any expiration dates on defibrillation pads and batteries, and replace as necessary After use, make sure that all accessories are replaced and that the machine is in proper working order before placing it back in service. If at any time the machine fails to work properly or warning indicators are recognized, discontinue use, place it out of service and contact the manufacturer immediately.",
        "High-Performance CPR": "High-performance CPR refers to providing high-quality chest compressions as part of a well-organized team response to a cardiac arrest. Coordinated, efficient, effective teamwork is essential to minimize the time spent not in contact with the chest to improve patient outcomes. Think about all of the activities performed during a resuscitation. For example: \uf0a7 AED pads are applied. \uf0a7 AED must charge. \uf0a7 Pocket mask or BVM may need to be repositioned. \uf0a7 Airway may need to be reopened. \uf0a7 Other personnel arrive on scene. \uf0a7 Responders switch positions. \uf0a7 Advanced airway may need to be inserted. \uf0a7 Pulse checks may be done, but unnecessarily. All of these activities could affect your ability to maintain contact with the patient\u2019s chest.",
        "High-Performance CPR - Science Note": "Current research indicates that survival following resuscitation is significantly affected by the quality of CPR performed. One important aspect is minimizing interruptions in chest compressions, which helps to maximize the blood flow generated by the compressions.",
        "Chest Compression Fraction": "Chest compression fraction, or CCF, is the term used to denote the proportion of time that chest compressions are performed. It represents the fraction of time spent performing compressions, that is, the time that the responders are in contact with the patient\u2019s chest, divided by the total time of the resuscitation, beginning with the arrival on scene until the ROSC. Expert consensus identifies a CCF of at least 60 percent to promote optimal outcomes, with a goal of 80 percent. To achieve the best CCF percentage, a coordinated team approach is needed, with each member assuming pre-assigned roles, anticipating the next action steps for yourself and other team members. This coordinated team approach also includes integrating and assimilating additional personnel, such as paramedics or a code team, who arrive on scene. To further your understanding of high-performance CPR, consider the example of an automotive racing team. Each crew member has a specific role when the race car arrives in the pit area. They are supervised by a leader, who keeps the crew on task and gets the race car back on the track. The quality, efficiency and swiftness of the crew\u2019s actions can ultimately affect the outcome of how the race car performs. The same is true for a team response to CPR. All team members should have specific roles during a resuscitation. Based on available resources, potential roles include the following: \uf0a7 Team leader \uf0a7 Compressor \uf0a7 Responder managing the airway \uf0a7 Responder providing ventilations \uf0a7 Responder managing the AED \uf0a7 Recorder Keep in mind that there are no national protocols in place for high-performance CPR. How you function within a team setting, including how additional personnel assimilate into the team, may vary depending on your local protocols or practice.",
        "Integration of More Advanced Personnel": "During resuscitation, numerous people may be involved in providing care to the patient. Responders must work together as a team in a coordinated effort to achieve the best outcomes for the patient. Characteristics of effective teamwork include well-defined roles and responsibilities; clear, closed-loop communication; and respectful treatment of others. Coordination becomes even more important when more advanced personnel, such as an advanced life support team or code team, arrive on the scene. This coordination of all involved is necessary to: \uf0a7 Ensure that all individuals involved work as a team to help promote the best outcome for the patient. \uf0a7 Promote effective perfusion to the vital organs. \uf0a7 Minimize interruptions of chest compressions, which have been shown to improve survival. Ultimately, it is the team leader who is responsible for this coordination. When more advanced personnel arrive on scene, it is the team leader who communicates with advanced personnel, providing them with a report of the patient\u2019s status and events. The team leader also sets clear expectations, prioritizes, directs, acts decisively, encourages team input and interaction, and focuses on the big picture.",
        "Crew Resource Management": "During resuscitation, crew resource management helps to promote effective and efficient teamwork. Crew resource management is a communication process that centers around the team leader, who coordinates the actions and activities of team members so that the team functions effectively and efficiently. For example, when new individuals arrive on the scene or when team members switch roles during an emergency, it is the team leader who is responsible for coordinating these activities. During resuscitation, the team leader directs and coordinates all the working elements, including team members, activities and actions, as well as equipment, to focus on providing high-quality CPR, the goal of any resuscitation effort. Crew resource management also guides team members to directly and effectively communicate to a team leader about dangerous or time-critical decisions. It was developed as a result of several airline disasters as a way to prevent future incidents. Crew resource management has been shown to help avoid medical errors in healthcare. To effectively communicate via crew resource management, team members should get the attention of the team leader, and state their concern, the problem as they see it and a solution. Working together, the team should then be sure to obtain direction from the team leader.",
        "PROVIDING CPR/AED FOR CHILDREN AND INFANTS - CPR/AED Differences Between Children and Adults": "When performing CPR on a child, there are some subtle differences in technique. These differences include opening the airway, compression depth, the ratio of compressions to ventilations depending on the number of responders, and AED pads and pad placement.",
        "PROVIDING CPR/AED FOR CHILDREN AND INFANTS - Airway": "To open the airway of a child, you would use the same head-tilt/chin-lift maneuver as for an adult. However, you would only tilt the head slightly past a neutral position, avoiding any hyperextension or flexion in the neck. Table 13-2 illustrates airway and ventilation differences for an adult and child.",
        "PROVIDING CPR/AED FOR CHILDREN AND INFANTS - Compressions": "The positioning and manner of providing compressions to a child are also very similar to an adult. Place your hands in the center of the exposed chest on the lower half of the sternum and compress at a rate of between 100 and 120 compressions per minute. However, the depth of compression is different. For a child, compress the chest only about 2 inches, which is 1\u20443 the anterior-posterior diameter of the chest, instead of at least 2 inches, but no more than 2.4 inches, as you would for an adult. For smaller children, you may need to compress the chest with only one hand. Ensure you are able to compress the chest about 2 inches.",
        "Compressions-to-Ventilations Ratio": "When you are the only responder, the ratio of compressions to ventilations for a child is the same as for an adult, that is, 30 compressions to 2 ventilations (30:2). However, in two-responder situations, this ratio changes to 15 compressions to 2 ventilations (15:2).",
        "Compressions-to-Ventilations Ratio - Science Note": "Most child-related cardiac arrests occur as a result of a hypoxic event such as an exacerbation of asthma, an airway obstruction or a drowning. As such, ventilations and appropriate oxygenation are important for a successful resuscitation. In these situations, laryngeal spasm may occur, making passive ventilation during chest compressions minimal or nonexistent. Therefore, it is critical to correct the oxygenation problem by providing high-quality CPR prior to leaving the child or infant. Based on local protocols or practice, it is permissible to provide two ventilations prior to initiating CPR after the primary assessment if a hypoxic event is suspected.",
        "Compressions-to-Ventilations Ratio - AEDs": "AEDs work the same way regardless of the patient\u2019s age, but there are differences in the pads used for children as well as the pad placement based on the size of the child. For children over the age of 8 years and weighing more than 55 pounds, you would continue to use adult AED pads, placing them in the same location as for an adult\u2014one pad to the right of the sternum and below the right clavicle, with the other pad on the left side of the chest on the midaxillary line a few inches below the left armpit. However, for children 8 years of age or younger or weighing less than 55 pounds, use pediatric AED pads if available. Be aware that some AEDs use a switch or key instead of changing pads, so follow the directions from the AED manufacturer on how to care for pediatric patients with their device. At no time should the AED pads touch each other when applied. If it appears that the AED pads would touch each other based on the size of the child\u2019s chest, use an anterior and posterior pad placement as an alternative. Apply one pad to the center of the child\u2019s chest on the sternum and one pad to the child\u2019s back between the scapulae.",
        "CPR/AED DIFFERENCES FOR INFANTS": "Like with children, several differences need to be addressed when providing CPR to an infant. These differences include the primary assessment (assessing the level of consciousness and checking the pulse), opening the airway, compression depth, the ratio of compressions to ventilations depending on the number of responders and AED pad placement.",
        "Primary Assessment Variations: Infant": "When assessing the infant\u2019s level of consciousness, you should shout, \u201cAre you okay?\u201d or use the infant\u2019s name if known, and tap the bottom of the foot rather than the shoulder as part of the \u201cshout-tap-shout\u201d sequence. Another variation for the infant involves the pulse check. For an infant, check the brachial pulse with two fingers on the inside of the upper arm. Be careful not to use your thumb because it has its own detectable pulse. You will need to expose the arm to accurately feel a brachial pulse.",
        "Primary Assessment Variations: Infant - Science Note": "AVPU is not as accurate in infants and children as it is in adults. The pediatric assessment triangle\u2014Appearance, Effort of breathing, and Circulation\u2014can give you a more accurate depiction of an infant\u2019s status. Regardless of what tool is used, the recognition of an unresponsive infant is the priority.",
        "Primary Assessment Variations: Infant - Airway": "To open the airway of an infant, use the same head-tilt/chin-lift maneuver as you would for an adult or child. However, only tilt the head to a neutral position, taking care to avoid any hyperextension or flexion in the neck. Be careful not to place your fingers on the soft tissues under the chin or neck to open the airway.",
        "Primary Assessment Variations: Infant - Compressions": "Although the rate of compressions is the same for an infant as for an adult or child, the positioning and manner of providing compressions to an infant are different because of the infant\u2019s smaller size. Positioning also differs based on the number of responders involved.",
        "CRITICAL FACTS 7": "In the absence of pediatric pads or a pediatric setting on the AED, you may use adult pads for the child. Be sure that the pads will not touch each other if considering a traditional pad placement on the anterior chest. Use the anterior and posterior pad placement if the pads may touch each other. Remember: because the energy supplied by pediatric pads is reduced, they would not be effective for an adult patient and should not be used. Always follow local protocols, medical direction and the manufacturer\u2019s instructions.",
        "CPR/AED Differences: Adult and Child\nADULTCHILD ( Age 1 through onset of puberty)": "Compressions\nHand position Hands centered on lower half of sternum Hands centered on lower half of sternum\nCompression rateBetween 100 and 120 compressions per minuteBetween 100 and 120 compressions per minute\nCompression depthAt least 2 inches (but no more than 2.4 inches)About 2 inches (or 1/3 the anterior-posterior diameter of the chest)\nCompression/ventilation ratio \u2022One-responder CPR: 30:2 \u2022Two-responder CPR: 30:2 \u2022One-responder CPR: 30:2 \u2022Two-responder CPR: 15:2\nAED\nAED pads Adult pads: age > 8 years, weight > 55 pounds \u2022Pediatric pads: age 1\u20138 years, weight < 55 pounds \u2022Adult pads if pediatric pads not available\nAED pad placement \u2022Upper right chest below right clavicle to the right of sternum \u2022Left side of chest several inches below left armpit on midaxillary line \u2022Upper right chest below right clavicle to the right of sternum \u2022Left side of chest several inches below left armpit on midaxillary line \u2022If pads risk touching each other\u2014anterior/posterior placement The firm, flat surface necessary for providing compressions is also appropriate for an infant. However, that surface can be above the ground, such as a stable table or countertop. Often it is easier for the responder to provide compressions from a standing position rather than kneeling at the patient\u2019s side. Compressions are delivered at the same rate for adults and children, that is, at a rate of at least 100 per minute to a maximum of 120 compressions per minute. However, for an infant, only compress the chest about 1\u00bd inches (or 1/3 the anterior-posterior diameter of the chest).",
        "CPR Differences - One-Responder": "CPR To perform compressions when one responder is present, place two fingers from your hand closest to the infant\u2019s feet in the center of the exposed chest, just below the nipple line on the sternum. The fingers should be oriented so that they are parallel, not perpendicular to the sternum. Responders may use either their index finger and middle finger or their middle finger and fourth finger to provide compressions. Fingers that are more similar in length tend to make the delivery of compressions easier. The ratio of compressions to ventilations is the same for an adult or child, that is, 30 compressions to 2 ventilations (30:2).",
        "CPR Differences - Two-Responder": "CPR When two responders are caring for an infant in cardiac arrest, the positioning of the responders and the method of performing chest compressions differ from that of an adult or child. The responder performing chest compressions will be positioned at the infant\u2019s feet while the responder providing ventilations will be at the infant\u2019s head. Compressions are delivered using the encircling thumbs technique. To provide compressions using this technique:\n\uf0a7 Place both thumbs on the center of the infant\u2019s exposed chest side by side, just below the nipple line.\n\uf0a7 Have the other fingers encircling the infant\u2019s chest toward the back, providing support.\nWhile positioned at the infant\u2019s head, the responder providing ventilations will open the airway using two hands and seal the mask using the E-C technique. With two responders, the ratio of compressions to ventilations changes to that of a child, that is, 15 compressions to 2 ventilations (15:2).",
        "AED Differences": "While the need to deliver a defibrillation for an infant occurs less often than for an adult, the use of an AED remains a critical component of infant cardiac arrest care. As with a child patient, use pediatric AED pads if available. Keep in mind that similar to a child, some AEDs use a switch or key instead of changing pads, so follow the directions from the AED manufacturer on how to care for pediatric patients with their device. When applying the pads, place one pad in the center of the anterior chest and the second pad in the posterior position centered between the scapulae. Just as with a child, if no pediatric pads are available, use adult AED pads. Table 13-5 summarizes the differences in CPR and AED for adults, children and infants.\nPediatric Consideration\u2014  \nPoor Perfusion  \nWhen a child or an infant is not breathing normally and has a pulse less than or equal to 60 beats per minutes, perform compressions (CPR) if there are signs of poor perfusion. Recheck breathing and pulse every 2 minutes. If there is no pulse, provide CPR.\nAdditional Resources\nWhile it is rare in the professional setting to be alone with a child or infant, there is a slight change of when you should call for additional resources when you are alone. After determining that an adult is unresponsive and you are alone, you should immediately call for additional resources and get an AED. With children, it is more important to provide about 2 minutes of CPR before leaving them to call for additional resources or get an AED unless the arrest is witnessed and believed to be cardiac in origin.",
        "CPR/AED Differences: Adult, Child and Infant\n\nADULT\nCHILD (Age 1 through onset of puberty)": "\nINFANT (Birth to age 1)\n\nCompressions\nHand position\nHands centered on lower half of sternum\nHands centered on lower half of sternum\nOne responder: Two fingers centered on sternum, just below nipple line\nTwo responders: Thumbs centered on chest side by side, just below nipple line.\n\nCompression rate\nBetween 100 and 120 compressions per minute\nBetween 100 and 120 compressions per minute\nBetween 100 and 120 compressions per minute\n\nCompression depth\nAt least 2 inches, but no more than 2.4 inches\nAbout 2 inches (or 1/3 the anterior-posterior diameter of the chest)\nAbout 1\u00bd inches (or 1/3 the anterior-posterior diameter of the chest)\n\nCompression/ventilation ratio\n\u2022One-responder CPR: 30:2\n\u2022Two-responder CPR: 30:2\n\u2022One-responder CPR: 30:2\n\u2022Two-responder CPR: 15:2\n\u2022One-responder CPR: 30:2\n\u2022Two-responder CPR: 15:2\n\nAED\nAED pads\nAdult pads: age > 8 years, weight > 55 pounds\n\u2022Pediatric pads: age 1 to 8 years, weight < 55 pounds\n\u2022Adult pads if pediatric pads not available\n\u2022Pediatric pads\n\u2022Adult pads if pediatric pads not available",
        "PUTTING IT ALL TOGETHER": "When the heart stops beating, or beats too ineffectively to circulate blood to the brain and other vital organs, this is called cardiac arrest. Irreversible brain damage is likely to occur after about 8 to 10 minutes from lack of oxygen. By starting CPR immediately, and using an AED, you can help keep the patient\u2019s brain and other vital organs supplied with oxygen and help the heart restore an effective, pumping rhythm. By summoning more advanced medical personnel, you can increase the cardiac arrest patient\u2019s chances for survival. A patient who is unconscious, not breathing normally and has no pulse is in cardiac arrest and needs immediate CPR. When performing CPR, always remember the following points regarding the quality and maximum effectiveness of CPR:\n\uf0a7\tChest compressions should be given fast, smooth and deep.\n\uf0a7\tLet the chest fully recoil or return to its normal position after each compression before starting the downstroke of the next compression.\n\uf0a7\tMinimize any interruptions in chest compressions.If two responders are available, begin two-responder CPR as soon as possible. Change positions about every 2 minutes and continue CPR. Once you start CPR, do not stop unnecessarily. The heart\u2019s electrical system controls the pumping action of the heart. Damage to the heart from disease or injury can disrupt the heart\u2019s electrical system, resulting in an abnormal heart rhythm that can stop circulation. The two most common treatable abnormal rhythms initially present in patients suffering sudden cardiac arrest are V-fib and V-tach. An AED is a portable electronic device that analyzes the heart\u2019s rhythm and delivers an electrical shock to the heart, called defibrillation. Defibrillation disrupts the electrical activity of V-fib and V-tach long enough to allow the heart to develop an effective rhythm on its own. AEDs are used in conjunction with CPR. Use an AED as soon as one becomes available. The sooner the shock is administered, the greater the likelihood of the patient\u2019s survival. AEDs are appropriate for use on adults, children and infants in cardiac arrest. When using an AED, follow your local protocols and the manufacturer\u2019s operating instructions, and be aware of AED precautions and special situations.",
        "Preventing Coronary Heart Disease": "Recognizing a heart attack and getting the necessary care as soon as possible may prevent a patient from going into cardiac arrest. However, preventing a heart attack in the first place is even more effective\u2014there is no substitute for prevention. Heart attacks are usually the result of disease of the heart and blood vessels. Coronary heart disease (CHD) develops slowly. Deposits of cholesterol, a fatty substance made by the body and present in certain foods, build up on the inner walls of the arteries. As the arteries that carry blood to the heart get narrower, less oxygen-rich blood flows to the heart. This reduced oxygen supply to the heart can eventually cause a heart attack. Although a heart attack may seem to strike suddenly, many people gradually put their hearts in danger from cardiovascular disease. Because cardiovascular disease develops slowly, people may not be aware of it for many years. Fortunately, it is possible to slow the progress of cardiovascular disease by making lifestyle changes. Behavior that can harm the heart and blood vessels may begin in early childhood. Junk food, which is high in cholesterol and saturated fats but has little real nutritional value, can contribute to cardiovascular disease. Cigarette smoking also greatly contributes to cardiovascular disease and to other diseases. Many factors increase a person\u2019s chances of developing cardiovascular disease. These are called risk factors. Some of them you cannot change. For instance, although more women than men die each year from cardiovascular disease in the United States, heart disease generally affects men at younger ages than it does women. Ethnicity also plays a role in determining the risk for heart disease. African-American and Native American/American Indian populations statistically have higher rates of heart disease than do other U.S. populations. A family history of heart disease also increases the risk.",
        "Altering Risk Factors": "Many risk factors can be altered, however. Cigarette smoking; uncontrolled diabetes, high blood cholesterol or high blood pressure; obesity; and lack of regular exercise all increase the risk of heart disease. When you combine one risk factor, such as smoking, with others, such as high blood pressure and lack of regular exercise, the risk of heart attack is much greater. It is never too late to take steps to control risk factors, thereby improving your chances for living a long and healthy life. It is important to know how to perform CPR and use an AED. However, since the chances of surviving cardiac arrest are poor, the best way to deal with cardiac arrest is to be aware of risk factors and take steps to help prevent it, including exercise and quitting smoking."
    },
    {
        "KEY TERMS": "Cardiogenic shock: The result of the heart being unable to supply adequate blood circulation to the vital organs, resulting in an inadequate supply of nutrients; caused by trauma or disease., Dilation: The process of enlargement, stretching or expansion; used to describe blood vessels., Distributive shock: A type of shock caused by inadequate distribution of blood, either in the blood vessels or throughout the body, leading to inadequate volumes of blood returning to the heart., Hypoglycemic shock: A type of shock that is a reaction to extremely low blood glucose levels., Hypoperfusion: A life-threatening condition in which the circulatory system fails to adequately circulate oxygenated blood to all parts of the body, resulting in inadequate tissue perfusion; also referred to as shock., Hypovolemic shock: A type of shock caused by an abnormal decrease in blood volume., Metabolic shock: A type of shock that is the result of a loss of body fluid, which can be due to severe diarrhea, vomiting or a heat-related illness., Neurogenic shock: A type of distributive shock caused by trauma to the spinal cord or brain, where the blood vessel walls abnormally constrict and dilate, preventing relay of messages and causing blood to pool at the lowest point of the body., Obstructive shock: A type of shock caused by any obstruction to blood flow, usually within the blood vessels, such as a pulmonary embolism., Psychogenic shock: A type of shock that is due to factors such as emotional stress that cause blood to pool in the body in areas away from the brain, which can result in fainting (syncope)., Respiratory shock: A type of shock caused by the failure of the lungs to transfer sufficient oxygen into the bloodstream; occurs with respiratory distress or arrest., Septic shock: A type of distributive shock that occurs when an infection has spread to the point that bacteria are releasing toxins into the bloodstream, causing blood pressure to drop when the tissues become damaged from the circulating toxins., Shock: A life-threatening condition that occurs when the circulatory system fails to provide adequate oxygenated blood to all parts of the body, resulting in inadequate tissue perfusion; also referred to as hypoperfusion.",
        "INTRODUCTION": "Injuries and medical emergencies can become life threatening as a result of shock. When the body experiences injury or sudden illness, it responds in a number of ways. Survival depends on the body\u2019s ability to adapt to the physical stresses of injury or illness. When the body\u2019s measures to adapt fail, the injured or ill person can progress into a life-threatening condition called shock. Shock complicates the effects of injury or sudden illness. In this chapter, you will learn to recognize the signs and symptoms of shock and how to provide care to minimize it.",
        "WHAT IS SHOCK?": "Shock, or hypoperfusion, is a progressive condition in which the circulatory system fails to adequately circulate oxygenated blood to all parts of the body, resulting in inadequate tissue perfusion. When vital organs, such as the brain, heart and lungs, do not receive sufficient oxygenated blood, the body begins a series of responses to protect those organs. The amount of blood circulating to the less important tissues of the arms, legs and skin is reduced so that more can go to the vital organs. This reduction in blood circulation to the skin causes a person in shock to appear pale or ashen (grayish) and feel cool. While, in the short term, this can protect the body\u2019s most crucial organs, if the situation is not treated quickly, shock can lead to death. When the body is healthy, three conditions are necessary to maintain adequate blood flow: \uf0a7 The heart must be working well. \uf0a7 The blood vessels must be intact and able to adjust blood flow and pressure. \uf0a7 An adequate amount of blood must be circulating in the body. Injury or sudden illness can interrupt normal body functions. In cases of minor injury or illness, this interruption is brief, because the body is able to compensate quickly. With more severe injuries or illnesses, however, the body is unable to adjust. When the body is unable to meet its demands for oxygen because the blood fails to circulate adequately, shock occurs.",
        "WHY SHOCK OCCURS": "Shock results from inadequate delivery of oxygenated blood to the body\u2019s tissues. There are several possible reasons for shock to occur. It can be the result of: \uf0a7 Severe bleeding or loss of fluid from the body through excessive vomiting and diarrhea. \uf0a7 Failure of the heart to pump enough oxygenated blood. \uf0a7 Abnormal dilation of the vessels. \uf0a7 Impaired blood flow to the organs and cells.",
        "WHY SHOCK OCCURS - The Heart": "The condition and functioning of the heart can have a significant impact on the likelihood of shock. If the heart rate is too slow, the rate of new oxygenated blood cells reaching each part of the body will not be enough to keep up with demand. If the heart beats too rapidly (ventricular tachycardia [V-tach]) or if the heartbeat becomes erratic (ventricular fibrillation [V-fib]), the oxygenated blood is not sent throughout the body as it should be. Damage to the heart can lead to weak and ineffective contractions; this can be related to disease (e.g., diabetes or cardiovascular disease), poisoning or respiratory distress.",
        "WHY SHOCK OCCURS - Blood Vessels": "If blood vessels are not able to adequately constrict or become abnormally dilated, even though the blood volume is adequate and the heart is beating well, the vessels are not filled completely with blood. Since oxygen is absorbed into the body through the walls of the blood vessels, this condition leads to less oxygen being available to the body. Abnormal dilation of the blood vessels can be caused by a spinal cord injury, or by infection or anaphylaxis.",
        "WHY SHOCK OCCURS - Blood": "Insufficient blood volume can lead to shock. Also, if the levels of some components of the blood, such as plasma or fluids, become too low, blood flow will be impaired and shock can result. These conditions can occur due to bleeding, severe vomiting, diarrhea and burns.",
        "WHY SHOCK OCCURS - Chest and Airway": "Shock can also occur following any injury to the chest, obstruction of the airway or any other respiratory problem that decreases the amount of oxygen in the lungs. This means insufficient oxygen enters the bloodstream.",
        "TYPES OF SHOCK": "There are four major types of shock: hypovolemic, obstructive, distributive and cardiogenic. All cause a drop in blood pressure and have the same outcome if not treated quickly.",
        "Hypovolemic": "Hypovolemic shock is due to a severe lack of blood and fluid within the body. Hemorrhagic shock is the most common type of hypovolemic shock. It results from blood loss, either through external or internal bleeding, which causes a decrease in total blood volume.",
        "CRITICAL FACTS": "Shock, or hypoperfusion, is a progressive condition in which the circulatory system fails to adequately circulate oxygenated blood to all parts of the body. There are several possible reasons for shock to occur. It can be the result of severe bleeding or loss of fluid, failure of the heart to pump enough oxygenated blood, abnormal dilation of the vessels, and impaired blood flow to the organs and cells.",
        "Obstructive": "Obstructive shock is caused by some type of obstruction to blood flow, usually within the blood vessels, such as a pulmonary embolism, tension pneumothorax or cardiac tamponade.",
        "Distributive": "Distributive shock refers to any type of shock caused by inadequate distribution of blood either in the blood vessels or throughout the body, leading to inadequate volumes of blood returning to the heart. It includes the following:",
        "Neurogenic shock": "Neurogenic shock is caused by spinal cord or brain trauma. The blood vessel walls normally constrict and dilate to circulate the blood throughout the circulatory system. In neurogenic shock, the messages are not relayed, and the blood pools at the lowest point of the body.",
        "Anaphylaxis": "Anaphylaxis (also referred to as anaphylactic shock) occurs as a result of exposure to an allergen. It is a whole-body reaction that causes dilation (enlargement, stretching or expansion) of the blood vessels and constriction (closing) of the airways, which in turn causes blood to pool and trouble breathing. The airways may close completely from inflammation. For more information on anaphylaxis, refer to Chapter 16.",
        "Septic shock": "Septic shock occurs when an infection has spread to the point that bacteria are releasing toxins into the bloodstream. The blood pressure drops when the tissues become damaged from the circulating toxins.",
        "Cardiogenic": "Cardiogenic shock is the result of the heart being unable to supply adequate blood circulation to the vital organs, resulting in an inadequate supply of oxygen and nutrients. Disease, trauma or injury to the heart causes this type of shock.",
        "Other Types of Shock": "Other types of shock include hypoglycemic, metabolic, psychogenic and respiratory shock. Hypoglycemic shock is a reaction to extremely low blood glucose levels. Metabolic shock is the result of a loss of body fluid, which can be due to severe diarrhea, vomiting or a heat-related illness. Psychogenic shock is due to factors such as emotional stress that cause blood to pool in the body in areas away from the brain, which can result in fainting (syncope). Respiratory shock is the failure of the lungs to transfer sufficient oxygen into the bloodstream and occurs with respiratory distress or arrest.",
        "SIGNS AND SYMPTOMS OF SHOCK": "Because this is a progressive condition, the signs and symptoms you see will depend on what stage of shock the person is in, and this will change over time (Fig. 18-1). At first, the signs and symptoms may seem minor, but responding to them promptly will increase the patient\u2019s chance of survival.",
        "Early Signs and Symptoms of SHOCK": "You may observe that: \uf0a7 The patient expresses feelings of apprehension and anxiety. \uf0a7 The patient\u2019s body temperature is slightly lower than normal. \uf0a7 The patient is breathing quickly. \uf0a7 The patient\u2019s pulse is slightly increased. \uf0a7 The patient\u2019s blood pressure is normal or slightly decreased. \uf0a7 The patient\u2019s skin is pale or ashen (grayish) and cool. \u2022 Apprehension and anxiety\n\u2022 Slightly lower body temperature\n\u2022 Rapid breathing\n\u2022 Slightly increased pulse\n\u2022 Slightly decreased or normal blood pressure\n\u2022 Pale, ashen, cool skin",
        "CRITICAL FACTS 1": "There are four major types of shock: hypovolemic, obstructive, distributive and cardiogenic. All cause a drop in blood pressure and have the same outcome if not treated quickly. Other types of shock include hypoglycemic, metabolic, psychogenic and respiratory shock. Early signs and symptoms of shock may include feelings of apprehension and anxiety; slightly low body temperature; rapid breathing; slight increase in pulse rate; normal or slightly decreased blood pressure; and pale, ashen and cool skin.",
        "Later Signs and Symptoms of SHOCK": "You may observe that:\n\uf0a7\tThe patient is listless and confused, and may have difficulty speaking.\n\uf0a7\tThe patient\u2019s breathing has slowed down and is shallow and irregular.\n\uf0a7\tThe patient\u2019s blood pressure is decreasing; diastolic blood pressure may reach zero.\n\uf0a7\tThe patient\u2019s pulse is rapid, but the pulse is weak and irregular.\n\uf0a7\tThe patient\u2019s skin is pale, cold and clammy, and the body temperature is much lower than normal.\n\uf0a7\tThe patient\u2019s pupils are dilated and slow to respond to light. \u2022 Listlessness and confusion\n\u2022 Slow, shallow, irregular breathing\n\u2022 Decreasing blood pressure\n\u2022 Rapid but weak and irregular pulse\n\u2022 Pale, cold and clammy skin\n\u2022 Lower than normal blood pressure\n\u2022 Dilated pupils",
        "Pediatric Considerations of SHOCK": "Early signs of shock may be absent in young children or infants, because their bodies can compensate for some of the factors that cause shock by maintaining blood pressure at normal levels. If the conditions continue, however, the situation can suddenly deteriorate into severe shock. Because a child is smaller than an adult, blood volume is less, and losing what seems like a small amount of blood can be serious, making children more susceptible to shock. Do not wait for signs and symptoms of shock to develop when treating a young child or infant, but treat promptly based on your assessment of the injuries or trauma.",
        "CRITICAL FACTS 2": "Later signs and symptoms of shock can include listlessness; confusion; difficulty speaking; irregular breathing; decreased blood pressure (diastolic blood pressure may reach zero); rapid yet weak or irregular pulse; pale, cold and clammy skin with a low body temperature; and dilated pupils.",
        "PROVIDING CARE of SHOCK": "Once you have assessed the patient and determined that there are signs and symptoms of shock present, quick response is essential:\n\uf0a7\tTake steps to control any severe, life-threatening bleeding and prevent further blood loss.\n\uf0a7\tEnsure the patient\u2019s airway is open and clear. Perform a primary assessment and call for more advanced medical personnel. Administer supplemental oxygen based on local protocols, and provide appropriate ventilatory support.\n\uf0a7\tSince you may not be sure of the patient\u2019s condition, leave them in a supine position.\n\uf0a7\tIf you see any suspected broken bones or dislocated or damaged joints, immobilize them to prevent movement after ensuring other life-threatening conditions have been addressed. Broken bones or dislocated or damaged joints can cause more bleeding and damage.\n\uf0a7\tCover the patient with a blanket to prevent loss of body heat. It is important not to overheat the patient\u2014your goal should be to maintain a normal body temperature. If the patient is lying on cold ground and if it is possible to do so without causing harm, you may want to put a blanket under the patient as well.\n\uf0a7\tTalk to the patient in a calm and reassuring manner to reduce the harmful effects of emotional stress. If you can help the patient rest in a comfortable position and reduce the pain, this will also be beneficial; pain intensifies the body\u2019s reactions and can accelerate the progression of shock.\n\uf0a7\tDo not give any food or drinks, even if the patient asks for them. The patient is likely to be thirsty due to the fluid loss. However, depending on the condition, surgery may be needed and it is better for the patient\u2019s stomach to be empty if that is the case. More advanced emergency medical personnel will be able to provide fluid replacement intravenously if appropriate.\n\uf0a7\tTreat any specific injuries or conditions, and have the patient transported to a hospital as soon as possible.",
        "PUTTING IT ALL TOGETHER": "Any condition or trauma situation where the body\u2019s ability to get oxygenated blood to the vital organs is compromised can lead to shock. Left untreated, shock is a progressive condition that can be fatal. Shock can be caused by loss of blood or body fluids, when the heart is not pumping blood effectively, by over-dilation of the blood vessels or by damage to the chest or airways. If any of these conditions are present, it is important to watch the patient for signs and symptoms of shock. These include decreasing blood pressure; increasing heart rate; increasing respiratory rate; pale or ashen, cool, clammy skin; pupils that are dilated and slow to respond; and anxiety and apprehension at first, turning into confusion and listlessness as shock progresses.\nTo treat shock, first control any severe, life-threatening bleeding that may be present. Ensure the patient has an open and clear airway and is breathing. Call for more advanced medical personnel and transport the patient to a hospital as soon as possible. Administer supplemental oxygen or artificial ventilation as appropriate. Keep the patient in a supine position. Splint any broken bones or joints and keep the patient warm by covering the patient with a blanket. Reassure and comfort the patient; try to keep the patient comfortable and reduce any pain. Do not give food or drink."
    },
    {
        "Introduction": "The purpose of this chapter is to teach you the remaining skills to perform cardiopulmonary resuscitation (CPR). CPR consists of three major skills: the C (circulation) skills, the A (airway) skills, and the B (breathing) skills. In Chapter 7, Airway Management, you learned the airway and breathing skills. These airway and breathing procedures may be lifesaving for a patient who has stopped breathing and whose heart is still beating. In most cases, however, by the time you arrive on the scene, the patient has not only stopped breathing, but the heart has stopped beating as well. If the patient has no heartbeat and is not breathing or only gasping, rescue breathing alone will not save the patient\u2019s life. Forcing air into the lungs is useless unless the circulatory system can carry the oxygen in the lungs to all parts of the body. In this chapter, you will learn the C (circulation) skills. If the patient\u2019s heart has stopped, you can maintain or restore circulation manually through the use of chest compressions (closed-chest cardiac massage). According to recent studies, it is important to restore circulation before starting rescue breathing. Therefore, in this chapter you will learn to perform the circulation skills before you perform the airway and breathing skills (a CAB sequence). To maintain both a heartbeat and ventilation, chest compressions and rescue breathing must be done together. By combining the circulation, airway, and breathing skills, you will be able to perform CPR. Statistics show that about 70% of the patients who experience cardiac arrest are in a state of ventricular fibrillation\u2014a condition in which the heart muscle is quivering and not effectively pumping blood. Therefore, this chapter covers the theory and the steps you need to learn to use an automated external defibrillator to defibrillate these patients.",
        "Anatomy and Function of the Circulatory System": "The circulatory system consists of a pump (the heart), a network of pipes (the blood vessels), and fluid (blood). After blood picks up oxygen in the lungs, it travels to the heart, which in turn pumps the oxygenated blood to the rest of the body. In Chapter 6, The Human Body, you learned how the heart functions as a pump. The heart, which is about the size of your fist, is located in the chest between the lungs. The cells of the body absorb oxygen and nutrients (glucose) from the blood and produce waste products (including carbon dioxide) that the blood carries back to the lungs. In the lungs, the blood exchanges the carbon dioxide for more oxygen. Blood then returns to the heart to be pumped out again. Other metabolic waste products are removed by the kidneys and liver. The human heart consists of four chambers, two on the right side of the heart and two on the left side. Each upper chamber is called an atrium. The right atrium receives blood from the veins of the body; the left atrium receives highly oxygenated blood from the lungs. The bottom chambers are known as the ventricles. The right ventricle pumps deoxygenated blood to the lungs; the left ventricle pumps highly oxygenated blood throughout the body. The most muscular chamber of the heart is the left ventricle, which needs the most power because it must force blood to all parts of the body. The four chambers of the heart work together in a well-ordered sequence to pump blood to the lungs and to the rest of the body. One-way valves in the heart and veins allow the blood to flow in only one direction through the circulatory system. The arteries carry blood away from the heart at high pressure; therefore, the walls of arteries are thick. The main artery carrying blood away from the heart, the aorta, is quite large (about 1 inch [2.5 cm] in diameter), but arteries become smaller in diameter farther away from the heart. These smaller arteries eventually branch into the capillaries, the smallest pipes in the circulatory system. Some capillaries are so small that only one blood cell at a time can go through them. At the capillary level, oxygen passes from the blood cells into the cells of body tissues, and carbon dioxide and other waste products pass from the tissue cells to the blood cells, which then return to the lungs. Veins are the thin-walled pipes of the circulatory system that carry blood back to the heart. The four major artery locations are as follows: the neck (carotid arteries); the wrist (radial arteries); the arm (brachial arteries); and the groin (femoral arteries). The locations of these arteries are shown in Figure 8-2. Because these arteries lie between a bony structure and the skin, you can use them to measure the patient\u2019s pulse. A pulse is generated when the heart contracts and sends a pressure wave through the artery. The carotid pulse is measured on either side of the neck, the radial pulse is taken at the thumb side of the wrist, the brachial pulse is taken on the inside of the upper arm, and the femoral pulse is taken at the groin. Blood has several components plasma (a clear, straw-colored fluid), red blood cells, white blood cells, and platelets. The red blood cells give blood its red color. Red blood cells carry oxygen from the lungs to the body and bring carbon dioxide back to the lungs. The white blood cells are called infection fighters because they devour bacteria and other disease-causing organisms. Platelets start the blood-clotting process",
        "Locations for assessing the patient\u2019s pulse.": "A. Neck (carotid pulse). B. Wrist (radial pulse). C. Arm (brachial pulse). D. Groin (femoral pulse).",
        "Cardiac Arrest": "Cardiac arrest occurs when the heart stops contracting and no blood is pumped through the blood vessels. Without a supply of blood, the cells of the body will die because they cannot get any oxygen or nutrients and they cannot eliminate waste products. As the cells die, organ damage occurs. Some organs are more sensitive to low oxygen levels than others. Brain damage begins within 4 to 6 minutes after the patient has gone into cardiac arrest. Within 8 to 10 minutes, the damage to the brain may become irreversible. Cardiac arrest may have many different causes, including the following: Heart and blood vessel diseases such as heart attack and stroke. Respiratory arrest, if untreated. Medical emergencies such as epilepsy, diabetes, allergic reactions, electric shock, and poisoning. Drug overdose. Drowning. Suffocation. Trauma and shock caused by massive blood loss. A patient who has experienced cardiac arrest is unconscious and is not breathing or only gasping. You cannot feel a pulse and the patient looks dead.Regardless of the cause of cardiac arrest, the initial treatment is the same: provide CPR.",
        "Words of Wisdom": "Certain physiologic and lifestyle factors can increase the chance that a person will have a heart attack. These factors include high blood pressure, uncontrolled diabetes, obesity, high blood cholesterol or lipids, and high stress. These factors can affect your patients, but they can also affect you. Developing and maintaining a healthy lifestyle will be beneficial in reducing your chance of experiencing a heart attack.",
        "Components of CPR": "The technique of CPR requires three types of skills: C (circulation) skills, A (airway) skills, and B (breathing) skills. From the airway and breathing skills that were detailed in Chapter 7, Airway Management, you learned how to check patients to determine whether the airway is open and to correct a blocked airway by using the head tilt\u2013chin lift or jaw-thrust maneuver. You learned how to check patients to determine whether they are breathing. You also learned to correct the absence of breathing by performing rescue breathing. To perform CPR, you combine the A (airway) and B (breathing) skills with C (circulation) skills in a CAB sequence. You begin by checking for the patient\u2019s pulse. With practice, you will be able to check for a pulse at the same time you are checking for signs of breathing. This helps to reduce the time it takes to begin treating the patient. If the patient has no pulse, you must restore the patient\u2019s circulation by starting external chest compressions. The airway and breathing techniques you learned previously will then be used to push oxygen into the patient\u2019s lungs. External chest compressions move the oxygenated blood throughout the body. By compressing the patient\u2019s sternum (breastbone), you change the pressure in the patient\u2019s chest and force enough blood through the system to sustain life for a short period of time. CPR by itself cannot sustain life indefinitely. However, once it is recognized that the patient is pulseless and is not breathing or only gasping, start CPR as soon as possible to give the patient the best chance for survival. By performing all three parts of the CPR sequence, you can keep the patient alive until an AED is available and more advanced medical care can be delivered. In many cases, the patient will need defibrillation and medication to be successfully resuscitated from cardiac arrest.",
        "CPR: Words of Wisdom": "Patients who are experiencing cardiac events\u2014as well as their family members and friends\u2014will usually be fearful and anxious about the episode. It is important for you to demonstrate a caring attitude and to acknowledge those feelings. Although your primary goal is to ensure that the patient receives appropriate and timely care, you should understand that compassion is an important part of your care for patients experiencing a cardiac event.",
        "The Cardiac Chain of Survival": "In most cases of cardiac arrest, CPR alone is not enough to save lives, but it is the first treatment in the out-of-hospital chain of survival presented by the American Heart Association (AHA). The five links in the chain include:\n1. Recognition of cardiac arrest and activation of the emergency response system\n2. Immediate CPR with emphasis on high-quality chest compressions\n3. Rapid defibrillation\n4. Basic and advanced emergency medical services (EMS) care\n5. Advanced life support (ALS) and postarrest care\nAs an emergency medical responder (EMR), you can help the patient by providing early CPR with an emphasis on high-quality chest compressions and by making sure that the EMS system has been activated. Some EMRs are trained in the use of automated external defibrillators. By keeping these links of the chain strong, you will help keep the patient alive until early ALS care can be administered by paramedics and hospital personnel. Just as an actual chain is only as strong as its weakest link, the chain of survival is only as good as its weakest link. Your actions in performing early CPR are vital to giving cardiac arrest patients their best chance for survival",
        "The Cardiac Chain of Survival - Words of Wisdom": "Patients with chest pain are often in denial as to the reason for their chest pain. Many people will try to deny that their pain could be caused by a cardiac event. They may tell you that they are experiencing indigestion or that they have a cold. This denial often results in long delays before the patient decides to call 9-1-1. Treat any patient with chest pain as if his or her pain could be caused by a significant heart problem.",
        "When to Start CPR": "CPR should be started on all nonbreathing, pulseless patients, unless they are obviously dead or they have a do not resuscitate (DNR) order that is valid in your jurisdiction. (DNR orders are discussed more fully later in this chapter.) Few reliable criteria exist to determine death immediately. As discussed in Chapter 4, Medical, Legal, and Ethical Issues, the following criteria are reliable signs of death and indicate that CPR should not be started: 1. Decapitation. Decapitation occurs when the head is separated from the rest of the body. When this occurs, there is obviously no chance of saving the patient. 2. Rigor mortis. This is the temporary stiffening of muscles that occurs several hours after death. Rigor mortis indicates the patient has been dead for a prolonged period of time and cannot be resuscitated. 3. Evidence of tissue decomposition. Tissue decomposition or actual flesh decay occurs only after a person has been dead for more than 1 day. 4. Dependent lividity. Dependent lividity is the red or purple color that appears on the parts of the patient\u2019s body that are closest to the ground. It is caused by blood seeping into the tissues on the dependent, or lower, part of the person\u2019s body. Dependent lividity occurs after a person has been dead for several hours. If any of the preceding signs of death are present in a pulseless, nonbreathing person, do not begin CPR. If none of these signs is present, you should activate the EMS system and then begin CPR. It is far better to start CPR on a person who is later declared dead by a physician than to withhold CPR from a patient whose life might have been saved.",
        "When to Stop CPR": "You should discontinue CPR only when:\n1. Effective spontaneous circulation and ventilation are restored or the patient begins to move.\n2. Resuscitation efforts are transferred to another person with an equal or higher level of training who continues CPR.\n3. A physician orders you to stop.\n4. The patient is transferred to properly trained EMS personnel.\n5. Reliable criteria for death (as previously listed) are recognized.\n6. You are too exhausted to continue resuscitation, environmental hazards endanger your safety, or continued resuscitation would place the lives of others at risk.",
        "External Cardiac Compression": "External Chest Compressions on an Adult\nAn adult patient in cardiac arrest is unconscious, has no carotid pulse, and is not breathing or only gasping. If you suspect that the patient has experienced cardiac arrest, check the carotid pulse and look for no breathing or only gasping. To check the carotid pulse, place your index and middle fingers on the larynx (Adam\u2019s apple). Slide your fingers into the groove between the larynx and the muscles at the side of the neck. Keep your fingers there for at least 5 seconds but no more than 10 seconds to be sure the pulse is absent and not just slow. At the same time, look for signs of chest movement and feel for air exchange. If there is no carotid pulse in an unresponsive, nonbreathing patient, you must begin chest compressions. For chest compressions to be effective, the patient must be lying on a firm, horizontal surface. If the patient is on a soft surface, such as a bed, it is impossible to compress the chest. Immediately place all patients needing CPR on a firm, level surface. To position yourself so that you can perform chest compressions effectively, stand or kneel beside the patient\u2019s chest and face the patient. Place the heel of one hand in the center of the patient\u2019s chest, on the lower half of the sternum. Place the heel of your other hand on top of the hand on the chest and interlock your fingers. 1. Place the heel of your hand in the center of the chest, on the lower half of the sternum.\n Place your other hand on top of your first hand and interlock your fingers.\n, It is important to locate and maintain the proper hand position while applying chest compressions. If your hands are too high, the force you apply will not produce adequate chest compressions. If your hands are too low, the force you apply may damage the liver. If your hands slip sideways off the sternum and onto the ribs, the compressions will not be effective and you may damage the ribs and lungs.\n After you have both hands in the proper position, compress the chest of an adult at least 2 inches (5 cm) straight down. For compressions to be effective, stay close to the patient\u2019s side and lean forward so that your arms are directly over the patient. Keep your back straight and your elbows stiff so you can apply the force of your whole body to each compression, not just your arm muscles. Between compressions, make sure you completely release pressure on the chest to allow maximum filling of the patient\u2019s heart. Never lean on the chest during compressions. Compressions must be rhythmic and continuous. Each compression cycle consists of one downward push followed by a rest so that the heart can refill with blood. Push hard and push fast. Compressions should be at the rate of 100 to 120 compressions per minute in all patients\u2014adults, children, and infants. After every 30 chest compressions, give two rescue breaths (1 second per breath). Practice on a manikin until you can compress the chest smoothly and rhythmically.",
        "Performing Adult Chest Compressions": "Step 1. Place the heel of your hand in the center of the chest, on the lower half of the sternum. Step 2\nPlace your other hand on top of your first hand and interlock your fingers.\nStep 3\nCompress the chest of an adult at least 2 inches (5 cm) straight down.",
        "Chest Compressions - Treatment": "Do not let your fingers touch the chest wall; your fingers could dig into the patient, causing injury. Interlocking your fingers will help avoid this.",
        "External Chest Compressions on an Infant": "Infants (children younger than 1 year) who have experienced cardiac arrest will be unconscious, not breathing or only gasping, and will have no pulse. To check for cardiac arrest, begin by checking responsiveness. If the infant is unresponsive, check the brachial pulse and look, listen, and feel for signs of breathing. If a pulse is absent and there are no signs of breathing, begin CPR starting with chest compressions. To check an infant\u2019s circulation, feel for the brachial pulse on the inside of the upper arm. Use two fingers of one hand to feel for the pulse and use your other hand to maintain the head tilt. If the infant has no pulse and is not breathing or only gasping, begin CPR starting with chest compressions. Draw an imaginary horizontal line between the two nipples and place your index finger just below the imaginary line in the center of the chest. Place your middle and ring fingers next to your index finger. Use your middle and ring fingers to compress the sternum at least one-third the depth of the chest (about 1.5 inches [4 cm]). Compress the sternum at a rate of 100 to 120 times per minute. If you are the only rescuer, give two rescue breaths (1 second per breath) after every 30 chest compressions. If two rescuers are present, give two rescue breaths after every 15 chest compressions. When you perform chest compressions, place the infant on a solid surface such as a table or cradle the infant in your arm. You do not need to use much force to achieve adequate compressions on infants because they are so small and their chests are so flexible.",
        "External Chest Compressions on a Child": "The signs of cardiac arrest in a child (from age 1 year to the onset of puberty [age 12 to 14 years]) are the same as those for an adult. Determine if the child is responsive. If the child is unresponsive, simultaneously check the carotid pulse and for no breathing and for gasping. If there is no pulse, no breathing, and only gasping, the patient is in cardiac arrest. Check the carotid pulse by placing two or three fingers on the larynx. Slide your fingers into the groove between the Adam\u2019s apple and the muscle. Feel for the carotid pulse with one hand.\n\nTo perform chest compressions on a small child, place the heel of one hand in the center of the chest, on the lower half of the sternum. In larger children, perform chest compressions with two hands, as with the adult. Compress the sternum at least one-third the depth of the chest (about 2 inches [5 cm]). Compress the chest at a rate of at 100 to 120 times per minute. If you are the only rescuer present, give two rescue breaths after every 30 chest compressions. If two rescuers are present, give two rescue breaths after every 15 compressions.",
        "One-Rescuer Adult CPR": "In Chapter 7, Airway Management you learned how to open the airway and perform rescue breathing. Now that you have learned how to check for circulation and do chest compressions, you are ready to put all your skills together to perform CPR. If you are the only trained person at the scene, you must perform one-rescuer CPR. Follow the steps in Skill Drill 8-2: \n1. Establish unresponsiveness Step 1. Ask the patient, \u201cAre you okay?\u201d Gently shake the patient\u2019s shoulder. If you do not get a response, call for additional help, activate the EMS system, and send someone to get an AED if one is available. \n2. Position the patient so he or she is flat on his or her back on a hard surface. Position yourself so that your knees are alongside the patient\u2019s chest.\n3. Determine pulselessness by checking the carotid pulse and simultaneously checking for no breathing or only gasping. Check the pulse and breathing for no more than 10 seconds Step 2.\n 4. If the patient has no pulse and is not breathing or only gasping, begin chest compressions. Place the heel of one hand in the center of the chest, on the lower half of the sternum. Place your other hand on top of the first. Lock your fingers together and pull upward so that the only thing touching the patient\u2019s chest is the heel of your hand Step 3. 5. Lean forward so your shoulders are directly over your hands and the patient\u2019s sternum. Keep your arms straight and compress the sternum at least 2 inches (5 cm), using the weight of your body. Relax between compressions, allowing the chest to fully recoil. Give 30 compressions at a rate of 100 to 120 compressions per minute, and count each one out loud as follows: \u201cOne and two and three and\u2026.\u201d Each set of 30 compressions should take between 15 and 18 seconds to complete. 6. After 30 chest compressions, open the airway using a head tilt\u2013chin lift or a jaw-thrust maneuver if you suspect a head or spinal injury Step 4. Give two rescue breaths (1 second each). Ensure that each breath produces visible chest rise Step 5. 7. Continue the cycles of 30 chest compressions and two breaths until additional personnel arrive, an AED arrives, or the patient starts to move\n\nWhen performing one-rescuer CPR\u2014whether the patient is an adult, child, or infant\u2014deliver chest compressions and rescue breathing at a ratio of 30 compressions to two breaths. Immediately give two rescue breaths after each set of 30 chest compressions. Because you must interrupt chest compressions to ventilate, you should perform each series of 30 chest compressions in approximately 18 seconds (a rate of 100 to 120 compressions per minute). Although one-rescuer CPR can keep the patient alive, two-rescuer CPR is preferable because it is less exhausting for the rescuers. Whenever possible, CPR for an adult should be performed by two rescuers.",
        "One-Rescuer Adult CPR - Words of Wisdom": "If you do not have a partner with you to help perform CPR, do not wait for another rescuer to arrive. Call 9-1-1 to activate EMS and then begin one-rescuer CPR immediately!",
        "Performing One-Rescuer Adult CPR": "Step 1 Establish unresponsiveness by shouting and gently shaking the shoulder.\nStep 2 If the patient is unresponsive, simultaneously check the carotid pulse and check for signs of breathing. Take no more than 10 seconds to do this. If the patient is unresponsive, activate the EMS system.\n Step 3 If breathing and pulse are absent, begin a cycle of 30 chest compressions at a rate of 100 to 120 compressions per minute. Compress the chest at least 2 inches (5 cm) and release the pressure on the chest after each compression.\nStep 4 After 30 compressions, open the airway with a head tilt\u2013chin lift or a jaw-thrust maneuver if you suspect a head or spinal injury.\nStep 5 Give two rescue breaths over 1 second. Watch for chest rise to ensure air is going into the lungs. Continue cycles of 30 compressions and two rescue breaths until an AED arrives, patient care is assumed by other providers, or the patient starts to move.",
        "Two-Rescuer Adult CPR": "In many cases, a second trained person will be on the scene to help you perform CPR. Two-rescuer CPR is more effective than one-rescuer CPR. One rescuer delivers chest compressions while the other performs rescue breathing. Chest compressions and ventilations can be given more regularly and without interruption. However, to avoid rescuer fatigue\u2014which may result in less effective chest compressions\u2014the two rescuers should switch roles after every five cycles of CPR (about every 2 minutes). Two rescuers should be able to switch roles quickly, interrupting CPR for 5 seconds or less. In any circumstance, CPR should not be interrupted for longer than 10 seconds. In two-rescuer CPR, one rescuer delivers ventilations (mouth-to-mouth, bag-mask, or mouth-to-mask breathing) and the other gives chest compressions. If possible, position yourselves on opposite sides of the patient\u2014one rescuer near the head and the other near the chest. The sequence of steps is the same as for one-rescuer CPR, but the tasks are divided.Skill Drill 8-3\n\n1. Rescuer One establishes unresponsiveness. Rescuer Two moves to the patient\u2019s side to be ready to deliver chest compressions. Rescuer One activates the EMS system Step 1. 2. If the patient is unresponsive, Rescuer One determines pulselessness. Rescuer One simultaneously checks for signs of circulation and breathing by checking the carotid pulse and watching for chest rise for no more than 10 seconds Step 2. If the patient has no pulse and is not breathing or only gasping, continue to Step 3. 3. The rescuers begin CPR, starting with chest compressions. Rescuer Two performs 30 chest compressions at a rate of 100 to 120 compressions per minute Step 3. 4. Rescuer One opens the airway with a head tilt\u2013chin lift or, in the case of a trauma or if a head or spinal injury is suspected, a jaw-thrust maneuver Step 4. 5. Rescuer One gives two ventilations of 1 second each and observes for visible chest rise Step 5. 6. Continue CPR for five cycles of 30 compressions and two ventilations (about 2 minutes). After 2 minutes of CPR, the rescuers switch.positions. The switch time should take no longer than 5 seconds. 7.Continue cycles of 30 chest compressions and two ventilations until an AED arrives, ALS personnel take over, or the patient starts to move. Compressions and ventilations should remain rhythmic and uninterrupted. By counting out loud, Rescuer Two can continue to deliver compressions at the rate of 100 to 120 compressions per minute, briefly pausing as Rescuer One delivers two rescue breaths. Once you and your partner establish a smooth pattern of CPR, you should limit interruptions in CPR to 10 seconds or less, such as when reassessing or moving the patient. A skill performance sheet titled Two-Res cuer Adult CPR is shown in Figure 8-9 for your review and practice.",
        "Performing Two-Rescuer Adult CPR": "Step 1 Establish responsiveness and lack of breathing. Step 2\nIf the patient is unresponsive, simultaneously check the carotid\npulse and check for no breathing and only gasping. This should take\nno more than 10 seconds.\n Step 3: Perform 30 chest compressions. Step 4 Open the airway using the head tilt\u2013chin lift or jaw-thrust maneuver. Step 5: Perform rescue breathing; give two breaths. Continue cycles of 30 compressions and two rescue breaths until an AED arrives, care is assumed by other providers, or the patient starts to move.",
        "Two-Rescuer Adult CPR - Words of Wisdom": "When you have a patient who is in cardiac arrest, always be prepared for vomiting. It is a frequent event, and your preparation for it can be lifesaving.",
        "Switching Positions During CPR": "If you and your partner must continue to perform two-rescuer CPR for any length of time, the rescuer performing chest compressions will become tired. Once a rescuer gets tired, the effectiveness of chest compressions decreases. Therefore rescuers should switch positions after every five cycles of CPR (about every 2 minutes). This will improve the quality of chest compressions and give the patient the best chance for survival. A switch allows the person giving compressions (Rescuer Two) to rest his or her arms. Switching positions should be accomplished as smoothly and quickly (5 seconds or less) as possible to minimize the break in rate and regularity of compressions and ventilations. There are many orderly ways to switch positions. Learn the method practiced in your EMS system. One method is as follows:\n1. As Rescuer Two tires, he or she says the following out loud (instead of counting): \u201cWe\u2014will\u2014switch\u2014this\u2014time.\u201d One word is spoken as each compression is done. These words replace the counting sequence for the first five compressions. After 25 more chest compressions (a total of 30 compressions), Rescuer One completes two ventilations and moves to the chest to perform compressions. Rescuer Two moves to the head of the patient to maintain the airway and ventilation. Rescuer One then begins chest compressions. Practice switching positions until you can do it smoothly and quickly. Switching positions is much easier if the rescuers work on opposite sides of the patient.",
        "One-Rescuer Infant CPR": "An infant is defined as anyone younger than 1 year. The principles of CPR are the same for adults and infants. In actual practice, however, you must use slightly different techniques for an infant. Follow these steps for one-rescuer infant CPR: 1. Position the infant faceup on a firm, flat surface. 2. Establish the infant\u2019s level of responsiveness. An unresponsive infant is limp. Gently shake or tap the infant to determine whether he or she is unconscious. Call for additional help if the patient is unconscious. Activate the EMS system. 3. If the infant is unresponsive, simultaneously check the brachial pulse and check for signs of no breathing or only gasping. The brachial pulse is on the inside of the arm. You can feel it by placing your index and middle fingers on the inside of the infant\u2019s arm, halfway between the shoulder and the elbow. Check for at least 5 seconds but no more than 10 seconds. Assess for breathing by looking at the infant\u2019s chest and abdomen. 4. If the infant has no pulse and is not breathing or only gasping, begin chest compressions. An infant\u2019s heart is located relatively higher in the chest than an adult\u2019s heart. Imagine a horizontal line drawn between the infant\u2019s nipples. To correctly position your fingers for chest compressions, imagine a line between the infant\u2019s nipples. Place your index finger in the middle of the sternum and just below the nipple line and your middle and ring fingers next to your index finger. Raise your index finger so that your middle finger and ring fingers remain in contact with the chest. 5. Perform chest compressions on an infant using two fingers in the middle of the chest just below the nipple line. Compress the chest at least one-third the depth of the chest (about 1.5 [4 cm] inches) at a rate of 100 to 120 compressions per minute. 5. With your fingers in the correct location, compress the chest 30 times with the pads of your fingertips. Compress the chest at least one-third the depth of the chest (about 1.5 inches [4 cm]) at a rate of 100 to 120 compressions per minute. 6. Open the infant\u2019s airway. This step is best done by the head tilt\u2013chin lift maneuver. Gently tilt the infant\u2019s head to a neutral or slight sniffing position. Tilting it too far can obstruct the airway. 7. Give two breaths, each lasting 1 second. To breathe for an infant, place your mouth over the infant\u2019s mouth and nose. Because an infant has very small lungs, you should give only very small puffs of air, just enough to make the chest rise. Do not use large or forceful breaths. 8. Continue compressions and ventilations. If you are alone, give 30 compressions and two breaths. Continue to give 30 compressions followed by two rescue breaths until other providers arrive to take over the care of the infant or the infant begins to move.",
        "Two-Rescuer Infant CPR": "If you are performing two-rescuer infant CPR, use the two-thumb/encircling hands technique for chest compressions. This technique is done by placing both thumbs side by side over the lower half of the infant\u2019s sternum and encircling the infant\u2019s chest with your hands. Compress the sternum at a rate of 100 to 120 compressions per minute. When you are performing two-rescuer infant CPR, perform a compression-to-ventilation ratio of 15 to 2. Rescuers should switch roles after 10 cycles of CPR (about 2 minutes) when using a compression to ventilation ratio of 15:2.",
        "One-Rescuer and Two-Rescuer Child CPR": "A child is defined as a person between age 1 year and the onset of puberty (age 12 to 14 years). The steps for child CPR are essentially the same as for an adult; however, some steps may require modification for a child. These variations are as follows:\n1.\nUse less force to compress the child\u2019s chest.\n2.\nIn small children, use only one hand to depress the sternum at least one-third the depth of the chest (about 2 inches [5 cm]). Use two hands in larger children.\n3.\nUse less force to ventilate the child. Ventilate only until the child\u2019s chest rises.\nFollow these steps to administer CPR to a child:\n1.\nEstablish the child\u2019s level of responsiveness. Tap and gently shake the shoulder and shout, \u201cAre you okay?\u201d If a second rescuer is available, have him or her activate the EMS system and get an AED if available. 2. Place the child faceup on a firm, flat surface. 3. Check for circulation and simultaneously check for signs of no breathing or only gasping. Locate the larynx with your index and middle fingers. Slide your fingers into the groove between the larynx and the muscles at the side of the neck to feel for the carotid pulse. Check for at least 5 seconds but no more than 10 seconds. 4. If the child has no pulse and is not breathing or only gasping, begin chest compressions. 5. Begin a cycle of 30 chest compressions. Compress the chest at least one-third the diameter of the chest (approximately 2 inches [5 cm] in most children) at a rate of 100 to 120 compressions per minute. Count the compressions out loud: \u201cOne and two and three and\u2026.\u201d In between compressions, allow the chest to fully recoil. 6. After 30 compressions, open the airway. Use the head tilt\u2013chin lift maneuver or, if the child is injured, use the jaw-thrust maneuver. Maintain an open airway. 7. Give two rescue breaths. Blow slowly for 1 second, using just enough force to make the chest visibly rise. Allow the lungs to deflate between breaths. 8. Coordinate chest compressions and ventilations in a 30:2 ratio for one rescuer and 15:2 for two rescuers, making sure the chest rises with each ventilation. 9. After five cycles (about 2 minutes) of CPR, assess for signs of breathing or a pulse. If the child has no pulse and you have an AED, apply it now. 10.If you are alone with no communications device, perform 2 minutes of CPR before leaving the patient to activate the EMS system. 11. Continue until other EMS providers arrive to take over the care of the patient or the patient starts to move. A skill performance sheet titled One-Rescuer Child CPR is shown in Figure 8-14 for your review and practice. In large children, remember that you may need to use two hands to achieve an adequate depth of compression. When you are performing two-rescuer CPR on a child, administer 15 compressions followed by two rescue breaths.",
        "Signs of Effective CPR": "It is important to know the signs of effective CPR so you can assess your efforts to resuscitate the patient. The signs of effective CPR are as follows:\n1. A second rescuer feels a carotid pulse while you are compressing the chest.\n2. The patient\u2019s skin color improves (from blue to pink).\n3. The chest visibly rises during ventilations.\n4. Compressions and ventilations are delivered at the appropriate rate and depth.\nIf some of these signs are not present, evaluate and alter your technique to try and achieve these signs.",
        "Complications of CPR - Broken Ribs": "If your hands slip to the side of the sternum during chest compressions or if your fingers rest on the ribs, you may break a patient\u2019s ribs while delivering a compression. To prevent this complication, use proper hand positioning and do not let your fingers come in contact with the ribs. If you hear a cracking sound while performing CPR, check and correct your hand position but continue CPR. Sometimes you may break bones or cartilage even when using proper CPR technique.",
        "Complications of CPR - Gastric Distention": "Bloating of the stomach is called gastric distention. It is caused when too much air is blown too fast and too forcefully into the stomach. A partially obstructed airway, which allows some of the air you breathe into the patient\u2019s airway to go into the stomach rather than into the lungs, can also cause gastric distention. Gastric distention causes the abdomen to increase in size. A distended abdomen pushes on the diaphragm and prevents the lungs from inflating fully. Gastric distention also often causes regurgitation. If regurgitation occurs, quickly turn the patient to the side, wipe out the mouth with your gloved fingers, and then return the patient to a supine position. You can prevent gastric distention by making sure you have opened the airway completely. Do not blow excessive amounts of air into the patient (deliver each breath over a period of 1 second). Be especially careful if you are a large person with a large lung capacity and the patient is smaller than you.",
        "Complications of CPR - Regurgitation": "Regurgitation (passive vomiting) is a common occurrence during CPR, so you must be prepared to manage this complication. You can minimize the risk of regurgitation by minimizing the amount of air that enters the patient\u2019s stomach. Regurgitation commonly occurs if the patient has experienced cardiac arrest. When cardiac arrest occurs, the muscle that keeps food in the stomach relaxes. If there is any food in the stomach, it backs up, causing the patient to vomit. If the patient regurgitates as you are performing CPR, immediately turn the patient onto his or her side to allow the vomitus to drain from the mouth. Clear the patient\u2019s mouth of remaining vomitus, first with your fingers and then with a clean cloth (if one is handy). Use suction if it is available. The patient may experience frequent episodes of regurgitation, so you must be prepared to take these actions repeatedly. EMS units carry a mechanical suction machine that can clear the patient\u2019s mouth. However, you cannot wait until the mechanical suction machine arrives before beginning or resuming CPR. You must manage the regurgitation as it occurs so that CPR is not delayed. Do your best to clear any vomitus from the patient\u2019s airway. If the airway is not cleared, two complications may arise: The patient may breathe in (aspirate) the vomitus into the lungs. You may force vomitus into the lungs with the next artificial ventilation. It takes a strong stomach and the realization that you are trying to save the patient\u2019s life to continue with resuscitation after the patient has regurgitated\u2014but you must continue. Remove the vomitus from the patient\u2019s mouth with a towel, the patient\u2019s shirt, your gloved fingers, or a manual suction unit if available. As soon as you have cleared away the vomitus, continue rescue breathing.",
        "Voices of Experience": "When emergency medical responders arrived, they found Paul unconscious and unresponsive. Paul, my friend of 10 years, was 70 years old and very physically fit. One day, while mowing the lawn, he began experiencing shortness of breath. He went inside to rest and felt better. Later that day, he had the same problem when he walked up the stairs. Paul called his doctor and made an appointment to be seen in his office the next week. The following day, while eating breakfast, he began to complain of chest pain. Paul\u2019s wife, Donna, called 9-1-1 and help was on the way, but before they arrived, Paul\u2019s wife says, \u201cHe turned green and that was it.\u201d When emergency medical responders arrived, they found Paul unconscious and unresponsive. With the ambulance still on the way, they immediately began to administer professional rescuer CPR. A pulse check was done and they opened his airway, but Paul had no pulse and was not breathing. The team initiated compressions and an AED was attached, \u201cShock advised, stand clear of patient.\u201d A shock was delivered. Paul had been in cardiac arrest for 4 minutes and 30 seconds. Two weeks after Paul\u2019s incident, I sat at a local restaurant listening to this story. As Paul\u2019s wife spoke, it sent chills up my spine. Paul was in cardiac arrest for over 4 minutes. Yet, due to rapid implementation of the cardiac chain of survival and the actions of the EMRs, my friend sat beside his wife with tears in his eyes that day thanking me for teaching others the lifesaving skills that had saved his life.\n\nAs you study the material in this textbook, consider the following: Will you someday be the Paul whose life is saved by someone, or will you be a lifesaver yourself and save someone\u2019s Paul?",
        "Creating Sufficient Space for CPR": "As an EMR, you will frequently find yourself alone with a patient in cardiac arrest. One of the first steps you must take is to create or find a space where you can perform CPR. Ask yourself, \u201cIs there enough room in this location to perform effective CPR?\u201d To perform CPR effectively, you need 3 to 4 feet (approximately 1 m) of space on all sides of the patient. This will provide you with enough space so that rescuers can change places, advanced life support procedures can be implemented, and an ambulance stretcher can be brought in. If there is not enough space around the patient, you have two options: 1. Quickly rearrange the furniture in the room or arrange objects at the scene to make space.2. Quickly drag the patient into an area that has more space; for instance, out of the bathroom and into the living room but not into a hallway. Space is essential to a smooth rescue operation for a cardiac arrest patient. It takes a minimal amount of time to either clear a space around the patient or move the patient into a larger area.",
        "Early Defibrillation by EMRs": "According to the AHA, about 424,000 people in the United States die each year of coronary heart disease in an out-of-hospital setting. As mentioned previously, more than 70% of all out-of-hospital cardiac arrest patients have an irregular heart electrical rhythm called ventricular fibrillation. This condition, often referred to as V-fib, is the rapid, disorganized, and ineffective vibration of the heart. An electric shock applied to the heart will defibrillate it and reorganize the vibrations into effective heartbeats. A patient in cardiac arrest stands the greatest chance for survival when early defibrillation is available.\n\nAs an EMR, you are often the first emergency health care provider to reach a patient who has collapsed in cardiac arrest. When you perform effective CPR, you are helping to keep the patient\u2019s brain and heart supplied with oxygen until a defibrillator and advanced life support (ALS) providers arrive at the scene.\n\nTo get defibrillators to cardiac arrest patients more quickly, increasing numbers of EMS systems are equipping EMRs with automated external defibrillators (AEDs). These machines accurately identify ventricular fibrillation and advise you to deliver a shock if needed. Such equipment allows you to combine effective CPR with early defibrillation to restore an organized heartbeat in a patient. AEDs may be appropriate for your community if you work to strengthen all links of the cardiac chain of survival. The links of the chain of survival include the following:\nRecognition of cardiac arrest and activation of the EMS system\nImmediate CPR with emphasis on high-quality chest compressions\nRapid defibrillation \n Basic and advanced EMS care \n Advanced life support and post arrest care,",
        "Performing Automated External Defibrillation": "The steps for using an AED are listed in Skill Drill 8-4:\n1. If CPR is in progress when you arrive, check the effectiveness of the chest compressions by checking for a pulse Step 1. It is important to limit the amount of time compressions are interrupted. If the patient is responsive, do not apply the AED.\n2. If the patient is unresponsive, begin providing chest compressions as soon as possible Step 2. Perform compressions and rescue breaths at a ratio of 30 compressions to two breaths, continuing until an AED arrives and is ready for use. It is important to start chest compressions and use the AED as soon as possible. Compressions provide vital blood flow to the heart and brain, improving the patient\u2019s chance of survival. If the cardiac arrest is witnessed, attach the AED as soon as it is available.\n3. Turn on the AED. Remove clothing from the patient\u2019s chest area. Apply the pads to the chest: one just to the right of the breastbone (sternum) just below the collarbone (clavicle), the other on the left lower chest area with the top of the pad 2 to 3 inches (5 cm to 8 cm) below the armpit. Be sure that the pads are attached to the patient cables (and that they are attached to the AED in some models). Plug in the pads connector to the AED Step 3.\n4. Stop CPR.\n5. State aloud, \u201cClear the patient,\u201d and ensure that no one is touching the patient.\n6. Push the analyze button, if there is one, and wait for the AED to determine if a shockable rhythm is present.\n7. If a shock is not advised, perform five cycles (about 2 minutes) of CPR beginning with chest compressions. Then reassess the patient\u2019s pulse and reanalyze the cardiac rhythm. If a shock is advised, reconfirm that no one is touching the patient and push the shock button. After the shock is delivered, immediately resume CPR, beginning with chest compressions Step 4.\n8. After five cycles (about 2 minutes) of CPR, reanalyze the patient\u2019s cardiac rhythm. Do not interrupt chest compressions for more than 10 seconds Step 5.\n9. Repeat the cycle of 2 minutes of CPR, one shock (if indicated), and 2 minutes of CPR.\n10. Arrange for transport, and contact medical control as needed. AEDs vary in design and operation, so learn how to use your specific AED. You must have the training required by your medical director to practice automated external defibrillation. Practice until you can perform the procedure quickly and safely. Because the recommended guidelines for using the AED change, always follow the most current CPR and Emergency Cardiac Care (ECC) guidelines.",
        "Procedure for Automated External Defibrillation": "Step 1 Check for responsiveness by shouting and gently shaking the shoulder. If the patient is unresponsive, simultaneously check the carotid pulse and check for signs of breathing or only gasping. If pulse is absent and there are no signs of breathing, proceed to Step 2. Begin cycles of 30 compressions and two breaths. Use the AED as soon as it is available. If cardiac arrest is witnessed, proceed to Step 3. Step 4 Turn on the AED. Apply the adhesive pads and connect them to the AED. Press the analyze button. If your AED has voice prompts, follow the verbal instructions. Do not touch the patient. Allow the AED to analyze the rhythm.\n\nIf a shock is advised, press the button to defibrillate the patient. If no shock is advised, perform five cycles of CPR. Step 5 As soon as the shock is delivered, begin CPR starting with chest compressions. Perform five cycles of CPR (about 2 minutes). After 2 minutes of CPR, go back to Step 3 to reanalyze the cardiac rhythm.",
        "Automated External Defibrillation - Special Populations": "You can safely use AEDs in pediatric patients using the pediatric-sized pads and a dose-attenuating system (energy reducer). However, if these items are unavailable, use an adult AED. During CPR, the AED should be applied to infants or children after the first five cycles of CPR have been completed. Cardiac arrest in children is usually the result of respiratory failure; therefore, oxygenation and ventilation are vitally important. After the first five cycles of CPR, use the AED to deliver shocks in the same manner as with an adult patient. If the child is between 1 month and 1 year of age (an infant), a manual defibrillator is preferred to an AED; however, manual defibrillation is a paramedic-level skill. Therefore, call for paramedic backup immediately if you suspect an infant may be in cardiac arrest. If paramedic backup with a manual defibrillator is not available, an AED equipped with a pediatric dose attenuator is preferred. If neither is available, an AED",
        "Automated External Defibrillation - Treatment": "When preparing to defibrillate a patient, be alert for the following situations:\nIf the patient is wet, dry the patient before initiating defibrillation. This will ensure that the defibrillation pads stick to the patient\u2019s chest and that the full shock is delivered safely.\nIf the patient has excessive hair on his chest and a razor is available, quickly shave the area where the pads will be placed.\nIf the patient has a pacemaker, you may need to reposition one of the defibrillation pads so that it is not placed directly over the pacemaker.\nIf the patient has a transdermal medication patch on his or her chest, remove the patch and wipe the skin before defibrillating the patient.",
        "CPR Training": "As an EMR, you should successfully complete a CPR course through a recognized agency such as the Emergency Care and Safety Institute or the AHA. You should also regularly update your skills by successfully completing a recognized recertification course. You cannot achieve proficiency in CPR unless you have adequate practice on adult, child, and infant manikins. Your department should schedule periodic reviews of CPR theory and practice for all EMRs.",
        "Legal Implications of CPR": "Advance directives, living wills, and durable powers of attorney for health care are legal documents that specify the patient\u2019s wishes regarding specified medical procedures. These documents are explained in Chapter 4, Medical, Legal, and Ethical Issues. You may sometimes wonder whether you should start CPR on a person who has an advance directive or a living will. Because you are not in a position to determine whether the advance directive or living will is valid, CPR should be started on all patients unless signs of obvious death are present (such as rigor mortis, tissue decay, or decapitation) or a resuscitation attempt would put you in harm\u2019s way. If a patient has an advance directive or living will, the physician at the hospital will determine whether you should stop CPR. Follow your department\u2019s protocols regarding advance directives, living wills, and do not resuscitate (DNR) orders. Do not hesitate to begin CPR on a pulseless, nonbreathing patient. Without your help, the patient will certainly die. Make sure you perform a careful assessment of the patient before beginning CPR. Another potential legal pitfall is abandonment\u2014the discontinuation of CPR without the order of a licensed physician or without turning the patient over to someone who is at least as qualified as you are. If you avoid these pitfalls, you need not be overly concerned about the legal implications of performing CPR. Your most important protection against a possible lawsuit is to become thoroughly skilled in the theory and practice of CPR.",
        "Prep Kit Ready for Review": "\nThe circulatory system transports oxygenated blood from the lungs to the rest of the body. Each beat of the heart produces a pulse, which can be felt at various sites on the body, such as the inside of the wrist (radial), the neck (carotid), the inside of the upper arm (brachial), and the groin (femoral).\n Cardiac arrest occurs when the heart stops contracting and no blood is pumped through the blood vessels. Brain damage begins within 4 to 6 minutes after the patient has experienced cardiac arrest. Within 8 to 10 minutes, the damage to the brain may become irreversible.\n The chain of survival includes five links that are essential to successful emergency cardiac care: (1) recognition of cardiac arrest and activation of the emergency response system; (2) immediate high-quality CPR; (3) rapid defibrillation; (4) basic and advanced emergency medical services (EMS); and (5) advanced life support (ALS) and post cardiac arrest care. \nWhen you arrive at an emergency scene, first assess the area for potential safety hazards. If the scene is unsafe, make it as safe as possible for yourself and the patient. As you approach the patient, look for possible causes of illness or injury. Next, establish unresponsiveness. If he or she is unresponsive, simultaneously check for signs of circulation and breathing by checking the pulse and watching for chest rise. If the patient has no pulse and is not breathing or only gasping, begin cardiopulmonary resuscitation (CPR) with chest compressions, followed by rescue breathing.\nBasic life support for adults and children follows the same general steps: Check responsiveness, circulation, airway, and breathing. Intervene at any point if the patient\u2019s airway is obstructed, the patient is not breathing or only gasping, or the patient has no pulse. \nUse the jaw-thrust maneuver to open the airway if you suspect a head or spinal injury and the head tilt\u2013chin lift maneuver if you do not suspect a head or spinal injury.\nRescue breathing should be performed at a rate of one breath every 5 to 6 seconds (10 to 12 breaths per minute) for adults and one breath every 3 to 5 seconds (12 to 20 breaths per minute) for children and infants.\nChest compressions should be performed at a rate of 100 to 120 compressions per minute for adults and children. Perform 30 compressions and two breaths for adults and for one-rescuer CPR. Perform 15 compressions and two breaths for two-rescuer child and infant CPR. \nBasic life support for infants is similar to that provided for adults and children. The techniques may vary somewhat, but the same general steps apply: check responsiveness, simultaneously check circulation and for the absence of breathing or just gasping. Intervene at any point if the infant\u2019s airway is obstructed, the infant is not breathing or only gasping, or the infant has no pulse.\nOpen an infant\u2019s airway by using the head tilt\u2013chin lift maneuver if you do not suspect a spinal injury. Be careful not to hyperextend the neck, which could obstruct the airway.\nIf the infant has no pulse, begin CPR. If you are alone, use two fingers to compress the chest 30 times, at a rate of 100 to 120 compressions per minute, to a depth equal to at least one-third the depth of the chest. After 30 compressions, give two breaths. If two rescuers are present, use the two-thumb/encircling hands technique and provide 15 compressions to two breaths.\nThe single most important cardiac arrest survival factor is early defibrillation. The indications for using an automated external defibrillator (AED) are that the patient is unresponsive, pulseless, and not breathing or only gasping. After determining that a patient is in cardiac arrest, begin immediate CPR and apply the AED as soon as possible.\nOnce you turn on the AED and attach it to the patient\u2019s bare chest, the AED will analyze the heart rhythm and advise whether a shock is indicated. If a shock is advised, ensure that no one is touching the patient, deliver the shock, and immediately perform CPR for 2 minutes before reanalyzing the patient\u2019s rhythm. If no shock is advised, perform CPR for 2 minutes and then reanalyze the patient\u2019s rhythm. Continue CPR and rhythm analysis until advanced life support personnel arrive.",
        "Vital Vocabulary": "automated external defibrillator (AED): A portable, battery-powered device that recognizes ventricular fibrillation and advises when a countershock is indicated. The device delivers an electric shock to patients with ventricular fibrillation., brachial pulse: The pulse on the inside of the upper arm., cardiac arrest: Sudden cessation of breathing and heart function., carotid pulse: The pulse taken on either side of the neck., chest compression: A means of applying artificial circulation by applying rhythmic pressure and relaxation on the lower half of the sternum; also called external cardiac compressions., child: A person between the age of 1 year and the onset of puberty (age 12 to 14 years)., circulatory system: The heart and blood vessels, which together are responsible for the continuous flow of blood throughout the body., femoral pulse: The pulse taken at the groin., gastric distention: Inflation of the stomach caused when excessive pressures are used during artificial ventilation and air is directed into the stomach rather than the lungs., infant: A person younger than 1 year., one-rescuer CPR: Cardiopulmonary resuscitation performed by one rescuer., plasma: The fluid part of the blood that carries blood cells, transports nutrients, and removes cellular waste materials., platelets: Microscopic disc-shaped elements in the blood that are essential to the process of blood clot formation, the mechanism that stops bleeding., pulse: The wave of pressure created by the heart as it contracts and forces blood out into the major arteries., radial pulse: Pulse located on the inside of the wrist on the thumb side., two-rescuer CPR_9: Cardiopulmonary resuscitation performed by two rescuers., ventilation: The movement of air in and out of the lungs., ventricular fibrillation: An uncoordinated muscular quivering of the heart; the most common abnormal rhythm causing cardiac arrest; also called V-fib."
    },
    {
        "CPR Compression to Ventilation Ratios": "The cheat sheet outlines CPR compression-to-ventilation ratios based on age and number of rescuers. For one rescuer, the ratio is 30:2 for adults, children, and infants, while for neonates it is 3:1. With two rescuers, the ratio remains 30:2 for adults but becomes 15:2 for children and infants. Neonates do not receive AED, and CPR is recommended if their heart rate falls below 60 bpm. If a patient is hypothermic, rescuers should check the pulse for 45\u201360 seconds before starting CPR and limit to three AED cycles. Once compressions begin, they should be continued until return of spontaneous circulation (ROSC).",
        "High Performance 'Pit Crew' CPR": "This section explains the High Performance 'Pit Crew' CPR approach, which involves a sequence of steps for both airway clear and obstructed scenarios. In the airway clear scenario, rescuers perform compressions, use an AED if available, attempt two successful ventilations, place an OPA, and continue compressions and ventilations until return of spontaneous circulation (ROSC) or obvious signs of life are observed. If ventilation doesn't go in, rescuers readjust and try a second ventilation, remove the OPA, perform compressions and AED, look in the mouth, and attempt ventilation again. If two successful ventilations occur with the OPA in place, the process continues. In the airway obstructed scenario, rescuers follow similar steps but prioritize removing the OPA, performing compressions and AED, looking in the mouth, attempting ventilation, and repeating until either two successful ventilations or ROSC are achieved.",
        "CPR in transport - Treatable CPR": "This section lists treatable conditions requiring CPR during transport, along with their causes and actions to take. Conditions include hypoxia caused by asthma, COPD, CHF, anaphylaxis, or tension pneumothorax; hypovolemia due to trauma, GI bleed, or ruptured abdominal aortic arch; known acidosis from sepsis, diabetic ketoacidosis, or post-workout; hyperkalemia resulting from kidney failure, pressure sores, crush injury, or burns; hypothermia from submersion, cold weather, or being found on the floor; toxins from ingestion, injection, or inhalation; tamponade (cardiac) following cardiac surgery, infection, IV drug use, or trauma; tension pneumothorax from trauma, COPD, asthma, or Marfan's syndrome; thrombosis (pulmonary) from sudden death, IVDU, pregnancy, fractures, flights, bed rest, or cancer; and thrombosis (coronary) from sudden death or coronary artery disease. For each condition, the action recommended is consulting medical oversight (CliniCall).",
        "Oxygen Cylinder Calculations": "This section provides formulas for calculating the duration of flow from oxygen cylinders. The formula is Duration of Flow = (gauge pressure - 200 psi) x C / Flow Rate (lpm), where C is the cylinder constant. For D-cylinders, C = 0.16 L/psi, E-cylinders have C = 0.28 L/psi, and M-cylinders have C = 1.56 L/psi."
    },
    {
        "ASA & Nitro (Cardiac Chest Pain)": "This section provides guidelines for administering ASA and Nitroglycerin (Nitro) in cases of suspected cardiac chest pain. It outlines the indications, contraindications, and administration details for both medications. For ASA, the indications include chest pain suspected to be cardiac in nature, with contraindications such as inability to chew or swallow tablets, taking a full dose already, allergy to ASA/NSAIDs, previous asthma triggered by ASA/NSAIDs, and pediatric patients. Cautions include recent internal bleeding, known bleeding diseases, anticoagulant use, recent surgery, and possibility of pregnancy. Administration is recommended before transport and vital signs, with a dosage of 162 mg (two 81 mg tablets) chewed. Nitro can only be administered via EMR, with indications similar to ASA. Contraindications include systolic blood pressure below 110 mmHg, heart rate below 50 bpm or above 150 bpm, use of Cialis within 48 hours, Viagra/Levitra within 24 hours, and hypersensitivity to nitrates. Cautions include the potential for hypotension and ensuring the patient will not fall. Administration involves a single dose of 0.4 mg sublingually. Entonox may be considered if Nitro is contraindicated, with specific instructions for discontinuation if hospital arrival is not imminent."
    },
    {
        "National EMS Education Standard Competencies": "Shock and Resuscitation\nApplies a fundamental knowledge of the causes, pathophysiology, and management of shock, respiratory failure or arrest, cardiac failure or arrest, and postresuscitation management. Pathophysiology\nApplies fundamental knowledge of the pathophysiology of respiration and perfusion to patient assessment and management.",
        "Introduction Shock (hypoperfusion) is defined as inadequate cellular perfusion.": "Any compromise in perfusion can lead to cellular injury or death.\nIn the early stages, the body attempts to maintain homeostasis.",
        "Pathophysiology": "Diffusion is a passive process in which molecules move from an area with a higher concentration of molecules to an area of lower concentration.\nOxygen and carbon dioxide move across the walls of the alveoli. In cases of poor perfusion (shock): \nTransportation of carbon dioxide out of tissues is impaired.\nResults in a dangerous buildup of waste products, which may cause cellular damage Shock is a state of collapse and failure of the cardiovascular system that leads to inadequate circulation.\nEarly recognition can save lives.\nRequires immediate recognition and rapid treatment Cardiovascular system consists of three parts:\nPump (heart)\nSet of pipes (blood vessels or arteries)\nContents (the blood) FIGURE 13-1 The cardiovascular system consists of three parts: the pump (heart), the container (vessels), and the contents (blood). The blood carries oxygen and nutrients through the vessels to the capillary beds, where they diffuse into the tissue; in exchange, waste products diffuse into the bloodstream. \u00a9 Jones & Bartlett Learning. Blood pressure is the pressure of blood within the vessels at any moment in time.\nSystolic: peak arterial pressure\nDiastolic: pressure in the arteries while the heart rests between heartbeats Pulse pressure is the difference between the systolic and diastolic pressures.\nIt signifies the amount of force the heart generates with each contraction.\nA pulse pressure less than 25 mm Hg may be seen in patients with shock. Blood flow through the capillary beds is regulated by the capillary sphincters.\nUnder the control of the autonomic nervous system\nRegulation of blood flow is determined by cellular needs. Perfusion also requires adequate:\nOxygen exchange in the lungs\nNutrients in the form of glucose in the blood\nWaste removal, primarily through the lungs Mechanisms are in place to help support the respiratory and cardiovascular systems when the need for perfusion of vital organs is increased.\nIncludes the autonomic nervous system and hormones Hormones are triggered when the body senses pressure falling.\nCause an increase in: \nHeart rate \nStrength of cardiac contractions\nPeripheral vasoconstriction\nThis response causes all the signs and symptoms of shock.",
        "\u201cPerfusion triangle.\u201d": "When a patient is in shock, one or more of the three parts is not working properly. FIGURE 13-2 The heart, the blood vessels, and the blood represent the three parts of perfusion (the perfusion triangle). \u00a9 Jones & Bartlett Learning.",
        "Many different shocks result from three basic causes:": "Pump failure\nPoor vessel function\nLow fluid volume \u00a9 Jones & Bartlett Learning. FIGURE 13-3 There are three basic causes of shock and impaired tissue perfusion. A. Pump failure occurs when the heart is damaged by disease or injury, or when an obstruction prevents it from functioning. B. Low fluid volume, often a result of bleeding. C. The blood vessels can dilate excessively so that the blood within them is inadequate to fill the system. A, B, C: \u00a9 Jones & Bartlett Learning.",
        "Caused by inadequate function of the heart": "A major effect is the backup of blood into the pulmonary vessels.\nResulting buildup of pulmonary fluid is called pulmonary edema. Cardiogenic shock develops when the heart cannot maintain sufficient output to meet the demands of the body.\nCardiac output depends on adequate:\nContractility of the heart muscle\nAmount of blood to pump (preload)\nResistance to flow in peripheral circulation (afterload)",
        "Caused by a mechanical obstruction that prevents an adequate volume of blood from filling the heart chambers.": "Three of the most common examples: \nCardiac tamponade\nTension pneumothorax\nPulmonary embolism Cardiac tamponade\nCollection of fluid between the pericardial sac and the myocardium (pericardial effusion) becomes large enough to prevent ventricles from filling with blood.\nCaused by blunt or penetrating trauma\nSigns and symptoms are referred to as Beck triad. Tension pneumothorax\nCaused by damage to lung tissue\nAir normally held within the lung escapes into the chest cavity.\nThe lung collapses, and air applies pressure to the organs, including the heart and great vessels. Pulmonary embolism\nA blood clot that blocks the flow of blood through pulmonary vessels\nIf massive: \nCan result in complete backup of blood in the right ventricle\nLeads to catastrophic obstructive shock and complete pump failure",
        "Distributive Shock": "Results from widespread dilation of small arterioles, small venules, or both\nThe circulating blood volume pools in the expanded vascular beds.\nTissue perfusion decreases. Septic shock\t\nOccurs as a result of severe infections in which toxins are generated by bacteria or by infected body tissues\nToxins damage vessel walls, causing increased cellular permeability.\nVessel walls leak and are unable to contract well. Septic shock (cont\u2019d)\nWidespread dilation of vessels, in combination with plasma loss through the vessel walls, results in shock. Neurogenic shock\nUsually the result of high spinal cord injury\nNerve impulses to blood vessels below the level of the injury are blocked.\nAll vessels cut off from nerve impulses will dilate, causing the blood to pool. Anaphylactic shock\nOccurs when a person reacts violently to a substance to which he or she has been sensitized\nSensitization means becoming sensitive to a substance that did not initially cause a reaction.\nEach subsequent exposure tends to produce a more severe reaction. Psychogenic shock\nCaused by a sudden reaction of the nervous system\nProduces temporary, generalized vascular dilation\nResults in fainting (syncope) Psychogenic shock (cont\u2019d)\nLife-threatening causes include irregular heartbeat and brain aneurysm.\nNon\u2013life-threatening events include receipt of bad news or experiencing fear or unpleasant sights (such as blood).",
        "Hypovolemic Shock Result of an inadequate amount of fluid or volume in the circulatory system": "Hemorrhagic causes and nonhemorrhagic causes\nOccurs with severe thermal burns",
        "Stages in the progression of shock:": "Compensated shock: early stage when the body can still compensate for blood loss\nDecompensated shock: late stage when blood pressure is falling\nNo way to assess when effects are irreversible\nMust recognize and treat shock early Blood pressure may be the last measurable factor to change in shock.\nWhen a drop in blood pressure is evident, shock is well developed.\nParticularly true in infants and children\nWhen blood pressure drops in infants and children in shock, they are close to death. Also expect shock if a patient has any one of the following conditions:\nMultiple severe fractures\nAbdominal or chest injury\nSpinal injury\nA severe infection\nA major heart attack\nAnaphylaxis",
        "Scene Size-up Scene size-up": "Be alert to potential hazards to your safety.\nUse gloves and eye protection for trauma scenes or if bleeding is suspected.\nMechanism of injury/nature of illness",
        "Primary assessment": "Perform a rapid exam.\nDetermine the level of consciousness.\nIdentify and manage life-threatening concerns.\nDetermine priority of the patient and transport. Primary assessment (cont\u2019d)\nProvide high-flow oxygen to assist in perfusion.\nFor hypoperfusion, treat aggressively and provide rapid transport.\nRequest advanced life support (ALS) as necessary. Primary assessment (cont\u2019d)\nForm a general impression.\nAssess the airway to ensure it is patent.\nAssess breathing.\nAn increased respiratory rate is often an early sign of impending shock.\nAssess patient\u2019s circulatory status. Primary assessment (cont\u2019d)\nA rapid pulse suggests compensated shock.\nIn shock or compensated shock, the skin may be cool, clammy, or ashen.\nAssess for and identify any life-threatening bleeding and treat it at once. Primary assessment (cont\u2019d)\nDetermine if patient is high priority, if ALS is needed, and which facility to transport to.\nTrauma patients with shock or a suspicious MOI generally should go to a trauma center.",
        "History Taking History taking": "Determine the chief complaint.\nObtain a SAMPLE history.",
        "Secondary Assessment Secondary assessment": "Repeat the primary assessment, followed by focused assessment. \nIf a life-threatening problem is found, treat it immediately.\nObtain a complete set of baseline vital signs.\nUse monitoring devices.",
        "Reassessment": "Reassess the patient\u2019s:\nVital signs\nInterventions\nChief complaint\nABCs\nMental status Reassessment (cont\u2019d)\nDetermine what interventions are needed.\nFocus on supporting the cardiovascular system. \nTreat for shock early and aggressively by:\nProviding oxygen\nKeeping the patient warm",
        "Emergency Medical Care for Shock": "As soon as you recognize shock, begin treatment. \nFollow standard precautions.\nControl all obvious bleeding.\nMake sure the patient has an open airway.\nMaintain manual in-line stabilization if necessary, and check breathing and pulse. As soon as you recognize shock, begin treatment. (cont\u2019d)\nComfort, calm, and reassure the patient.\nNever allow patients to eat or drink anything prior to being evaluated by a physician.\nIf spinal immobilization is indicated, splint the patient on a backboard.\nProvide oxygen and monitor patient\u2019s breathing. As soon as you recognize shock, begin treatment. (cont\u2019d)\nPlace blankets under and over the patient.\nConsider the need for ALS.\nAccurately record the patient\u2019s vital signs approximately every 5 minutes throughout treatment and transport.",
        "Treating Cardiogenic Shock": "Patient cannot generate the necessary contraction to pump blood throughout the circulatory system.\nPatients may present with chest pain.\nPatients in cardiogenic shock should not receive nitroglycerin; they are hypotensive. Patients usually have:\nLow blood pressure \nWeak, irregular pulse\nCyanosis about lips/underneath fingernails\nAnxiety \nNausea Place the patient in a position that eases breathing as you give high-flow oxygen.\nAssist ventilations as necessary.\nProvide prompt transport.\nConsider meeting ALS en route to hospital.",
        "Treating Obstructive Shock": "For cardiac tamponade:\nIncreasing cardiac output is the priority.\nApply high-flow oxygen.\nSurgery is the only definitive treatment. For tension pneumothorax:\nApply high-flow oxygen to prevent hypoxia.\nChest decompression is required.\nAsk for ALS early in call if available, but do not delay transport.",
        "Treating Septic Shock Hospital management is required.": "Use standard precautions and transport.\nAdminister high-flow oxygen.\nVentilatory support may be necessary.\nUse blankets to conserve body heat.\nNotify \u201csepsis team\u201d if available.",
        "Treating Neurogenic Shock Emergency treatment:": "Obtain and maintain a proper airway.\nProvide spinal immobilization.\nAssist inadequate breathing.\nConserve body heat.\nEnsure the most effective circulation.\nTransport promptly.",
        "Treating Anaphylactic Shock Administer epinephrine.": "Promptly transport the patient.\nProvide high-flow oxygen and ventilatory assistance en route.\nA mild reaction may worsen suddenly.\nConsider requesting ALS backup, if available.",
        "Treating Psychogenic Shock": "In an uncomplicated case of fainting, once the patient collapses, circulation to the brain is restored.\nPsychogenic shock can worsen other types of shock.\nIf the patient falls, check for injuries. If the patient reports being unable to walk after a fall, suspect another problem.\nTransport the patient promptly.",
        "Treating Hypovolemic Shock Control all obvious external bleeding.": "Keep the patient warm.\nRecognize internal bleeding and provide aggressive support. \nSecure and maintain an airway, and provide respiratory support.\nTransport as rapidly as possible.",
        "Older patients have more serious complications than younger ones.": "Illness is not just a part of aging.\nMany older patients take medications that mask or mimic signs of shock. Treating Shock in Older Patients"
    },
    {
        "National EMS Education Standard Competencies": "Pathophysiology\nApplies fundamental knowledge of the pathophysiology of respiration and perfusion to patient assessment and management. Medicine\nApplies fundamental knowledge to provide basic emergency care and transportation based on assessment findings for an acutely ill patient. Cardiovascular\nAnatomy, signs, symptoms, and management of\nChest pain\nCardiac arrest Anatomy, physiology, pathophysiology, assessment, and management of\nAcute coronary syndrome\nAngina pectoris\nMyocardial infarction\nAortic aneurysm/dissection Anatomy, physiology, pathophysiology, assessment, and management of (cont\u2019d)\nThromboembolism\nHeart failure\nHypertensive emergencies",
        "Cardiovascular disease has been the leading killer of Americans since 1900.": "Accounts for 1 of every 3 deaths",
        "EMS can help reduce deaths by:": "Encouraging healthy lifestyle\nEarly access to medical care\nMore CPR training of laypeople\nIncreased use of evolving technology in dispatch and cardiac arrest response",
        "Introduction": "EMS can help reduce deaths by (cont\u2019d): \nPublic access to defibrillation devices\nRecognizing need for advanced life support (ALS)\nThe use of cardiac specialty centers when they are available",
        "Anatomy and Physiology": "Heart\u2019s job is to pump blood to supply oxygen-enriched red blood cells to tissues.\nDivided into left and right sides\nUpper chambers (atria) receive incoming blood.\nLower chambers (ventricles) pump outgoing blood. FIGURE 17-1 The heart is a four-chambered muscle that pumps blood to all parts of the body. \u00a9 Jones & Bartlett Learning. One-way valves keep blood flowing in the proper direction.\nThe aorta, the body\u2019s main artery, receives blood ejected from left ventricle. FIGURE 17-2 A. The right side of the heart receives oxygen-poor blood from the venous circulation. B. The left side of the heart receives oxygen-rich blood from the lungs through the pulmonary veins. A, B: \u00a9 Jones & Bartlett Learning. Heart\u2019s electrical system controls heart rate and coordinates atria and ventricles.\nElectrical impulses start at the SA node.\nPasses from the atria to the ventricles\nAutomaticity allows spontaneous contraction without a stimulus from a nerve source. Electrical conduction system of the heart FIGURE 17-3 The electrical conduction system of the heart controls most aspects of heart rate and enables the four chambers to work together.\nAV = atrioventricular; SA = sinoatrial. \u00a9 Jones & Bartlett Learning Autonomic nervous system (ANS) controls involuntary activities.\nThe ANS has two parts:\nSympathetic nervous system\nParasympathetic nervous system The myocardium must have a continuous supply of oxygen and nutrients to pump blood.\nCardiac output is increased by increasing the heart rate or stroke volume.\nIn the normal heart, increased blood is delivered to the myocardium by dilating the coronary arteries. Coronary arteries are blood vessels that supply blood to heart muscle.\nCoronary arteries start at the first part of the aorta:\nRight coronary artery\nLeft coronary artery FIGURE 17-4 Blood flow to the heart. A. Coronary arteries (anterior view). B. Coronary arteries (posterior view). A, B: \u00a9 Jones & Bartlett Learning. Arterioles and capillaries are smaller vessels.\nCapillaries connect arterioles to venules.\nVenules are the smallest branches of the veins.\nVenae cavae return deoxygenated blood to the heart. Blood consists of:\nRed blood cells, which carry oxygen\nWhite blood cells, which fight infection\nPlatelets, which help blood to clot\nPlasma, which is the fluid cells float in Blood pressure is the force of circulating blood against artery walls.\nSystolic blood pressure\nThe maximum pressure generated by left ventricle\nDiastolic blood pressure\nThe pressure against artery walls while the left ventricle is at rest A pulse is felt when blood passes through an artery during systole.\nPeripheral pulses felt in the extremities\nCentral pulses felt near the body\u2019s trunk Carotid Femoral Brachial Radial Posterior tibial Dorsalis pedis FIGURE 17-7 Common pulse points. A. The carotid pulse is felt in the neck. B. The femoral pulse is felt in the groin area. C. The brachial pulse is felt on the inside of the upper arm. D. The radial pulse is felt on the thumb side of the wrist.  E. The posterior tibial pulse is felt on the inside of the ankle. F. The dorsalis pedis pulse is felt on the top of the foot. A-F: \u00a9 Jones & Bartlett Learning. Cardiac output is the volume of blood that passes through the heart in 1 minute.\nPerfusion is the constant flow of oxygenated blood to tissues.\nIf perfusion fails, cellular and eventually patient death occur.",
        "Arteries supply oxygen to different parts of the body:": "Right and left carotid\t\nRight and left subclavian\nBrachial\nRadial and ulnar\nRight and left iliac\nRight and left femoral\nAnterior and posterior tibial and peroneal",
        "Pathophysiology": "Chest pain usually stems from ischemia, which is decreased blood flow.\nIschemic heart disease involves a decreased blood flow to one or more portions of the heart.\nIf blood flow is not restored, the tissue dies. Atherosclerosis is the buildup of calcium and cholesterol in the arteries. FIGURE 17-8 In atherosclerosis, calcium and cholesterol\nbuild up inside the walls of the coronary blood vessels,\ncausing an obstruction in blood flow to the heart. \u00a9 Jones & Bartlett Learning. A thromboembolism is a blood clot floating through blood vessels.\nIf a clot lodges in a coronary artery, acute myocardial infarction (AMI) results. Coronary artery disease is the leading cause of death in the United States.\nControllable AMI risk factors:\nCigarette smoking, high blood pressure, high cholesterol, diabetes, lack of exercise, and obesity\nUncontrollable AMI risk factors:\nOlder age, family history, atherosclerotic coronary artery disease, race, ethnicity, and being male Acute coronary syndrome (ACS) is caused by myocardial ischemia.\nAngina pectoris\nAcute myocardial infarction (AMI) Angina pectoris occurs when the heart\u2019s need for oxygen exceeds supply.\nCrushing or squeezing pain\nDoes not usually lead to death or permanent heart damage\nShould be taken as a serious warning sign Unstable angina\nOccurs in the absence of a significant increase in oxygen demand\nStable angina\nOccurs in response to exercise or activity that increases demand on the heart muscle\nTreat angina patients like AMI patients. AMI pain signals actual death of cells in heart muscle.\nOnce dead, cells cannot be revived.\n\u201cClot-busting\u201d (thrombolytic) drugs or angioplasty within the first few hours prevents damage.\nImmediate transport is essential. Signs and symptoms of AMI\nWeakness, nausea, sweating\nChest pain, discomfort, or pressure \nLower jaw, arm, back, abdomen, or neck pain\nIrregular heartbeat and syncope (fainting)\nShortness of breath (dyspnea)\nNausea/vomiting\nPink, frothy sputum\nSudden death AMI pain differs from angina pain.\nNot always due to exertion\nLasts 30 minutes to several hours\nNot always relieved by rest or nitroglycerin\nAMI patients may not realize they are experiencing a heart attack. AMI and cardiac compromise physical findings:\nFear, nausea, poor circulation\nFaster, irregular, or bradycardic pulse\nDecreased, normal, or elevated blood pressure\nNormal or rapid and labored respirations\nPatients express feelings of impending doom. Three serious consequences of AMI:\nSudden death\nCardiogenic shock\nCongestive heart failure (CHF) Dysrhythmia: heart rhythm abnormalities\nPremature ventricular contractions\nTachycardia\nBradycardia\nVentricular tachycardia\nVentricular fibrillation Defibrillation restores cardiac rhythms.\nCan save lives\nInitiate CPR until a defibrillator is available.\nAsystole\nAbsence of all heart electrical activity \nReflects a long period of ischemia\nNearly all patients will die. Cardiogenic shock\nOften caused by heart attack\nHeart lacks power to force enough blood through circulatory system.\nInadequate oxygen to body tissues causes organs to malfunction.\nRecognize shock in its early stages. Congestive heart failure\nOften occurs a few days following heart attack\nIncreased heart rate and enlargement of left ventricle no longer make up for decreased heart function\nLungs become congested with fluid.\nMay cause dependent edema. Hypertensive emergencies\nSystolic pressure greater than 180 mm Hg\nCommon symptoms\nSudden, severe headache\nStrong, bounding pulse\nRinging in the ears Hypertensive emergencies (cont\u2019d)\nCommon symptoms\nNausea and vomiting\nDizziness\nWarm skin (dry or moist)\nNosebleed\nAltered mental status \nSudden pulmonary edema Hypertensive emergencies (cont\u2019d)\nIf untreated, can lead to stroke or dissecting aortic aneurysm.\nTransport patients quickly and safely.\nConsider ALS assistance. Aortic aneurysm is weakness in the wall of the aorta.\nSusceptible to rupture\nDissecting aneurysm occurs when inner layers of aorta become separated.\nPrimary cause: uncontrolled hypertension Aortic aneurysm (cont\u2019d)\nSigns and symptoms\nVery sudden chest pain\nComes on full force\nDifferent blood pressures\nMay be difficult to tell the difference between a dissecting aneurysm and AMI\nTransport patients quickly and safely.",
        "Scene Size-up Scene safety": "Ensure the scene is safe.\nFollow standard precautions.\nNature of illness (NOI)\nObtain clues from dispatch, the scene, patient, family members, bystanders.",
        "Form a general impression.": "If unresponsive and not breathing, begin CPR and call for AED. \nAirway and breathing\nOxygen saturation less than 95%: apply oxygen via nasal cannula at 4 L/min\nNot breathing or inadequate breathing: 100% oxygen with bag-mask device\nPulmonary edema: bag-mask device or CPAP Circulation\nCheck pulse, skin, capillary refill.\nConsider treatment for cardiogenic shock.\nTransport decision\nDecision based on ability to stabilize life threats during primary assessment\nTransport in a stress-relieving manner.",
        "History Taking": "Investigate the chief complaint (eg, chest pain, difficulty breathing).\nObtain a SAMPLE history from a responsive patient.\nUse OPQRST.",
        "Secondary Assessment Physical examination": "Focus on cardiac and respiratory systems.\nCirculation\nRespirations\nVital signs\nMeasure and record the patient\u2019s vital signs.\nIf available, use pulse oximetry.",
        "Reassessment Reassess vital signs at least every 5 minutes or when patient\u2019s condition changes significantly.": "If cardiac arrest occurs, perform CPR immediately until an AED is available.\nReassess your interventions.\nProvide rapid patient transport.",
        "Emergency Medical Care for Chest Pain or Discomfort": "Ensure a proper position of comfort.\nGive oxygen if indicated.\nDepending on protocol, prepare to administer low-dose aspirin and assist with prescribed nitroglycerin. Aspirin\nPrevents blood clots from forming or getting bigger\n81 mg chewable tablets\nRecommended dose: 162 mg (two tablets) to 324 mg (four tablets) Nitroglycerin \nAvailable forms\nSublingual pill\nSublingual spray\nSkin patch applied to chest Nitroglycerin \nMechanism of action:\nRelaxes blood vessel walls\nIncreases blood flow and oxygen supply to heart\nDecreases workload of heart\nDilates blood vessels Nitroglycerin \nSide effects:\nDecreased blood pressure\nSevere headache Nitroglycerin \nContraindications:\nSystolic blood pressure <100 mm Hg\nHead injury\nUse of erectile dysfunction drugs within 24 hours\nMaximum prescribed dose has been given.",
        "For an ECG to be reliable and useful, electrodes must be placed in consistent positions.": "Basic principles should be followed to minimize artifact in the signal. Guiding principles:\nMay need to shave body hair\nRub electrode site with alcohol swab before application.\nAttach electrodes to ECG cables before placement.\nConfirm electrode placement. FIGURE 17-10 Limb electrode placement for cardiac monitoring. \u00a9 Jones & Bartlett Learning. FIGURE 17-11 12-lead ECG electrode placement. \u00a9 Jones & Bartlett Learning. Once electrodes are in place, switch on the monitor.\nPrint a sample rhythm strip.\nIf strip shows artifact, confirm electrodes are firmly applied and cable is plugged in.",
        "Many open-heart operations have been performed in the last 40 years.": "Coronary artery bypass graft \nChest or leg blood vessel is sewn from the aorta to a coronary artery beyond the point of obstruction.\nPercutaneous transluminal coronary angioplasty \nA tiny balloon is inflated inside a narrowed coronary artery.",
        "Patients who have had open-heart procedures may or may not have long chest scars.": "Treat chest pain in a patient who has had any of these procedures the same as a patient who has never had heart surgery. \nSome patients have implanted cardiac pacemakers to maintain a regular cardiac rhythm and rate.",
        "Cardiac pacemakers": "Maintain regular cardiac rhythm and rate\nDeliver electrical impulse through wires in direct contact with the myocardium\nImplanted under a heavy muscle or fold of skin in the upper left portion of the chest",
        "Cardiac pacemakers (cont\u2019d)": "This technology is very reliable.\nPacemaker malfunction can cause syncope, dizziness, or weakness due to an excessively slow heart rate.\nTransport patients promptly. FIGURE 17-12 A pacemaker, which is typically inserted under the skin in the left upper portion of the chest, delivers an electrical impulse to regulate the heartbeat. \u00a9 Carolina K. Smith, MD/Shutterstock.",
        "Automatic implantable cardiac defibrillators": "Used by some patients who have survived cardiac arrest due to ventricular fibrillation\nMonitor heart rhythm and shock as needed.\nTreat chest pain patients with these devices like other patients having an AMI.\nElectricity is low so it will not affect rescuers.",
        "Heart Surgeries and Cardiac Assistive Devices": "External defibrillator vest\nA vest with built-in monitoring electrodes and defibrillation pads worn by the patient \nAttached to a monitor\nUses high-energy shocks\nDo not touch the patient if devices warns it is about to deliver a shock. \nVest should remain in place while CPR is being performed unless it interferes with compressions. Left ventricular assist devices (LVADs)\nUsed to enhance the pumping of the left ventricle\nMost common ones have an internal pump and external battery pack.\nMost patient will not have a palpable pulse.\nTransport all supplies and battery packs with the patient.",
        "Cardiac Arrest The complete cessation of cardiac activity": "Absence of a carotid pulse\nWas terminal before CPR and external defibrillation were developed in the 1960s\nHigh-quality CPR, early defibrillation, and access to advanced care can improve outcomes.",
        "Analyzes electrical signals from heart": "Identifies ventricular fibrillation\nAdministers shock to heart when needed FIGURE 17-15 A. Automated external defibrillators vary in their design, features, and operation. Jones & Bartlett Learning.",
        "AED models:": "All require some operator interaction.\nMost have a computer voice synthesizer advising steps to take.\nMost are semiautomated. FIGURE 17-15 B. Automated external defibrillators vary in their design, features, and operation. Photographee.eu/Shutterstock.",
        "Advantages of AED use:": "Quick delivery of shock\nEasy to operate\nALS providers do not need to be on scene.\nRemote, adhesive pads safe to use\nLarger pad area = more efficient shocks",
        "Other considerations": "Not all patients in cardiac arrest require shock.\nAll patients in cardiac arrest should be analyzed with an AED.\nAsystole indicates no electrical activity.\nPulseless electrical activity usually refers to a state of cardiac arrest that exists despite an organized electrical complex.",
        "Early defibrillation": "Few cardiac arrest patients survive outside a hospital without a rapid sequence of events.\nChain of survival:\nEarly recognition and activation of EMS\nImmediate bystander CPR\nRapid defibrillation\nBasic and advanced EMS\nALS and postarrest care\nRecovery",
        "Automated External Defibrillation": "FIGURE 17-16 The six links of the chain of survival. Data from American Heart Association.",
        "Early defibrillation (cont\u2019d)": "CPR prolongs period during which defibrillation can be effective.\nHas resuscitated patients with cardiac arrest from ventricular fibrillation\nNontraditional first responders are being trained in AED use.",
        "ALS and postarrest care": "Continue ventilation.\nMaintain oxygen saturation.\nAssure blood pressure >90 mm Hg.\nTargeted temperature management upon arrival to the hospital\nAdvanced assessment techniques and interventions\nRecovery\nMay take a year or longer",
        "Integrating the AED and CPR": "Work the AED and CPR in sequence.\nDo not touch the patient during analysis and defibrillation.\nCPR must stop while AED performs its job.",
        "AED maintenance": "Maintain as manufacturer recommends.\nRead the operator\u2019s manual.\nDocument AED failure.\nCheck equipment daily at beginning of shift.\nAsk manufacturer for maintenance checklist.\nReport AED failures to manufacturer and US Food and Drug Administration (FDA).",
        "Medical direction should approve written protocol for AED use.": "Continuing education with skill competency review is generally required for EMS providers.",
        "Emergency Medical Care for Cardiac Arrest": "Preparation\nMake sure the electricity injures no one.\nDo not defibrillate patients in pooled water. \nDo not defibrillate patients touching metal. Preparation (cont\u2019d)\nCarefully remove nitroglycerin patch and wipe with dry towel before shocking.\nShave hairy chest to increase conductivity.\nDetermine the NOI and/or MOI.\nCall for ALS assistance in a tiered system. FIGURE 17-18 Automated external defibrillator (AED) algorithm. CPR indicates cardiopulmonary resuscitation. \u00a9 Jones & Bartlett Learning. Begin chest compressions and attach AED as soon as available with witnessed cardiac arrests. \nFollow local protocol for patient care after AED use.\nAfter AED protocol is completed, one of the following is likely:\nPulse regained\nNo pulse regained and no shock advised\nNo pulse regained and shock advised Wait for ALS and continue shocks and CPR on scene.\nIf ALS is not responding and protocols agree, begin transport when:\nThe patient regains a pulse.\n6 to 9 shocks are delivered.\nAED gives three consecutive messages (every 2 min of CPR) advising no shock. Cardiac arrest during transport:\nStop the vehicle.\nBegin CPR if AED is not immediately available\nCall for ALS support. \nAnalyze rhythm.\nDeliver shock, if indicated, and resume CPR.\nContinue resuscitation per local protocol. Coordination with ALS personnel\nIf AED available, do not wait for ALS.\nNotify ALS of cardiac arrest.\nDo not delay defibrillation.\nFollow local protocols for coordination.",
        "Management of Return of Spontaneous Circulation Monitor for respirations.": "Provide oxygen via bag-mask device at 10 breaths/min.\nMaintain SpO2 between 95% and 99%. \nAssess blood pressure.\nSee if patient can follow simple commands.\nImmediately begin transport if ALS is not en route per local protocol."
    },
    {
        "definition of pe": "blood clot obstructing arterial pulmonary circulation",
        "most common causes of pe": "dvt (deep vein thrombosis)",
        "common signs/symptoms of pe": "tachycardia, tachypnea, anxiety, restlessness, sudden dyspnea, clear lung sounds, decrease spo2 levels, cough, dizziness, syncope, chest pain, signs of dvt, diaphoresis",
        "common causes of blood clots": "recent surgery, pregnancy or recent childbirth, use of oral contraceptives (i.e. birth control), history of blood clots, atrial fibrillation, recent prolonged travel, sedintary lifestyle or long periods without movement",
        "treatment/management of pe": "support abcs, supplemental oxygen, ventilatory assistance, rapid transport",
        "pe is a common cause of:": "shock and cardiac arrest",
        "signs/symptoms of dvt": "leg pain, non-traumatic bruising on leg, redness/swelling of leg, affected area warm to the touch",
        "cause of pe": "a blood clot obstructs blood flow in the arterial pulmonary circulation",
        "most common cause for blood clots resulting in pe's": "dvts (deep vein thrombosis)",
        "common causes for dvt resulting in pe": "recent surgery, pregnancy or childbirth, oral contraceptive use (i.e. birth control), history of blood clots (i.e., stroke), atrial fibrillation, recent prolonged travel or airplane ride, extended period of time without movement",
        "type of shock most commonly associated with pes": "obstructive",
        "pe falls under what category of the h's and t's?": "thrombosis (pulmonary)",
        "definitive treatment for pe": "thrombolytics, anticoagulants, thrombectomy",
        "most common ecg findings with pe": "tachycardia",
        "common 12-lead ecg findings (paramedic only):": "s1q3t3 pattern, rbbb, diffuse st depression/inverted t-waves, right atrial enlargement (peaked t-wave in lead ii), right ventricular strain pattern (inverted t-waves in v1-v4, ii, iii, avf)"
    },
    {
        "___ refers to ischemic chest pain.": "angina pectoris",
        "___ refers to an inadequate blood supply to an organ or tissue.": "ischemia",
        "what is the typical dose of nitroglycerin for angina?": "0.4 mg",
        "true or false: chest pain is the only symptom of a heart attack?": "false",
        "___ refers to tissue death as a result of ischemia.": "infarction",
        "contraindications for nitroglycerin": "hypotension, erectile dysfunction medication",
        "contraindications for aspirin": "allergy, recent gi bleeding",
        "what medications are used to treat chest pain?": "aspirin, nitroglycerin, oxygen",
        "function of aspirin for chest pain": "anti platelet",
        "function of nitroglycerin": "vasodilator",
        "process of fatty plaque buildup in a blood vessel": "atherosclerosis",
        "____ refers to the narrowing of a blood vessel": "stenosis",
        "what is a thrombus?": "blood clot",
        "what is infarction?": "death of tissue caused by ischemia",
        "chest pain caused by ischemia of cardiac myocytes": "angina pectoris",
        "_____ chest pain changes with breathing": "pleuritic",
        "_____ refers to the muscle layer of the heart": "myocardium",
        "cariogenic pulmonary edema is a sign of ____ sided heart failure": "left",
        "pitting edema and jugular vein distention are signs of ____ sided heart failure.": "right",
        "treatments for ischemic chest pain include:": "aspirin, nitroglycerin, oxygen if needed, analgesics",
        "what is ischemia?": "inadequate perfusion",
        "death of tissue as a result of inadequate perfusion": "infarction",
        "dose for sublingual ntg": "0.4 mg",
        "ntg administration may cause a life threatening drop in bp when combined with ____ inhibitors": "phosphodiesterase (pde)",
        "atypical chief complaints are common in which populations": "women, elderly, diabetic",
        "____ refers to fatty plaque buildup within the wall of a coronary artery": "atherosclerosis",
        "narrowing of a blood vessel can also be referred to as ____": "stenosis",
        "during which phase of contraction are the coronary arteries perfused?": "diastole",
        "myocardial infarction caused by a complete occlusion of a coronary artery that results in st segment elevation?": "stemi",
        "ischemic chest pain that occurs at rest without ecg or cardiac enzyme changes": "unstable angina",
        "which coronary artery supplies the inferior wall of the heart and the right ventricle?": "right coronary artery (rca)",
        "which coronary artery supplies the anterior wall of the heart?": "left anterior descending (lad)",
        "which coronary artery supplies the lateral wall of the left ventricle?": "left circumflex (lcx)",
        "what is the most important piece of information to identify a stemi?": "12 lead ecg",
        "what does st segment depression on an ecg represent in the context of ischemic chest pain?": "subendocardial ischemia",
        "this stemi mimic is the result of inflammation of the pericardium and may result in widespread, concave st elevation.": "pericarditis",
        "what treatment is standard of care for stemi (in the hospital)?": "percutaneous intervention (pci)",
        "signs of myocardial ischemia other than chest pain are known as ______": "anginal equivalents",
        "_______ is a blanket term that includes unstable angina, stemi, and nstemi": "acute coronary syndrome",
        "treatments for ischemic chest pain:": "aspirin, nitroglycerin, oxygen if needed, narcotic analgesics",
        "leads ii, iii, and avf look at the ____ wall of the heart": "inferior",
        "death of heart tissue due to ischemia": "infarction",
        "1 mm or more of st elevation in ____ contiguous limb leads is positive for stemi": "2 or more",
        "cariogenic pulmonary edema is most likely to be the result of ___ ventricular infarct": "left",
        "criteria to identify stemi in the presence of lbbb": "sgarbossa"
    },
    {
        "hypovolemic shock": "hypoperfusion (lack of blood supply) of the body's vital tissues and organs due to a loss of fluid. causes include severe dehydration and/or blood loss (also called hemorrhagic shock)",
        "in the presence of a severe hemorrhage what is the priority?": "stop of the bleeding. while airway and breathing come before circulation in an a,b,c assessment, in trauma, a massive hemorrhage is a life threat which if not corrected immediately will make the patient's airway or respiratory status inconsequential.",
        "artery": "high pressure, relatively thick walled vessel that carries blood from the heart to the lungs, organs, and peripheral tissues. the majority of arteries carry oxygenated blood (exception: pulmonary arteries).",
        "arterial bleed": "due to high pressure, an arterial bleed will generally involve rapid spurting. blood is generally a bright red color.",
        "vein": "a relatively thinner walled vessel that is of lower pressure. brings blood from the lungs, tissues, and peripheral tissues back to the heart. most veins are deoxygenated (exception: pulmonary veins).",
        "venous bleed": "venous bleed will involve pooling of blood that is generally a darker red color.",
        "capillary": "microscopic blood vessels that allow for the exchange of nutrients/oxygen to the tissues and the removal of waste such as co2.",
        "capillary bleed": "oozing of blood. small bleed should generally stop on their own with little intervention. most capillary bleeds will respond to direct pressure and bandaging.",
        "hemoptysis": "coughing up of blood. (hem/o = blood) (-ptysis = spitting up)",
        "hematochezia": "blood, generally bright red, that is mixed with stool. (hem/o = blood) (chez/o = defecate)",
        "melena": "dark black and  tarry stool indicated of blood that has remained in the bowel/gi tract for some time.",
        "stages of shock": "compensated shock. decompensated shock. irreversible shock.",
        "compensated shock": "the body responds to the poor perfusion by increasing heart rate, contraction strength, and vasoconstriction of peripheral vessels. these adaptations can temporarily maintain normal blood pressure and delay decompensated shock.",
        "compensated shock (signs and symptoms)": "increased heart rate. normal blood pressure. anxiety/restlessness/combativeness. thirst. weakness. air hunger/elevated respiratory rate. cool and clammy skin peripherally. may be cyanotic or pale peripherally as well.",
        "decompensated shock": "the bodies mechanism of compensating for poor perfusion have been exhausted and the body begins to shock further signs of poor perfusion.",
        "decompensated sock (signs and symptoms)": "peripheral pulses may be gone. failure to maintain blood pressure (~systolic <90). altered mental status or loss of consciousness. slow respirations or apnea.",
        "irreversible shock": "if decompensated shock is not corrected immediately, poor perfusion of body tissues and organs will leads to wide spread cell death, irreversible damage that will kill the patient.",
        "adult systolic blood pressure": "systolic range is 90 to 120 (adults).  <90 is indicative of hypotension or low blood pressure.",
        "perfusion": "refers to the body's ability to deliver blood to all organs and tissues.",
        "hypoperfusion": "inadequate distribution of blood to the body's tissues."
    },
    {
        "what is the term for when the atria or ventricles contract?": "systole",
        "the more blood the ventricles are filled with, the more they stretch, and in turn, the harder they contract. what is this principle called?": "frank-starling principle",
        "what is unique about that pulmonary veins?": "they are the only veins in the body that carry oxygenated blood",
        "what is stroke volume?": "the amount of blood ejected from the ventricles in a single beat/contraction",
        "what is the normal range for an adult's heart rate?": "60-100 beats per minute",
        "what are the four valves of the heart called?": "right side: tricuspid and pulmonary\nleft side: mitral and aortic",
        "when the atria are in systole, the ventricles are in______________.": "diastole",
        "a visual representation of the electrical activity of the heart is called what?": "an electrocardiogram (ecg)",
        "what part of the central nervous system regulates involuntary body functions like respiration and heartbeat?": "the autonomic nervous system (ans) is responsible for maintaining involuntary body functions that are performed whether you are thinking about them or not.",
        "what part of the conduction system is responsible for setting the rate the heart beats at?": "the sa (sinoatrial) node",
        "what part of the cardiac conduction system is considered the primary pacemaker of the heart?": "the sa (sinoatrial) node",
        "true or false: if the sa node fails to set the pace, the next part of the conduction system will take over as the primary pacemaker.": "true",
        "what is the primary function of the av node?": "to briefly delay the electrical impulse so that there is time for adequate ventricular filling.",
        "true or false: the intrinsic rate of the ventricles/purkinje fibers is faster than that of the av node": "false. the intrinsic rate of the ventricles/purkinje fibers (20-40) is slower than that of the av node (40-60). the further down the conduction system you go, the slower the intrinsic rate.",
        "what are the names of the two atrioventricular valves? which side is each valve located on?": "the tricuspid valve (right) and the mitral valve (left).",
        "what is the intrinsic rate of the ventricles/purkinje fibers?": "20-40 bpm",
        "how is cardiac output calculated?": "stroke volume x heart rate",
        "what is the term for the relaxation phase of the cardiac cycle?": "diastole",
        "what part of the cardiac conduction system is responsible for innervating the ventricles?": "the purkinje fibers",
        "what happens to the heart rate when the sympathetic nervous system is stimulated?": "it increases",
        "when a cell reverses its polarity to create an action, this is called ________________.": "depolarization",
        "when looking at an ecg, what wave represents ventricular repolarization?": "the t-wave",
        "what cranial nerve has branches that extend to the heart? what part of the nervous system is this nerve primarily associated with?": "the vagus nerve; parasympathetic",
        "what do chronotropic factors effect?": "the rate at which the heart contracts",
        "what are the two normal heart sounds associated with the cardiac cycle?": "s1 and s2 (lub-dub)",
        "what part of the heart sets the intrinsic rate of beats per minute and is considered the pacemaker of the heart?": "the sa (sinoatrial) node",
        "which node slows conduction slightly to allow time for the atria to contract?": "the av (atrioventricular) node",
        "a normal heart rate for an adult is considered to be between ___ - ___ beats per minute.": "60-100",
        "where in the heart are the purkinje fibers located?": "the purkinje fibers encircle the ventricles",
        "where in the heart is the sa node located?": "in the wall of the right atrium",
        "what causes the s1 sound during the cardiac cycle? s2?": "s1 is caused by the closure of the atrioventricular valves. s2 is caused by the closure of the semilunar valves.",
        "at it's resting potential, is a cardiac myocyte more positive or negative within the cell?": "at resting potential, a cardiac myocyte is more negative inside the cell.",
        "a change  in what causes gated ion channels to open or close during the action potential of a cardiac myocyte?": "a change in voltage",
        "what is the term for the amount of blood pumped out of the heart with each heart beat?": "stroke volume",
        "during which part of the cardiac cycle do chambers contract?": "systole",
        "what is it called when a cell reverses its polarity briefly?": "depolarization",
        "during what period can a cardiac myocyte not be stimulated to produce an action, no matter what?": "the absolute refractory period",
        "what is the primary neurotransmitter of the parasympathetic nervous system?": "acetylcholine",
        "what is needed to break down acetylcholine and allow muscles to relax after contraction?": "acetylcholinesterase",
        "the heart has two kinds of receptors, what are they called?": "alpha receptors and beta receptors",
        "when the sympathetic nervous system is stimulated, what is the result on the heart and vasculature?": "the heart pumps harder and faster, and vasculature constricts.",
        "where is the carotid sinus located?": "at  the bifurcation of the common carotid artery just below the angle of the mandible and about at the level of the thyroid cartilage.",
        "dromotropic factors affect what?": "the conduction speed of the cardiac system.",
        "what is the typical cardiac output for an adult?": "5-6 liters per minute",
        "what is the frank-starling principle?": "the frank-starling principle states that when left ventricular volume increases, so does the force of ventricular contraction. so, the more blood that fills the ventricle, the more the ventricle stretches, and the harder it will contract."
    },
    {
        "what is pulmonary edema?": "the accumulation of fluid within the lungs and air spaces",
        "pulmonary edema is primarily related to what disease?": "congestive heart failure (chf)",
        "there are 2 types of pulmonary edema. what are they?": "high pressure (cardiogenic) and high permeability (noncardiogenic)",
        "what is the most common cause?": "coronary heart disease",
        "general symptoms of pulmonary edema": "dyspnea, fatigue, exercise intolerance, fluid retention (edema), chest pain, orthopnea, restlessness, anxiety, confusion, limited word sentences",
        "assessment: lung sounds": "crackles; start in the bases and move up with worsening symptoms",
        "assessment: skin signs/ perfusion": "pale/ cyanotic, cool skin, delayed cap refill, weak distal pulses, decreased urinary output",
        "classic sign of pulmonary edema": "frothy, blood-tinged sputum",
        "what is key with patient's experiencing pulmonary edema?": "reassurance",
        "maintain systolic blood pressure at what level (or above)": "100 systolic or above",
        "maintain o2 saturation at what level (or above)": "94% or above",
        "basic prehospital treatment": "oxygenation and maintain adequate perfusion",
        "pulmonary edema is related to what disease?": "congestive heart failure (chf)",
        "what is the goal with patient's experiencing pulmonary edema?": "reassurance",
        "3 important interventions/ diagnostic interventions": "oxygen, vascular access, monitor with 12-lead",
        "interventions: alert patient": "cpap (or other non-invasive positive pressure ventilation); nitroglycerin (if systolic blood pressure above minimum)",
        "how does cpap help with pulmonary edema?": "decreases venous return and preload; improves gas exchange",
        "how does nitroglycerin help with pulmonary edema?": "decreases preload with peripheral vasodilation",
        "what is occurring during left ventricle failure?": "pressure within the pulmonary veins is increasing which causes blood to backup into the lungs; pulmonary edema and poor gas exchange are present",
        "what is occurring during right ventricle failure?": "blood backs up into the venae cavae; this causes congestion of the venous system",
        "describe high pressure (cardiogenic) pulmonary edema": "caused by heart failure; dysfunction of either the left or right ventricle, chronic hypertension, cardiac diseases, or dysrhythmias",
        "describe high permeability (noncardiogenic) pulmonary edema": "caused by acute hypoxemia; \"leaky capillaries\"",
        "what dysrhythmias can be caused with high pressure": "ventricular tachycardia and supraventricular tachycardia",
        "examples of possible causes of high permeability": "inhaled toxins or near submersion (this can damage alveolar tissue)",
        "what medication can be used with cpap?": "nitroglycerin",
        "if the patient is on cpap and their gcs drops to 3, what do you do?": "take cpap off immediately; intubation is indicated",
        "when must cpap be removed?": "patient becomes altered or blood pressure drops",
        "how does lasix help pulmonary edema?": "used to remove toxins and promote excretion of excess amounts of electrolytes (and fluids)"
    },
    {
        "how many chambers in the heart?": "4. 2 atrium and 2 ventricles",
        "where does the heart receive its blood from?": "the coronary arteries",
        "what does the left coronary artery supply blood to?": "left ventricle, intraventricular septum, \npart of the right ventricle, and conduction system.",
        "what does the right coronary artery supply blood to?": "right atrium, right ventricle, and conduction system.",
        "what does the left coronary artery branch into?": "anterior descending, and circumflex artery",
        "what does the right coronary artery branch into?": "posterior descending, and the marginal artery.",
        "how is the st segment measured?": "at the j point/ from the end of the s wave, to the beginning of the t wave.",
        "what does stemi stand for?": "st segment elevation myocardial infarction",
        "what does nstemi stand for?": "non st segment elevation myocardial infarction",
        "what are the three phases of myocardial infarction and how does it correlate on a ekg?": "ischemia due to lack of oxygen. (st depression/t wave inversion\ninjury ( elevation of the st segment)\nnecorsis of heart muscle- q wave \u22650.04 seconds.",
        "how is stemi diagnosed?": "st segment elevation \u22651mm in two or more contiguous leads except in leads v2, and v3.",
        "how is nstemi diagnosed?": "st depression or t wave inversion can be seen. nstemi mostly caught with elevated lab values. such as ckmb, or troponin",
        "what leads look at the lateral aspect of the heart?": "lead 1, avl, v5-v6",
        "what leads look at the inferior aspect of the heart?": "lead ii, iii, avf",
        "what leads look at the septal aspect of the heart?": "v1-v2",
        "what leads look at the anterior aspect of the heart?": "v3-v4",
        "what are the two types of stroke?": "ischemic and hemorrhagic",
        "what are the two types of ischemic stroke?": "thrombotic and embolic",
        "what is the path of treatment for acs in ems?": "aspirin 324 mg po\nnitroglycerine 0.4 mg sl (unless inferior stemi is present)\nmorphine/fentanyl- 2-8 mg iv, or 50-100 mcg respectivley.\nserial 12 leads\ntransport to hospital with pci capabilities",
        "what reperfusion techniques are used by the \nhospital to treat acs?": "fibrinolytic drugs\npci (percutaneous coronary intervention)\ncabg (coronary artery bypass grafting)",
        "what common ekg rhythm is seen post pci?": "accelerated idioventricular rhythm",
        "what is the path of treatment for stroke in ems?": "manage airway and breathing as needed\nstroke assessment/ check cbg\niv therapy (ideally 20g or larger above the wrist)\nearly notification to the hospital\nif permitted, manage hypertension with beta blockers."
    },
    {
        "introduction": "hypotension refers to a lower than normal blood pressure. blood pressure is an important component of tissue perfusion. inadequate blood pressure prevents oxygen and vital nutrients from reaching body tissues",
        "lessons and concepts": "blood pressure is a critical component of tissue perfusion. adequate blood pressure is necessary to supply vital organs with oxygen and other essential nutrients. blood pressure is the result of both cardiac output and vascular resistance. cardiac output is the amount of blood pumped by the heart. vascular resistance is the result of vascular tone (smooth muscle contraction in peripheral blood vessels). when blood pressure drops, the body will often compensate for the reduced perfusion by increasing cardiac output and/or vascular resistance. hypotension is generally defined as a blood pressure below 90/60. any systolic pressure below 90 indicates hypotension. mean arterial pressure under 65 indicates hypotension. mean arterial pressure (map) is an average pressure during a complete cardiac cycle. formula is dbp (diastolic pressure) + 1/3 pulse pressure. pulse pressure is the difference between systolic and diastolic pressure. example - for a blood pressure of 110/70. map = 70 + 1/3*(110-70) = 70 + 40/3 = 83.33333.",
        "shock": "in ems, the word \"shock\" refers to hypoperfusion, a state of insufficient blood supply to vital organs. there are 4 categories of shock: hypovolemic shock occurs when there is insufficient blood volume, may be a result of: dehydration, blood loss from a traumatic event (hemorrhagic shock). think of this as a fluid problem. cardiogenic shock occurs when cardiac output does not meet the body's needs, may be a result of: heart failure, acute myocardial infarction. typically presents with cool, dry extremities. think of this as a pump problem. distributive shock occurs when vascular tone is lost and blood vessels relax. this leads to decreased vascular resistance and decreased tissue perfusion, may be a result of: septic shock occurs when blood vessels relax in response to widespread infection. neurogenic shock occurs when sympathetic (fight or flight) output is lost due to central nervous system injury. anaphylaxis is an inflammatory reaction to an allergy that leads to widespread vasodilation. typically presents as warm skin, swelling, and tachycardia. think of this as a pipe or container problem. obstructive shock occurs when something is obstructing circulation, may be a result of: tension pneumothorax or pulmonary embolism. commonly presents with signs and symptoms of chf (jvd, pulmonary edema, peripheral swelling).",
        "signs and symptoms": "initial signs and symptoms of shock may include: pale, cool, and/or diaphoretic (sweaty) skin. distributive shock may present with warm extremities. delayed capillary refill time. anxiety or a sense of impending doom. tachycardia.",
        "compensated vs decompensated shock": "this is almost exactly what it sounds like. is the body taking measures to correct poor perfusion? and are those measures working? compensated shock: when the body's compensatory mechanisms successfully maintain adequate tissue perfusion and blood pressure (tachycardia, delayed capillary refill, etc.). decompensated shock: when the body's compensatory mechanisms fail (hypotension with signs and symptoms of shock; organ failure begins). irreversible shock: when organ damage and the build-up of toxic metabolic byproducts will almost certainly lead to death.",
        "autonomic control": "activation of the sympathetic nervous system. release of epinephrine and norepinephrine in response to hypoperfusion. increased vascular tone from alpha receptor activation. smooth muscle contraction in blood vessels. \"shunting\" of blood to central organs. increased cardiac output from beta receptor activation. increase in heart rate. increase in contractility (force of heart's contraction).",
        "vital organs": "vital organs need adequate pressure. brain: inadequate perfusion initially leads to altered mental status. prolonged and severe hypoperfusion leads to death or brain cells and failure to maintain vital tasks. heart: heart muscle is perfused primarily during diastole (heart relaxation). if the heart doesn't get its own blood, it will not have the resources needed to pump blood to the rest of the body. kidneys: kidneys are responsible for maintaining ph balance, clearing certain toxins from the blood, and maintaining electrolyte concentrations. hypoperfusion of the kidneys leads to a lack or urine production. toxic accumulation of waste products, electrolyte disturbances, and disregulation of ph begin to harm other organs through the body.",
        "orthostatic hypotension": "orthostatic hypotension refers to a drop in blood pressure when a patient sits or stands. this is very common in patients who are dehydrated or otherwise hypovolemic. due to a lack of rapid compensation when blood volume moves toward the lower extremities and away from vital organs. this is commonly associated with syncope and postural dizziness.",
        "recognition": "initial assessment for signs of impaired circulation. skin color, temperature and nature. pale, cool, or diaphoretic (sweaty) skin may indicate hypotension. check for a radial pulse. an absent radial pulse is indicative of a low blood pressure. however, do not assume pressure is adequate because a pulse is present. capillary refill time. mental status exam. obtain a blood pressure with an appropriate size of cuff. manual pressure may be more accurate.",
        "treatment and management": "initial basic treatments for hypoperfusion. position patient supine if airway management permits. trendelenburg position has been proven to be harmful and is now highly discouraged except in specific situations. elevation of patients legs is not routinely recommended. administer oxygen as needed. keep the patient warm (particularly important in hemorrhagic shock). in hemorrhagic shock, bleeding control is the first priority. always request als if available. im epinephrine for anaphylaxis. permissive hypotension in trauma with blood loss. patients with hypotension secondary to hemorrhagic shock may benefit from permissive hypotension. this means limiting crystalloid (iv fluid) administration and allowing a mild state of hypotension in a controlled setting. the goal is to permit clotting and avoid dilution of the patient's blood. permissive hypotension is for bleeding patients, not for isolated traumatic brain or spine injuries. always investigate the underlying cause of hypotension and treat appropriately.",
        "scenario": "you and your emt partner are dispatched to the home of a 47-year-old male complaining of weakness. the patient reports they called 911 after becoming so weak that they were unable to get out of bed. you observe that the patient has been incontinent of urine and notice a foul odor. the patient is sitting up in bed and protecting their own airway. the patient reports a history of frequent urinary tract infections. on arrival you observe that the patient appears pale and diaphoretic. initial vitals signs are as follows: bp 86/38; hr 116; spo2 90% on room air; respirations 26 and non-labored. lung sounds are clear in all fields. your initial treatment for hypotension is to lie the patient flat, keep them warm, and to administer 4l oxygen by nasal cannula. you direct your partner to obtain a blood glucose and a temperature while you establish an 18ga iv in the patient's right ac. temperature is 102.4f, blood glucose is 218. because the patient is febrile, you elect to avoid the use of blankets or other warming measures. you and your partner prepare the patient for transport. follow-up vitals are as follows: bp 98/50; hr 108; spo2 98% on 4l; respirations 26 and non-labored. you transport the patient to the local er who continuing to monitor vital signs every 5 minutes. you make a sepsis alert in accordance with your local protocol with a clinical impression of a possible urinary tract infection and clinical sepsis. the patient later receives iv fluids, antibiotics, and treatment for a bladder infection.",
        "tips and tricks": "always remember initial bls treatments for hypotension and clinical shock. be sure to perform a thorough assessment to determine the underlying cause of the problem.",
        "volume replacement": "iv fluids to increase blood volume are particularly beneficial in the treatment of hypovolemic and distributive shock 20cc/kg fluid bolus is standard for treatment of hypotension 30cc/kg in sepsis (dependent on local protocol) 10cc/kg in neonates large bore iv access preferred, but any access is better than none always be sure to assess for volume overload by auscultating lung sounds and observing for signs of abdominal distention",
        "permissive hypotension": "patients with hypotension secondary to hemorrhagic shock may benefit from permissive hypotension this means limiting crystalloid (iv fluid) administration and allowing a mild state of hypotension in a controlled setting the goal is to permit clotting and avoid dilution of the patient's blood permissive hypotension is for bleeding patients, not for isolated traumatic brain or spine injuries always investigate the underlying cause of hypotension and treat appropriately",
        "initial signs and symptoms of shock": "initial signs and symptoms of shock may include: pale, cool, and/or diaphoretic (sweaty) skin delayed capillary refill time anxiety or a sense of impending doom tachycardia cariogenic shock may present with bradycardia",
        "autonomic control: compensation for shock": "activation of the sympathetic nervous system release of epinephrine and norepinephrine in response to hypoperfusion increased vascular tone from alpha receptor activation smooth muscle contraction in blood vessels \"shunting\" of blood to central organs increased cardiac output from beta receptor activation increase in heart rate increase in contractility (force of heart's contraction)",
        "vital organs need adequate pressure": "brain inadequate perfusion initially leads to altered mental status prolonged and severe hypoperfusion leads to death or brain cells and failure to maintain vital tasks heart heart muscle is perfused primarily during diastole (heart relaxation) if the heart doesn't get its own blood, it will not have the resources needed to pump blood to the rest of the body kidneys kidneys are responsible for maintaing ph balance, clearing certain toxins from the blood, and maintaining electrolyte concentrations hypoperfusion of the kidneys leads to a lack or urine production toxic accumulation of waste products, electrolyte disturbances, and disregulation of ph begin to harm other organs through the body",
        "permissive hypotension in trauma with blood loss": "patients with hypotension secondary to hemorrhagic shock may benefit from permissive hypotension this means limiting crystalloid (iv fluid) administration and allowing a mild state of hypotension in a controlled setting the goal is to permit clotting and avoid dilution of the patient's blood permissive hypotension is for bleeding patients, not for isolated traumatic brain or spine injuries",
        "pressors": "pressors are primarily used in ems for the treatment of cardiogenic shock also beneficial for treatment of distributive shock in combination with fluids epinephrine, norepinephrine, and/or dopamine depending on local protocol pressors may be given as a drip or as a push dose always investigate the underlying cause of hypotension and treat appropriately"
    },
    {
        "introduction": "what is chf? congestive heart failure (chf) refers to a condition where the heart cannot pump enough blood to meet the body's requirements. it results from any disorder that impairs ventricular filling or ejection of blood to the systemic circulation. the heart fails to meet the systemic demands of the circulatory system and often individuals develop various types of edema which result in the backup of excessive fluid in portions of the body. chf is estimated to affect 26 million people worldwide. about 6.2 million are diagnosed in the united states, and nearly 379,800 (13.4%) of death certificates mentioned chf.",
        "types of heart failure": "the types of heart failure include: left-sided heart failure, heart failure with reduced ejection fraction (hfref): \"systolic failure\", heart failure with preserved ejection fraction (hfpef): \"diastolic failure\", right-sided heart failure, and biventricular heart failure.",
        "causes of chf": "chf is often developed by unhealthy behaviors that can damage the heart including: smoking tobacco, unhealthy diet, poor physical activity levels, excessive alcohol usage. other medical conditions can contribute to risk factors for developing chf including: various types of heart disease(s) including mi, cad, cardiomyopathy, etc., diabetes, hypertension, obesity.",
        "symptoms of chf": "chf is not a curable disease (unless a complete heart transplant is done), although it is treatable with lifestyle changes and healthcare assistance it can improve and extend the quality of life for those suffering from the disease. chf often results in numerous symptoms that can impact individuals day to day life including: shortness of breath while doing daily activities, orthopnea (shortness of breath while lying down flat), chest pain(s), chronic cough, weight gain, edema (swelling) in legs, feet, ankles, stomach, or lower back, increased fatigue or weakness daily.",
        "ems and chf": "ems may be called upon for multiple different symptoms or issues related to chf. individuals may be suffering from chf related issues causing complaints including: respiratory distress, chest pain, peripheral edema, abdominal pain.",
        "lessons and concepts": "the heart is one of the most important organs of the body, as it supplies oxygen-rich blood throughout the body. without this, cells begin to lack oxygen (ischemia) and cell death will shortly follow in which some cases the damage is irreversible. damage to the heart from various conditions can result in the weakening of the myocardium, resulting in failure of the heart.",
        "anatomy of chf": "the heart has its own ability to create its own electrical impulse spontaneously generated by special cells only found within the heart (automaticity). the impulse generated causes the myocardium to contract creating a \"pump force\" pushing blood to other areas throughout the heart and circulatory system.",
        "the circulatory system": "the circulatory system is responsible for delivering oxygen and nutrients to the body's cells and removing waste products. the system includes the heart, blood vessels, and blood.",
        "the respiratory system": "chf specifically can impact the respiratory system not only due to increase oxygen demands and physical exertion from the disease, but also because of fluid crossing the alveolar membrane which normally does not occur at baseline resulting pulmonary edema.",
        "physiology of chf": "chf is caused by structural abnormalities of the heart. this structural damage begins to cause issues with the heart's ability to function properly in multiple different areas.",
        "recognition": "many millions of people live with chf on a daily basis experiencing a variety of symptoms depending on the severity, extent and progression of the disease.",
        "signs and symptoms of chf": "depending on the extent of the issues or event, s/s will vary. signs and symptoms can include: difficulty breathing (dyspnea) at rest or upon varying levels of exertion, tachypnea, tachycardia, cardiac arrhythmias, anxiety or restlessness, cough: often with pink colored, \"frothy sputum\" in some circumstances.",
        "treatment and management": "chf treatments will heavily vary based on the presenting findings and condition severity present on arrival. decompensated heart failure is defined as a clinical syndrome in which a structural or functional change in the heart leads to its inability to eject and/or accommodate blood within physiological pressure levels, thus causing a functional limitation and requiring immediate therapeutic intervention.",
        "transport considerations": "be aware that some facilities will not have the capability to continuously treat severe hf patients. patients may require intensive care capabilities due to severity of incident.",
        "scenario": "a 75-year-old male complaining of difficulty breathing, the caller (staff member) notes he noted development of issues yesterday and this afternoon they can hear \"gurgling\" when he breaths.",
        "tips and tricks": "as always: scene safety, request additional resources, c-spine and abc's take first priority (in that order)! be aware of trick questions that may ask for \"highest priority\" options first where any of the following may not have been addressed yet!",
        "causes and risk factors": "chf is often developed by unhealthy behaviors that can damage the heart including: smoking tobacco, unhealthy diet, poor physical activity levels, excessive alcohol usage. other medical conditions can contribute to risk factors for developing chf including: various types of heart disease(s) including mi, cad, cardiomyopathy, etc., diabetes, hypertension, obesity.",
        "symptoms": "chf is not a curable disease (unless a complete heart transplant is done), although it is treatable with lifestyle changes and healthcare assistance it can improve and extend the quality of life for those suffering from the disease. chf often results in numerous symptoms that can impact individuals day to day life including: shortness of breath while doing daily activities, orthopnea (shortness of breath while lying down flat), chest pain(s), chronic cough, weight gain, edema (swelling) in legs, feet, ankles, stomach, or lower back, increased fatigue or weakness daily.",
        "anatomy of the heart": "the heart has three separate layers within the walls of it, with each being composed of different as well as having varying levels of thickness. the layers include: pericardium, myocardium, endocardium.",
        "coronary vessels": "the coronary arteries supply oxygen enriched blood to the cells of the heart with the coronary vessels carrying the deoxygenated blood back to the venous system.",
        "hearts electrical system": "the heart has its own ability to create its own electrical impulse spontaneously generated by special cells only found within the heart (automaticity). the impulse generated causes the myocardium to contract creating a \"pump force\" pushing blood to other areas throughout the heart and circulatory system.",
        "systemic circulation": "systemic circulation goes around the whole body to deliver oxygen/nutrients to cells of tissues/organs. systemic circulation starts at the with blood flowing into the aorta from the left ventricle and ends at superior/inferior vena cava filling the right atrium.",
        "pulmonary circulation": "pulmonary circulation goes from the heart to the lungs where carbon dioxide and oxygen are exchanged so that the waste (co2) is exhaled and blood is reoxygenated to be circulated into systemic circulation.",
        "left-sided heart failure": "left-sided heart failure often results from left-sided heart failure: due to the left ventricle failing resulting in increased fluid pressure with blood backing up into the pulmonary circulation ultimately putting strain on the right ventricle. damage to the right ventricle can also occur from infarction, cad, chronic ischemia, and other conditions.",
        "right-sided heart failure": "right-sided heart failure often results from left-sided heart failure: due to the left ventricle failing resulting in increased fluid pressure with blood backing up into the pulmonary circulation ultimately putting strain on the right ventricle. damage to the right ventricle can also occur from infarction, cad, chronic ischemia, and other conditions. both causes result in fluid backing up into the venous system resulting in pooling of blood into the gi tract, legs, ankles, etc.",
        "biventricular heart failure": "biventricular heart failure: both ventricles are damaged in which both left and right-sided heart failure symptoms will be exhibited.",
        "the heart and its structures": "the heart has four chambers: atria, ventricle(s), valve(s). the atria or upper chambers of the heart are \"receiving chambers\" that take in blood and send it to the ventricles.",
        "layers of the heart": "the heart has three separate layers within the walls of it, with each being composed of different as well as having varying levels of thickness. layers (outermost to innermost): pericardium, myocardium, endocardium",
        "ekgs": "the ekg or also known as ecg (electrocardiogram) shows the electrical stimulation as the impulse travels through the pathway.",
        "blood": "blood is composed of these parts: rbc's, wbc's, plasma, platelets",
        "types of vessels": "arteries: carry blood away from the heart. contain large portion of muscle within their walls due to the pressure that the heart creates upon pumping. capillaries: small, thin walled vessels. found at end-organ tissues, cellular level to allow for diffusion of molecules, oxygen, nutrients, waste, etc. veins: carry blood back to heart.",
        "pathway in systemic and pulmonary circulation": "arteries, arterioles, capillaries, venules, veins",
        "layers of a vessel": "tunica externa (adventitia): external layer of the vessel. provides structural support an shape to the vessel. tunica media: middle layer. composed of elastic and muscular tissues which regulate internal diameter of he vessel. tunica intima: innermost layer. composed of endothelial line to provide a frictionless pathway to promote adequate blood flow.",
        "gas exchange and diffusion": "the main goal of the respiratory system is to provide oxygen for the cells of the body and get rid of carbon dioxide byproducts of metabolism. gas exchange within the respiratory tract as well as other parts of the body occurs by diffusion.",
        "blood vessel pressure gradients and osmosis": "within our blood vessels at the capillary level, the thin cell layer exist allowing for oxygen, nutrients, waste products, fluids and other particles to cross freely between the cells of tissues and the circulatory system.",
        "decompensated heart failure": "decompensated heart failure (dhf) is defined as a clinical syndrome in which a structural or functional change in the heart leads to its inability to eject and/or accommodate blood within physiological pressure levels, thus causing a functional limitation and requiring immediate therapeutic intervention.",
        "sympathetic crashing acute pulmonary edema (scape)": "scape is caused by an abrupt increase in sympathetic tone and release of catecholamines that can precipitate flash pulmonary edema."
    },
    {
        "introduction": "cardiovascular disease is a common disease process that is seen in the pre-hospital setting. as obesity as well as other risk factors continue to rise, it is apparent cardiovascular disease is not going away. in this study guide, we will focus mainly on heart failure both left and right-sided. we will discuss the basic anatomy and physiology of the cardiovascular system, the pathophysiology of heart failure, signs and symptoms of heart failure, treatment of heart failure and review some scenarios.",
        "lessons and concepts": "anatomy: the heart is a muscular organ. its located in the center of the chest in the mediastinum, located anterior to the spine and posterior to the sternum. tissue layers: from inner to outer endocardium, myocardium, and pericardium. the endocardium lines the heart's chambers and is bathed with blood. myocardium: thick middle layer of the heart. the cells contain unique electrical properties similar to smooth muscle. these cells have specialized structures to rapidly conduct electrical impulses from one cell to another, causing the heart to contract. pericardium: protective sac surrounding the heart. consists of two layers, visceral pericardium (epicardium) and parietal pericardium (outermost layer). chambers: the heart has four chambers, right atrium, right ventricle, left atrium, and left ventricle. the atrium is the superior chambers receiving blood. the atrium is separated by the interatrial septum. the ventricles are the inferior chambers pumping blood out. ventricles are separated by the intraventricular septum. both septa contain fibrous connective tissues as well as contractile muscle. valves: the heart contains two pairs of valves, atrioventricular valves, and semilunar valves made of endocardial and connective tissue. atrioventricular valves control blood flow between the atrium and the ventricles. these valves are the tricuspid valve and mitral valve. semilunar valves- regulate blood flow between the ventricles and the arteries into which they empty. these valves are the pulmonary valve and the aortic valve. these valves permit the one-way movement of blood and prevent backflow. list of valves in order: tricuspid, pulmonary, mitral, and aortic.",
        "peripheral circulation": "three layers to veins and arteries: tunic intima: single cell layer thick. tunica media: middle layer. consists of elastic fibers and muscle giving the vessel the ability to recoil in response to a change in pressure inside and outside the vessel. tunica adventitia: outermost layer. gives the vessel the strength to withstand the pressures generated by the heart's contractions. arterial system: arteries branch into arterioles, controlling blood flow to various organs. arterioles divide into capillaries which are the connection points between the arteries and the veins. the vascular system is then able to exchanges, gases, nutrients, and fluids through the thin capillary walls. venous system: transports blood from the peripheral tissues back to the heart.",
        "physiology": "path of blood flow the right atrium receives deoxygenated blood from the inferior and superior vena cava. superior vena cava receives deoxygenated blood from the head and upper extremities. inferior vena cava receives deoxygenated blood from everywhere below the heart. the right atrium pumps this deoxygenated blood through the tricuspid valve into the right ventricle. the right ventricle pumps this deoxygenated blood through the pulmonic valve to the pulmonary arteries and onto the lungs. blood receives the oxygen from inspiration and co2 (carbon dioxide) is offloaded into the alveoli. the blood is now oxygenated. oxygenated blood then travels through the pulmonary veins into the left atrium. the left atrium will then pump oxygenated blood through the mitral valve into the left ventricle. the left ventricle pumps this oxygenated blood through the aortic valve into the aorta. the aorta will then pump this oxygenated blood into systemic circulation. cardiac cycle: sequence of events that occurs from the end of one heart contraction to the end of the next contraction. diastole: first phase of the cardiac cycle is the relaxation phase. this is when the ventricles are filling with blood. blood is entering the ventricles through the tricuspid and mitral valves. the pulmonic and aortic valves are closed in this stage. systole: the second phase of the cardiac cycle is the contraction phase. atria contract first to finish emptying the blood into the ventricles. the pressure in the ventricles increases until it exceeds the pressure in the aorta and pulmonary arteries. the atrioventricular valves are now closed and the semilunar valves are open. the normal ventricle ejects two-thirds of the blood it contains at the end of systole. this ratio is known as ejection fraction. the amount of blood ejected is known as stroke volume stroke volume relies on three factors- preload, contractility, and afterload. the pressure in the filled ventricle at the end of diastole is preload. preload influences the force and amount of the next contraction. starlings law states that the more the myocardial muscle is stretched, the greater the contraction. however, if stretched too far the muscle will start to weaken and the heart won't pump properly. afterload is the resistance against which the ventricle must contract. cardiac output: stroke volume x heart rate. defined as the amount of blood the heart can pump in one minute. nervous control on the heart: the nervous system utilizes the autonomic nervous system to regulate the heart through the sympathetic and parasympathetic components. sympathetic is the fight or flight. the neurotransmitter for the sympathetic system is norepinephrine. norepinephrine when released increases heart rate and cardiac contractile force by working on the beta receptors. the sympathetic system has two principal receptors (alpha and beta). alpha receptors are located in the peripheral blood vessels and are responsible for vasoconstriction. bets receptors are primarily located in the heart and affect the heart rate can contractile force. parasympathetic: rest and digest. controls the heart through the vagus nerve. the primary neurotransmitter is acetylcholine. when released, acetylcholine will slow the heart rate and atrioventricular conduction.",
        "heart failure pathophysiology": "clinical syndrome in which the heart's mechanical performance is compromised so that the cardiac output cannot meet the body's demands. heart failure is divided into two categories, left-sided heart failure, and right-sided heart failure. different etiologies include valvular, coronary, or myocardial disease. other factors include sepsis, hypertension, pe, excess alcohol or drug use, or excess salt and fluid intake left ventricular failure: occurs when the left ventricle fails as an effective forward pump causing a back pressure of blood into the pulmonary circulation, resulting in pulmonary edema. the pressure in the left atrium rises which causes an increase in pressure in the pulmonary capillaries. when the pressure in the pulmonary capillaries is too. high, it forces blood plasma into the alveoli, resulting in pulmonary edema. an increase in pulmonary edema decreases oxygenation causing hypoxia right ventricular failure: occurs when the right ventricle fails as an effective forward pump causing a back pressure of blood into the systemic circulation and venous congestion. this leads to edema build-up in the body's tissues most common cause of right-sided heart failure is left-sided heart failure.",
        "recognition": "left-sided heart failure signs and symptoms: shortness of breath with or without exertion, orthopnea, wheezing, crackles, cyanosis, tachypnea, chest pain, cough (pink frothy sputum). right-sided heart failure signs and symptoms: peripheral edema, distended abdomen (ascites), jvd, weight gain, chest pain.",
        "treatment and management": "right-sided heart failure: abcs, vitals, transport to the nearest appropriate facility, or call for als intercept. left-sided heart failure: abcs, vitals, position patient in high fowlers position, this usually provides minor relief in shortness of breath, cpap if the patient can tolerate it. transport rapidly to the nearest appropriate facility or call for als intercept. continue to monitor spo2 and the patient's work of breathing. look for improvements in spo2 or the patient's work of breathing.",
        "scenario 1": "you are dispatched to a call for a person complaining of pain in their legs. patient is unable to tolerate the pain anymore and is wanting evaluation down at the hospital. the patient ran out of their \"water pill\" three weeks ago. scene: you arrive on the scene at a nicely kept house and the wife guides you to the patient. your patient is a 62-year-old male sitting on the recliner appearing uncomfortable. the patient is 5'5 and weighs currently 300 lbs. patient reports he normally weighs 280 lbs but has gained twenty pounds in the last week. the airway is patent and the patient can speak in full sentences without difficulty. breathing is unlabored with clear and equal lung sounds in all fields. skin is pwd, no hemorrhage noted, radial pulses are strong and regular. during your head to toe, you note the patient's abdomen to be distended and has pitting edema in both lower extremities. pt reports he ran out of his water pill which he believes is called lasix about 2-3 weeks ago. the patient rates his pain as a 5/10 in his lower legs. pmh includes copd, right-sided heart failure, and hypertension. allergies: none. medications: albuterol, lasix, lisinopril. vitals: 160/100, hr 80 and regular. respiratory rate of 17 and unlabored. spo2: 98% cbg 140 and a temp of 98.2 f. treatment: you assist the patient to the stretcher and secure him with seatbelts. you place an ice pack on his legs and reports minor relief with the pain. transport: you can consider als intercept if available, or transport to the nearest appropriate facility. takeaway: this patient has not been on his lasix. the patient is starting to retain fluid which accounts for his abdominal distention and pitting lower extremity edema. this patient will be treated with lasix shortly. if als intercept is unavailable, we can keep them comfortable with ice or heat packs in the meantime.",
        "scenario 2": "you are dispatched to a call for an elderly female feeling short of breath. pt woke up from sleep and reported it felt like she was drowning. scene: you arrive on the scene of a nicely kept residence and see a 72 y/o female in the tripod position on the bed. airway: patent, but patient is only able to speak in 1-2 word sentences. breathing: breathing is labored and tachypneic. lung sounds reveal crackles in all fields. skin is pale cool and clammy. radial pulses are strong and bounding. no hemorrhage was noted. head to toe exam reveals lower extremity edema, the abdomen is soft non-tender. pt has no complaints of chest pain at this time. vitals: 180/90. hr 120 regular. respiratory rate of 30 and labored. spo2 80% on room air. cbg of 160 mg/dl. temp of 98.2 f. treatment: this patient is sick and needs noninvasive positive pressure ventilation. consider calling for als intercept early. consider the use of cpap. starting setting is generally 5 cm/h2o. if needed, meet up with als intercept. if als is unavailable, transport emergent to the nearest appropriate facility. takeaway: patients with left-sided heart failure will often have pulmonary edema. the earlier cpap is placed on these patients, the better the outcome will bed. non-invasive positive pressure ventilation will force the alveoli to open and push out the fluid.",
        "tips and tricks": "remember, left-sided heart failure backs up into the lungs. right-sided heart failure backs up into the lower extremities, abdomen, etc."
    },
    {
        "introduction": "pulmonary edema is the accumulation of fluid in the lungs and air spaces. occurs when fluid from blood plasma migrates into lung parenchyma. impairs diffusion of oxygen into the pulmonary capillaries. consequence related to congestive heart failure (chf).",
        "pathophysiology": "high pressure (cardiogenic) heart failure. result from dysfunction of the left or right ventricle, chronic hypertension, cardiac diseases (myocarditis), or dysrhythmias. ventricular tachycardia. supraventricular tachycardia. high permeability (noncardiogenic). acute hypoxemia. example: inhaled toxins or near-submersion damages alveolar tissue; fluid moves into the lungs and can damage the pulmonary capillaries. most common cause of chf is coronary heart disease. ventricular pumping function is decreased which causes a decrease in cardiac output (co). with the decrease in ventricular pumping function, there is an increase in blood that is left in the ventricle which causes pressure to build in the left or right heart circulatory pathways. left ventricle failure: pressure inside the pulmonary veins increase causes blood to backup into the lungs. pulmonary edema is present along with poor gas exchange. right ventricle failure: blood backs up into the venae cavae. causes congestion of the venous system. in someone with chronic chf, compensatory mechanisms (offset) redistribute blood to organs and the body adapts to a decrease in heart function. attempt to improve co by changing preload, cardiac contractility, and/or heart rate. may worsen heart failure. may be caused by an mi, lung infections, submersion, narcotic overdose, liver or kidney disease, high altitude pulmonary edema (hape), or burns.",
        "recognition": "general. dyspnea. fatigue. exercise intolerance. fluid retention (lead to pulmonary or peripheral edema). chest pain (tightness or discomfort) with an increased work of breathing. orthopnea (elevated upper body to aid with breathing). trouble concentrating, restlessness, anxiety, unexplained confusion (result of hypoxia). limited word sentences. symptoms can present after travel. lung sounds. crackles: starting in the bases and progressing upwards with an increase in severity. if crackles are heard at the end of inspiration: fluid has moved out of the capillaries. increase in diffusion space between alveoli and capillaries. alveolar walls are now swollen. fluid has started to move into alveoli. right ventricle failure: pedal edema. jvd. sacral edema. cardiogenic shock. may be present in patients presenting with signs/symptoms of pulmonary edema, chf, and an mi. acute systolic dysfunction. signs of poor perfusion. weak, distal pulses. cool skin. delayed cap refill. decreased urinary output. acidosis. systemic/ pulmonary congestion. tachypnea. labored breathing. crackles bilaterally. may be wheezing, known as 'cardiac asthma'. pale or cyanotic skin. hypoxemia. frothy, blood-tinged sputum. classic sign of severe pulmonary edema.",
        "prehospital treatment": "goals: decrease respiratory distress and/or work of breathing. adequate oxygenation and perfusion. supportive efforts in order to decrease workload of the heart. **reassurance** is key with these patients. if the patient appears to be having symptoms related to chf and pulmonary edema, it has been instructed via protocols to follow care based off of acute coronary syndromes. focus is on lowering blood pressure. oxygen. vascular access. monitor with 12-lead (evaluate for the possibility of an mi). the focus with managing heart failure is to improve gas exchange and co. with a blood pressure > 100 mm hg: supplemental oxygen (saturations >94% desired). position of comfort for the patient. if a patient is alert: noninvasive positive-pressure ventilation, positive end-expiratory pressure, bilevel positive airway pressure, and continuous positive airway pressure (cpap) is beneficial for the following reasons: decreasing venous return and preload (this reduces pulmonary edema). improving gas exchange.",
        "in-hospital treatment": "history. physical exam. chest radiograph. labs. arterial and venous blood samples show the patient's ability to oxygenate and ventilate. 12-lead. brain natriuretic peptide elevation. used to diagnose chf if not already clear. left and right-sided hemodynamic monitoring. evaluate pressures within the heart. show effectiveness of treatment. determine whether the patient requires pharmacologic intervention or a combination of pharmacologic and mechanical intervention. aquapheresis. helps to remove fluid overload without large changes in electrolytes. morphine. used in the treatment of acute chf. intra-aortic balloon pump. reduce afterload. may improve overall perfusion. patients with ejection fraction of <30% and a life expectancy >6 months. may receive an implanted intracardiac device. left ventricular assist device. biventricular assist device.",
        "scenario": "dispatch info: code 3 response, rp reporting 'my husband can't breathe!', call disconnected. scene info: you arrive on scene of a private residence, no stairs into or out of the home. patient info: patient is a 67 year old male. aox4, gcs15. skin signs pale, cool, and diaphoretic. patient is seated in a chair next to the kitchen table. patient has his hands on his knees and is in clear distress with rapid respirations. patient is unable to give account of events due to inability to form more than 3 word sentences. the patient's wife states 'we were sitting here at the table eating dinner and out of nowhere he started having a really hard time breathing. it's getting worse! help him!'. fire captain on scene came across discharge paperwork and reported a medical history of chf and recent abnormal heart rhythm. patient's wife denied medication allergies. unable to report current medications. patient's difficulty breathing appears to be rapidly worsening. treatment info: transport info:",
        "tips and tricks": "stay calm; use a calming voice and do procedures quickly although efficiently. as ems providers, patients trust us. take a moment to try to talk with the patient and attempt to coach their breathing. keep these patients in an upright position. do not lay patients flat and try not to move the patients in a supine position. use of end tidal co2 can not only track respirations but also determine adequacy of each breath.",
        "lessons and concepts": "pathophysiology: high pressure (cardiogenic) heart failure. result from dysfunction of the left or right ventricle, chronic hypertension, cardiac diseases (myocarditis), or dysrhythmias. ventricular tachycardia. supraventricular tachycardia. high permeability (noncardiogenic) acute hypoxemia. example: inhaled toxins or near-submersion damages alveolar tissue; fluid moves into the lungs and can damage the pulmonary capillaries.",
        "signs and symptoms": "general: dyspnea. fatigue. exercise intolerance. fluid retention (lead to pulmonary or peripheral edema). chest pain (tightness or discomfort) with an increased work of breathing. orthopnea (elevated upper body to aid with breathing). trouble concentrating, restlessness, anxiety, unexplained confusion (result of hypoxia). limited word sentences. symptoms may present after travel.",
        "lung sounds": "crackles: starting in the bases and progressing upwards with an increase in severity. if crackles are heard at the end of inspiration: fluid has moved out of the capillaries. increase in diffusion space between alveoli and capillaries. alveolar walls are now swollen. fluid has started to move into alveoli.",
        "right ventricle failure": "pedal edema. jvd. sacral edema.",
        "cardiogenic shock": "can be present with patients showing signs of pulmonary edema, chf, and an mi. acute systolic dysfunction. signs of poor perfusion. weak, distal pulses. cool skin. delayed cap refill. decreased urinary output. acidosis.",
        "systemic/pulmonary congestion": "tachypnea. labored breathing. crackles bilaterally. may be wheezing, known as 'cardiac asthma'. pale or cyanotic skin. hypoxemia. frothy, blood-tinged sputum. classic sign of severe pulmonary edema.",
        "treatment and management": "prehospital treatment: goals: decrease respiratory distress and/or work of breathing. adequate oxygenation and perfusion. supportive efforts in order to decrease workload of the heart. *reassurance* is key with these patients.",
        "prehospital treatment details": "if the patient appears to be having symptoms related to chf and pulmonary edema, it has been instructed via protocols to follow care based off of acute coronary syndromes. focus is on lowering blood pressure. oxygen. vascular access. monitor with 12-lead (evaluate for the possibility of an mi).",
        "in hospital treatment": "history. physical exam. chest radiograph. labs. arterial and venous blood samples show the patient's ability to oxygenate and ventilate. 12-lead. brain natriuretic peptide elevation. used to diagnose chf if not already clear.",
        "in hospital treatment details": "left and right sided hemodynamic monitoring. evaluate pressures within the heart. show effectiveness of treatment. determine whether the patient requires pharmacologic intervention or a combination of pharmacologic and mechanical intervention. aquapheresis. helps to remove fluid overload without large changes in electrolytes.",
        "medications": "morphine. used in the treatment of acute chf. intra-aortic balloon pump. reduce afterload. may improve overall perfusion.",
        "device implantation": "patients with ejection factors of <30% and a life expectancy >6 months. may receive an implanted intracardiac device. left ventricular assist device. biventricular assist device.",
        "patient assessment": "patient is seated in a chair next to the kitchen table. patient has his hands on his knees and is in clear distress with rapid respirations. patient is unable to give account of events due to inability to form more than 3 word sentences.",
        "treatment info": "transport info: tips and tricks: stay calm; use a calming voice and do procedures quickly although efficiently. as ems providers, patients trust us. take a moment to try to talk with the patient and attempt to coach their breathing.",
        "overview": "pulmonary edema is the accumulation of fluid in the lungs and air spaces. occurs when fluid from blood plasma migrates into lung parenchyma. impairs diffusion of oxygen into the pulmonary capillaries. consequence related to congestive heart failure (chf).",
        "causes of chf": "most common cause of chf is coronary heart disease. ventricular pumping function is decreased which causes a decrease in cardiac output (co). with the decrease in ventricular pumping function, there is an increase in blood that is left in the ventricle which causes pressure to build in the left or right heart circulatory pathways.",
        "left ventricle failure": "left ventricle failure: pressure inside the pulmonary veins increase causes blood to backup into the lungs. pulmonary edema is present along with poor gas exchange.",
        "compensatory mechanisms": "in someone with chronic chf, compensatory mechanisms (offset) redistribute blood to organs and the body adapts to a decrease in heart function. attempt to improve co by changing preload, cardiac contractility, and/or heart rate. may worsen heart failure.",
        "causes of pulmonary edema": "may be caused by an mi, lung infections, submersion, narcotic overdose, liver or kidney disease, high altitude pulmonary edema (hape), or burns.",
        "right ventricular failure signs": "pedal edema. jvd. sacral edema.",
        "treatment steps": "if the patient appears to be having symptoms related to chf and pulmonary edema, and it is in accordance with your protocols, follow care based off of acute coronary syndromes. focus is on lowering blood pressure. oxygen. vascular access. monitor with 12 lead (evaluate for the possibility of an mi).",
        "oxygen therapy": "the focus with managing heart failure is to improve gas exchange and co. with a blood pressure > 100 mm hg: supplemental oxygen (saturations >94% desired). position of comfort for the patient. if a patient is alert: noninvasive positive-pressure ventilation, positive end-expiratory pressure, bilevel positive airway pressure, and continuous positive airway pressure (cpap) is beneficial to: decreasing venous return and preload (this reduces pulmonary edema). improving gas exchange.",
        "hemodynamic monitoring": "left and right sided hemodynamic monitoring. evaluate pressures within the heart. show effectiveness of treatment. determine whether the patient requires pharmacologic intervention or a combination of pharmacologic and mechanical intervention.",
        "aquapheresis": "helps to remove fluid overload without large changes in electrolytes.",
        "morphine": "used in the treatment of acute chf.",
        "intra-aortic balloon pump": "reduce afterload. may improve overall perfusion.",
        "implanted devices": "patients with ejection factors of <30% and a life expectancy >6 months. may receive an implanted intracardiac device. left ventricular assist device. biventricular assist device.",
        "case study": "dispatch: code 3 response, rp reporting 'my husband can't breathe!', call disconnected. arrival: you arrive on scene of a private residence, no stairs into or out of the home. patient is a 67 year old male. aox4, gcs15. skin signs pale, cool, and diaphoretic."
    },
    {
        "introduction": "coronary artery disease (cad) results in restricted blood supply to the heart, usually though narrowing of the coronary arteries. cad is the most common type of heart disease, which is the leading cause of death in the united states. cad is the underlying background that leads to myocardial infarctions (heart attacks) and other causes of ischemic chest pain.",
        "lessons and concepts": "the myocardium (heart muscle) is supplied by its own network of blood vessels, as the heart wall is too thick to receive oxygen and nutrients directly from the ventricles. anytime these coronary vessels fail to meet the demand of the heart muscle, a patient may experience ischemic chest discomfort. this can manifest as chest pain, shortness of breath, nausea, dizziness, weakness, or a number of other symptoms. the root cause of cad is usually a process called atherosclerosis. atherosclerosis is a process of fatty plaque buildup within the lining of a blood vessel that restricts blood flow through the vessel. stenosis refers to narrowing of the blood vessel. if a plaque ruptures, this can lead to rapid blood clot (thrombus) formation. this blood clot restricts blood flow to the myocardium (heart muscle). the result is an infarction, referring to tissue death caused by ischemia.",
        "important terms": "ischemia refers to an inadequate blood supply to a tissue. angina or angina pectoris refers to chest pain caused by ischemia. myocardial infarction refers to death of heart tissue as a result of inadequate tissue perfusion. myocardial infarctions are often referred to as heart attacks. myocardium is the muscle layer of heart tissue. thrombus is a blood clot. these occur in blood vessels when a fatty plaque ruptures and activates clotting factors. atherosclerosis is a process of fatty plaque buildup within the lining of a blood vessel that restricts blood flow through the vessel. coronary arteries are blood vessels on the heart's surface that deliver oxygen and nutrients to the heart.",
        "recognition": "the hallmark symptom of cad is chest pain. this may radiate to the arms, neck, jaw, back or abdomen. usually worsens on exertion. certain populations are more likely to experience an atypical presentation. these populations include females, diabetics, and elderly patients. the chief complaint may be nausea, anxiety, shortness of breath, or another symptom. may be associated with other signs and symptoms of heart failure. left-sided heart failure can result in respiratory distress with cariogenic pulmonary edema (wet lungs). right-sided heart failure can result in swelling of extremities, pitting edema, and jugular vein distention (jvd). look for pale or diaphoretic (sweaty) skin as indications of impaired circulation. chest pain patients can usually be put into one of two main categories: stable ischemic heart disease leads to ischemic chest discomfort during periods of increased exertion or stress. stable angina refers to chest pain that is relieved by rest or nitroglycerin. acute coronary syndrome (acs) comes with chest pain (usually sudden onset) that is not relieved by rest and is not stable. there are three sub-categories: unstable angina refers to chest pain at rest. nstemi or nste-acs is one type of heart attack. stemi is a serious heart attack that can be diagnosed on an ecg.",
        "treatment and management": "initial management begins with addressing any immediate life threats and managing any problems that compromise airway, breathing, or circulation. consider the need for oxygen and positive pressure ventilatory support. position patient to support breathing and/or circulation. obtain baseline vital signs. obtain a 12-lead ecg as soon as possible. even though an emt is not trained to interpret ecgs, an emt may obtain one so that it is available to a trained provider. in many ems systems, you may transmit an ecg to the receiving hospital. always obtain an ecg for pain or any complaint above the umbilicus (belly button). obtain patient history and perform detailed patient assessment. visualize and palpate the chest. listen to lung sounds. screen for cardiac and/or respiratory history. at the emt level, treatments for chest pain include: supplemental oxygen to maintain 90% saturation or higher (or per protocol). american heart association (aha) recommends titrating to 90%. unnecessary oxygen can restrict coronary blood flow. 162-325mg of aspirin (usually 2 or 4 81mg chewable baby aspirin). goal is to slow the formation of blood clots (anti-platelet). aspirin is also an nsaid (pain reliever) but not given for this purpose. patients are often instructed to take aspirin by 911 operator. contraindications include allergy and active gi bleeding. assist patient to self-administer their own prescribed nitroglycerin (usually 0.4mg sublingual tablets). nitroglycerin is a vasodilator that can reduce workload on the heart and increase blood flow to the myocardium. contraindications include hypotension, bradycardia, and concurrent medications for erectile dysfunction (within 24-48 hours). transport to an appropriate facility per local protocol. chest pain patients should generally be taken to larger, more capable hospitals.",
        "scenario": "you and your emt partner are dispatched to the home of a 74-year-old female complaining of chest pain, shortness of breath, and nausea. an als ambulance is also en route but is further away. you arrive to the well-kept home of an elderly couple and find the patient seated in a recliner. the patient appears diaphoretic (sweaty) and appears to be breathing heavily. you direct your partner to obtain baseline vital signs while you begin your primary assessment. airway: the patient appears to be breathing spontaneously through a patent airway. breathing: you note rapid breathing and immediately listen for lung sounds. you hear clear lung sounds throughout. the patient is breathing at a rate of 34/minute and has an initial spo2 of 94%. circulation: you feel for a radial pulse and assess skin color. you also check for peripheral swelling and jugular vein distention (jvd). you feel a strong radial pulse with pink, warm and diaphoretic skin. you do not note any peripheral swelling or jvd. your partner reports baseline vitals as follows: bp 98/42, hr 94 and regular, spo2 of 94%. you direct your partner to obtain a 12-lead ecg while you move on to your secondary assessment. you obtain a full sample history. the patient reports a history of high blood pressure that is managed with medication. she denies any other medical history. you prepare to administer initial treatments for chest pain. after confirming the patient has not already taken aspirin and confirming they have no allergies and no active gi bleeding, you administer 324 mg of aspirin. the patient does not have a prescription for ntg to assist with. you elect to withhold oxygen per your protocol because the patient is not hypoxemic. while awaiting als transport, you carefully monitor your patient for any changes and obtain repeat vitals signs every 5 minutes with no changes. on arrival of als, you provide a thorough verbal report to the responding paramedic and provide a 12-lead ecg. the paramedic determines that the patient is having a stemi (type of heart attack) and places defibrillator pads on the patient preemptively. they request you ride with the patient to the hospital as an extra crew member. during emergency transport, the paramedic obtains iv access and administers 3 doses of nitroglycerin. care is transferred to a hospital that urgently takes the patient for stent placement. the patient makes a full recovery with no lasting damage to their heart. key takeaways: initial treatment and management significantly speeds up the patient\u2019s ultimate arrival at definitive care. obtaining an ecg is crucial even if you are unable to interpret it. remember to perform a detailed assessment before administering treatments. the only exception is a threat to airway, breathing, or circulation (e.g. oxygen when necessary).",
        "tips and tricks": "always remember to focus on the abcs. drugs and treatments come after a primary assessment. if something compromises the airway or breathing, treat it. remember to ask about drug allergies and drug contraindications. for example, always ask about active gi bleeding prior to giving aspirin. always obtain an ecg.",
        "coronary anatomy": "coronary arteries are perfused directly from the aorta during diastole, and are located on the surface of the heart. left main coronary artery (lmca). left anterior descending (lad) supplies the anterior heart. septal branches perfuse the septum. diagonal branches extend across the anterior surface of the heart. left circumflex (lcx) perfuses the lateral wall of the left ventricle. left marginal branch off of lcx. sometimes supplies posterior/inferior also in a left dominant heart. right coronary artery (rca) supplies the right side of heart. branches supply the sa and av nodes. right marginal branch supplies the lateral wall of right ventricle. posterior descending supplies posterior/inferior aspects (right dominant). posterior descending usually connects with lad. multiple variants exist that alter which coronary artery perfuses different aspects of the heart.",
        "important terms to remember": "ischemia refers to an inadequate blood supply to a tissue. angina or angina pectoris refers to chest pain caused by ischemia. myocardial infarction refers to death of heart tissue as a result of inadequate tissue perfusion. myocardial infarctions are often referred to as 'heart attacks'. myocardium is the muscle layer of heart tissue. thrombus is a blood clot. these occur in blood vessels when a fatty plaque ruptures and activates clotting factors. atherosclerosis is a process of fatty plaque buildup within the lining of a blood vessel that restricts blood flow through the vessel. coronary arteries are blood vessels on the heart's surface that deliver oxygen and nutrients to the heart.",
        "types of chest pain": "chest pain patients can usually be put into one of two main categories. stable ischemic heart disease leads to ischemic chest discomfort during periods of increased exertion or stress. stable angina refers to chest pain that is relieved by rest or nitroglycerin. acute coronary syndrome (acs) comes with chest pain (usually sudden onset) that is not relieved by rest and is not stable. there are three sub-categories: unstable angina refers to chest pain at rest. ecg will look normal. no elevated cardiac biomarkers. no infarction. nstemi or nste-acs is one type of 'heart attack'. ecg may show st segment depression, inverted t waves, conduction delays, and/or new arrhythmias. blood work will show elevated cardiac biomarkers (troponin). this is a subendocardial infarction. stemi is a serious heart attack that can be diagnosed on an ecg.",
        "stemi criteria": "2 or more contiguous leads with more than 1mm st elevation. contiguous means the leads look at a similar location. e.g. i and avl or iii and avf. threshold is 2 mm is v2 and v3 for anterior stemi. 2.5 mm for men younger than 40. 1.5 mm for women. new lbbb",
        "ecg findings to look for": "st-segment elevation indicates transmural (full-thickness) ischemia. usually caused by complete occlusion of a coronary artery. st segment depression indicates subendocardial (partial thickness) ischemia of the myocardium. pay special attention to st segment morphology. st segments should be concave. straight or convex st segments are highly suspicious of an emergency. think \"smiley face\" (concave) vs frowning face (convex). new or growing q waves indicate infarction of cardiac tissue. inverted t waves (except where normal) indicate ischemia."
    },
    {
        "introduction": "the term shock is frequently used to describe someone in emotional distress. in emergency medicine, shock has a very specific and important meaning that should not be confused with other uses of the word. shock is the failure of the body to provide blood flow (perfusion) to its tissues and vital organs. this is a life-threatening condition which requires early identification to prevent progressively worse outcomes, as interventions and treatment cannot be delayed. perfusion in the body relies on three pillars: the pump (heart), the vessels, and the fluid (blood). shock is when one or more of these pillars fail. shock is defined by and broken in to four to six categories (i.e., the causes of shock): cardiogenic, hypovolemic, obstructive, distributive, anaphylactic, neurogenic, septic",
        "pathophysiology": "cardiogenic shock occurs when a patient's heart fails to pump the blood to all tissues and organs in the body. there are multiple disease processes that can lead to this condition. the most common cause is severe left ventricular failure due to a myocardial infarction (heart attack) or congestive heart failure. cardiac output (ml/min) is defined as volume of blood that is ejected from the heart over 1 min. it is determined by the following equation: stroke volume (ml) x heart rate (bpm)",
        "identification": "one of the most important actions to accomplish with respects to shock is early recognition and activation of medical resources. this is within any medical provider's scope. the following clinical information can help identify a patient at risk for or in cardiogenic shock. signs: poor perfusion (poor skin color, cold extremities, capillary refill > 2 sec., hypotension, etc.), cyanosis, poor oxygen saturations, adventitious lung sounds/pulmonary edema, cough with or without white/pink foam*, altered mental status or confusion, altered level of consciousness and cardiac arrest. symptoms: chest pain or discomfort, difficulty breathing, shortness of breath, dizziness history: coronary artery disease, myocardial infarction, heart failure, hypertension medications: nitroglycerin, diuretics, beta blockers, calcium channel blockers, ace inhibitors *the presence of pulmonary edema is a useful sign to differentiate between cardiogenic shock from other types of shock in the field.",
        "treatment": "prehospital basic treatment of cardiogenic shock patients is important but limited. lead with and return to airway, breathing, and circulation. when suspicion of cardiogenic shock is high, we should be prepared for airway obstruction (pulmonary edema w/ secretions) and hypoxia. therefore, airway management, suctioning and supplemental oxygenation with possible positive pressure ventilation (ppv) may be necessary. also, keep the patient warm because hypoperfusion is going to compromise the patient's ability to warm themselves. the patient's circulation will be compromised due to pump failure but this life threat cannot be directly fixed prehospitally by basic or even advanced providers. early activation of als and transport resource to a capable hospital is a priority for these patients.",
        "treating common causes of cardiogenic shock": "treating a possible cause of cardiogenic shock prior to the development of hypoperfusion can make an important difference in patient outcomes. we will review treatment for the two most common causes, myocardial infarction or chf. ischemic chest pain (suspected myocardial infarction) early identification of signs/symptoms a, b, cs administration of aspirin 324 mg (chew/oral) assist with prescribed nitroglycerin (sub lingual) early activation of als/transport rapid transport and early notification to hospital with cath lab capabilities (follow your local protocols and ensure no allergy/contraindication to a medication)",
        "scenario": "you are part of a two person emt crew working on a bls ambulance. it is 0700 hrs and you are dispatched to a breathing problems. you are the closest bls unit and an als ambulance is also dispatched. information: 54-year-old male, complaining of difficulty catching his breath. you arrive first to find a male sitting upright in a chair, he appears to be working to catch his breath, no obvious life threats at this time. you have your partner gather vital signs. patient is able to speak with mild difficulty, he states that he woke from bed around 0400 and hasn't been able to catch his breath. he states that he has felt similarly before but never this bad or for this long. when you ask the patient is, he has chest pain is says he does not. he is alert and oriented to ppte. you repeat your question, this time asking whether he has chest discomfort. he says he has mild chest discomfort over his left pectoral region, that gets worse when he lays down.",
        "questions and answers": "1. is this considered ischemic chest pain? a. yes. it is important to keep in mind there are different ways to describe chest pain and some patients will feel it differently than others. moreover, some patients will outright deny chest pain even when it is present because of the fear of an associated heart attack. if you suspect a possible chest pain, don't just take the first answer, ask more questions and get the patient to describe the experience in their own words. 2. what would be an appropriate intervention for this patient? a. nitroglycerin 0.4 mg sublingual b. supplemental oxygen therapy c. aspirin 324 mg oral d. b and c e. none of the above performing b and c simultaneously would be appropriate. the patient is hypoxic and has sob and a rapid respiratory rate and adventitious lung sounds (crackles) supplemental oxygen indicated. the patient is also experiencing ischemic chest discomfort/pain aspirin administration indicated.",
        "answers": "1. yes. it is important to keep in mind there are different ways to describe chest pain and some patients will feel it differently than others. moreover, some patients will outright deny chest pain even when it is present because of the fear of an associated heart attack. if you suspect a possible chest pain, don't just take the first answer, ask more questions and get the patient to describe the experience in their own words. 2. performing b and c simultaneously would be appropriate. the patient is hypoxic and has sob and a rapid respiratory rate and adventitious lung sounds (crackles) supplemental oxygen indicated. the patient is also experiencing ischemic chest discomfort/pain aspirin administration indicated. 3. b or code 3. patients experiencing suspected ischemic chest discomfort or pain need rapid als treatment and transport to a hospital. 4. the patient is hypotensive with a recent blood pressure below 90 systolic. this is a common contraindication for nitroglycerin due to the risk of dropping the patient's blood pressure. 5. the patient described in this scenario has a suspected myocardial infarction and is demonstrating signs of poor perfusion, hypoxia, and pulmonary edema. the patient is also clinically bradycardic (slow heart rate < 60 bpm). this presentation gives a high suspicion of heart failure and cardiogenic shock. 6. this patient is demonstrating signs of pulmonary edema secondary to a suspected myocardial infarction. excessive fluid resuscitation can stress this condition and make it worse since the left ventricle is already unable to keep up with normal preload. acute administration of fluid bolus (~250 ml) to improve pressure to ~90 systolic may be appropriate follow local protocols. 7. you should prioritize airway, breathing and circulation for this decompensating patient. even with your appropriate interventions he is worsening. if the patient is able to bear it cpap should be a priority. there is a high risk of secretions due to pulmonary edema (crackles), be prepared to suction. while some protocols call for titrating oxygen for patients in ischemic chest discomfort, this patient is in respiratory distress and needs high flow supplemental oxygen. if his respiratory rate becomes ineffective, he cannot tolerate the cpap, or goes unconscious/significant decrease in mentation, ppv with a bvm may be indicated."
    },
    {
        "introduction": "cardiac tamponade occurs when excess liquid, liquid-like substance, or gas accumulates in the area between the pericardial sac and the heart. there is normally a small amount of fluid between the layers of the pericardial sac to provide lubrication during contraction, but during a medical emergency or existing medical abnormality, this space can fill with a substance. as it fills, the abnormal presence of fluid around the heart will exert pressure and decrease ability for the heart to refill during the relaxation phase of contraction (diastole). this reduction in filling will significantly decrease the ability to eject blood from the heart, decreasing perfusion, and posing a serious life threat to the patient.",
        "note": "if left untreated, cardiac tamponade will likely result in obstructive shock (hypoperfusion) and death. note: during a cardiac tamponade air, blood, serum, puss or a combination will fill the intrapericardial space",
        "causes": "the cause of cardiac tamponade can be subacute or acute. subacute causes take time to develop while acute causes happen suddenly. it is important to understand that whether the cause of the tamponade is subacute or acute, they both have lethal potential, posing the same life threat to the patient. the difference between these two categories is the onset of symptoms, which will likely be gradual (days or weeks) for subacute causes and rapid (within minutes) for acute causes. subacute causes can tend to have symptomology that is more difficult to identify and easier to miss.",
        "subacute causes of cardiac tamponade": "pericarditis (infection/inflammation of the pericardium), neoplasm (malignant or benign cancer), renal disease (rare), hypothyroidism (rare), autoimmune disease",
        "acute causes of cardiac tamponade": "myocardial infarction (heart attack), traumatic injury (penetrating, nonpenetrating, or cpr), iatrogenic (e.g., surgical error, failure of sutures, radiation of the chest area). caution: depending on the nature of an acute cause, it is possible for their symptoms to manifest at a slower rate. e.g., a slow bleed from a traumatic injury",
        "possible findings": "signs: blunt or penetrating trauma to the thorax, signs of recent open-heart surgery (zipper scar on sternum), signs of infection (e.g., fever), becks triad: distended jugular veins (early sign), muffled heart sounds, narrowing pulse pressure (systolic - diastolic)/hypotension, tachycardia, tachypnea, pulsus paradoxus (drop in systolic pressure of >10 mmhg during inspiration), poor perfusion, pale skin, cold skin, cyanosis, altered mental status, loss of consciousness/fainting, vomiting, cough. note: a pulse pressure of less than 25% of systolic pressure is considered abnormal",
        "symptoms": "chest pain (common chief complaint), dyspnea (common chief complaint), orthopnea, lightheadedness, weakness, nausea, upper right quadrant abdominal pain. note: quality of chest pain and other symptoms will depend the underlying cause. note: be prepared to encounter signs and symptoms of possible underlying cause. e.g., myocardial infarction or traumatic injury",
        "assessment": "the prehospital assessment should start with the airway, breathing, circulation and life threats. a cardiac tamponade is a potentially fatal condition. therefore, it should be considered for any patient who presents with medical history or signs and symptoms that would increase our index of suspicion. if you suspect a cardiac tamponade, your questions should focus on determining the cause of the tamponade. this is not only important to identify but will help decide what prehospital treatments may be necessary.",
        "treatment": "definitive treatment for a cardiac tamponade is pericardiocentesis (aspiration of fluid with a needle) or surgery. therefore, scene time should be minimized and rapid transport to a capable hospital prioritized. basic life support should focus on airway, breathing, and circulation. activate als early. keep in mind, if you are in the immediate vicinity of a capable facility and have bls transport options, it may be more appropriate to transport the patient than wait for als resources. follow your local protocols. if signs of shock/hypoperfusion are present the patient is at a high risk of entering cardiac arrest, be prepared to resuscitate and perform cpr.",
        "possible basic life support interventions": "airway management (unconscious/severe shock/cardiac arrest), hypoxia and dyspnea: provide supplemental oxygen, positive pressure ventilation (e.g., respiratory or cardiac arrest), trauma: manage traumatic injuries, control bleeding, spinal immobilization, treat cardiac chest pain, cpr. note: interventions will be generally supportive and depend largely on the underlying cause",
        "scenario": "you are part of a two person bls ambulance dispatched to a 22 y/o female, sick person. dispatch states that the patient has been ill for almost one week. you arrive to find a female, sitting, head down, clutching her chest in a bed. she appears to be in significant discomfort. there are no immediate life threats and the scene is safe. upon seeing the state of your patient and clear discomfort, you call for als resources. the patient states that she woke up 5 hours ago to horrible chest pain, that was sharp and she feels like her heart is racing. she has had a fever for the last week and been treating it with over-the-counter antipyretics. she is recently started to have difficulty breathing and a cough. your partner has acquired a set of vitals: hr is 110 bpm and irregular radial pulse. rr are 22 breath/min, rapid, with clear and equal lung sounds in all fields. blood pressure is 90/70. oxygen saturation is 95% on room air.",
        "cardiac tamponade": "in prehospital medicine, emphasis is placed on medical conditions that are most common and/or the most life-threatening. cardiac tamponade is a condition that is relatively rare but a very serious surgical emergency which can be easily overlooked or misdiagnosed. this study guide will explore the anatomy and causes of cardiac tamponades, how to identify high risk patient or patients in crisis and what actions can be done prehospitally to achieve the best possible outcome for patients at the emt-advanced scope.",
        "possible advanced life support interventions": "advanced airway management, iv access, pain management, hypotension/hypoperfusion: fluid bolus",
        "ecg interpretation": "ecg and 12 lead can be useful in cardiac monitoring and ruling out or in potential other differential diagnoses such as myocardial infarction. keep in mind, an ecg prehospitally should not be used to diagnose a cardiac tamponade. research shows that ecg presentations during a cardiac tamponade are generally inconclusive but can include: ectopy (late sign), st elevation is possible, low qrs and t wave voltage, electrical alternans (weak than normal voltages)"
    },
    {
        "introduction": "cardiac conduction system emt cardiac conduction system  this study guide covers the pathophysiology and electrophysiology of the cardiac conduction system. we will discuss how the heart's electrical activity relates to the cardiac cycle and various factors that affect both these systems.",
        "topic areas": "\u2022 anatomy of the cardiac conduction systems \u2022 brief overview of how electrical activity appears on an ecg \u2022 the cardiac cycle \u2022 cardiac output \u2022 s1/s2 heart sounds \u2022 unique characteristics of myocytes \u2022 influence of the parasympathetic nervous system on the cardiac conduction system",
        "physiology": "\u2022 the heart is composed of two types of cells, those with a mechanical function, like contractility, and those with an electrical component \u2022 the cardiac conduction system consists of a network of electrical (pacemaker) cells embedded in the myocardial contractile cells1 \u2022 when the conduction system is electrically stimulated, it causes the filaments of the mechanical cells to slide together and produce a contraction \u2022 this network of cardiac conduction cells has four unique characteristics that differentiate them from any other type of cell in the human body: \u2022 automaticity - the ability of cardiac pacemaker cells to produce an electrical impulse without outside stimulation \u2022 excitability - the ability of the cardiac cells to respond to stimuli \u2022 conductivity - the ability of the cardiac cell to receive an electrical impulse and pass it directly to the adjoining cardiac cell \u2022 contractility - the ability of the cardiac cells to shorten or contract in response to an impulse",
        "characteristics of cardiac conduction cells": "\u2022 these characteristics allow the heart to produce and respond to its own stimuli \u2022 this allows the heart to continue beating even if it is removed from the body (as in the case of a transplant)2 \u2022 the cardiac conduction system is composed of six main parts:  \u2022 sa (sinoatrial) node \u2022 av (atrioventricular) node \u2022 bundle of his \u2022 right bundle branch \u2022 left bundle branch \u2022 purkinje fiber",
        "parts of the conduction system": "\u2022 each part plays a specific role, and stimulation within that anatomic region correlates to a step in the cardiac cycle \u2022 let's look at each portion of the conduction system individually:  \u2022 sa node: this is where it all begins \u2022 the sa node is the origin of electrical impulses and is considered the pacemaker of the heart4 \u2022 it is a specialized group of cells located at the top of the right atrium4 \u2022 av node: the av node lies on the floor of the right atrium  \u2022 it is responsible for a very brief delay in the electrical impulse as it travels from the atria to the ventricles",
        "the cardiac cycle": "\u2022 as the electrical impulse moves from the sa node to the purkinje fibers, it stimulates the contractions of the heart that create the cardiac cycle and pump blood throughout the body \u2022 this is called the cardiac cycle. \u2022 overview \u2022 the cardiac cycle is the repetitive pumping of the heart \u2022 it has two phases: systole and diastole  \u2022 systole is when the chamber contracts and ejects blood \u2022 diastole is when the chamber relaxes and fills with blood",
        "movement of blood": "\u2022 the cardiac cycle begins with deoxygenated blood entering the right atrium through the inferior and superior vena cava \u2022 then, atrial systole occurs; the atria contract, the atrioventricular valves (tricuspid and mitral) open, and blood passes into the ventricles1 \u2022 as the atria are in systole, the ventricles are in diastole \u2022 the ventricles remain relaxed and allow for blood to fill them",
        "output": "\u2022 the amount of blood pumped out of the heart with each contraction is called the stroke volume8 \u2022 the stroke volume can be multiplied by the number of heartbeats in a minute to calculate the cardiac output \u2022 cardiac output is the volume of blood pumped throughout the body each minute \u2022 a typical adult's cardiac output is between 5-6 liters per minute",
        "ecg/ekg": "\u2022 the electrical impulses of the cardiac conduction system can be viewed on an ecg \u2022 each part of the ecg corresponds with a region of the conduction system being activated \u2022 when the process is working as it should, this activation results in the contraction of the heart's chambers",
        "heart sounds": "\u2022 two sounds associated with the normal cardiac cycle can be auscultated over the chest  \u2022 these are called s1 and s2  \u2022 the closing of the heart valves creates these sounds; they are often referred to as a \u201club-dub\u201d sound",
        "ans effect on cardiac cycle": "\u2022 the autonomic nervous system (ans) is integral to the cardiac cycle \u2022 the ans tells the heart to go faster or slower and affects the strength of the contraction12 \u2022 although the ans can affect these factors, it cannot tell the heart to generate an electrical signal12",
        "receptors": "\u2022 the heart has both alpha receptors and beta receptors  \u2022 alpha (\u03b1) adrenoceptors stimulate smooth muscle contraction and vasoconstriction \u2022 beta (\u03b2) receptors cause smooth muscle relaxation and vasodilation",
        "scenario 1": "\u2022 dispatch info: you are dispatched to a 60 yo female complaining of chest discomfort and feeling lightheaded and dizzy. \u2022 scene info: when you arrive on scene, your patient is seated on her couch in her living room. she appears pale, diaphoretic, and anxious, though aox4. she has no obvious traumatic injury, gross neurological deficits, or external hemorrhage.",
        "sa node and av node": "\u2022 av node: the av node lies on the floor of the right atrium \u2022 it is responsible for a very brief delay in the electrical impulse as it travels from the atria to the ventricles \u2022 this pause is essential to give the ventricles enough time to fill with blood following the contraction of the atria",
        "bundle of his and bundle branches": "\u2022 bundle of his: located in the interventricular septum just inferior to the atria \u2022 this is where the contraction of the ventricles begins \u2022 right and left bundle branches: these two sections are located in the interventricular septum before branching into the right and left ventricles",
        "purkinje fibers": "\u2022 purkinje fibers: the last part of the conduction pathway \u2022 these fibers branch off the bundle branches and are responsible for the innervation of the ventricles4",
        "cardiac cycle": "\u2022 the cardiac conduction system begins at the sa node \u2022 the electrical impulse travels to the av node, where it is paused briefly \u2022 once through the av node, the impulse travels to the bundle of his, then branches off into the left and right bundle branches \u2022 the last part of the conduction system is the purkinje fibers which branch off the bundle branches and are responsible for innervating the ventricles",
        "heart rate": "\u2022 the sa node is considered the pacemaker of the heart \u2022 it produces a heart rate of 60-100 beats per minute, what we know as a normal sinus rhythm \u2022 should the sa node fail, the next section of the cardiac conduction system will assume responsibility for creating the electrical impulses to keep the heart beating1",
        "intrinsic heart rates": "\u2022 each subsequent section has a lower intrinsic heart rate6: \u2022 sa node: 60-100 bpm \u2022 av node: 40-60 bpm \u2022 ventricles/purkinje fibers: 20-40",
        "phases of the cardiac cycle": "\u2022 systole is when the chamber contracts and ejects blood \u2022 diastole is when the chamber relaxes and fills with blood \u2022 each set of chambers will go through systole and diastole at opposite times \u2022 this cycle takes about 0.8 seconds to complete and occurs at an average rate of 70-80 times per minute1",
        "cardiac output": "\u2022 the amount of blood pumped out of the heart with each contraction is called the stroke volume8 \u2022 the stroke volume can be multiplied by the number of heartbeats in a minute to calculate the cardiac output \u2022 cardiac output is the volume of blood pumped throughout the body each minute",
        "sympathetic and parasympathetic nervous systems": "\u2022 the ans is comprised of two systems: the sympathetic and parasympathetic nervous systems \u2022 sympathetic neurotransmitter: norepinephrine \u2022 when the sympathetic nervous system is stimulated (fight-or-flight), norepinephrine is released",
        "electrolytes": "\u2022 several common electrolytes within the body allow for cellular function they include: \u2022 sodium \u2022 potassium \u2022 calcium \u2022 chloride \u2022 magnesium",
        "action potentials": "\u2022 there are two types of action potentials seen in cardiac myocytes - one for the contractile cells and one for the pacemaker cells2 \u2022 they exhibit different action potentials, as they have different functions",
        "key takeaways": "\u2022 your patient is in pulsatile v-tach \u2022 this occurs when the ventricles become completely disassociated from the atria, and ectopic foci in the ventricles are setting the rate for the lower chambers",
        "scenario 2": "\u2022 dispatch info: you are dispatched to a 79 yo male complaining of a feeling lethargic, a bit dizzy, and easily out of breath for several days now.",
        "scenario 3": "\u2022 dispatch info: you are dispatched to a 54 yo male complaining of chest pain, feeling dizzy, and short of breath.",
        "the cardiac conduction system": "\u2022 the cardiac conduction system is composed of six main parts: \u2022 sa (sinoatrial) node \u2022 av (atrioventricular) node \u2022 bundle of his \u2022 right bundle branch \u2022 left bundle branch \u2022 purkinje fiber",
        "voltage-gated ion channels": "\u2022 electrolytes are moved in and out of the cardiac myocytes primarily by voltage-gated ion channels \u2022 these channels open or close based on the voltage of the cell."
    },
    {
        "introduction": "hypertension (htn) simply refers to a higher than normal blood pressure. hypertension is arguably the biggest risk factor of mortality worldwide with an increased risk of dozens of chronic health problems and an increased risk of medical emergencies such as stroke (cva) and heart attack (mi). emergency treatment of hypertension itself is not usually recommended in the field and treatment is aimed at correcting underlying causes and managing associated symptoms.",
        "lessons and concepts": "types of hypertension: primary, secondary, systemic, and pulmonary. primary (essential) hypertension occurs when pressure is the direct problem. this is the most common type and this is usually what a patient means if they state a history of high blood pressure. secondary hypertension occurs as a result of a medical problem or medication. symptoms resolve when the condition is managed. systemic hypertension affects the blood vessels supplied by the left ventricle. this is what we can measure with a blood pressure cuff. this is what hypertension refers to unless otherwise specified. pulmonary hypertension affects the blood vessels supplied by the right ventricle. generally requires more invasive monitoring. causes include heart disease, lung disease, and blood clots. may be prescribed pde inhibitors such as sildenafil (viagra).",
        "terminology": "systolic blood pressure (sbp) is the blood pressure during myocardial contraction. this is the \"top\" number. diastolic blood pressure (dbp) is the blood pressure during myocardial relaxation. this is the \"bottom\" number. blood pressure is affected by several physiological factors, including vascular tone (peripheral vascular resistance), overall blood volume, or cardiac output. vascular tone is the result of constriction and relaxation of vascular smooth muscle. contraction of vascular smooth muscle (vasoconstriction) increases pressure. relaxation of vascular smooth muscle reduces blood pressure. blood volume is largely regulated by the kidneys. sodium and electrolyte both contribute to blood volume regulation as well as urine output. cardiac output is affected by several cardiovascular factors, preload, afterload, contractility, and heart rate.",
        "preload": "the blood arriving to the heart before contraction. related to venous return. more preload = higher cardiac output.",
        "afterload": "the back pressure the heart must work against to move blood. closely related to arterial blood pressure. higher afterload = lower cardiac output.",
        "contractility": "how forcefully the heart muscle contracts. increased contractility = greater cardiac output and higher blood pressure.",
        "heart rate": "autonomic nervous system control. sympathetic nervous system (sns) output tends to increase blood pressure. alpha receptors on blood vessels lead to blood vessel constriction. beta receptors in the heart lead to increased heart rate and contractility. parasympathetic nervous system (psns) influence is limited to heart rate. psns receptors have minimal effect on contractility or vascular tone. muscarinic acetylcholine receptor activation leads to decrease in heart rate.",
        "hypertension and cariogenic pulmonary edema": "systemic hypertension may dramatically increase afterload on the left ventricle. this reduces left ventricular cardiac output. reduced output can cause or worsen fluid congestion around the lungs. severe congestive heart failure (chf) exacerbations frequently come with hypertension.",
        "hypertension in brain injury": "hypertension is a part of cushing's reflex which involves increased blood pressure and reflex bradycardia. hypertension, in this case, is caused by increased sympathetic output aimed at restoring perfusion of the brain.",
        "hypertension during pregnancy": "preeclampsia is a hypertensive complication of pregnancy. defined as new-onset hypertension (>140/90) after 20 weeks gestation. it may be accompanied by proteinuria and/or organ dysfunction. eclampsia is a life-threatening complication of preeclampsia. defined by new onset of tonic-clonic type seizures following preeclampsia. treated with magnesium sulfate and anti-seizure medication.",
        "normal blood pressure": "ideal blood pressure in an adult is around 110/70. hypertension is generally defined as an sbp over 140 or dbp over 90. every patient is different and variation from established values may be normal.",
        "recognition": "ensure you use a properly sized blood pressure cuff. cuffs that are too large generally underestimate blood pressure. cuffs that are too small generally overestimate blood pressure. a manual pressure may be more accurate than a machine. obtain pressure in both arms to ensure accuracy. assess for clinical symptoms. if hypertension causes clinical symptoms, it is termed symptomatic hypertension. symptoms such as headache, blurry vision, chest pain, sob, etc. if hypertension occurs without clinical symptoms, it is termed as asymptomatic. is the high pressure causing a concern, or is it simply a vital sign we notice. while concerning, hypertension in a patient with no symptoms may be normal. remember that hypertension may be a symptom of a different emergency.",
        "review of medications": "review the patient's medication list for medications used to treat hypertension. ace inhibitors (-pril) such as lisinopril. angiotensin receptor blockers (-sartan) such as losartan. diuretics such as hydrochlorothiazide, spironolactone, or furosemide. beta blockers (-lol) such as metoprolol. alpha blockers (-zosin) such as doxazosin. calcium channel blockers such as amlodipine.",
        "treatment and management": "do not treat hypertension directly unless ordered by a physician or if treatment is otherwise indicated by the patient's presentation. instead, treat the patient for their presenting signs and symptoms. pain management may relieve hypertension that is the result of pain. treat airway and breathing complications. consider cpap/bipap and nitrates for cardiogenic pulmonary edema. treat preeclampsia and eclampsia according to protocol. patients with symptomatic or otherwise concerning hypertension should always be transported to the emergency room. be sure to perform a thorough assessment and consider that hypertension may be a symptom of a life-threatening emergency (example: stroke).",
        "scenario": "you and your emt partner are dispatched to a skilled nursing facility for a report of a 72-year-old male with increased shortness of breath and high blood pressure. nursing staff report a 4-hour history of increased shortness of breath and report a blood pressure of 184/100. the patient has a documented history of congestive heart failure, primary hypertension, type 2 diabetes, and copd. the patient takes aspirin, lisinopril, insulin, prednisone, albuterol as needed, and hydrochlorothiazide. on arrival, the patient is found in a tripod position with obvious labored breathing at a rate of 32 breaths/minute and visible accessory muscle use. initial vitals are: bp 194/110; hr 112; spo2 87% on 4l home oxygen; respirations 32/minute. patient is speaking in 2-3 word sentences and too distressed to provide history. on auscultation you hear fine crackles in the upper fields with no audible air movement in the bases. after identifying inadequate oxygenation you apply a nrb at 15lpm while your partner obtains a 12-lead ecg. oxygen saturation rises to 90% on high flow oxygen but the labored breathing persists and the patient's appearance and overall condition remain unchanged. you prepare to administer cpap in accordance with your local protocol. you transport emergency to your local er. your patient continues to improve en route and vitals on arrival to the er are as follows: bp 156/90; hr 96; spo2 100% on high flow oxygen; respirations 20/minute. the patient is now able to speak in complete sentences and appears calm. auscultation reveals clear uppers with fine crackles in the bases.",
        "tips and tricks": "treat the patient for their symptoms, not their blood pressure. consider life threatening causes of hypertension. always encourage transport to the er for symptomatic hypertension. always obtain an ecg if able.",
        "physiological factors": "preload- the blood arriving to the heart before contraction. related to venous return. more preload = higher cardiac output. afterload - the back pressure the heart must work against to move blood. closely related to arterial blood pressure. higher afterload = lower cardiac output. contractility - how forcefully the heart muscle contracts. increased contractility = greater cardiac output and higher blood pressure. heart rate. autonomic nervous system control. sympathetic nervous system (sns) output tends to increase blood pressure. alpha receptors on blood vessels lead to blood vessel constriction. beta receptors in the heart lead to increased heart rate and contractility. parasympathetic nervous system (psns) influence is limited to heart rate. psns receptors have minimal effect on contractility or vascular tone. muscarinic acetylcholine receptor activation leads to decrease in heart rate.",
        "medications": "review the patient's medication list for medications used to treat hypertension. ace inhibitors (-pril) such as lisinopril. angiotensin receptor blockers (-sartan) such as losartan. diuretics such as hydrochlorothiazide, spironolactone, or furosemide. beta blockers (-lol) such as metoprolol. alpha blockers (-zosin) such as doxazosin. calcium channel blockers such as amlodipine."
    },
    {
        "introduction": "acute pulmonary embolism (pe) is a high-mortality medical emergency that occurs when a blood clot becomes lodged in a patient's pulmonary circulation. pe is also a common cause of sudden cardiac arrest. as always, treatment is focused on supporting airway, breathing, and circulation within a clinician's scope of practice. not all pes are as obvious as one might think.",
        "lessons and concepts": "background of pulmonary embolism. deep vein thrombosis (dvt) is a condition of undesired blood clot formation in the veins of the patient's extremities. these clots almost always originate in the legs. an embolism occurs when a clot breaks away from the blood vessel and enters systemic circulation. an embolism originating in the leg will travel through the inferior vena cava (ivc) and enter the patient's right atrium. next, it will travel through the right ventricle and out through the pulmonary artery. once the clot leaves the heart, it will eventually get trapped in the arterial pulmonary circulation.",
        "pathophysiology": "when a blood clot becomes trapped in the pulmonary circulation, it obstructs the flow of blood to a portion of the lung tissue. small clots may obstruct small peripheral arteries, causing mild symptoms. in many cases, several small clots break loose at once and occlude several small arteries. a larger clot may obstruct a larger blood vessel such as the right pulmonary artery or the left pulmonary artery. when a massive blood clot obstructs the main pulmonary artery, it is called a saddle embolism and carries a very high risk of sudden death. this occludes blood flow to both lungs at once.",
        "respiratory effects": "because blood is unable to make it to the lungs, blood is now unable to pick up oxygen or offload carbon dioxide in the affected area. a patient may experience shortness of breath due to high co2, low oxygen, or both. because the affected portion of the lungs is still ventilated but not adequately perfused, we use the term \"dead space\" to describe the affected territory. as time goes on, affected lung tissue may infarct (die).",
        "cardiovascular effects": "if a blood clot is large enough, it will obstruct a large volume of blood that would normally circulate through the lungs. this is a type of obstructive shock. it creates a backlog of blood and ultimately leads to right ventricular failure if the heart's muscle cannot overcome the resistance. this may lead to signs and symptoms associated with right ventricular heart failure, including: distention of the jugular veins (jvd), swelling of extremities, fluid accumulation in the abdomen. as the right ventricle begins to swell, it shifts the heart's interventricular septum and may ultimately occlude the left ventricle as well. this will lead to hypotension and eventually cardiac arrest if untreated.",
        "cardiovascular effects signs and symptoms": "distention of the jugular veins (jvd)\nswelling of extremities\nfluid accumulation in the abdomen",
        "recognition": "pulmonary embolism may present with a variety of chief complaints, making it challenging to conclusively identify in the prehospital setting. common complaints reported in patients with pe include: chest pain - often pleuritic in nature, shortness of breath (sob), cough, especially coughing up blood (hemoptysis), dizziness or syncope. examination may reveal: tachycardia, tachypnea, unexplained hypoxia (secondary to hypoxemia), signs of right ventricular heart failure (e.g. jvd). major hemodynamic compromise may also be present (e.g. hypotension). signs of dvt such as unilateral painfully or swollen legs.",
        "recognition common complaints": "chest pain - often pleuritic in nature\nshortness of breath (sob)\ncough, especially coughing up blood (hemoptysis)\ndizziness or syncope",
        "recognition examination may reveal": "tachycardia\ntachypnea\nunexplained hypoxia (secondary to hypoxemia)\nsigns of right ventricular heart failure (e.g. jvd)",
        "stable vs. unstable": "it is important to differentiate whether there is hemodynamic compromise. hemodynamically stable pe presents with adequate blood pressure and no major impairment of a patient's circulation. this is usually the case with smaller emboli and carries a lower risk. unlikely to present with definitive signs in the field, but they should always be transported for evaluation. hemodynamically unstable pe presents with a major circulatory compromise. hypotension or a sudden drop in normal bp.",
        "treatment and management": "prehospital care always begins with assessing and supporting the abcs. supplemental oxygen is indicated if a patient presents with oxygen saturation < 94%. or per local protocol. ventilatory support may be necessary in severe cases. treat for shock if signs and symptoms are present. initiate rapid transport for any patient with serious symptoms or hemodynamic compromise. e.g. hypoxia, hypoxemia, hypotension, altered mental status, or signs of clinical deterioration.",
        "treatment and management prehospital care": "assessing and supporting the abcs\nsupplemental oxygen if oxygen saturation < 94%\nventilatory support may be necessary in severe cases\ntreat for shock if signs and symptoms are present",
        "scenario": "dispatch info: you and your emt partner are dispatched to the home of a 42-year-old female with the chief complaint of sob. scene info: on arrival, you note that the patient is protecting her own airway, but breathing rapidly and speaking in 3-5 word sentences. patient info: you note that the patient's skin is pale and cool to the touch, with cyanosis around the lips.",
        "tips and tricks": "while some pulmonary emboli are obvious, many present with mild symptoms that still need care and evaluation in the emergency room. remember that the early concerns are for obstructive shock and impaired gas exchange rather than ischemia of the lung tissue itself. always remember to focus on the abcs and administer oxygen aggressively if needed. rapid transport should be initiated for any patient with severe symptoms or hemodynamic compromise.",
        "examination": "examination may reveal: tachycardia, tachypnea, unexplained hypoxia (secondary to hypoxemia), signs of right ventricular heart failure (e.g. jvd), major hemodynamic compromise may also be present (e.g. hypotension), signs of dvt such as unilateral painfully or swollen legs.",
        "medical history": "a complete medical history may reveal: history of dvt or pe, risk factors of dvt such as: lower limb fracture, recent childbirth, long periods without movement (e.g. travel or hospitalization), history of blood clots elsewhere (e.g. prior stroke), oral contraceptive use (e.g. birth control).",
        "12-lead ecg": "12-lead ecg - while there are no ecg patterns diagnostic of pe, you are likely to find some of the following: tachycardia is the most common ecg finding in acute pe, right ventricular strain pattern, inverted t-waves in early precordial and inferior leads (v1-4, ii, iii, avf), right bundle branch block (rbbb), right atrial enlargement (peaked t-wave in lead ii), s1q3t3 pattern, dominant s-wave in lead i, pathologic q, and inverted t-wave in lead iii.",
        "non-specific signs of ischemia": "diffuse st depression, inverted t-waves, etc. any patient with symptoms suspicious of pe should be transported to a facility capable of diagnostic imaging and blood work.",
        "iv therapy": "obtain large bore iv access if possible, without delaying care or transport. ensure your iv meets local requirements for a ct scan with contrast. avoid large volumes of iv fluid.",
        "pressure support": "as stated above, avoid excessive use of iv fluids. pressers may be indicated (depending on local protocols) for hypotension that does not improve with patient positioning or small fluid bolus.",
        "definitive management": "definitive management of a pe occurs in the hospital. this may include: administration of anticoagulants (\"blood thinners\"), thrombolytics (\"clot-busting\" drugs) for unstable patients. if the hospital is capable, patients may also receive endovascular treatment or surgical intervention.",
        "treatment info": "at this point, you place the patient on a non-rebreather mask and note that oxygen saturation climbs to 92%. in your assessment, the patient tells you they suddenly became short of breath when doing some remodeling around her home.",
        "differential diagnosis": "should include acute coronary syndrome (acs) and acute pe at minimum. this history of dvt, pleuritic-type chest pain, and sudden onset of sob of accompanying hypoxia lead you to believe pe is more likely.",
        "transport info": "you elect to administer spirit per local protocol, which is unlikely to help or hurt if this patient is, in fact, suffering from a pe. because of your assessment and clinical impressions, you decide to take the patient to a large hospital with the capability of a ct scan and start a large-bore iv en route."
    },
    {
        "introduction": "in the human body, there are many possible medical emergencies that can occur. to help prioritize the approach to prehospital emergency medicine, emphasis is placed on the most frequent emergencies and the most lethal emergencies. an aortic aneurysm is not an infrequent emergency for americans, but can be lethal and if overlooked by providers, can have detrimental effects on patient outcome. this study guide will review the different types of aortic aneurysm, the risk factors, the signs and symptoms, and treatment at the emt-basic scope.",
        "the aorta and aneurysm": "the aorta is the largest artery in the body and conveys blood to the peripheral tissues and vital organs. it starts at the heart, as the ascending aorta. the ascending aorta is sometimes described as a subclass of the thoracic aorta, which includes the portion of the aorta in the chest wall or thorax. once it crosses through the diaphragm, it becomes the abdominal aorta which ends when it splits into the iliac arteries. an aneurysm is when a blood vessel is dilated past its normal size. this involves the weakening of the vessel wall which forms a fragile balloon like expansion. there are generally two types of aortic aneurysms, thoracic aneurysm and abdominal aortic aneurysm (aaa or triple a). ascending aortic aneurysm is generally considered a subtype of thoracic aneurysm. an abdominal aortic aneurysm is the most common type of aneurysm.",
        "possible complications": "because of the weakening of the vessel wall, dissection and/or rupture can occur. a dissection is when the inner layer of the aorta tears, creating a false cavity or false lumen. during a rupture, all layers of the aorta tear. the size of the aneurysm has a positive relationship for risk of dissection/rupture. i.e., as size increases, so does risk of dissection or rupture. these complications are lethal.",
        "risk factors": "there are a variety of risk factors for aortic aneurysm. being aware of risk factors can help prioritize patient history questions, develop differential diagnoses and index of suspicion. risk factors include: \n* atherosclerosis (hardening of the arteries)\n* marfans syndrome (connective tissue disorder)\n* loeys-dietz syndrome (connective tissue disorder)\n* history of smoking\n* family history\n* hypertension\n* aortic valve abnormalities\n* being male (greater risk of aaa)\n* being white (greater risk of aaa)\n* age (> 40-50 years)\n* history of aneurysms\n* pregnancy",
        "causes": "there is a portion of aortic aneurysms that do not have a known cause or are idiopathic. there are families with a history of aortic aneurysms with no known reason. that said, the following are some potential causes: \n* atherosclerosis\n* marfan syndrome\n* loeys-dietz syndrome\n* hypertension\n* infection and/or inflammation of blood vessels\n* aortic valve abnormalities\n* traumatic injury",
        "possible findings": "this section contains possible signs and symptoms for aortic and thoracic aneurysms. the majority of aortic and thoracic aneurysm have no obvious signs/symptoms. a sign for thoracic aneurysms is tenderness of the chest. a sign for an abdominal aneurysm is pulse near the umbilicus.",
        "symptoms (thoracic aneurysm)": "symptoms of thoracic aneurysm include: \n* sharp, sudden chest or back pain\n* shortness of breath\n* difficulty breathing\n* difficulty swallowing",
        "symptoms (abdominal aneurysm)": "symptoms of abdominal aneurysm include: \n* deep, throbbing pain, back or side\n* pain in buttocks, groin or legs",
        "signs and symptoms of dissection": "unlike the aneurysms themselves, the lethal complications of dissection and/or rupture have some common signs and symptoms. that said, these conditions can present with little to no outward signs or complaints, increasing the chance the condition is overlooked. signs of dissection include: \n* hypertension\n* hypotension (late sign most likely indicating full rupture)\n* discrepancy when comparing bilateral blood pressures of >20 mmhg\n* extremity weakness\n* loss of peripheral pulse (arms or legs)\n* altered mental status\n* syncope\n* hoarseness\n* muffled heart tones (cardiac tamponade secondary to dissection/rupture)\n* signs of a stroke\n* signs of a heart attack. symptoms of dissection include: \n* severe pain in neck, chest, or back\n* pain may move as dissection moves\n* tearing chest pain that radiates to the back\n* pain in arms or legs\n* paresthesia (pins and needles)\n* extremity weakness\n* the intense need to defecate\n* symptoms of a stroke\n* symptoms of a heart attack",
        "signs and symptoms of rupture": "signs of rupture include: \n* sudden signs of shock or hypoperfusion\n* cold, clammy skin\n* pale skin\n* hypotension\n* loss of peripheral pulses\n* altered mental status\n* syncope or sudden loss of consciousness\n* muffled heart tones\n* thoracic trauma\n* hemoptysis (spitting/coughing of blood)\n* hematoma\n* abdominal\n* posterior\n* left subclavicular region\n* cardiac arrest. symptoms of rupture include: \n* severe chest, back, or abdominal pain\n* dyspnea\n* dysphagia\n* the intense need to defecate",
        "treatment": "definitive treatment for aortic aneurysms will depend on the risk of dissection or rupture. patients who are asymptomatic and have small, low risk aneurysms may be monitored since the risk of surgery may be considered too high. patients who are symptomatic and/or have high risk of dissection or rupture will have emergency surgery. basic interventions include: \n* rapid identification of patients who are at risk of an aortic aneurysm/dissection/rupture\n* be familiar with risk factors, signs and symptoms, and supportive interventions\n* maintain airway, breathing, circulation\n* position of comfort\n* treat hypoxia and/or dyspnea\n* supplemental oxygen\n* positive pressure ventilation\n* transport decision to definitive care (emergency vascular surgery)",
        "scenario": "you are dispatched as part of a two-person bls response vehicle to a person complaining of chest pain. an als ambulance is also dispatched but delayed. dispatch info includes a 55-year-old male, with no history of a heart attack. you arrive to find a male in 9/10 sudden chest pain. he states that it started in his chest but is now in his back and he says it feels like a tearing sensation.",
        "signs (dissection)": "hypertension, hypotension (late sign most likely indicating full rupture), discrepancy when comparing bilateral blood pressures of >20 mmhg, extremity weakness, loss of peripheral pulse (arms or legs), altered mental status, syncope, hoarseness, muffled heart tones (cardiac tamponade secondary to dissection/rupture), signs of a stroke, signs of a heart attack.",
        "symptoms (dissection)": "severe pain in neck, chest, or back, pain may move as dissection moves, tearing chest pain that radiates to the back, pain in arms or legs, paresthesia (pins and needles), extremity weakness, the intense need to defecate, symptoms of a stroke, symptoms of a heart attack.",
        "signs (rupture)": "sudden signs of shock or hypoperfusion, cold, clammy skin, pale skin, hypotension, loss of peripheral pulses, altered mental status, syncope or sudden loss of consciousness, muffled heart tones, thoracic trauma, hemoptysis (spitting/coughing of blood), hematoma, abdominal, posterior, left subclavicular region, cardiac arrest.",
        "symptoms (rupture)": "severe chest, back, or abdominal pain, dyspnea, dysphagia, the intense need to defecate.",
        "basic and advanced life support interventions": "rapid identification of patients who are at risk of an aortic aneurysm/dissection/rupture, be familiar with risk factors, signs and symptoms, supportive interventions, maintain airway, breathing, circulation, position of comfort, treat hypoxia and/or dyspnea, supplemental oxygen, positive pressure ventilation, iv access, pain management (if within advanced scope), transport decision to definitive care (emergency vascular surgery).",
        "symptoms": "symptoms for thoracic aneurysm include: \n* sharp, sudden chest or back pain\n* shortness of breath\n* difficulty breathing\n* difficulty swallowing\nsymptoms for abdominal aneurysm include: \n* deep, throbbing pain, back or side\n* pain in buttocks, groin or legs",
        "ecg findings": "generally, ecg findings are non-specific and cannot be used to identify the presence of an aortic aneurysm or dissection prehospitally. that said, they are important to acquire because they can identify other conditions, rule out conditions, or identify possible side effects of aortic aneurysm and its complications. a full 12 lead must be done to help rule out a myocardial infarction."
    },
    {
        "introduction": "everyday around the world, people have myocardial infractions as well as strokes. in ems, we treat signs and symptoms enroute to the hospital, but what happens to the patient once we have transitioned care over to the emergency physician? the patient will undergo reperfusion therapy.",
        "reperfusion therapy": "in cardiology, reperfusion therapy is defined as a therapy used to restore blood flow through a suspected or known occluded coronary artery on immediate diagnosis and includes intravenous thrombolysis, primary angioplasty, intracoronary thrombolysis, and immediate coronary artery bypass grafting surgery. reperfusion therapy for ischemic strokes is similar with the objective of trying to restore blood flow to regions of the brain that are ischemic, but not yet infarcted. the two forms of reperfusion therapy are iv thrombolysis, or mechanical clot retrieval, depending on the size and location of clot.",
        "lessons and concepts": "anatomy of the heart: the heart is composed of three tissue layers starting from the innermost layer, endocardium, myocardium, and pericardium. the endocardium lines the inner chamber of the heart. the myocardium is the thick middle layer of the heart. the myocardium contains specialized structures that help rapidly conduct electrical impulses to help the heart contract. the pericardium is a protective sac that surrounds the heart.",
        "anatomy of the heart": "four chambers and the path of blood flow- two atrium and two ventricles. the right atrium receives deoxygenated blood which pumps the blood through the tricuspid valve into the right ventricle. the right ventricle then pumps the blood through pulmonary arteries and into the pulmonary capillaries where the blood will become oxygenated. the oxygenated blood then travels through the pulmonary veins and into the left atrium. the left atrium then pumps oxygenated blood through the mitral valve and into the left ventricle. the left ventricle will then pump the oxygenated blood through the aortic valve into the aorta and into systemic circulation.",
        "coronary circulation": "the heart does not receive is blood from the endocardium, but from the coronary arteries. the coronary arteries originate in the aorta, just above the leaflets of the aortic valve. the main coronary arteries lie on the surface of the heart, and small penetrating arterioles supply the myocardial muscle.",
        "cardiac cycle": "sequence of events that occurs between the end of one heart contraction and the end of the next heart contraction. 1. diastole: ventricular filling occurs in this stage through the tricuspid and mitral valves. 2. systole: atria contract first to finish emptying blood into the ventricles. ventricles will then contract to pump blood into pulmonary and systemic circulation.",
        "electrocardiograph": "ecg graph paper: 1 small box= 0.04 seconds, 1 large box=0.20 seconds, 1 mm per box vertical, this is used to calculate st elevation and st depression.",
        "ekg interpretation": "p wave- the first component of the ekg. p wave corresponds to atrial depolarization/contraction. pr interval- beginning of the p wave to the beginning of the qrs complex. represents the time it takes for the electrical impulse takes to travel from the atria to the ventricles. normal pr interval is below 0.20 seconds.",
        "myocardial infarction": "death of a portion of the heart muscle due to prolonged deprivation of oxygenated blood. most often associated with atherosclerotic heart disease. left coronary artery obstruction- anterior, lateral, or septal infarcts. right coronary artery- inferior, posterior, and right ventricle infarcts.",
        "types of myocardial infarctions": "stemi (st. segment elevation myocardial infarction). stemi is classified by 1mm of st segment elevation in two contiguous leads. i.e. i and avl. ii, avf. v5-v6. this type of infarction is classified as transmural, the entire thickness of the myocardium becomes destroyed. nstemi- (non-st segment elevation myocardial infarction). presence of st depression or inverted t waves on an ekg.",
        "cardiac enzymes": "heart will start to release certain enzymes when injury occurs to the cardiac muscle. ck-mb (creatine kinase myocardial band)- this lab is considered a cardiac maker. in response to the damaged tissue, ck begins to rise post infarction and peaks at 24 hours.",
        "stroke and cerebral hemorrhage": "stroke is defined as injury or death of the tissue in the brain. this occurs due to a lack of oxygen in the brain. two causes of strokes. 85% of strokes are infarction, 15% of strokes are hemorrhage.",
        "types of strokes": "occlusive: cerebral artery blood flow is blocked. by a clot or other foreign material. this blocks oxygen from getting to the brain. infarcted tissue will continue to swell and can cause icp.",
        "recognition of acs/stroke": "signs and symptoms of acs: chest pressure, diaphoresis, nausea, weakness, arm/neck/jaw or pain, shortness of breath.",
        "treatment and management of acs/stroke": "ems treatment for acs: serial 12 leads- obtain several 12 leads to trend. asa (aspirin) 324 mg of asa po. nitroglycerine 0.4 mg sl. morphine/fentanyl (2- 8 mg of morphine iv) (50-100 mcg of fentanyl iv). transport to the nearest hospital with pci capabilities.",
        "hospital treatment": "fibrinolysis- example of fibrinolysis medications are rtpa (activase). can reperfuse all ischemic tissue and much of the injured myocardial tissue. time window for fibrinolysis- generally 6 hours from start of symptoms.",
        "percutaneous coronary intervention (pci)": "catheter is placed through the radial or femoral artery and advanced into the heart. from there, they will use contrast dye to visualize the coronary arteries (process is called an angiogram).",
        "coronary artery bypass grafting (cabg)": "this technique is used when damage is greater than what pci can perform. patient is placed on a cardiopulmonary bypass pump and heart is stopped.",
        "stroke treatment for ems": "manage airway as needed. stroke assessment/ check cbg. iv therapy. early notification to the hospital. if permitted, manage hypertension as indicated with beta blockers (metoprolol, labetalol, etc.).",
        "hospital treatment of strokes": "fibrinolytic therapy with tpa. mechanical thrombectomy to retrieve the clot.",
        "scenario": "dispatched to a priority one chest complaint at a local residence. patient is a 50-year-old male who developed chest pressure while performing yard work.",
        "stroke scenario": "dispatched to a priority one stroke at a local care home. ems was requested by the care staff after they did their nightly patient checks on the patient and found her watching tv and appeared to have facial droop on the right side."
    },
    {
        "introduction": "an acute myocardial infarction (ami) or also referred to as a myocardial infarction (mi) is irreversible damage to the heart muscle (myocardium) due to a lack of oxygen. this irreversible damage not only can be fatal, but can result in development of other health conditions as well as worsening of pre-existing conditions. ami is one of the leading causes of death in the developed world.",
        "annual death rates": "worldwide: estimated 3 million\nusa: estimated 1 million",
        "stemi and nstemi": "the presence of either of these key findings may indicate a myocardial ischemic event is occurring if present.",
        "preventable risk factors": "smoking/alcohol use\ndiabetes\nhtn (hypertension)\nobesity\nsedentary lifestyle\npoor diet and exercise\ndevelopment of vascular diseases (cad, pad)",
        "ems and ami": "ems plays a huge role in recognition, treatment and management of patients suffering from an ami. this includes all levels of providers playing a key role for these patients. many different conditions, symptoms, and illnesses can mimic similar symptoms of an ami. ami understanding and management heavily relies on many different factors including:\nanatomy and physiology of the cardiovascular system\nmedication availability and usage\nekg interpretation\nknowing and understanding mimicking conditions\ntreatment and transport of patients suffering from an ami",
        "other conditions": "other conditions can fall into the ami and/or chest pain category of ems treatment which will be discussed later:\nangina pectoris\nacute coronary syndrome (acs)",
        "lessons and concepts": "cardiovascular system:\nthe heart:\natrium: upper chambers to heart, send blood to ventricle(s).\nright atrium: receives blood from superior and inferior vena cava.\nleft atrium: receive blood from pulmonary veins.\nventricle: lower chambers of heart, send blood to pulmonary and systemic circulation.\nright ventricle: delivers blood to pulmonary arteries.\nleft ventricle: delivers blood to systemic circulation, produces pulse felt externally and blood pressure.",
        "the vascular system": "blood parts: when blood comes in contact with oxygen or oxygen is bound to hemoglobin it produces red color. when blood appears blue in color, this is because blood is without oxygen causes the blue appearance.\nwhole blood: name for all the blood contents combined in normal blood flow in our bodies.\nred blood cells (rbc) or erythrocytes help transport oxygen to the cells of our body and help assist with carrying co2 out of the body. rbcs are made in bone marrow.\nhemoglobin: transport protein on rbcs that oxygen binds too, has potentially for up to four oxygen molecules to bind to one rbc.",
        "types of vessels": "arteries: vessels that carry blood away from heart with oxygenated blood.\narterioles: smaller arteries that branch into capillaries at end organs, tissue, etc.\ncapillaries: thin membraned vessels, allow for diffusion of oxygen, carbon dioxide, nutrients, waste products to exit and enter cells.\nvenules: connection from capillaries to veins.\nveins: vessels that care deoxygenated blood back to the heart, low pressure system that does not have any major force to allow for blood to flow through.",
        "the conduction system": "the heart\u2019s myocytes are unique cells that produce there own electrical impulses to stimulated contraction of the heart and production of a heart beat. myocytes are the only cells in the body that can produce this unique ability on their own.",
        "pathophysiology of an ami": "with an ami, a lack in oxygen (typically causes by reduced or stoppage of blood flow) to the cells of the heart has caused infarction (local tissue death) due to prolonged cardiac ischemia (lack of blood supply).",
        "coronary arteries": "rca (right coronary artery): main artery from aorta to supply right side of heart as well as the bottom of the left ventricle and back of intraventricular septum.\nlca (left coronary artery): main artery from aorta to supply left side of heart.",
        "modifiable risk factors": "modifiable risk factors, like discussed above, can again increase risk of ami from occurring.",
        "angina pectoris": "angina pectoris or stable angina is chest pain typically due to cad.",
        "acs (acute coronary syndrome)": "acs (acute coronary syndrome) is a term that encompasses unstable angina, nstemi and stemi all in one.",
        "recognition": "signs and symptoms of an ami: can vary heavily from patient to patient, with some potentially not even having or describing chest discomfort as a symptom.",
        "ekg interpretation": "12-lead ekgs for ems are the only way, besides patient presenting state, that we can decipher whether an ischemic cardiac event is occurring.",
        "treatment and management": "response: consider any scene safety concerns, need for additional resources and response to scene (emergent/non emergent)\nassessment: consider where the patient is found and what they appear to have been doing (i.e. yard work, physical activity, resting, etc.).",
        "scenario": "medic 21 and truck 21 are dispatched to a high priority chest pain call.",
        "key takeaways": "patient was treated swiftly and effective, transported to appropriate facility that has capabilities to manage patient.",
        "tips and tricks": "testing tips\nscene safety, c-spine, and abcs first!\nif there is any concerns with any of the following, treat them first in order as the question allows or reads!"
    },
    {
        "introduction": "ecg is an important tool in the assessment of a patient's cardiovascular status. permits early identification of certain types of heart attack. provides insight into dozens of other emergencies. not universally available in all ems systems but its use has grown substantially in the past decade.",
        "lessons and concepts": "ecg and ekg refer to the same terminology. electrocardiogram (english) and elektrokardiogram (german).",
        "equipment": "many ems organizations carry cardiac monitors with 12-lead ecg capability. 3-lead ecg involves equipment with 3 limb electrodes. provides leads i, ii, and iii. adding a 4th electrode permits 3 additional augmented leads. provides leads avl, avf, and avf. 6-lead ecg may be referred to as a quick 6. 6 additional precordial leads produce a full 12-lead ecg.",
        "cardiac monitoring vs 12-lead ecg": "cardiac monitoring allows a paramedic to continuously monitor the patient's heart rate and rhythm. this permits early identification of arrhythmias and electrical abnormalities which may require immediate treatment. this may also identify abnormalities that explain a patient's symptoms. generally looks at a single lead (commonly lead ii) at a time. 12-lead ecg involves assessment of electrical information in 12 different leads (angles) of the heart.",
        "identify certain types of myocardial infarction (heart attack)": "dozens of medical emergencies will affect a 12-lead ecg.",
        "electrical movement: upward and downward deflections": "an upward deflection on an ecg lead indicates that a wave of positive charge (depolarizing myocytes) is traveling toward that lead. or a wave of negative charge (repolarizing myocytes) moving away. conversely, a downward deflection reflects a wave of positive charge (depolarizing myocytes) moving away from a lead.",
        "a 12-lead ecg": "a 12-lead ecg simply looks at the heart from 12 different angles and gives us a view of the electrical movement through the heart. this view of electrical movement allows us to infer a great deal of information about the patient's cardiac health.",
        "heart electrical anatomy": "the sa node is often called the pacemaker node. it is located in the right atrium and controls the heart rate in a sinus rhythm. the sa node has a theoretical maximum discharge rate of (220-age). the av node creates a delay between atrial and ventricular depolarization. this affects the pr interval and allows the atria to contract before the ventricles.",
        "the bundle of his": "the bundle of his is the only electrical route to the ventricles in a normal heart. this is because the atria and ventricles are electrically isolated (insulated) from each other except through the bundle of his.",
        "waves and intervals and segments": "define waves and intervals and segment. a wave is an upward or downward deflection that represents an electrical event in the heart. an interval is the time between two events (eg pr interval, qt interval, etc). a segment is the length between two specific points (eg st segment).",
        "the p wave": "the p wave reflects depolarization of cardiac myocytes through the atria.",
        "the pr interval": "the pr interval reflects the delay of depolarization though the av node.",
        "the qrs complex": "the qrs complex reflects ventricular depolarization. in a normal ecg it should be narrow.",
        "a q wave": "a q wave is an initial negative deflection, if the first deflection is negative. usually reflects depolarization of the septum.",
        "the r wave": "the r wave is the initial upward deflection of the qrs complex.",
        "the s wave": "the s wave is the downward deflection after the r wave.",
        "the st segment": "the st segment is scrutinized when assessing for signs of ischemia. st segment elevation may reflect transmural (full thickness) ischemia. st segment depression may reflect sub-endocardial (deep) ischemia.",
        "the t wave": "the t wave reflects ventricular repolarization.",
        "axis": "axis referees to the overall direction of electrical movement through the heart.",
        "leads and surfaces": "inferior wall: leads ii, iii, and avf. anterior wall: leads v1 and v2 turned the septal leads. leads v3 and v4 termed the anterior leads.",
        "artifact": "artifact refers to electrical interference that makes ecg interpretation very difficult. electrical interference can come from a variety of sources (power chairs, electric blankets, etc).",
        "rate": "there are several methods to calculate heart rate from an ecg or rhythm strip. remember that ecg shows electrical movement only. always confirm that a physical pulse matches the monitor.",
        "stemi": "stemi refers to a specific type of heart attack accompanied by st segment elevation. also called occlusion myocardial infarction.",
        "stemi mimics": "acute pericarditis. left bundle branch block (lbbb). left ventricular hypertrophy. benign early repolarization.",
        "scenario": "you and your paramedic partner respond to the home of a 74-year-old male complaining of chest pain.",
        "tips and tricks": "always obtain a 12-lead ecg where there in concern for a patient's cardiovascular status. a good rule of thumb is to obtain an ecg anytime the patient's complain is above the waist (altered mental status, respiratory distress/shortness of breath, nausea/abdominal pain)."
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "Medical \u2013 Pulmonary Edema/CHF",
        "overview": "Heart failure is generally divided into left ventricular failure and right ventricular failure.\n\nLeft ventricular heart failure is the inability of the left ventricle to adequately move blood into the systemic circulation. In left ventricular failure, an imbalance in the output of the two sides of the heart occurs. The left ventricle is unable to move all the blood delivered to it from the right side of the heart. Left ventricular followed by left atrial pressure rises and is transmitted back to the pulmonary circulation. When the pressure in the pulmonary vessels becomes too high, blood serum is forced into the alveoli, resulting in pulmonary edema.\n\nIn right ventricular heart failure the right side of the heart fails to function as an adequate pump, which leads to back pressure which leads to back pressure into the venous circulation. This is most commonly caused by left heart failure, which subsequently progresses to right heart failure.\n\nThe patient\u2019s symptoms should assist in determining left versus right heart failure, or both. Signs of left sided heart failure include rales / crackles, tachypnea while right -sided failure will create JVD, ascites, and peripheral edema.\n\nThe management goal of patients with HF involves decreasing cardiac workload by reducing both preload and afterload.",
        "hpi": "Congestive heart failure\n Past medical history\n Medications (digoxin, lasix, Bumex)\n\uf0a7 Erectile dysfunction meds: Cialis\u00ae (Tadalafil), Viagra\u00ae (Sildenafil), Levitra\u00ae (Vardenafil HCl)\n Cardiac history\n Myocardial infarction",
        "signs and symptoms": "Respiratory distress, rales\n Apprehension, orthopnea\n Jugular vein distention\n Pink, frothy sputum\n Peripheral pitting edema\n Diaphoresis\n Tripod positioning\n Inability to speak in full sentences\n Accessory muscle usage with respiration\n Hypotension, shock\n Chest pain",
        "considerations": "Myocardial Infarction\n Asthma\n Anaphylaxis\n Aspiration\n COPD\n Pleural effusion\n Pneumonia\n Pulmonary Embolus\n Pericardial Tamponade",
        "conditional guideline pulmonary edema": "Pulmonary edema with SBP greater than or equal to100 mmHg\n\nIf SBP less than 100 mmHg, see Cardiogenic SHOCK protocol.",
        "procedures": "1. Perform general patient management.     \n2. Support life -threatening problems.     \n3. Administer oxygen to maintain SPO2 94 - 99%     \n4. CPAP is the preferred airway management over endotracheal intubation. Consider intubation for severe respiratory distress / pending respiratory failure.  \n5. Transport the patient immediately positioned in an upright position.    \n6. Monitor pulse oximetry.     \n7. Place patient on cardiac monitor and obtain/interpret 12 lead ECG.  \n8. Establish an IV / lock of normal saline at KVO.   \n9. Give NITROGLYCERIN.\na. SBP greater than 180: Give NITROGLYCERIN, 2 tablets, 0.4 mg SL and 2 inches of Nitropaste 2%. If respiratory distress persists and SPB greater than 180 and HR greater than or equal to 60 bpm, repeat nitroglycerin, 1 tablets SL every 5 minutes.   \nb. SBP 100 \u2013 180: Give NITROGLYCERIN , 1 tablet, 0.4 mg SL and 1 inch of Nitropaste 2%. If respiratory distress persists and SPB greater than or equal to 100 mmHg and HR greater than or equal to 60 bpm, repeat nitroglycerin, 1 tablet SL every 5 minutes.   \n10. If available, administer CPAP with 5 - 10 cmH20 PEEP. If no CPAP available, continue with next step.    \n11. If obvious pulmonary edema noted on exam, consider LASIX 0.5 \u2013 1.0 mg / kg slow IVP, if systolic BP > 90 mmHg.  \n12. If wheezing is present, consider bronchodilator therapy, ALBUTEROL 5.0 mg and ATROVENT 0.5 mg via nebulizer with 6 - 8 liters of Oxygen. Treatment should only be administered ONCE.   \n13. Consider FENTANYL titrated to pain relief at 1 mcg / kg IV/IM, not to exceed 50 mcg per single dose. May repeat every 10 minutes.   \n14. Transport and perform ongoing assessment as indicated.",
        "assessment of edema": "+1 Slight pitting, disappears rapidly (2 mm)\n+2 Deeper pit, disappears in 10 - 15 seconds (4 mm)\n+3 Pit is noticeably deep and may last more than a minute. The extremity is fuller and swollen (6 mm)\n+4 The pit is very deep, lasts 2 - 5 minutes, and the extremity is grossly distorted (8 mm)",
        "pearls": "1. The possibility of myocardial infarction should be assessed in all patients presenting with HF.\n2. If the patient is currently taking daily diuretics, double the patient\u2019s normal prescribed dose.\n3. In left ventricular failure, the apical pulse is usually displaced laterally and downward. There may additionally be a paradoxically split S2 / S3 gallop.\n4. In right ventricular failure, S3 is often heard with a holosystolic murmur of tricuspid regurgitation.\n5. Advise the receiving facility of CPAP initiation early so they can have CPAP ready on arrival.\n6. Upon arrival at hospital, advocate for patient to remain on CPAP and do not remove CPAP until hospital equivalent respiratory therapy is ready to be placed on patient."
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "ECMO for Cardiac Arrest",
        "overview": "Out-of-hospital cardiac arrest in the U.S. has a mortality rate greater than 90% and results in excess of 300,000 deaths per year. Many of those who do survive suffer significant neurologic morbidity. Some patients may benefit from Extracorporeal Membrane Oxygenation (ECMO) intervention. Minimizing out of hospital time is one key factor which may translate to improvements in survival. Not all facilities offer this therapy and not all patients can qualify. Despite potentially minimal increase in transport time, bypassing facilities for ECMO may provide improvements in outcome.",
        "patient selection inclusion criteria": "* Age 15 -70\n* Witnessed Cardiac Arrest\n* Arrest time <30 Minutes including transport time\n* Persistent VF/VT or recurrent VF with intermittent ROSC",
        "patient selection exclusion criteria": "* >5 min without CPR\n* Asystole\n* Inability to perform and maintain mechanical or high quality manual chest compressions\n* Unwitnessed Arrest\n* Pulmonary Embolism\n* Irreversible pre-existing conditions (ESRD, advanced malignancy, renal disease, neurologic disability)\n* Weight <140 kgs\n* DNR or SNF (Skilled Nursing Facility)\n* Weight >140 kgs",
        "participating facilities hca": "* Chippenham Medical Center\n* Henrico Doctors\u2019 Hospital -Forest",
        "participating facilities bon secours": "* St. Mary\u2019s Hospital",
        "participating facilities vcu health": "* VCU (MCV Campus)",
        "procedure": "1. Perform initial patient assessment. If persistent VF/VT (or AED identifies shockable rhythm), deliver initial shock.\n2. If persistent shockable rhythm, continue resuscitation per guidelines while en route to destination facility.\n3. If suspected pulmonary embolus as an etiology, continue resuscitation per guidelines while en route to destination facility.\n4. Maintain mechanical chest compressions or high quality manual chest compressions.\n5. Alert destination facility of incoming patient who may benefit from ECMO.\n6. Transport patient to destination facility which provides ECMO strategy.",
        "pearls": "1. Keep in mind that, though the patient may meet the above inclusion criteria, the patient may have other factors outside the scope of this protocol that excludes them. Implementation of ECMO at the facility will be up to physician discretion."
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "Medical \u2013 Bradycardia",
        "overview": "Brady-arrhythmias can be caused by two mechanisms: depression of sinus nodal activity or conduction system blocks. In both situations, subsidiary pacemakers take over and pace the heart, provided the pacemaker is located above the bifurcation of the Bundle of His, and the rate is generally adequate to maintain cardiac output. The need for emergent treatment is guided by two considerations: evidence of hypoperfusion and the potential of the rhythm to degenerate into a more profound bradycardia or Asystole.",
        "hpi": "* Past medical history\n* Medications (Beta Blockers, Calcium channel blockers, Clonidine, Digitalis)\n* Pacemaker",
        "signs and symptoms": "* Heart rate < 60 bpm\n* Chest pain\n* Respiratory distress\n* Hypotension or shock\n* Altered mental status\n* Syncope",
        "considerations": "* Acute myocardial infarction\n* Hypoxia\n* Hypothermia\n* Sinus bradycardia\n* Athletes\n* Head injury (elevated ICP) or stroke\n* Spinal cord lesion\n* Sick sinus syndrome\n* AV blocks (1st, 2nd, or 3rd degree)",
        "pearls": "1. Symptomatic 2nd and 3rd degree heart block should be treated with transcutaneous pacing, avoid Atropine.\n2. In the setting of AMI or suspected acute cardiac ischemia, transcutaneous pacing should be first, only if the patient is showing profound symptoms of poor perfusion.\n3. Electrical capture during transcutaneous pacing is defined as an electrical stimulus marker followed by a wide QRS complex, with no underlying intrinsic rhythm, followed by a T-wave. This should occur for each electrical complex.\n4. Mechanical capture is confirmed when the patient\u2019s pulse matches the displayed pace rate. Because pacing stimuli generally causes muscular contractions that can be mistaken for a pulse, you should never take a pulse on the left side of the body to confirm mechanical capture. Pectoral muscle contractions due to pacing also do not indicate mechanical capture. To avoid mistaking muscular response to pacing stimuli for arterial pulsations, use ONLY: (1) right femoral artery or (2) right brachial for confirming mechanical capture.\n5. Acute myocardial infarcts can present with hypotension and brady-arrhythmias. Obtain 12-Lead ECG.\n6. If hypotension exists with bradycardia, treat the bradycardia.\n7. If blood pressure is adequate, monitor only.\n8. Treatment of bradycardia is based upon the presence or absence of significant signs and symptoms (symptomatic vs. asymptomatic)."
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "Medical - Supraventricular Tachycardia (including atrial fibrillation)\n- Medical - Tachycardia\n- Medical - Ventricular Tachycardia with a Pulse",
        "overview": "OVERVIEW:\nTachycardia's can be classified in several ways, based on the appearance of the QRS complex, heart rate, and regularity. ACLS professionals should be able to recognize and differentiate between sinus tachycardia, narrow -complex Supraventricular Tachycardia (SVT), and wide -complex tachycardia. Because ACLS providers may be unable to distinguish between supraventricular and v entricular rhythms, they should be aware that most wide -complex (broad -complex) tachycardias are ventricular in origin.",
        "signs and symptoms": "Signs and Symptoms\n- QRS < 0.12 ms",
        "hpi": "HPI\n- Past medical history\n- Medications: (Aminophylline, Diet Pills, Thyroid Supplements, Decongestants, Digoxin)\n- Diet (caffeine, chocolate)"
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "Medical \u2013 Chest Pain \u2013 Cardiac Suspected",
        "overview": "Non-traumatic chest discomfort is a common pre-hospital patient complaint. It always should be considered life-threatening until proven otherwise. The discomfort may be caused by acute myocardial infarction (AMI) or angina pectoris, which is a sign of inadequate oxygen supply to the heart muscle. Risk factors which increase the likelihood of heart disease include > 50 years of age, history of hypertension, diabetes mellitus, hypercholesterolemia, smoking, and strong family history of coronary artery disease.",
        "hpi": "* Age\n* Medications\n* PMH (MI, Angina, DM, HTN)\n* Allergies (ASA, Morphine)\n* Recent physical exertion\n* Onset\n* Quality (crushing, sharp, dull, constant, etc.)\n* Region/ Radiation / Referred\n* Severity (1 - 10)\n* Time (duration / repetition)\n* Erectile dysfunction medications such as: Viagra\u00ae (Sildenafil), Levitra\u00ae (Vardenafil), Cialis\u00ae (tadalafil)",
        "signs and symptoms": "* CP (pressure, aching, burning, indigestion and / or tightness)\n* Location (sub-sternal, epigastric, arm, jaw, neck, shoulder)\n* Radiation of pain\n* Pale, diaphoresis\n* Shortness of breath\n* Nausea, vomiting, dizziness\n* Non-specific illness",
        "considerations": "* Trauma vs. Medical\n* Angina vs. MI\n* Pericarditis\n* Mitral valve prolapse\n* Pulmonary embolism\n* Asthma / COPD\n* Pneumothorax\n* Aortic dissection or aneurysm\n* GI reflux, hiatal hernia\n* Esophageal spasm\n* Chest wall injury or pain\n* Pleural pain\n* Musculo-skeletal pain",
        "procedures": "1. Perform general patient management. \uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7\n2. Support life-threatening problems associated with airway, breathing, and circulation. \uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7\n3. Treat dysrhythmias. Be prepared to initiate CPR and defibrillation, if necessary. \uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7\n4. Administer supplemental oxygen to maintain SPO2 94 - 99% \uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7\n5. Obtain patient history. Reassure the patient. \uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7\n6. Place patient on cardiac monitor. \uf0b7 \uf0b7 \uf0b7 \uf0b7\n   a. Obtain a 12 lead ECG, <10 minutes of pt arrival. \uf0b7 \uf0b7 \uf0b7 \uf0b7\n   b. Consider ALS rendezvous, especially when the 12-lead indicates the patient is experiencing a STEMI. \uf0b7 \uf0b7\n   c. When a 12 lead ECG indicates \u201c***ACUTE MI***\u201d notify closest appropriate Emergency PCI center (cath hospital) in < 5 minutes. \uf0b7 \uf0b7 \uf0b7 \uf0b7\n7. Transport as soon as feasible. \uf0b7 \uf0b7 \uf0b7 \uf0b7\n8. Administer ASPIRIN 324 mg to chew. \uf0b7 \uf0b7 \uf0b7 \uf0b7\n9. Establish an IV of normal saline at KVO. \uf0b7 \uf0b7 \uf0b7\n10. If history consistent with cocaine associated chest pain and 12 lead not indicative of STEMI, administer MIDAZOLAM 5 mg IV. Alternatively administer DIAZEPAM 2.5 - 5 mg IV. Skip to step 14 \uf0b7 \uf0b7\n11. Administer NITROGLYCERIN.\n    a. Assist patient with PRESCRIBED NITROGLYCERIN. If the pain persists and B/P > 100 mmHg systolic, repeat nitroglycerin 0.4 mg SL in 3 to 5 minutes (up to total of three SL doses). \uf0b7 \uf0b7 \uf0b7 \uf0b7\n    b. Administer nitroglycerin 0.4 mg SL. If the pain persists and B/P > 100 mmHg systolic, repeat nitroglycerin 0.4 mg SL in 3 to 5 minutes (up to total of three SL doses). \uf0b7 \uf0b7 \uf0b7\n12. If pain persists following administration of nitroglycerin SL, apply one (1) inch of nitroglycerin paste. \uf0b7 \uf0b7 \uf0b7\n13. If pain persists following administration of a minimum of 3 SL nitroglycerin and nitroglycerin paste, consider FENTANYL titrated to pain relief at 1 mcg / kg IV/IM, not to exceed 100 mcg per single dose. May repeat every 10 minutes. Alternatively, administer MORPHINE 0.1 mg / kg IV at 1 mg / min., not to exceed 10 mg, titrated to effect. \uf0b7 \uf0b7\n14. Transport to appropriate hospital. Patients with ECGs consistent with STEMI should be transported ONLY to PCI CAPABLE HOSPITALS. \uf0b7 \uf0b7 \uf0b7 \uf0b7\n15. Transport and perform ongoing assessment as indicated. \uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7",
        "acute cocaine toxicity management": "If 12-lead ECG does not indicate AMI and chest discomfort due to cocaine is suspected per HPI, administer Midazolam 5 mg slow IVP, or alternatively Valium 2.5 \u2013 5.0 mg slow IVP.",
        "cardiac causes chest discomfort": "Ischemic\n* Angina\n* Myocardial infarction\n* Aortic stenosis\n* Hypertrophic cardiomyopathy\n* Coronary vasospasm\nNon-Ischemic\n* Pericarditis\n* Aortic dissection\n* Mitral valve prolapse",
        "non cardiac causes chest discomfort": "Gastro-esophageal\n* Reflux esophagitis\n* Esophageal spasm\n* Esophageal perforation\n* Gastritis\n* Peptic ulcer disease\nPulmonary\n* Pneumothorax\n* Pulmonary embolism\n* Pleuritis\n* Neoplasm\n* Bronchitis\nMusculoskeletal\n* Costochondritis\n* Rib fracture\n* Compression radiculopathy\nDermatologic\n* Herpes zoster",
        "ecg lead elevation reciprocal depression": "SEPTAL V1, V2 NONE\nANTERIOR V3, V4 NONE\nANTERO-SEPTAL V1, V2, V3, V4 NONE\nLATERAL I, aVL, V5, V6 II, III, aVF\nANTERO-LATERAL I, aVL, V3, V4, V5, V6 II, III, aVF\nINFERIOR II, III, aVF I, aVL\nINFERO-LATERAL II, III, aVF, V5, V6 I, aVL, V1, V2\nPOSTERIOR NONE V1, V2, V3, V4",
        "pearls": "1. Many patients with an acute coronary syndrome do not have classic textbook symptoms. As age progresses, chest discomfort declines in frequency as the presenting symptom.\n2. Women are more likely to have atypical presentations. Do not overlook vague complaints such as discomfort in the epigastric area, shortness of breath, back, jaw, and heartburn.\n3. Ongoing chest discomfort that has been present for an extended period of time may still represent angina. Further questioning may reveal that the pain is actually intermittent since onset rather than constant.\n4. Although most acute MI develop ECG changes, up to 1/3 do not develop any changes at all.\n5. Do not attribute cardiac symptoms to other chronic underlying conditions, (i.e. hiatal hernia or esophageal spasm) without a thorough assessment. A new cardiac condition may have developed."
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "LVAD Patient Management",
        "overview": "Left Ventricular Assist Device (LVAD) is a surgically implanted mechanical pump that augments the left ventricular function. The degree of augmentation is patient specific. Depending on the level of augmentation, the patient may have a palpable pulse and a blood pressure; others may have no discernable pulse or an abnormal blood pressure. Cardiac arrest in patients on mechanical support with cardiac circulatory devices such as LVAD and TAH is a new phenomenon brought about by the increased use of this therapy in patients with end-stage heart failure. The American Heart Association scientific statement highlights the recognition and treatment of cardiovascular collapse or cardiopulmonary arrest in an adult or pediatric patient who has a ventricular assist device or total artificial heart. The research performed by the AHA has not found any indication that CPR in these patients will cause harm. As such, it is recommended that CPR be given to all patients when indicated.",
        "signs and symptoms": "LVAD Patient\nAltered Mental Status\n* Confusion\n* Weakness, dizziness\nAbsent pulse\n* Pale, cool, clammy skin\n* Delayed capillary refill\n* Indeterminable BP\n* Hypotension",
        "considerations": "LVAD Patient\nHypovolemia\n* Sepsis\n* Neurogenic Shock\n* Anaphylaxis\n* Dysrhythmia\n* Device failure",
        "procedure": "1. Perform general patient management.\n2. Support life threatening problems associated with airway, breathing, and circulation.\n3. Perform general patient assessment. Include ETCO2, blood glucose, temperature, and SPO2. Administer oxygen to maintain SPO2 94 - 99%\n4. Assess status of patient perfusion i.e does the patient have normal skin color and cap refill. If normal, treat for non-LVAD causes of patient\u2019s problem within scope of practice.\n5. If LVAD problem suspected, attempt to trouble shoot:\n   * Attempt to restart LVAD\n   * Is driveline connected?\n   * Power source connected?\n   * Need to replace system controller\n6. If possible, contact patient\u2019s LVAD coordinator as soon as possible.\n7. If unable to trouble shoot LVAD proceed to section 8.\n8. While assessing the patient, CPR indicators are inadequate perfusion with one or more of the following:\n   * ETCO2 of less than 20 mm Hg\n   And/Or\n   * Mean Arterial Pressure (MAP) of less than 50\n   * Patient is in obvious cardiac arrest\n9. If indicated, begin CPR.\n10. Establish an IV of normal saline KVO. Establish a second IV if time permits.\n11. If there is a FLOW ALARM, administer Normal Saline 20 mL/kg bolus. Monitor ETCO2 and other signs of perfusion to help determine effectiveness of fluid bolus.\n12. If alarms still sounding and inadequate perfusion after IV initial fluid bolus and/or CPR, consider:\n    a. Administration of Norepinephrine infusion 0.1-0.5 mcg/kg/min for hypotension. Titrate to level of consciousness or ETCO2 > 20 mmHg.\n    b. If Norepinephrine unavailable, consider Dopamine 10- 20 mcg/kg/min for hypotension. Titrate to level of consciousness ETCO2 > 20 mmHg.\n13. Obtain 12 Lead\n14. Obtain EKG and treat any abnormal rhythms per guidelines.\n15. Transport and perform ongoing assessment as indicated. Patient condition may require transport to closest LVAD center.",
        "pearl": "It is possible for patients in a low -flow state to have abnormally low EtCO2 readings, despite correct placement of their advanced airway adjunct. It may be necessary to rely on other confirmatory methods than simply evaluating EtCO2 to confirm proper tube placement."
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "Cardiac Arrest \u2013 Unknown Rhythm (i.e. BLS)",
        "possible causes of pulseless arrest": "*Alcohol, Abuse, Acidosis*\n*Toxidromes, Trauma, Temperature, Tumor*\n*Endocrine, Electrolytes, Encephalopathy*\n*Infection, Intussusception*\n*Insulin*\n*Psychogenic, Porphyria, Pharmacological*\n*Oxygenation, Overdose, Opiates*\n*Space occupying lesion, Sepsis, Seizure, Shock*\n*Uremia*",
        "pearls": "1. If airway is maintainable initially with a BVM, delay rescue airway insertion until after initial defibrillation. The best airway is an effective airway with the least potential complications.\n2. Continue CPR while AED is charging.\n3. CPR should not be stopped for any reason, if at all avoidable, other than to check for rhythm post -defibrillation. Any stop of compressions should be kept as short as possible, preferably a maximum of 10 seconds.\n4. Rescue airway placement should be performed during compressions.\n5. Pay close attention to rate of manual ventilation. The rate should be maintained at 8 - 10 breaths per minute. Hyperventilation should be avoided because it decreases preload, cardiac output, coronary perfusion, and cerebral blood flow. The oxygenation goal is to maintain a SPO2 of 94 - 99% throughout resuscitation."
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "Medical \u2013 Abdominal Aortic Aneurysm Dissectio (Aortic Dissection and AAA)",
        "overview": "Aortic Aneurysms (AA) are a degenerative and progressively slow process where the walls of the aorta weaken and expand due to the systemic pressures of the circulatory system. The formation of aneurysms can be attributed to atherosclerosis, infection, trauma, hypertension, and inherited disorders. AAs generally form in the abdominal section of the aorta and present with weak or absent pulses in the lower extremities, cooler temperatures in the lower extremities, a central abdominal mass that can sometimes have pulsations, and abdominal and/ or back pain. If the aneurysm ruptures, chance of survival is very low and requires immediate surgical intervention. Aortic Dissections usually occur in the thoracic cavity when the aortic intima is torn away, exposing the media layer. The pulse pressure from the systemic circulation then begins to dissect the two layers of the aortic wall and creates a false lumen or pouch in the wall of the aorta. Conditions associated with the formation of an aortic dissection include: hypertension, Marfan\u2019s Syndrome, aortic valve abnormalities, immune disorders, atherosclerosis, and patients in the third trimester of pregnancy. When left untreated, about 33% of patients die within the first 24 hours, and 50% die within 48 hours. The 2-week mortality rate approaches 75% in patients with undiagnosed ascending aortic dissection.1",
        "hpi": "* Age\n* Medications\n* Viagra\u00ae, Levitra\u00ae, Cialis\u00ae\n* PMH (MI, Angina, DM, HTN)\n* Allergies (ASA, Morphine)\n* Onset\n* Quality (crushing, sharp, dull, constant, etc.)\n* Region / Radiation / Referred\n* Severity (1 \u2013 10)\n* Time (duration / repetition)",
        "signs and symptoms": "* Weak / absent pulses in lower extremities\n* Cooler temperatures in lower extremities\n* Central abdominal mass with possible pulsations\n* Anterior chest / upper back pain\n* \u201cTearing\u201d sensation in back or chest\n* Tachycardia\n* Hypertension",
        "considerations": "* Trauma vs. Medical\n* Angina vs. MI\n* Pericarditis\n* Pulmonary embolism\n* Asthma / COPD\n* Pneumothorax\n* GI reflux, hiatal hernia\n* Esophageal spasm\n* Chest wall injury or pain\n* Pleural pain",
        "procedures": "1. Perform general patient management.     \n2. Support life -threatening problems associated with airway, breathing, and circulation.     \n3. Administe r oxygen to maintain SPO2 94 - 99%     \n4. Obtain VS in both arms and assess distal pulses.     \n5. Place the patient on a monitor and obtain (BLS) /interpret (ALS) 12 lead ECG ; Refer to appropriate Cardiac Patient Care Protocol as needed. DO NOT administer ASA if acute MI is present in conjunction with suspected AAA or aortic dissection.    \n6. Establish two IV of normal saline and titrate to a systolic B/P > 90 mmHg. Do not delay transport to establish second IV.   \n7. Administer FENTANYL 1mcg / kg IN / IV / IM or MORPHINE 2.5 - 5.0 mg IV / IM as needed, per Pain Management Patient Care Protocol.   \n8. Administer ONDANS ETRON (Zofran) as needed per Medical - Nausea and Vomiting protocol.    \n9. Consider LEVOPHED Infusion 0.1-0.5 mcg / kg / minute for hypotension. Titrate to systolic B/P > 90 mmHg  \n10. Transport and perform ongoing assessment as indicated.",
        "pearls": "1. Treatment goals are to maintain systolic BP 90 \u2013120 mmHg and heart rate between 50 - 80 bpm.\n2. Do not delay transport for any reason if possible, interventions should be done enroute to appropriate facility.\n3. Abdominal mass may not be palpable in obese patients.\n4. Physical examination may reveal a murmur of aortic insufficiency.\n5. Type A dissection occurs in the ascending aorta, while a Type B dissection occurs just distal to the left subclavian artery."
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "Medical \u2013 ST Elevation Myocardial Infarction (STEMI)",
        "overview": "Prompt diagnosis and treatment offer the greatest potential benefit for myocardial salvage in the first hours of STEMI; and early, focused management of unstable angina and NSTEMI reduces adverse events and improves outcome.\nThus, it is imperative that healthcare providers recognize patients with potential ACS in order to initiate the evaluation, appropriate triage, and management as expeditiously as possible; in the case of STEMI, this recognition also allows for prompt notification of the receiving hospital and preparation for emergent reperfusion therapy.\nPotential delays to therapy occur during 3 intervals: from onset of symptoms to patient recognition, during prehospital transport, and during emergency department (ED) evaluation.",
        "hpi": "* Age\n* Medications\n* PMH (MI, Angina, DM, HTN)\n* Allergies (ASA, Morphine)\n* Recent physical exertion\n* Onset\n* Quality (crushing, sharp, dull, constant, etc.)\n* Region / Radiation / Referred\n* Severity (1  - 10)\n* Time (duration / repetition)\n* Viagra\u00ae, Levitra\u00ae, Cialis\u00ae",
        "signs and symptoms": "* CP (pressure, aching, and / or tightness)\n* Location (sub-sternal, epigastric, arm, jaw, neck, shoulder)\n* Radiation of pain\n* Pale, diaphoresis\n* Shortness of breath\n* Nausea / vomiting, dizziness\n* Non-specific illness",
        "considerations": "* Trauma vs. Medical\n* Angina vs. MI\n* Pericarditis\n* Pulmonary embolism\n* Asthma / COPD\n* Pneumothorax\n* Aortic dissection or aneurysm\n* GI reflux, hiatal hernia\n* Esophageal spasm\n* Chest wall injury or pain\n* Pleural pain",
        "lead elevation reciprocal depression": "SEPTAL V1, V2 NONE\nANTERIOR V3, V4 NONE\nANTERO -SEPTAL V1, V2, V3, V4 NONE\nLATERAL I, aVL, V5, V6 II, III, aVF\nANTERO -LATERAL I, aVL, V3, V4, V5, V6 II, III, aVF\nINFERIOR II, III, aVF I, aVL\nINFERO -LATERAL II, III, aVF, V5, V6 I, aVL, V1, V2\nPOSTERIOR NONE V1, V2, V3, V4",
        "procedures": "1. Perform general patient management. **\uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7**\n2. Support life-threatening problems associated with airway, breathing, and circulation. **\uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7**\n3. Administer oxygen to maintain SPO2 94 - 99% **\uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7**\n4. Establish an IV of normal saline per patient assessment. **\uf0b7 \uf0b7 \uf0b7**\n5. Obtain 12 lead ECG. **\uf0b7 \uf0b7 \uf0b7 \uf0b7**\na. If 12 lead reads, \u201c***AMI***, the patient should be immediately transported to the closest PCI capable hospital. AIC must notify receiving facility ASAP. **\uf0b7 \uf0b7 \uf0b7 \uf0b7**\nb. If 12 lead is consistent with STEMI, and capability exists, transmit 12 lead to PCI center . **\uf0b7 \uf0b7 \uf0b7 \uf0b7**\n6. Transport immediately. **\uf0b7 \uf0b7 \uf0b7 \uf0b7**\na. If actual transport time is greater than 45 minutes to a PCI center, consider use of aeromedical. **\uf0b7 \uf0b7 \uf0b7 \uf0b7**\n7. Place patient on cardiac monitor and monitor pulse oximetry. **\uf0b7 \uf0b7**\n8. If no contraindications, administer ASA 324 mg PO. **\uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7**\n9. If confirmed STEMI and/or significant cardiac history, administer NITROGLYCERIN 0.4 mg SL. If the pain persists and B/P > 100 mmHg systolic, repeat nitroglycerin 0.4 mg SL in 3 to 5 minutes (up to total of three SL doses). **\uf0b7 \uf0b7 \uf0b7**\n10. If pain persists, refer to General \u2013 Pain Control protocol . **\uf0b7 \uf0b7 \uf0b7 \uf0b7 \uf0b7**\n11. Transport and perform ongoing assessment as indicated. **\uf0b7 \uf0b7 \uf0b7 \uf0b7**",
        "pearls": "1. Recognized PCI centers in the ODEMSA region include (in alphabetical order):\n    Chippenham Hospital, Henrico Doctors\u2019 Hospital (Forest), Memorial Regional Medical Center, Southside Regional Medical Center, St. Francis Medical Center, St. Mary\u2019s Hospital, VA McGuire\u2019s Medical Center, VCU Medical Center.\n2. In right-sided infarctions, a prophylactic fluid bolus will assist with pre-load.\n3. Decreasing time from diagnosis to definitive treatment (cath) is essential.\n4. Designated Emergency Percutaneous Coronary Intervention Centers will have the service available on a 24 hrs per day basis and will not divert STEMI patients unless there is a catastrophic event affecting hospital operations.\n5. Patients who have had ROSC from a cardiac arrest and have an ECG consistent with a STEMI should be transported to the closest Emergency Percutaneous Coronary Intervention Center."
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "Medical \u2013 Hypotension/Shock (Non-trauma) (CARDIOGENIC SHOCK)",
        "overview": "Shock is defined as a state of inadequate tissue perfusion. This can lead to:\n- Acidosis\n- Cellular metabolism derangements\n- End-organ damage\n- Death\nEarly in shock, patients compensate with:\n- Increased sympathetic nervous system stimulation\n- Tachycardia\n- Tachypnea\nLater, compensatory mechanisms fail, causing:\n- Decreased mental status\n- Hypotension\n- Death\nEarly cellular injury may be reversible with prompt treatment.",
        "signs and symptoms": "- Blood loss (vaginal or gastrointestinal)\n- Fluid loss (vomiting, diarrhea)\n- Cardiac ischemia (MI, HF)\n- Restlessness, confusion\n- Weakness, dizziness\n- Weak, rapid pulse\n- Pale, cool, clammy skin\n- Delayed capillary refill\n- Difficulty breathing\n- Hypotension\n- Coffee-ground emesis\n- Tarry stools",
        "considerations": "- AAA, ectopic pregnancy\n- Fever, infection\n- Medications, allergic reaction\n- Pregnancy\n- Shock\n- Hypovolemic, cardiogenic, septic, neurogenic, anaphylactic\n- Ectopic pregnancy, dysrhythmia, pulmonary embolus, tension pneumothorax\n- Medication effect, overdose, vaso-vagal\n- Physiologic (pregnancy)",
        "procedures": "1. Perform general patient management. (EMR: \u221a, EMT: \u221a, A: \u221a, I: \u221a, P: \u221a)\n2. Assess mechanism of injury or nature of illness. (EMR: \u221a, EMT: \u221a, A: \u221a, I: \u221a, P: \u221a)\n3. Administer Oxygen to maintain SPO2 94-99%. (EMR: \u221a, EMT: \u221a, A: \u221a, I: \u221a, P: \u221a)\n4. If shock is present, without pulsating masses, refer to Shock protocol. (EMR: \u221a, EMT: \u221a, A: \u221a, I: \u221a, P: \u221a)\n5. Obtain 12 lead ECG:\n    a. Place patient on cardiac monitor and interpret. (A: \u221a, I: \u221a)\n6. Initiate IV of Normal Saline KVO. Establish second IV if time permits. (A: \u221a, I: \u221a, P: \u221a)\n7. Administer Normal Saline 20 mL/kg bolus twice. Caution should be used in patients with a history of renal failure and HF. Reassess for overload. (A: \u221a, I: \u221a, P: \u221a)\n8. If patient has not responded to boluses, contact medical control to consider administration of LEVOPHED 0.1-0.5 mcg/kg/min for hypotension that remains after fluid bolus. Titrate to maintain adequate peripheral perfusion. (A: \u221a, I: \u221a)\n9. Transport promptly in position of comfort. Reassess as needed. (EMR: \u221a, EMT: \u221a, A: \u221a, I: \u221a, P: \u221a)",
        "classes of shock": "- Hypovolemic: Cause: Hemorrhage, burns, dehydration.\n- Distributive: Cause: Neurogenic shock, sepsis, anaphylaxis, severe hypoxia, metabolic shock.\n- Cardiogenic: Cause: Myocardial necrosis, arrhythmias.\n- Obstructive: Cause: Pulmonary embolism, tension pneumothorax, cardiac tamponade.",
        "pearls": "1. Circulatory failure is due to inadequate cardiac function.\n2. Cardiogenic shock should be considered when MI is suspected and there is no volume-related shock.\n3. Pulmonary edema/HF may cause cardiogenic shock.\n4. Symptomatic tachycardia and bradycardia can cause cardiogenic shock."
    },
    {
        "document title": "Adult Cardiovascular Emergencies",
        "protocol title": "General \u2013 Cardiac Arrest",
        "overview": "Cardiac arrest can be caused by Ventricular Fibrillation (VF), pulseless Ventricular Tachycardia (VT), Pulseless Electric Activity (PEA), and asystole. VF represents disorganized electric activity, whereas pulseless VT represents organized electric activity of the ventricular myocardium. Neither of these rhythms generates significant forward blood flow. PEA encompasses a heterogeneous group of organized electric rhythms that are associated with either absence of mechanical ventricular activity or mechanical ventricular activity that is insufficient to generate a clinically detectable pulse. Asystole (perhaps better described as ventricular asystole) represents absence of detectable ventricular electric activity with or without atrial electric activity. The foundation of successful ACLS is high quality CPR, and, for VF / pulseless VT, attempted defibrillation within minutes of collapse. For victims of witnessed VF arrest, early CPR and rapid defibrillation can significantly increase the chance for survival to hospital discharge."
    },
    {
        "document title": "Pediatric Cardiovascular Emergencies",
        "protocol title": "Medical - Newborn/Neonatal Resuscitation",
        "overview": "The majority of newborns will require only warmth, stimulation, and occasionally some oxygen after birth. That treatment is recommended before attempting the more aggressive interventions of positive-pressure ventilation (PPV) and chest compressions.Remember that a newborn\u2019s cardiac output is rate dependent. Bradycardia usually is the result of hypoxia. Once the hypoxia is corrected, the heart rate may spontaneously correct itself. A \u201cnewborn\u201d is defined as within one month of age post delivery.",
        "procedure": "1. If obvious obstruction to spontaneous breathing or requires positive pressure ventilation, gently suction the newborn\u2019s mouth, then nostrils, with a bulb syringe for 3 to 5 seconds. Don\u2019t routinely suction an active baby. \n2. If meconium staining is present: - a. If the newborn is vigorous (strong respiratory effort, good muscle tone, and a heart rate greater than 100 bpm), no routine suctioning is required. - b. If the newborn is NOT vigorous (poor or absent respiratory effort, flaccid, lethargic), consider immediate MECONIUM ASPIRATION via endotracheal suctioning. Suctioning of meconium should not distract from the need for emergent oxygenation and ventilation of the newly born. In the patient with meconium aspiration and respiratory failure or apnea, quickly suction meconium and then begin BVM ventilations. \n3. If meconium staining is not present, rub the newborn\u2019s back vigorously. Simultaneously begin drying and warming measures. \n4. KEEP THE NEWBORN WARM AND DRY. \n5. Evaluate respirations, heart rate (apical pulse or pulse at the base of the umbilical cord), and state of oxygenation. Obtain 1 minute APGAR. \n6. If respirations are inadequate, HR > 100 bpm: - a. Initiate positive -pressure ventilation with a BVM NOT attached to oxygen. Deliver 40 to 60 breaths per minute. Use only enough volume to make the newborn\u2019s chest rise. \n7. If respirations are inadequate and HR less than 100 bpm:  - a. Initiate positive -pressure ventilation with a BVM on room air. If no increase in HR after 90 seconds, administer 100% oxygen. - b. If HR is below 60 bpm, begin compressions.",
        "apgar score \u2013 1st and 5th minute post birth": "| **Sign** | **0 Points** | **1 Point** | **2 Points** |\n|---|---|---|---|\n| **Activity (Muscle Tone)** | Flaccid | Some Flexion | Active Motion |\n| **Pulse** | Absent | < 100 | > 100 |\n| **Grimace (Reflex Irritability)** | No Response | Some | Vigorous |\n| **Appearance (Skin Color)** | Blue, Pale | Blue Extremities | Fully Pink |\n| **Respirations** | Absent | Slow, Irregular | Strong Cry |",
        "supportive care": "- Maintain airway. Suction as needed with bulb syringe. \n- Obtain blood glucose sample. If BGL is < 40 mg/dL, administer Dextrose 10% 2cc / kg (0.5 g / kg) slow IV / IO push. Repeat as necessary.\n- Maintain warmth via blankets and Porta -Warm mattress or skin -to-skin.",
        "procedure for making dextrose 10%": "In 50 ml syringe, mix 10 ml of Dextrose 50% with 40 ml Normal Saline. Mixture will yield 50 ml of Dextrose 10%\n| **Age** | **Pre-Term** | **Term** |\n------- | -------- | -------- |\n| **Weight (lb / kg)** | 3.3 lbs<br>1.5 kg | 6.6 lbs<br>3.0 kg |\n| **Epinephrine 1:10,000**<br>(1 mg / 10 ml) | 0.01 mg / kg | 0.015 mg | 0.03 mg |\n| **Dextrose 10%** | 2.0 ml / kg | 3.0 ml | 6.0 ml |",
        "pearls": "1. The primary measure of adequate initial ventilation is prompt improvement in heart rate.\n2. In the presence of thick meconium and an infant who is limp, aggressive suctioning is required.\n3. A 3:1 ratio of compressions to ventilations with 90 compressions and 30 breaths should be used to achieve approximately 120 events per minute to maximize ventilation at an achievable rate. Each event should be allotted approximately \u00bd second, with exhalation occurring during the first compression following, each ventilation.\n4. Arterial saturations of a term infant at birth can be as low as 60% and can require more than 10 minutes to reach saturations of > 90%. Hyperoxia can be toxic, particularly to the preterm baby."
    },
    {
        "document title": "Pediatric Cardiovascular Emergencies",
        "protocol title": "General \u2013 Cardiac Arrest",
        "overview": "During cardiac arrest, there is no effective pumping activity, pulse, or blood pressure.\n\nMost commonly, the rhythms that cause pulseless arrest are: ventricular fibrillation, ventricular tachycardia, pulseless electrical activity, or asystole. The ECG of ventricular fibrillation shows a fine to coarse zigzag pattern without discernible P waves or QRS complexes. Ventricular fibrillation / ventricular tachycardia is most commonly seen in patients with severe ischemic heart disease and is the most frequently encountered rhythm in sudden cardiac death in adults. Defibrillation is required to stop VF / VT. It constitutes the most important aspect of therapy for VF / VT. The sooner the shocks are given, the more likely they are to be successful.",
        "hpi": "* Estimated down time\n* Past medical history\n* Medications\n* Events leading to arrest",
        "signs and symptoms": "* Unresponsive, apneic, pulseless\n* Ventricular fibrillation or pulseless ventricular tachycardia on ECG\n* Asystole",
        "considerations": "* Renal failure / dialysis\n* DNR or living will\n* Artifact / Device failure\n* Cardiac\n* Endocrine / metabolic\n* Drugs\n* Respiratory Arrest",
        "possible causes of pulseless arrest": "**A** Alcohol, Abuse, Acidosis\n**T** Toxidromes, Trauma, Temperature, Tumor\n**E** Endocrine, Electrolytes, Encephalopathy\n**I** Infection, Intussusception\n**I** Insulin\n**P** Psychogenic, Porphyria, Pharmacological\n**O** Oxygenation, Overdose, Opiates\n**S** Space occupying lesion, Sepsis, Seizure, Shock\n**U** Uremia",
        "infant dosing chart": "Age     Term     6 months  \nWeight (lb/kg)     6.6 lb  3 kg     17.6 lb  \n8 kg  \nDefibrillation     2 joules / kg     6 joules     16 joules  \nDefibrillation     4 joules / kg     12 joules    32 joules  \nEpinephrine     1:10,000     (1 mg / 10 ml)     0.01 mg / kg     0.03 mg    0.08mg  \nAmiodarone     5 mg / kg     15 mg     40 mg  \nMagnesium     Sulfate     25 - 50 mg / kg     75 mg    200 mg",
        "pediatric dosing chart": "Age     1  \nyears     3  \nyears     6  \nyears     8  \nyears     10  \nyears     12  \nyears     14  \nyears  \nWeight (lb / kg)     22 lb 10  \nkg     30.8 lb     14 kg     44 lb 20  \nkg     55 lb 25  \nkg     75 lb 34  \nkg     88 lb 40  \nkg     110 lb  \n50 kg  \nDefibrillation     2 joules / kg 20  \njoules     28     \njoules     40     \njoules     50     \njoules     68     \njoules     80     \njoules     100  \njoules  \nDefibrillation     4 joules / kg 40  \njoules     56     \njoules     80     \njoules     100    \njoules     136     \njoules     160     \njoules     200  \njoules  \nEpinephrine     1:10,000     (1 mg / 10 ml)     0.01 mg / kg     0.1 mg 0.14  \nmg 0.2     \nmg 0.25     \nmg 0.34     \nmg 0.4     \nmg 0.5     \nmg  \nAmiodarone     5 mg / kg     50  \nmg     70     \nmg     100     \nmg     125     \nmg     170     \nmg     200     \nmg     250  \nmg  \nMagnesium     Sulfate     25 - 50 mg / kg     250  \nmg     350     \nmg     500     \nmg     625      \nmg     850     \nmg     1      \ngm     1.25    \ngm",
        "monitor operation note": "Ensure you are operating according to the specifications of the manufacturer of your particular monitor.",
        "pearls": "1. If airway maintainable initially with BVM, delay advanced airway insertion until after initial medication administration. The best airway is an effective airway with the least potential complications.\n2. Do not stop CPR to give ventilations once advanced airway has been secured.\n3. CPR should not be stopped for any reason, if at all avoidable, other than to check for rhythm change. Any stop of compressions should kept as short as possible, preferably a maximum of 10 seconds. IV / IO access and advanced airway placement should be performed while compressions are being performed.\n4. Pay close attention to rate of manual ventilation. Hyperventilation produces decrease in preload, cardiac output, coronary perfusion, and cerebral blood flow."
    },
    {
        "document title": "Pediatric Cardiovascular Emergencies",
        "protocol title": "Cardiac Arrest \u2013 Unknown Rhythm (i.e. BLS)",
        "possible causes of pulseless arrest": "* A Alcohol, Abuse, Acidosis\n* T Toxidromes, Trauma, Temperature, Tumor\n* E Endocrine, Electrolytes, Encephalopathy\n* I Infection, Intussusception\n* I Insulin\n* P Psychogenic, Porphyria, Pharmacological\n* O Oxygenation, Overdose, Opiates\n* S Space occupying lesion, Sepsis, Seizure, Shock\n* U Uremia",
        "pearls": "1. If airway is maintainable initially with a BVM, delay rescue airway insertion until after initial defibrillation. The best airway is an effective airway with the least potential complications.\n2. Continue CPR while AED is charging.\n3. CPR should not be stopped for any reason, if at all avoidable, other than to check rhythm immediately prior to defibrillation. Any stop of compressions should kept as short as possible, preferably a maximum of 10 seconds. Alternate airway placement should be performed during compressions.\n4. Pay close attention to rate of manual ventilation. Hyperventilation produces decrease in preload, cardiac output, coronary perfusion, and cerebral blood flow.\n5. AED\u2019s may be used for patients all ages. For children less than 8 years of age, use an AED equipped with a pediatric attenuator. If an AED with pediatric attenuator is not available, use a standard AED."
    },
    {
        "document title": "Pediatric Cardiovascular Emergencies",
        "protocol title": "Medical \u2013 Supraventricular Tachycardia (including atrial fibrillation) Medical \u2013 Tachycardia Medical \u2013 Ventricular Tachycardia with a Pulse",
        "overview": "Tachycardia is an abnormally fast rhythm of the heart. It is most commonly caused by a reentry mechanism that involves an accessory pathway or the AV conduction system.\nSVT is the most common tachyarrhythmia producing cardiovascular compromise during infancy.",
        "hpi": "* Past medical history\n* Medications, toxin ingestion (aminophylline, diet pills, thyroid supplements, decongestants, digoxin)\n* Drugs (nicotine, cocaine)\n* Congenital heart disease",
        "signs and symptoms": "* Respiratory distress\n* Syncope, near syncope\n* Heart rate:\n    * Child > 180 / min\n    * Infant > 220 / min\n* QRS < 0.08 seconds\n* Pale or cyanosis\n* Diaphoresis\n* Tachypnea\n* Vomiting\n* Hypotension\n* Altered mental status\n* Pulmonary congestion\n* Syncope",
        "considerations": "* Heart disease (congenital)\n* Hypo / hyperthermia\n* Hypovolemia\n* Anemia\n* Electrolyte imbalance\n* Anxiety, pain, emotional stress\n* Fever, infection, sepsis\n* Hypoxia\n* Hypoglycemia\n* Medication, toxin, drugs\n* Pulmonary embolus\n* Trauma",
        "infant dosing chart": "Infant Dosing Chart:\n| Age | Term | 6 months |\n|---|---|---|\n| Weight (lb / kg) | 6.6 lb / 3 kg | 17.6 lb / 8 kg |\n| Defibrillation | 2 joules / kg | 6 joules | 16 joules |\n| Defibrillation | 4 joules / kg | 12 joules | 32 joules |\n| Epinephrine 1:10,000 (1 mg / 10 ml) | 0.01 mg / kg | 0.03 mg | 0.08mg |\n| Amiodarone | 5 mg / kg | 15 mg | 40 mg |\n| Magnesium Sulfate | 25 - 50 mg / kg | 75 mg | 200 mg |\n\n| Age | 1 years | 3 years | 6 years | 8 years | 10 years | 12 years | 14 years |\n|---|---|---|---|---|---|---|---|\n| Weight (lb / kg) | 22 lb / 10 kg | 30.8 lb / 14 kg | 44 lb / 20 kg | 55 lb / 25 kg | 75 lb / 34 kg | 88 lb / 40 kg | 110 lb / 50 kg |\n| Defibrillation | 2 joules / kg | 20 joules | 28 joules | 40 joules | 50 joules | 68 joules | 80 joules | 100 joules |\n| Defibrillation | 4 joules / kg | 40 joules | 56 joules | 80 joules | 100 joules | 136 joules | 160 joules | 200 joules |\n| Epinephrine 1:10,000 (1 mg / 10 ml) | 0.01 mg / kg | 0.1 mg | 0.14 mg | 0.2 mg | 0.25 mg | 0.34 mg | 0.4 mg | 0.5 mg |\n| Amiodarone | 5 mg / kg | 50 mg | 70 mg | 100 mg | 125 mg | 170 mg | 200 mg | 250 mg |\n| Magnesium Sulfate | 25 - 50 mg / kg | 250 mg | 350 mg | 500 mg | 625 mg | 850 mg | 1 gm | 1.25 gm |",
        "pearls": "1. SVT is often diagnosed in infants because of symptoms of congestive heart failure. SVT usually presents differently in older children. Common signs and symptoms of SVT in infants include: poor feeding, rapid breathing, irritability, unusual sleepiness, pale or blue skin color, and vomiting. SVT is initially well tolerated in most infants and older children. It can, however, lead to heart failure and clinical evidence of shock, particularly if baseline myocardial function is impaired by congenital heart disease or cardiomyopathy. It can ultimately cause cardiovascular collapse.\n2. Approved vagal maneuvers include coughing, bearing down as if attempting a bowel movement. Carotid sinus massage and / or ocular massage is not approved.",
        "amiodarone drip": "(5 mg / kg over 40 minutes)\nDilute calculated volume of Amiodarone in 50 ml D 5W\nUsing a 60 gtts / mL administration set, flow infusion at 60 gtts. (1 mL / min, 1 gtt / sec)"
    },
    {
        "document title": "Pediatric Cardiovascular Emergencies",
        "protocol title": "Medical - Bradycardia",
        "overview": "Bradycardia is the most common dysrhythmia in the pediatric population. Bradycardia, in pediatric patients, typically is the result of some form of respiratory depression and initial treatment should be directed to ensuring that the patient is breathing adequately and providing supplemental oxygenation and ventilation as needed. Since the etiology of bradycardia is usually hypoxemia, initial management is ventilation and oxygenation while perfusion is maintained with chest compressions in children with a heart rate of less than 60 beats per minute. Symptomatic bradycardia is defined in pediatrics as hypotension or other signs and/or symptoms of poor perfusion, with a (relative to age) bradycardia. Most bradycardia is hypoxia related, and will usually respond to oxygenation.",
        "hpi": "* Past medical history\n* Foreign body exposure\n* Respiratory distress or arrest\n* Apnea\n* Possible toxic or poison Environmental exposure\n* Congenital disease\n* Medication (maternal or infant)",
        "signs and symptoms": "* Heart rate < 60 bpm\n  * Delayed capillary refill or cyanosis\n  * Mottled, cool skin\n  * Hypotension or arrest\n  * Altered mental status",
        "considerations": "* Respiratory effort\n* Respiratory obstruction\n* Foreign body, secretions\n* Croup, epiglottitis\n* Hypovolemia\n* Hypothermia\n* Infection, sepsis\n* Medication, toxin\n* Hypoglycemia\n* Trauma",
        "pearls": "1. Pharmacological treatment of bradycardia is based upon the presence or absence of significant signs and symptoms (symptomatic vs. asymptomatic).\n2. Although noninvasive pacing may be attempted, typically bradycardias of hypoxic etiology do not respond. First line therapy is prompt airway support, ventilation and oxygenation.\n3. Capture thresholds in children are similar to those in adults. Studies indicate no relationship between body surface area, weight, and capture thresholds and although many children will achieve capture between 50 - 100 mA, higher current requirements are possible. The pacing rate must be set high enough to perfuse the patient.\n4. Electrical capture during transcutaneous pacing is defined as an electrical stimulus marker followed by a wide QRS complex, with no underlying intrinsic rhythm, followed by a T-wave. This should occur for each electrical complex.\n5. Mechanical capture is confirmed when the patient\u2019s pulse matches the displayed pace rate.  Because pacing stimuli generally causes muscular contractions that can be mistaken for a pulse, you should never take a pulse on the left side of the body to confirm mechanical capture. Pectoral muscle contractions due to pacing also do not indicate mechanical capture. To avoid mistaking muscular response to pacing stimuli for arterial pulsations, use ONLY the (1) Femoral artery or (2) Right brachial or radial artery for confirming mechanical capture."
    }
]