Heart disease complicates more than 1 percent of all pregnancies and is now the leading cause of indirect maternal deaths—accounting for 20 percent of all cases (Simpson, 2012). In an analysis of maternal mortality in the United States between 1987 and 2005, the causes previously responsible for most maternal deaths—hemorrhage and hypertensive disorders—had progressively decreased rates, whereas deaths attributable to cardiovascular diseases had the greatest percentage increase (Berg, 2010). Similarly, in the United Kingdom, the rate of maternal mortality due to cardiac disease increased from 1.65 to 2.31 per 100,000 births between 1997–1999 and 2006–2008 (Centre for Maternal and Child Enquiries, 2011). Cardiovascular diseases also account for significant maternal morbidity and are a leading cause of obstetrical intensive care unit admissions (Small, 2012).
The increasing prevalence of cardiovascular diseases complicating pregnancy is likely due to a number of causes, including higher rates of obesity, hypertension, and diabetes. Indeed, according to the United States National Center for Health Statistics, almost half of adults aged 20 and older have at least one risk factor for cardiovascular disease (Fryar, 2012). And as shown in Figure 49-1, the prevalence of these risk factors among reproductive-aged women is dramatic. Other related factors include delayed childbearing. From 1970 to 2006 the proportion of first births to women aged 35 years or older increased nearly eightfold (Mathews, 2009). Finally, as discussed subsequently, an increasing number of patients with congenital heart disease are now becoming pregnant.
Physiological Considerations in Pregnancy
The marked pregnancy-induced anatomical and functional changes in cardiac physiology can have a profound effect on underlying heart disease (Chap. 4, Cardiovascular System). Some of these changes are listed in Table 49-1. Importantly, cardiac output increases approximately 40 percent during pregnancy. Almost half of this total increase takes place by 8 weeks and is maximal by midpregnancy (Capeless, 1989). The early increase stems from augmented stroke volume that results from decreased vascular resistance. Later in pregnancy, resting pulse and stroke volume increase even more because of increased end-diastolic ventricular volume that results from pregnancy hypervolemia. This along with an increase in heart rate translates to increased cardiac output that continues to rise across pregnancy to average 40 percent higher at term. These changes are even more profound in multifetal pregnancy (Kametas, 2003; Kuleva, 2011).
TABLE 49-1Hemodynamic Changes in 10 Normal Pregnant Women at Term Compared with Repeat Values Obtained 12 Weeks Postpartum