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Some authorities recommend that women suffering from heart lesions be dissuaded from marriage. This, however, appears to be an extreme view, though, of course, when the lesion is serious and the compensation faulty, the dangers of childbearing should be carefully explained.

—J. Whitridge Williams (1903)


As Williams recognized more than a century ago, pregnancy in those with significant heart disease can be extremely hazardous and may lead to decompensation and death. In an analysis of maternal mortality in the United States between 2011 and 2013, the causes previously responsible for most maternal deaths—hemorrhage, hypertensive disorders, and embolism—continued to show declining rates. In contrast, deaths attributable to cardiovascular diseases were responsible for approximately 26 percent of all pregnancy-related deaths (Creanga, 2017). Cardiovascular diseases also account for significant maternal morbidity and are a prominent reason for obstetrical intensive care unit admissions (Small, 2012).

The rising prevalence of cardiovascular diseases complicating pregnancy is likely multifactorial and includes the higher rates of obesity, hypertension, and diabetes (Klingberg, 2017). Indeed, according to the National Center for Health Statistics, almost half of adults aged 20 and older have at least one risk factor for cardiovascular disease (Fryar, 2012). Another related reason is delayed childbearing. Last, as discussed subsequently (Congenital Heart Disease), an increasing number of women with congenital heart disease are now becoming pregnant.


Cardiovascular Physiology

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 takes place by 8 weeks’ gestation and is maximal by midpregnancy (Capeless, 1989). This early rise stems from augmented stroke volume, which results from lowered vascular resistance. Later in pregnancy, resting pulse and stroke volume are even higher because of greater end-diastolic ventricular volume that results from pregnancy hypervolemia. These changes translate to a cardiac output that enlarges across pregnancy to average 40 percent higher at term. These adaptations are even more profound in multifetal pregnancies (Kametas, 2003; Kuleva, 2011). Importantly, intrinsic left ventricular contractility does not change. Thus, normal left ventricular function is maintained during pregnancy. Namely, pregnancy is not characterized by hyperdynamic function or a high cardiac-output state.

TABLE 49-1Hemodynamic Changes in 10 Normal Pregnant Women at Term Compared with Repeat Values Obtained 12 Weeks Postpartum

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