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In an analysis of maternal mortality in the United States between 2011 and 2013, deaths related to hemorrhage, hypertensive disorders, and embolism showed declining rates. In contrast, deaths attributable to cardiovascular diseases are rising and are responsible for one fourth of all pregnancy-related mortalities (Creanga, 2017; Petersen, 2019). Recent development of state-level maternal mortality review committees have emphasized this issue and highlighted the relatively protracted timeline of illness. Up to a year after delivery, cardiac events were among the leading causes of death for women in Texas in 2013 (Texas Maternal Morbidity Task Force, 2020). These disorders account also for significant maternal morbidity and are a common reason for intensive care unit admissions (Small, 2012).

Cardiovascular disease complicates 1 to 4 percent of pregnancies in the United States (American College of Obstetricians and Gynecologists, 2019). The increasing prevalence is likely multifactorial and includes the higher rates of obesity, hypertension, and diabetes (Klingberg, 2017). 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 (p. 927), an increasing number of women with congenital heart disease are now becoming pregnant.

The importance of heart disease and its adverse effect on pregnancy morbidity and mortality led the American College of Obstetricians and Gynecologists to create a Task Force on Pregnancy and Heart Disease. Its purpose is to emphasize the prevalence and effect of heart disease in pregnancy, provide guidance for risk factor identification, outline common cardiovascular disorders, provide recommendations for management, and develop a comprehensive interpregnancy plan. Multidisciplinary care is essential (Quinones, 2021).


Cardiovascular Physiology

The marked pregnancy-induced anatomical and functional changes in cardiac physiology can have a profound, negative effect on underlying heart disease. These changes are discussed in detail in Chapter 4 (p. 62), and some are listed in Table 52-1 (Clark, 1989). 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 augmented pregnancy blood volume. These adaptations are even more profound in multifetal pregnancies (Ghi, 2019). Intrinsic left ventricular contractility does not change, and thus normal left ventricular function is maintained during pregnancy. Namely, pregnancy is not characterized by hyperdynamic function or a high cardiac-output state.

TABLE 52-1Hemodynamic Changes in 10 Normal Pregnant Women at Term Compared with Repeat Values Obtained 12 Weeks Postpartum

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