According to the Centers for Disease Control and Prevention, heart disease is the leading cause of death in women who are 25 to 44 years old (Kung and colleagues, 2008). Cardiac disorders of varying severity complicate approximately 1 percent of pregnancies and contribute significantly to maternal morbidity and mortality rates. For example, Chang and co-workers (2003) reported that cardiomyopathy alone was responsible for 8 percent of 4200 pregnancy-related deaths in the United States from 1991 to 1999. From Brazil, Avila and associates (2003) reported the maternal mortality rate to be 2.7 percent in 1000 pregnancies complicated by heart disease. In addition to maternal mortality, cardiac disorders accounted for 7.6 percent of severe obstetrical morbidities diagnosed during hospitalization for delivery in the United States from 1991 to 2003 (Callaghan and associates, 2008).


The marked pregnancy-induced hemodynamic alterations can have a profound effect on underlying heart disease. These are further detailed in Chapter 5, Cardiovascular System. The most important is that cardiac output is increased by as much as 50 percent during pregnancy. Capeless and Clapp (1989) have shown that almost half of this total increase takes place by 8 weeks, and it is maximized by midpregnancy. 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 diastolic filling from pregnancy hypervolemia. These changes are even more profound in multifetal pregnancy (Kametas and colleagues, 2003).


An important study by Clark and colleagues (1989) contributed greatly to the understanding of cardiovascular physiology during pregnancy. Using right-sided heart catheterization, these investigators measured hemodynamic function in 10 healthy primigravid women. Pregnancy values were compared with those measured again at 12 weeks postpartum. As shown in Table 44-1, near term the cardiac output in the lateral recumbent position increased 43 percent because of increased pulse rate and augmented stroke volume as the result of ventricular dilatation. Systemic and pulmonary vascular resistance were concomitantly decreased. Importantly, there was no change in intrinsic left ventricular contractility. Despite these changes, normal left ventricular function is maintained during pregnancy—specifically, hyperdynamic function or a high cardiac-output state does not develop (see Fig. 5-10).

Table Graphic Jump Location
Table 44-1. Hemodynamic Changes in 10 Normal Pregnant Women at Term Compared with Their 12-Week Postpartum Values 

Recent noninvasive studies have elucidated further the maternal adaptation to the “natural volume overload state.” For example, possible controlling-gene expression/function of signaling molecules that mediate reversible eccentric hypertrophy have been described ...

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