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 (p. 958), an increasing number of women with congenital heart disease are now becoming pregnant.
he marked pregnancy-induced anatomical and functional changes in cardiac physiology can have a profound efect on underlying heart disease (Chap. 4, p. 60). 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). his 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. hese changes translate to a cardiac output that enlarges across pregnancy to
TABLE 49-'. Hemodynamic Changes in 10 Normal Pregnant Women at Term Compared with Repeat Values Obtained 12 Weeks pregnant women because they do not take into account the spherical remodeling characteristic of normal pregnancy (Savu, 2012; Stewart, 2016).
Adjusting for these geometrical changes, Melchiorre and coworkers (2016) studied normal cardiac echocardiographic indings in 559 nulliparas at four points during pregnancy and again at 1 year postpartum. At term, signiicant chamber diastolic dysfunction and impaired myocardial relaxation were evident in approximately 18 and 28 percent of the women
Data from Clark, 1989.
average 40 percent higher at term. hese adaptations are even more profound in multifetal pregnancies (Kametas, 2003; Kuleva, 2011). Importantly, intrinsic left ventricular contractility does not change. hus, normal left ventricular function is maintained during pregnancy. Namely, pregnancy is not characterized by hyperdynamic function or a high cardiac-output state.
Women with underlying cardiac disease may not always accommodate these changes, and ventricular dysfunction leads to cardiogenic heart failure. A few women with severe cardiac dysfunction can experience evidence of heart failure before midpregnancy. In others, heart failure may develop after 28 weeks' gestation, when pregnancy-induced hypervolemia and cardiac output reach their maximum. In most, however, heart failure develops peripartum, when labor, delivery, and several common obstetrical conditions add undue cardiac burdens. Some of these include preeclampsia, hemorrhage and anemia, and sepsis.
Ventricular volumes and mass accrue to accommodate pregnancy-induced hypervolemia. his is reflected by greater end-systolic and end-diastolic dimensions. At the same time, however, septal thickness and ejection fraction are unchanged. his is because these alterations are accompanied by substantive ventricular remodeling-plasticiy-which is characterized by eccentric expansion of left-ventricular mass that averages 30 to 35 percent near term. All of these adaptations return to prepregnancy values within a few months postpartum.