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Hemodynamic adaptations of pregnancy are geared to augment blood flow to the developing fetoplacental unit. These alterations may stress the maternal cardiovascular system, leading to signs and symptoms similar to those seen in heart disease. Women with preexisting cardiovascular disease are particularly at risk, as they may exhibit marked clinical deterioration during the course of pregnancy.

Blood volume begins to increase as early as 6 weeks of gestation and continues to rise until midpregnancy. The hormonally mediated increase in plasma volume is disproportionately higher than the red cell mass, resulting in the so-called physiologic anemia of pregnancy. Cardiac output (CO) increases by 50% above the nonpregnant state as a result of increased stroke volume and heart rate (increases by 10–20 beats/min) and peaks in the mid-second trimester and plateaus thereafter. Myocardial contractility improves, left atrial and left ventricular chamber sizes increase, and peripheral vascular resistance falls (effects of progesterone, circulating prostaglandins, atrial natriuretic peptides, endothelial nitric oxide, and the low-resistance vascular bed of the placenta). For the majority of women, the systemic arterial pressure falls during the first trimester, reaches a nadir, and then remains stable during the second trimester, returning to pregestational levels before term. The reduction in diastolic pressure is more pronounced than the reduction in systolic pressure due to vasodilatory effects of progesterone that lead to a wide pulse pressure. Recent data, however, have suggested that obese or overweight women may experience higher systemic pressures in the first trimester with continual increase throughout pregnancy, as compared to normal-weight women. This relationship, however, remains under investigation.

These hemodynamic alterations may lead to sign and symptoms of normal pregnancy (Table 27–1). Reduced exercise tolerance and easy fatigability may partly be explained by a combination of weight gain and the physiologic anemia of pregnancy. Hyperventilation in pregnancy is likely related to the effect of progesterone on the respiratory center. It is important to differentiate hyperventilation from dyspnea, which is a common finding in heart failure. Bibasilar crackles in normal pregnancy may result from atelectasis that develops from basal compression of the lungs due to uterine enlargement and the subsequent increase in intra-abdominal pressure, which may also lead to orthopnea. Another common symptom in pregnancy is palpitations, which in most cases are due to the hyperdynamic circulation of pregnancy rather than arrhythmias.

Table 27–1.Common findings in normal pregnancy.

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