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Less than 5% (0.2%-4%) of pregnancies in the western world are complicated by cardiovascular diseases;1 however, the incidence of cardiovascular disease in pregnancy is increasing. This increase is due in part to the increasing prevalence of cardiovascular risk factors such as obesity, hypertension, and diabetes, as well as increasing age at first pregnancy and improved survival of patients with congenital heart disease, with many of these patients now reaching childbearing age. Because of this, cardiovascular disease is now one of the major causes of nonobstetric maternal mortality in the western world.
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PHYSIOLOGIC CHANGES IN PREGNANCY
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Several physiologic changes occur during a normal pregnancy to accommodate increasing metabolic demands of the mother and fetus. Hemodynamic changes include blood volume expansion, increase in cardiac output, and decrease in systemic vascular resistance. There are also changes in cardiac anatomy and blood vessels. These changes can put additional strain on patients with underlying heart disease or cardiovascular risk factors (Table 10-1).
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Cardiac output increases by 30% to 50% in normal pregnancy. This increase in cardiac output starts around the 5th gestational week and plateaus around 20 weeks. Early in pregnancy, cardiac output increases primarily due to an increase in stroke volume (Figure 10-1). However, in the third trimester, increases in heart rate contribute more to cardiac output as stroke volume plateaus. Heart rate increases throughout pregnancy by about 15 beats per minute, starting at around 20 weeks' gestation and increasing to up to 32 weeks' gestation. The heart rate stays high until 2 to 5 days postpartum and then gradually decreases. Late in pregnancy, cardiac output can be affected by posture, likely due to mechanical compression of the inferior vena cava by the gravid uterus, resulting in decreased venous return and, in turn, decreased stroke volume. Moving from the left lateral decubitus to supine position can decrease cardiac output by as much as 25% to 30%. This is felt to be the mechanism of supine hypotensive syndrome, a syndrome of hypotension, bradycardia, and occasionally syncope in pregnant women when supine.
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