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Pregnancy involves a number changes in anatomy, physiology, and biochemistry, which can challenge maternal reserves. A basic knowledge of these adaptations is critical for understanding normal laboratory measurements, knowing the drugs likely to require dose adjustments, and recognizing women who are predisposed to medical complications during pregnancy.
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With uterine enlargement and diaphragmatic elevation, the heart rotates on its long axis in a left-upward displacement. As a result of these changes, the apical beat (point of maximum intensity) shifts laterally. Overall, the heart size increases by approximately 12%, which results from both an increase in myocardial mass and intracardiac volume (approximately 80 mL). Vascular changes include hypertrophy of smooth muscle and a reduction in collagen content.
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Blood volume expansion begins early in the first trimester, increases rapidly in the second trimester, and plateaus at about the 30th week (Fig. 8–1). The approximately 50% elevation in plasma volume, which accounts for most of the increment, results from a cascade of effects triggered by pregnancy hormones. For example, increased estrogen production by the placenta stimulates the renin–angiotensin system, which, in turn, leads to higher circulating levels of aldosterone. Aldosterone promotes renal Na+ reabsorption and water retention. Progesterone also participates in plasma volume expansion through a poorly understood mechanism; increased venous capacitance is another important factor. Human chorionic somatomammotropin, progesterone, and perhaps other hormones promote erythropoiesis, resulting in the approximately 30% increase in red cell mass.
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The magnitude of the increase in blood volume varies according to the size of the woman, the number of prior pregnancies, and the number of fetuses she is carrying. This hypervolemia of pregnancy compensates for maternal blood loss at delivery, which averages 500–600 mL for vaginal and 1000 mL for caesarean delivery.
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Cardiac output increases approximately 40% during pregnancy, with maximum values achieved at 20–24 weeks' gestation. This rise in cardiac output is thought to result from the hormonal changes of pregnancy, as well as the arteriovenous-shunt effect of uteroplacental circulation.
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Stroke volume increases 25–30% during pregnancy, reaching peak values at 12–24 weeks' gestation (Fig. 8–2). Thus elevations in cardiac output after 20 weeks of gestation depend critically on the rise in heart rate. Maximum cardiac output is associated with a 24% increase in stroke volume and a 15% rise in heart rate. Cardiac output increases in labor in association with painful contractions, which increase venous ...