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Cardiovascular Changes in Normal Pregnancy
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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.
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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) is increased by 50% above the nonpregnant state as a product of increased stroke volume, along with an increased heart rate by 10–20 beats/min. CO 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). The systemic arterial pressure falls during the first trimester, remains stable during the second trimester, and returns to pregestational levels before term. The reduction in diastolic pressure is more pronounced than the reduction in systolic pressure, leading to a wide pulse pressure. Supine hypotensive or uterocaval syndrome may occur in 0.5–11% of pregnancies and is related to the acute occlusion of inferior vena cava by the gravid uterus in the supine position; it is characterized by significant decreases in blood pressure and heart rate. This contrasts with the tachycardia seen with hypotension in the nonpregnant state. Patients usually complain of lightheadedness, nausea, dizziness, and syncope in extreme cases. Symptoms are alleviated by changing to a left lateral recumbent position.
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Hemodynamic changes during labor and delivery are in part related to the fear, anxiety, and pain experienced by the patient at that stage. Additionally, uterine contractions displace 300–500 mL of blood with each contraction, further augmenting CO. Oxygen consumption increases 3-fold. These changes in CO are less pronounced if the patient remains in the supine position with leftward tilt and receives adequate analgesia. Immediately after delivery, relief of caval compression coupled with autotransfusion from the contracting uterus produces a further increase in CO. This may lead to acute cardiac decompensation in the immediate postpartum period. Most of these physiologic changes revert to prepregnancy levels by 2 weeks postpartum.
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Heart disease is surpassing other causes of maternal mortality in recent years. Cardiac disease complicates approximately 1% of all pregnancies. Pregnant patients with significant symptoms on exertion, such as patients in New York Heart Association (NYHA) functional classes III and IV (Table 27–1), have high event rates and may succumb to complications of heart disease, such as heart failure, arrhythmias, and stroke. Patients with stenotic lesions (eg, mitral or aortic stenosis) and minimal baseline symptoms (NYHA ...