A healthy heart adapts well to the marked demands of pregnancy, but congenital or acquired heart disease may present or worsen in the gravid woman due to the cardiovascular changes associated with increased cardiac workload. Estrogen mediates an increase in cardiac output by six weeks gestation via increased preload and stroke volume. Blood volume rises by 30% to 40% during pregnancy, peaking at the end of the second trimester. Cardiac output (CO) peaks in the third trimester, typically 30% to 50% above baseline. Total peripheral resistance declines by 20%. Systolic and diastolic blood pressures drop by 10 to 15 mm Hg in the first trimester then return to baseline in the second half of pregnancy; diastolic blood pressure declines more than systolic, so pulse pressure widens. The cardiac axis is shifted leftward, anterior and cephalad.
Blood flow distribution changes during pregnancy such that up to 25% of CO is directed to the uteroplacental unit (a new “end-organ”) and up to 20% to the kidneys. An increased proportion of CO supplies breast tissue, but cerebral blood flow remains at baseline proportions.
Cardiovascular adaptations lead to common complaints in pregnant women: palpitations, decreased exercise tolerance, and dizziness. A shift of the heart toward the chest wall may contribute to the experience of palpitations by the gravida, but palpitations may also represent increased sensitivity to mild sinus tachycardia, premature atrial or ventricular systoles, or, less likely, supraventricular tachycardia. It is postulated that the increase in blood volume may be associated with stretching of the myocardium, thereby potentially increasing myocardial irritability and predisposing to arrhythmias. While this is not clearly proven, both atrial and ventricular arrhythmias may occur in pregnancy just as they occur in the nonpregnant patient. By late pregnancy there is attenuated ability to increase cardiac output with exercise, and this combined with normal weight gain of pregnancy can lead to decreased exercise tolerance. Beyond midpregnancy the gravid uterus causes aortocaval compression in the supine position, decreasing CO by 30%, and venous return, leading to dizziness and dyspnea (termed supine hypotensive syndrome) in some women. Pertinent exam findings include systolic flow murmur by midpregnancy, mammary soufflé, point of maximal impulse (PMI) displaced leftward and cephalad, and mild bilateral lower-extremity edema. Heart rate increases but is not generally above 100 beats per minute. While the neck veins may appear full, jugular venous pulsation is not elevated. Electrocardiograms of pregnant women often will show left axis deviation, atrial enlargement and nonspecific ST-T wave changes, but such findings should be carefully interpreted within clinical context. The cardiac silhouette may be generous on chest radiograph. Increased cardiac output and volume of distribution in pregnant women necessitate careful attention to timing of intravenous contrast dye bolus for computed tomography pulmonary angiography (CT-PA), in order to avoid radiation exposure for an inconclusive study. Care should be taken to position pregnant woman in the left lateral decubitus (or at least with hip elevation to displace the pregnant uterus off the vena cava) when performing medical investigations or treating ill pregnant women to minimize such adverse hemodynamic effects.