INTRODUCTION

The management of cardiac disease in pregnancy is discussed in detail in the references listed below. Only a few major points can be covered in this brief section.

Cardiovascular Changes During Pregnancy

Normal physiologic changes during pregnancy can exacerbate symptoms of underlying cardiac disease even in previously asymptomatic individuals. Maternal blood volume rises progressively until the end of the sixth or seventh month. Stroke volume increases over the same time course as a result of the volume change and an increase in ejection fraction. The latter reflects predominantly a decline in peripheral resistance due to vasodilation and the low-resistance shunting through the placenta. The heart rate tends to rise in the third trimester. Overall, cardiac output increases by 30-50%; systolic blood pressure tends to rise slightly or remain unchanged, but diastolic pressure falls significantly.

High cardiac output causes alterations in the cardiac examination. A third heart sound is prominent and normal, and a pulmonary flow murmur is common. Electrocardiographic changes include rate-related decreases in PR and QT intervals, a leftward axis shift, inferior Q waves due to the more horizontal position of the heart, and nonspecific ST-T wave changes.

Management of Preexisting Conditions

The physiologic changes imposed by pregnancy can cause cardiac decompensation in patients with any significant cardiac abnormality, but the most severe problems are encountered in patients with valvular stenosis (especially mitral and aortic stenosis), congenital or acquired abnormalities associated with pulmonary hypertension or right-to-left shunting, congestive heart failure due to any cause, coronary heart disease, and hypertension. Valvular insufficiency or left-to-right shunting often diminishes because of the fall in peripheral resistance and is better tolerated.

Mitral stenosis becomes more hemodynamically severe owing to the increase in diastolic flow and the rate-related shortening of diastole. Left atrial pressures rise, and dyspnea or pulmonary edema can occur in previously asymptomatic individuals. The onset of atrial fibrillation often leads to acute decompensation. Patients with moderate to severe stenosis should have the condition corrected prior to becoming pregnant if possible. Patients who become symptomatic can undergo successful surgery, preferably in the third trimester. Balloon valvuloplasty is an attractive alternative, though radiation exposure to the fetus is unavoidable. Coarctation is usually well tolerated, but patients with symptoms should have corrective surgery before pregnancy. Patients with severe pulmonary hypertension and cyanotic congenital heart disease and those with severe aortic stenosis are at extremely high risk and should attempt to avoid pregnancy.

Asymptomatic arrhythmias should be closely observed unless underlying heart disease is present, in which case they should be treated with drugs. Paroxysmal supraventricular arrhythmias are quite common. Patients with Wolff-Parkinson-White syndrome may have more problems during pregnancy. Therapy is similar to that required for nonpregnant women.

Preexisting systemic hypertension is usually well tolerated and controllable, though the fetal morbidity rate is slightly increased. The incidence of preeclampsia and eclampsia (see Pregnancy Section) is increased.

Hydralazine and methyldopa are the antihypertensive agents for which there has been the greatest experience during pregnancy. Diuretics have also been used frequently, but concern has been raised that intravascular hypovolemia might impair uterine blood flow. Nonetheless, these agents are relatively safe. More recently, there has been considerable use of the combined a- ß-blocker labetalol and of calcium channel blockers, which have been proved effective and safe to both the mother and fetus. On the other hand, atenolol has been associated with lower fetal weights. ACE inhibitors and angiotensin II blockers are contraindicated in pregnancy because of the risk of fetal injury. ß-Blockers may retard fetal growth, but experience with them has been generally favorable. Little is known about the safety of most other antihypertensive agents.