Normal pregnancy is accompanied by changes in blood volume, heart rate, blood pressure, cardiac output, and ventilation. Cardiac output begins to rise during the first trimester, peaks at an approximate 40% increase by 20 to 24 weeks, then declines during the last 8 weeks of gestation. The increase in cardiac output during early pregnancy is primarily caused by an increase in stroke volume. As pregnancy advances, heart rate increases, whereas stroke volume falls to nonpregnant levels.
Immediately after delivery, with relief of compression on the inferior vena cava, cardiac output may increase as much as 10% to 20%. Following this transitory rise in cardiac output, values fall progressively to baseline levels. Nonpregnant levels are reached by the end of the second postpartum week. During the initial postpartum period, relative bradycardia is common.
Atrial premature contractions, ectopic atrial tachycardia, and paroxysmal supraventricular tachycardia (PSVT) may be recognized for the first time during pregnancy or may increase in frequency and severity during pregnancy in previously diagnosed patients. Similarly, the awareness of ventricular tachycardia may also increase during pregnancy. Potential reasons for these occurrences include increased myocardial irritability as a consequence of increased blood volume; increased sinus heart rate, which may cause altered myocardial refractoriness and altered reentry patterns; and increased cardiac excitability and numbers of α-adrenergic receptors secondary to increased estrogen levels. Regardless of the mechanism, the treatment of arrhythmias during pregnancy is complicated by concerns for fetal well-being, and therefore depends on the maternal hemodynamic response and severity of symptoms. Nonpharmacologic therapy is strongly preferred and includes observation, rest, recumbency, and reassurance. Vagal maneuvers may aid in both diagnosis and treatment, and esophageal pacing can be quite effective. Although almost all of the antiarrhythmic agents are labeled FDA pregnancy risk category C (i.e., risk cannot be ruled out), most of these drugs are well tolerated by mother and fetus and can be used if deemed necessary. The use of phenytoin is contraindicated because of the risk of teratogenesis, and amiodarone and bretylium should be reserved for life-threatening situations. Temporary and permanent pacing have been used during pregnancy safely, as has direct current cardioversion.
Most patients with valvular heart disease can successfully complete pregnancy. If necessary, there is ample experience with valvular surgery during pregnancy. Yet it is extremely important that women with known valvular heart disease be evaluated before pregnancy and that, if necessary, corrective surgery be performed before conception.
Mitral stenosis is by far the most common rheumatic valvular lesion encountered in pregnant women. Increased heart rate, blood volume, and transmitral flow are all associated with normal pregnancy and tend to exacerbate the severity of mitral stenosis. Mitral regurgitation generally poses little threat during pregnancy except in severe cases, when volume overload can produce congestive heart failure. Mild aortic stenosis is usually well tolerated. Cardiac catheterization is indicated during pregnancy when aortic stenosis is associated with left ventricular failure, syncope, or angina. Aortic regurgitation is often ameliorated during pregnancy because there is a reduction in total peripheral resistance.
Primary or secondary pulmonary hypertension, Eisenmenger’s syndrome, and cardiomyopathy with persistent left ventricular failure all pose an unacceptably high risk of maternal mortality. Women with these conditions should not become pregnant, and those who do conceive should be encouraged to terminate pregnancy in the first trimester.
Marfan’s syndrome is associated with aortic dissection and myxomatous degeneration of the aortic and mitral valves. Historically, these patients have been advised to avoid pregnancy. More recent reports, however, suggest a favorable outcome for women with Marfan’s syndrome who lack significant cardiovascular involvement.
Revision date: June 21, 2011
Last revised: by Andrew G. Epstein, M.D.