Optimal Management of a Pregnant Patient with Rheumatic Heart Disease

Abstract

Rheumatic heart disease remains the number one worldwide cause of maternal cardiac complications in pregnancy.1 Since symptoms of rheumatic fever typically do not present until the fourth or fifth decade, the pathophysiologic changes associated with pregnancy may cause as many as 25% of these women to first experience symptoms during pregnancy. For this reason, it is important that obstetric anesthesiologists remain aware of the disease, its complications, and management of valvular lesions throughout the birthing process. The normal physiologic changes of pregnancy cause unique problems to the mother with underlying cardiac disease.2 Intravascular volume and cardiac output (CO) increase while systemic vascular resistance (SVR) decreases to preserve normal mean arterial pressure (MAP). During labor, each uterine contraction results in an auto transfusion of blood, resulting in even higher CO.3 Likewise, pain and apprehension can lead to sympathetically mediated increases in SVR, heart rate (HR), and CO causing further stress.2 Yet, the greatest stress comes immediately after delivery when uterine contraction and involution can increase CO by as much as 80% above third trimester values.3 With all these changes, one must realize how valvular disease is affected during pregnancy. In general, regurgitant lesions are tolerated better due to the increase in intravascular volume and the decrease in SVR, thus improving forward flow of blood through the valves.2,3 In contrast, stenotic lesions are tolerated poorly due to the inability to increase CO through a stenotic valve in the setting of increased intravascular volume and increased preload.2 In patients with rheumatic heart disease, mitral stenosis is the most common heart lesion.1 When these patients become pregnant, the hypervolemia and increased HR can increase the transmitral pressure gradient, leading to increased left atrial volume and pressure. Pressure can be transmitted to the pulmonary vasculature, resulting in pulmonary edema and in severe cases pulmonary hypertension, a significant risk during pregnancy as it can cause right heart failure.4 Further, the chronically dilated left atrium has a propensity to disrupt the cardiac conducting system and cause supraventricular tachycardia, 1 a detrimental event in patients with mitral stenosis who rely on the atrial kick to augment preload. Overall, these factors often cause the previously undiagnosed and asymptomatic patient to develop symptoms during pregnancy, and, in severe cases, experience profound cardiac decompensation.