Background: Maternal heart disease complicates between 0.2%-3% of pregnancies3. Severe mitral stenosis (MS), which carries a fetal mortality up to 25%, is poorly tolerated by the parturient due to increased intravascular volume with limited ability to increase cardiac output 1,3. Understanding cardiovascular and hemodynamic changes that occur in these patients during pregnancy and delivery, particularly those undergoing neuraxial anesthesia(1), is paramount to delivering safe care.
Case Description: A 33-year-old G32002 female at 38 weeks gestation with gestational diabetes mellitus and moderate-severe rheumatic MS was transferred from an outside hospital for workup and management prior to delivery. The patient reported prior diagnosis of a "heart condition" at age 14 years in Micronesia. Her first pregnancy was an uncomplicated C-Section; her second pregnancy, also a C-Section, resulted in significant postpartum heart failure and pulmonary edema requiring intubation. She recovered, but declined to pursue follow-up. On arrival, the patient endorsed 2-pillow orthopnea with no dyspnea on exertion, significant edema, chest pain, or palpitations. TTE was significant for moderate-severe MS, moderate MR, mean mitral gradient of 10.2 mmHg, and mitral valve appearance consistent with rheumatic heart disease. Metoprolol was started per cardiology recommendations. Once in the operating room, an arterial line was placed. Then, an epidural was placed; after a negative test dose, incremental local anesthetic boluses were given while closely monitoring hemodynamic changes. Simultaneously a vasopressor infusion was uptitrated to maintain systemic vascular resistance.
Once a T4 dermatomal level to sharp stimulation was achieved, cesarean delivery was completed. Soon after delivery, mean arterial pressure rapidly dropped, despite increased phenylephrine dosing, and oxygen requirements increased. Norepinepherine infusion was initiated. After achieving hemodynamic stability, a dose of furosemide was given for presumed acute pulmonary edema. The parturient recovered from her acute post-delivery episode quickly and was taken to the ICU on low-dose phenylephrine infusion. Her vasoactive and oxygen requirements quickly resolved. Repeat echocardiogram indicated improved mean mitral gradient. The patient was discharged on post-delivery day 3 with cardiology follow up at 6 weeks.
Discussion: The main complication in the setting of MS is a relatively fixed stroke volume. Inability to increase cardiac output as intravascular volume increases leads to obstructive/congestive physiology, resulting from increasing left atrial pressure3,1. Epidural anesthesia has improved morbidity and mortality compared to general anesthesia in high-risk patients. Epidurals significantly blunt the large sympathetic surges that accompany delivery; however, they also create additional physiologic challenges in the parturient with MS1. Sympathectomy leads to decreased peripheral vascular resistance and hypotension with an inability for patients to tolerate reflex tachycardia1. These changes explain the significant decrease in MAP seen after cumulative boluses of the epidural. Finally, immediately postpartum, uterine involution leads to auto-transfusion, which can increase cardiac output by 75-80%2. This new volume, in the setting of an inability to adequately increase cardiac output, explains our second step-wise decrease in blood pressure, since the congestive physiology becomes further volume overloaded. Vigilant post-partum monitoring and follow-up is crucial, as most deaths occur during post-partum days 2-92.
References: Available on request.
