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Cesarean Delivery for Patient with Single Ventricle Physiology
Abstract Number: RF2AB-192
Abstract Type: Case Report Case Series
The number of parturients with single-vessel physiology is rising as nearly 85% of individuals born with congenital heart disease (CHD) are surviving into adulthood. 25% of maternal cardiac deaths are now related to CHD. The hemodynamic changes of pregnancy raise concerns for women with this altered physiology and creates unique challenges for the anesthesiologist.
A 21 year old G1P0 at 34 weeks gestation presented with intrauterine growth restriction and preeclampsia with severe features. She had a history of congenital tricuspid valve atresia treated with a lateral tunnel Fontan procedure with an intracardiac baffle. She had normal ventricular function and unobstructed Fontan flow without cyanosis or dysrhythmias. Two large bore IVs and an arterial line were placed on admission. The fetus did not tolerate a contraction stress test, so induction of labor was deferred. Maternal Fetal Medicine, Pediatric Cardiology, Obstetric Anesthesia, and Pediatric Cardiac Anesthesia discussed her care before proceeding with cesarean delivery. An epidural was placed and a total of 30 ml of 2% lidocaine with epinephrine was injected in 3 ml increments over 45 minutes until a T4 dermatomal level was achieved. The cesarean was completed with 500 ml of blood loss. Supplemental oxygen was provided throughout the case. After delivery, oxytocin was initiated at 15 units/hour. Intravenous fluid was restricted to 400 ml. She was admitted to the cardiac intensive care unit postoperatively for close monitoring. A post-partum echocardiogram was unchanged from prior and discharge was on post-operative day four.
Safe delivery in CHD patients is guided by their altered cardiac physiology. Cardiac output is dependent upon sinus rhythm, adequate preload and low-normal afterload and pulmonary vascular resistance (PVR). Cautious fluid boluses and left uterine displacement maintain preload. While bleeding and hypovolemia will decrease cardiac output, fluid overload can cause pulmonary edema. Excessive valsalva during labor should be minimized to avoid sudden changes in venous return. Telemetry, large bore IV access, and invasive blood pressure monitoring should be utilized. Supplemental oxygen and avoidance of acidosis prevent increased PVR. The sympathectomy of neuraxial anesthesia dilates the venous system and decreases the potential for large volume fluctuations but also decreases systemic vascular resistance and should be initiated gradually. In the setting of general anesthesia, positive pressure ventilation should be minimized to avoid reduced preload and cardiac output. Cardiodepressant induction agents should be avoided. In this patient, multi-disciplinary care, slow development of adequate epidural anesthesia, and appropriate monitoring allowed for a safe peripartum course.
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