(235) Paradoxical Response to Epinephrine Post-Mitral Replacement in a Patient With Pulmonic Insufficiency

Introduction: Epinephrine is a sympathomimetic agent with potent vasopressor and inotropic effects. Its primary application in the intensive care setting is augmentation of cardiac index (CI). Paradoxical reactions to epinephrine have been reported. The following describes a paradoxical response to epinephrine in a patient with suspected pulmonary hypertension (pHTN), pulmonic valve insufficiency (PI), and distributive shock after mitral valve replacement.

Description: A 53-year-old female with a history of ventricular septal defect (VSD) repair (age 7), mitral valve repair and atrial septal defect repair (age 32) was admitted following redo sternotomy for mitral valve replacement for severe mitral regurgitation. The surgery and immediate postoperative period were uneventful, the patient was extubated the following day. Within hours of extubation, and without a clear etiology, the patient had worsening hypotension, hyperlactatemia, and oliguria in the setting of a low systemic vascular resistance (SVR), high pulmonary arterial pressures (PAP), and a high CI on a moderate dose dobutamine infusion. An attempted dobutamine wean given her high CI was unsuccessful. In the setting of hypotension and low systemic vascular resistance, her dobutamine infusion was bridged to epinephrine. Soon thereafter and with no other clinical change, the patient’s CI dropped precipitously, and her systolic PAP significantly increased. Her epinephrine infusion was bridged back to dobutamine, and her CI rapidly improved. Her clinical decline progressed and, a transesophageal echo revealed moderate PI with a 40% pulmonic valve regurgitant fraction.

Discussion: Paradoxical reaction to epinephrine is infrequently reported in the literature. One animal study demonstrated a decrease in left ventricular volumes with low doses of epinephrine. In a different study, the ratio of pulmonary vascular resistance (PVR) to SVR increased with epinephrine administration. Given these findings, the etiology of her drop in CI after epinephrine initiation could be explained by an increase in PVR leading to worsening PI and decreased effective right ventricular output. Further research is warranted to elucidate the mechanisms underlying paradoxical responses to sympathomimetic agents in PI.