Angiotensin II In The Treatment Of Post Cardiopulmonary Vasoplegic Shock And Primary Graft Dysfunction

Abstract

Background Little is known about the use of Angiotensin II (AT-II) for the treatment of patients with primary graft dysfunction and post cardiopulmonary vasoplegia. Case A 59 year old Caucasian male, UNOS Status 4 secondary to Hypertrophic Cardiomyoptahy underwent orthotopic heart transplant at our center. The procedure was complicated by vasoplegia and primary graft dysfunction. Intraoperative left ventricular ejection fraction was estimated at 30-35% and profound hemodynamic instability continued despite maximal doses of norepinephrine, vasopressin, and epinephrine in addition to administration of methylene blue and initiation of veno-arterial ECMO (Table). AT-II was started to maintain appropriate hemodynamic parameters and facilitate eventual vasopressor weaning. The patient responded well to therapy (Table) and over the course of 24 hours was able to be weaned off of norepinephrine, vasopressin, and AT-II. Blood pressure was maintained with ECMO and minimal concentrations of epinephrine. The patient underwent ECMO decannulation on postop day 3 and had a prolonged 31-day hospital postoperative recovery before eventually discharging to a rehab facility. There were no thromboembolic events noted. Discussion AT-II is a non-catecholamine vasopressor that is FDA approved for the treatment of distributive shocks like post-CPB vasoplegia. Our case demonstrates that it can be safely utilized in patients experiencing concomitant primary graft dysfunction. Little is known about the use of Angiotensin II (AT-II) for the treatment of patients with primary graft dysfunction and post cardiopulmonary vasoplegia. A 59 year old Caucasian male, UNOS Status 4 secondary to Hypertrophic Cardiomyoptahy underwent orthotopic heart transplant at our center. The procedure was complicated by vasoplegia and primary graft dysfunction. Intraoperative left ventricular ejection fraction was estimated at 30-35% and profound hemodynamic instability continued despite maximal doses of norepinephrine, vasopressin, and epinephrine in addition to administration of methylene blue and initiation of veno-arterial ECMO (Table). AT-II was started to maintain appropriate hemodynamic parameters and facilitate eventual vasopressor weaning. The patient responded well to therapy (Table) and over the course of 24 hours was able to be weaned off of norepinephrine, vasopressin, and AT-II. Blood pressure was maintained with ECMO and minimal concentrations of epinephrine. The patient underwent ECMO decannulation on postop day 3 and had a prolonged 31-day hospital postoperative recovery before eventually discharging to a rehab facility. There were no thromboembolic events noted. AT-II is a non-catecholamine vasopressor that is FDA approved for the treatment of distributive shocks like post-CPB vasoplegia. Our case demonstrates that it can be safely utilized in patients experiencing concomitant primary graft dysfunction.