1261: LIBERATION FROM PROLONGED CATECHOLAMINE VASOPRESSOR EXPOSURE WITH 72-HOUR ANGIOTENSIN II INFUSION

Abstract

Introduction: Angiotensin II produces vasoconstriction independent of adrenergic receptors and has been used in refractory shock. We report 2 patients in the recovery phase of shock that were successfully separated from prolonged exposure to catecholamines using 72-hours of angiotensin II infusion. Description: Case 1. A 46-year-old man with aortic valve dehiscence and recurrent endocarditis underwent redo mechanical aortic and mitral valve replacements. While recovering from multiple postoperative complications, he persistently required norepinephrine 0.06 mcg/kg/min, vasopressin 0.04 unit/min, droxidopa 300 mg q4h, and midodrine 15 mg q6h to maintain MAP > 55 mmHg for several weeks. Angiotensin II was trialed at 10 ng/kg/min and within 15 minutes the MAP was 86 mmHg and norepinephrine discontinued, with vasopressin stopped an hour later. Droxidopa and midodrine were also stopped, and over the next 72 hours angiotensin II was gradually tapered off in increments of 1-2 ng/kg/min every 6-12 hours. After a long hospital stay and eventual reintubation, the family decided to withdraw cares and the patient expired. Case 2. A 52-year-old man was admitted with urinary sepsis. After 4 weeks of complex treatment, he was recovering but persistently required norepinephrine 0.08 mcg/kg/min, vasopressin 0.04 unit/min, and midodrine 15 mg q8h to maintain MAP > 60 mmHg for 2 weeks. Angiotensin II was trialed at 20 ng/kg/min and within 30 minutes the MAP was 101 mmHg and norepinephrine discontinued, with vasopressin discontinued within 12 hours. Over the next 72 hours, midodrine was discontinued and angiotensin II was gradually tapered off. After an additional 8 weeks in the hospital, the patient discharged back to a skill nursing facility. Discussion: Prolonged stimulation of adrenergic receptors may lead to tachyphylaxis to catecholamines, believed to be due to adrenoreceptor desensitization and internalization. In such scenarios, alternative mechanisms of vasoconstriction may be necessary to achieve MAP targets. Angiotensin II engages the angiotensin type I receptor for venous and arterial constriction. We suspect in these two cases, augmenting MAP through the renin-angiotensin pathway provided a holiday from exogenous catecholamines and an opportunity for adrenoreceptors to externalize and re-sensitize.