Brian Trethowan1, Christopher J Michaud2, Sarah Fifer3. 1. Department of Cardiac Anesthesia, Grand Rapids, MI. 2. Department of Pharmacy, Spectrum Health, Grand Rapids, MI. 3. Spectrum Health Medical Group, Grand Rapids, MI.
Abstract
OBJECTIVE: Describe a case of post-pneumonectomy vasoplegia managed with angiotensin II. Plasma renin activity was measured at specific time intervals to describe the relationship between endogenous renin activity and exogenous angiotensin II supplementation. DESIGN: Case report. SETTING: Spectrum Health Cardiothoracic Critical Care Unit. PATIENTS: Fifty-seven-year-old male. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Plasma renin activity at five pre-determined time points. Angiotensin II caused a significant increase in mean arterial pressure and a rapid reduction in catecholamine vasopressor doses from 0.75 to 0.31 mcg/kg/min norepinephrine equivalents. Plasma renin activity drawn immediately before angiotensin II initiation was 40 ng/mL/hr (normal, 0.6-3.0 ng/mL/hr) with resultant drop to 22 and 12 ng/mL/hr at 2 and 6 hours after angiotensin II initiation, respectively. The patient suffered no end-organ damage and achieved a positive outcome, discharging home on postoperative day 11. CONCLUSION: Exogenous angiotensin II reduced catecholamine vasopressor doses and had an apparent effect in reducing endogenous renin production in this case. Prospective research is warranted to determine the utility of angiotensin II and to better understand it effects on the dysfunctional renin-angiotensin-aldosterone system during vasoplegic shock.
OBJECTIVE: Describe a case of post-pneumonectomy vasoplegia managed with angiotensin II. Plasma renin activity was measured at specific time intervals to describe the relationship between endogenous renin activity and exogenous angiotensin II supplementation. DESIGN: Case report. SETTING: Spectrum Health Cardiothoracic Critical Care Unit. PATIENTS: Fifty-seven-year-old male. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Plasma renin activity at five pre-determined time points. Angiotensin II caused a significant increase in mean arterial pressure and a rapid reduction in catecholamine vasopressor doses from 0.75 to 0.31 mcg/kg/min norepinephrine equivalents. Plasma renin activity drawn immediately before angiotensin II initiation was 40 ng/mL/hr (normal, 0.6-3.0 ng/mL/hr) with resultant drop to 22 and 12 ng/mL/hr at 2 and 6 hours after angiotensin II initiation, respectively. The patient suffered no end-organ damage and achieved a positive outcome, discharging home on postoperative day 11. CONCLUSION: Exogenous angiotensin II reduced catecholamine vasopressor doses and had an apparent effect in reducing endogenous renin production in this case. Prospective research is warranted to determine the utility of angiotensin II and to better understand it effects on the dysfunctional renin-angiotensin-aldosterone system during vasoplegic shock.