Angiotensin II administration improves cerebral blood flow in cardiopulmonary arrest in swine.

Abstract

Cerebral blood flow during cardiopulmonary resuscitation is inadequate to meet cerebral metabolic demand. Adrenergic agonists improve cerebral blood flow, but clinical trials of increased doses in adults have not shown improved outcome from cardiac arrest. This may be due to adverse beta-agonist-mediated effects. The purpose of this study was to determine the effect of angiotensin II, a potent nonadrenergic vasopressor, on cerebral blood flow in cardiac arrest. Eleven immature swine were anesthetized and instrumented for regional blood flow measurements with radiolabeled microspheres. A sagittal sinus catheter was placed for blood gas determination. A blood flow measurement was performed in normal sinus rhythm and ventricular fibrillation induced. After 10 minutes of ventricular fibrillation, cardiopulmonary resuscitation was begun and a blood flow measurement performed. Angiotensin II at a dose of 50 micrograms/kg was administered intravenously at 13 minutes of ventricular fibrillation. A blood flow measurement was performed and defibrillation attempted. A fourth blood flow measurement was obtained if return of spontaneous circulation occurred. Total cerebral blood flow was 46.4 mL/min per 100 g in normal sinus rhythm. This fell to 6.9 mL/min per 100 g with cardiopulmonary resuscitation alone and rose to 30.8 mL/min per 100 g after the administration of angiotensin II. The improvement following angiotensin II was statistically different (P = .002). Cerebral blood flow further rose in the animals that had return of spontaneous circulation to 73.9 mL/min per 100 g. Angiotensin II in a dose of 50 micrograms/kg significantly improves cerebral blood flow in this model of cardiac arrest.