Angiotensin II improves myocardial blood flow in cardiac arrest.

Epinephrine is used to increase coronary perfusion pressure and improve myocardial blood flow during cardiac arrest. Alternative vasopressors may have hemodynamic advantages over epinephrine. The purpose of this investigation was to test the effect of the vasopressor angiotensin II on myocardial blood flow in a swine model of cardiac arrest. Eleven swine were anesthetized and instrumented for regional blood flows by radiolabeled microsphere technique. A baseline blood flow measurement (BFM), coronary sinus and aortic blood gases were obtained in normal sinus rhythm (NSR). Ventricular fibrillation (VF) was induced and mechanical CPR begun after 10 min of VF. A BFM and blood gases were obtained during CPR. Angiotensin II, 50 micrograms/kg, was administered at 13 min of VF. A repeat BFM and blood gases were obtained following angiotensin II. Defibrillation was attempted at 16.5 min of VF. If return of spontaneous circulation (ROSC) occurred a fourth BFM and blood gases were obtained. Myocardial blood flow was 134.2 +/- 40.1 ml/100 g per min during NSR. This fell to 15.1 +/- 19.9 with CPR alone, and rose to 66.9 +/- 69.8 following angiotensin II administration (P = 0.04; by two tailed T-test). Myocardial blood flow following ROSC further increased to 212.6 +/- 58.0. Angiotensin II in a dose of 50 micrograms/kg significantly increases myocardial blood flow in this model of cardiac arrest.