NOREPINEPHRINE-INDUCED HYPERTENSION FOLLOWING CARDIAC-ARREST - EFFECTS ON MYOCARDIAL OXYGEN USE IN A SWINE MODEL

Study objective: Recent studies suggest that norepinephrine-induced hy pertension early after cardiac arrest ameliorates cerebral hypoperfusi on and improves neurologic outcome. The purpose of this study was to e valuate the effects of early norepinephrine-induced hypertension on po stresuscitation myocardial blood flow and oxygen use. Design: Prospect ive, controlled laboratory study. Participants: Ten swine. Interventio ns: All animals underwent 10 minutes of ventricular fibrillation cardi ac arrest followed by 5 minutes of low-flow cardiopulmonary bypass (10 mL/kg.min), nonrepinephrine (0.12 mg/kg), and defibrillation. Animals then were assigned to a hypertension group (mean aortic pressure, 95 mm Hg) or a control group (mean aortic pressure, 75 mm Hg) by titratin g a norepinephrine infusion to attain the prescribed aortic pressure. Results: Myocardial blood flow, perfusion pressure, and oxygen metabol ism were compared between groups at different times using analysis of variance with a post-hoc Tukey test. Groups had siomilar myocardial bl ood flow during ventricular fibrillation, total defibrillation energy, and time to restoration of spontaneous circulation, the hypertension group had significantly elevated myocardial blood flow, 965+/-314 mL/m in.100 g versus 325+/-67 mL/min.100 g in the control group (P<.001), m yocardial oxygen consumption of 51.2+/-26.9 mL O2/min.100 g versus 6.4 +/-3.4 mL O2/min.100 g (P<.001), and myocardiual oxygen extraction of 46%+/-20% verus 14%+/-4% (P<.01). Conclusion: In the early resuscitati on period, increasing the norepinephrine dose to induce mild hypertens ion significantly increases oxygen use in the postichemic myocardium.