Optimal vasopressor drug therapy during resuscitation

Joseph P Ornato

doi:10.1186/cc6824

Abstract

Optimal vasopressor support during resuscitation should theoretically enhance aortic diastolic and coronary perfusion pressure as well as coronary and cerebral blood flow/oxygen delivery without increasing cellular oxygen demand. Intravenous vasopressor support, using 1 mg doses of epinephrine every 5 minutes in adults or vasopressin 40 IU, is recommended by American Heart Association Advanced Cardiac Life Support Guidelines to maximize oxygen delivery to the heart and brain and increase cellular high energy phosphate levels. Vasopressin offers theoretical advantages over epinephrine in that it does not increase myocardial oxygen demand significantly and its receptors are relatively unaffected by acidosis. However, unlike epinephrine, it is not a myocardial stimulant. Despite these differences in physiologic actions, two large randomized clinical trials yielded virtually identical overall survival to hospital discharge when these agents were compared during inhospital or out-of-hospital resuscitation in Canada and Europe, respectively. More recent clinical and experimental evidence suggests that a combination of vasopressin and epinephrine used during resuscitation can improve hemodynamics and perhaps survival. The verdict on a combination vasopressor strategy may soon come from a large (>2,000 patients) prospective clinical trial that is underway in France to clarify the role of combination vasopressin/epinephrine therapy in out-of-hospital resuscitation.

Highlights

In this issue of Critical Care, Stroumpoulis and coworkers [1] reported that a combination of vasopressin and epinephrine improve hemodynamics and return of spontaneous circulation (ROSC) in an experimental cardiac arrest model
Critical Care Vol 12 No 2 Ornato which looked promising in animal models, did not improve survival in clinical resuscitation trials is that the increased coronary perfusion pressure did not increase myocardial oxygen delivery sufficiently to offset the increased myocardial oxygen demand caused by epinephrine’s βadrenergic effects [7]
Vasopressin offers theoretical advantages over epinephrine in that it does not increase myocardial oxygen demand significantly and its receptors are relatively unaffected by acidosis

Summary

Introduction

In this issue of Critical Care, Stroumpoulis and coworkers [1] reported that a combination of vasopressin and epinephrine improve hemodynamics and return of spontaneous circulation (ROSC) in an experimental cardiac arrest model. If prompt defibrillation cannot be performed and/or is unsuccessful and the resuscitation team must administer advanced life support drugs, the odds of survival to hospital discharge are under 10% [6,7].

Results

Conclusion