• B Schwarz, P Mair, H Wagner-Berger, K H Stadlbauer, S Girg, V Wenzel, and K H Lindner.
• Department of Anaesthesiology and Critical Care Medicine, Leopold-Franzens-University, Innsbruck, Austria. birgit.schwarz@uibk.ac.at
• Acta Anaesthesiol Scand. 2003 Oct 1; 47 (9): 1114-8.

BackgroundAim of this experimental animal study was to investigate the influence of vasopressin and amiodarone on cardiopulmonary resuscitation (CPR) outcome in a pig model of hypothermic cardiac arrest.MethodsAfter surface cooling to a core temperature of 26 degrees C, ventricular fibrillation was induced in 14 12-16-week-old domestic pigs. After 15 min of untreated cardiac arrest, a manual closed chest CPR was started and pigs were randomly assigned to two treatment groups: Group 1 pigs (n = 7) received vasopressin 0.4 U kg-1 as initial drug therapy, followed by a combination vasopressin (0.4 U kg-1) and amiodarone (4 mg kg-1) as subsequent drug therapy. Subsequent drug therapy was administered in animals without permanent restoration of spontaneous circulation after a first series of electrical countershocks 10 min after drug administration. Group 2 pigs (n = 7) received saline placebo as initial drug therapy and saline placebo and amiodarone (4 mg kg-1) as subsequent drug therapy.ResultsVasopressin significantly increased coronary perfusion pressure and defibrillation success (successful defibrillation in five of seven Group 1 vs. none of seven Group 2 pigs, P = 0.02). Due to refibrillation within 30-150 s, the 60-min survival rate was not improved by vasopressin. Subsequent drug therapy with amiodarone had no further effect on defibrillation success or the refibrillation rate.ConclusionsData from this experimental animal model suggest that vasopressin and amiodarone may not be beneficial for treatment of ventricular fibrillation associated with severe hypothermia when concomitant measures at core rewarming are not applied.

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