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CRITICAL CARE AND TRAUMA

Vasopressin Improves Survival After Cardiac Arrest in Hypovolemic Shock

Wolfgang G. Voelckel, MD^*,, Keith G. Lurie, MD^*, Karl H. Lindner, MD, Todd Zielinski, MS^*, Scott McKnite, BS^*, Anette C. Krismer, MD, and Volker Wenzel, MD

*Cardiac Arrhythmia Center, Cardiovascular Division, Department of Medicine at the University of Minnesota, Minneapolis, Minnesota; and Department of Anesthesiology and Critical Care Medicine, Leopold-Franzens-University of Innsbruck, Innsbruck, Austria

Address correspondence and reprint requests to Keith G. Lurie, MD, Department of Medicine, Cardiac Arrhythmia Center, Cardiovascular Division, University of Minnesota, Box 508, Mayo, 420 Delaware St. SE, Minneapolis, MN 55455. Address e-mail to lurie002{at}maroon.tc.umn.edu

Survival after hypovolemic shock and cardiac arrest is dismal with current therapies. We evaluated the potential benefits of vasopressin versus large-dose epinephrine in hemorrhagic shock and cardiac arrest on vital organ perfusion, and the likelihood of resuscitation. In 18 pigs, 35% of the estimated blood volume was withdrawn over 15 min and ventricular fibrillation was induced 5 min later. After 4 min of cardiac arrest and 4 min of standard cardiopulmonary resuscitation, a bolus dose of either 200 µg/kg epinephrine (n = 7), 0.8 unit/kg vasopressin (n = 7), or saline placebo (n = 4) was administered in a blinded, randomized manner. Defibrillation was attempted 2.5 min after drug administration, and all animals were subsequently observed for 1 h without further intervention. Spontaneous circulation was restored in 7 of 7 vasopressin animals, in 6 of 7 epinephrine pigs, and in 0 of 4 placebo swine. At 5 and 30 min after return of spontaneous circulation, median (minimum and maximum) renal blood flow after epinephrine was 2 (0–31), and 2 (0–48) mL · 100 g^-1 · min^-1, respectively; and after vasopressin 96 (12–161), and 44 (16–105) mL · 100 g^-1 · min^-1, respectively (P < .01 between groups). Epinephrine animals developed a profound metabolic acidosis by 15 min after return of spontaneous circulation (mean arterial pH, 7.11 ± 0.01), and by 60 min all epinephrine-treated animals had died. The vasopressin pigs had (P = 0.015) less acidosis (pH = 7.26±0.04) at corresponding time points, and all survived 55 min (P < 0.01). In conclusion, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital organ perfusion, less metabolic acidosis, and prolonged survival. Based on these findings, clinical evaluation of vasopressin during hypovolemic cardiac arrest may be warranted.

Implications: The chances of surviving cardiac arrest in hemorrhagic shock are considered dismal without adequate fluid replacement. However, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital organ perfusion and prolonged survival in an animal model of suspended infusion therapy.

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999