Vasopressin improves survival after cardiac arrest in hypovolemic shock

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 per fusion, and the likelihood of resuscitation. In 18 pigs, 35% of the estimat ed blood volume was withdrawn over 15 min and ventricular fibrillation was induced 5 min later.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 ca rdiopulmonary resuscitation, a bolus dose of either 200 mu g/kg epinephrine (n = 7), 0.8 unit/kg vasopressin (n = 7), or saline placebo (n = 4) was ad ministered 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 p lacebo swine. At 5 and 30 min after return of spontaneous circulation, medi an (minimum and maximum) renal blood flow after epinephrine was 2 (0-31), a nd 2 (0-48) mL . 100 g(-1) . min(-1), respectively; and after vasopressin 9 6 (12-161), and 44 (16-105) mL . 100 g(-1) . min(-1), respectively (P <.01 between groups). Epinephrine animals developed a profound metabolic acidosi s 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 vas opressin pigs had (P = 0.015) less acidosis (pH = 7.26+/-0.04) at correspon ding time points, and all survived greater than or equal to 55 min (P < 0.0 1). in conclusion, treatment of hypovolemic cardiac arrest with vasopressin , but not with large-dose epinephrine or saline placebo, resulted in sustai ned vital organ perfusion, less metabolic acidosis, and prolonged survival. Based on these findings, clinical evaluation of vasopressin during hypovol emic cardiac arrest may be warranted.