The effects of epinephrine on outcomes of normothermic and therapeutic hypothermic cardiopulmonary resuscitation.

OBJECTIVE To investigate the effects of epinephrine when administered during either normothermic or therapeutic hypothermic cardiopulmonary resuscitation on postresuscitation myocardial and cerebral function and survival. DESIGN Prospective, randomized, placebo-controlled experimental study. SETTING University-affiliated animal research laboratory. SUBJECTS Thirty-two healthy male Sprague-Dawley rats. INTERVENTIONS Ventricular fibrillation was induced and untreated for 8 mins. The animals were then randomly assigned to one of four groups: normothermic placebo control; normothermic epinephrine; hypothermic placebo control; and hypothermic epinephrine. Hypothermia was initiated coincident with the start of cardiopulmonary resuscitation. The blood temperature was reduced and maintained at 32 ± 0.2°C and continued for 4 hrs after resuscitation. Normothermic animals were maintained at 37 ± 0.2°C. Either placebo or epinephrine (20 μg/kg) was administered 5 mins after the start of cardiopulmonary resuscitation and 3 mins before defibrillation. MEASUREMENTS AND MAIN RESULTS Postresuscitation cardiac output, ejection fraction, and myocardial performance index were measured hourly for 4 hrs after resuscitation; neurologic deficit scores were measured daily for 7 days, and durations of survival were observed for up to 3 mos. Except for three normothermic control animals, all animals were resuscitated. When epinephrine was administered during normothermic cardiopulmonary resuscitation, postresuscitation myocardial function was severely impaired when compared with the normothermic control group. However, postresuscitation myocardial function was significantly better in animals treated with epinephrine during hypothermic cardiopulmonary resuscitation when compared with hypothermic controls. This was associated with significantly fewer postresuscitation ventricular arrhythmias, less ST-segment elevation, better postresuscitation neurologic deficit scores, and longer duration of survival. CONCLUSIONS Epinephrine, when administered during normothermic cardiopulmonary resuscitation, significantly increases the severity of postresuscitation myocardial dysfunction and decreases the duration of survival. These detrimental effects of epinephrine, however, no longer exist when it is administered during therapeutic hypothermic cardiopulmonary resuscitation.