Abstract 2468: Hypothermia Minimizes the Detrimental Effects of Epinephrine During CPR
Epinephrine is administered during cardiac arrest to increase coronary perfusion and therefore favor return of spontaneous circulation (ROSC). Experimentally, the α1- and β adrenergic actions of epinephrine increase the severity of post resuscitation myocardial dysfunction and thereby reduce the duration of post resuscitation survival. We have previously demonstrated that therapeutic hypothermia after ROSC improves both post resuscitation myocardial and neurological function. In the present study, we investigated the combined effects of epinephrine and hypothermia. We hypothesized that hypothermia minimizes the detrimental effects of epinephrine on post resuscitation myocardial dysfunction and favors survival. Ventricular fibrillation (VF) was induced and untreated in 20 S-D rats, randomized into 4 groups: placebo control (Control), epinephrine (EPI), control hypothermic (C + H) and epinephrine hypothermic (EPI + H). Hypothermia was initiated coincident with start of CPR. The blood temperature was reduced and maintained at 32°C±0.2 with a cooling blanket and continued for 4 hours (hrs) after ROSC. Normothermic animals were maintained at 37°C±0.2. Either placebo or epinephrine was administered at 5 minutes after the start of CPR. Defibrillation was attempted after 8 minutes of CPR and 16 minutes of VF. Except for one control animal, all were resuscitated. Post resuscitation (PR) ejection fraction (EF), neurological deficit scores (NDS) and survivals were significantly greater after both epinephrine and hypothermia. These findings provide evidence that mild hypothermia minimized the adverse effects of epinephrine on post-resuscitation neurological and myocardial functions and favored better survival.