Introduction: High-dose epinephrine (HDE) improves hemodynamics during CPR, but does not improve outcome. Animal studies suggest that the lack of improvement after HDE may be due to increased myocardial oxygen demand during CPR and a hyperadrenergic state immediately post-resuscitation. Our hypothesis was that HDE plus beta-blocker(BB) during CPR would improve outcome compared with standard-dose epinephrine (SDE) or SDE+BB. Methods: Two minutes after ventricular fibrillation, 34 swine (3Q±1 kg) were provided with basic CPR for 12 minutes. Animals were randomly assigned to SDE (0.02 mg/kg), SDE+BB (0.04mg/kg prppranoloi), or HDE(0.20 mg/kg)+BB at 5, 8, and 11 minutes after initiation of CPR. Advanced life support was then provided, followed by 1 hour of ICU care. Data are expressed as meartfcSEM, and analyzed by ANOVA and Fisher's exact test. Results: SDE SDE+BB HDE+BB CPP,6'CPR,mmHg "2B±2 303338±3 CPP,10'CPR,mmHg 20±3 29±3 31 ±4 24-hr Survival 9/12 10/12 4/10 CPP, coronary perfusion pressureHDE+BB differs from SDE, p<0.05,HDE+BB differs from SDE and SDE+BB combined, p<0.05 Four of 6 HDE+BB nonsurvivors had ventricular tachycardia or severe SVT(>250/min) within 10 minutes of defibrillation vs 0/5 nonsurvivors in the other 2 groups (p=0.06). Similarly, aortic dastolic BP >120mmHg occurred in 4/6 HDE+BB vs 0/5 other nonsurvivors (p=0.06). All 24-hour survivors were normal or near-normal. Survival was dismal in pilot studies with higher propranolol closes. Conclusions: HDE+BB resulted in worse 24-hour survival despite excellent hemodynamics during CPR. A toxic hyperadrenergic state immediately post-resuscitation appears to be at least partially responsible for the poor outcome.
|Original language||English (US)|
|Journal||Critical care medicine|
|Issue number||1 SUPPL.|
|State||Published - Dec 1 1998|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine