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Carvedilol Mitigates Adverse Effects of Epinephrine During Cardiopulmonary Resuscitation

The Institute of Critical Care Medicine, Palm Springs, CA

Max Harry Weil, MD, PhD

The Institute of Critical Care Medicine, Palm Springs, CA, Keck School of Medicine, University of Southern California, Los Angeles, CA, Feinberg School of Medicine, Northwestern University, Chicago, IL, weilm{at}911research.org

Shijie Sun, MD

The Institute of Critical Care Medicine, Palm Springs, CA, Keck School of Medicine, University of Southern California, Los Angeles, CA

Wanchun Tang, MD

The Institute of Critical Care Medicine, Palm Springs, CA, Keck School of Medicine, University of Southern California, Los Angeles, CA

Xiangshao Fang, MD

The Institute of Critical Care Medicine, Palm Springs, CA

Introduction: Earlier studies have implicated the adverse effects of ß- and ₁-adrenergic receptors during cardiopulmonary resuscitation (CPR). Because carvedilol is both a nonselective ß- and ₁-selective adrenergic receptor-blocking agent, we hypothesized that pre-treatment with carvedilol would convert the actions of epinephrine to that of a selective a2-agonist.

Methods: Ventricular fibrillation (VF) was induced in Sprague-Dawley rats weighing approximately 500 g. Animals were randomized to 4 groups of 5 animals each: (1) placebo pretreatment and epinephrine treatment, (2) carvedilol pretreatment and placebo treatment, (3) carvedilol pretreatment and epinephrine treatment, and (4) placebo pretreatment and placebo treatment. Carvedilol (50 µg/kg) was injected as a bolus into the right atrium 15 minutes before VF was induced. VF was untreated for 8 minutes, after which CPR (chest compression and mechanical ventilation) was begun. Epinephrine (30 µg/kg) was injected into the right atrium 2 minutes after the start of CPR. Electrical defibrillation was attempted after 14 minutes of VF.

Results: All but 2 animals were successfully resuscitated. Approximately equivalent increases in coronary perfusion pressure from 23 ± 1 mm Hg to 30 ± 3 mm Hg were observed after the injection of epinephrine independently of carvedilol pretreatment. Carvedilol pretreatment followed by epinephrine treatment reduced early postresuscitation ventricular ectopy (116 ± 147 vs 834 ± 380, P < .01) and minimized increases in arterial blood lactate at 5 minutes after resuscitation (10.9 ± 2.1 mmol/L vs 17.4 ± 3.5 mmol/L, P < .01). The postresuscitation cardiac index measured 4 hours later was increased (307 ± 43 mL • min^-1• kg^-1 vs 210 ±6 mL • min^-1• kg^-1, P <.05). Left ventricular diastolic pressures were decreased (6 ± 1 vs 14 ± 1 mm Hg, P < .05). Animals pretreated with carvedilol survived longer (71 ± 1 vs 45 ± 22 hours, P < .05) and with less postresuscitation neurologic deficit.

Conclusion: After ß- and ₁-adrenergic blockade with carvedilol before inducing cardiac arrest, epinephrine administered during CPR yielded better postresuscitation myocardial and neurologic functions and significantly increased postresuscitation survival.

Key Words: adrenergic receptors • cardiac arrest • CPR • coronary perfusion pressure • ventricular fibrillation

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 10, No. 2, 113-120 (2005)
DOI: 10.1177/107424840501000205


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