Cardiac arrest: should we consider norepinephrine instead of epinephrine?

A patient scheduled for a laparoscopic cholecystectomy had an anaphylactic shock during induction of anesthesia. After the injection of vecuronium, an unusual fall of arterial pressure occurred, with bradycardia, enlargement of the QRS complex, then a circulatory arrest. Chest compressions were initiated, while intravenous epinephrine 1 mg was administered. The cardiac rhythm turned into a ventricular fibrillation (VF). Despite continuous chest compressions with repeated boluses of epinephrine and several external electric shocks, the patient remained in VF. Because of obviously beta-adrenergic adverse effects, epinephrine was replaced with norepinephrine. Return of spontaneous circulation was observed, with the recovering of sinusal activity. After staying for several weeks in intensive care unit because of multiorgan failure, the patient recovered without sequelae. Blood samples and cutaneous testing confirmed an allergy to vecuronium. This case report of a cardiac anaphylaxis with prolonged cardiac arrest illustrates the dual activity and adverse effects of epinephrine. Although vasoconstriction is mandated during cardiopulmonary resuscitation to provide an acceptable perfusion pressure to organs, beta-adrenergic stimulation seems deleterious to the heart. Experimental studies have shown that blocking the beta-adrenergic effects of epinephrine attenuates postresuscitation myocardial dysfunction or helps the return of spontaneous circulation after VF. Norepinephrine, a potent alpha-adrenergic drug nearly devoid of beta-adrenergic properties, could be an interesting alternative to epinephrine. It can improve organ perfusion during cardiopulmonary resuscitation and could be more efficient than epinephrine in case of VF.