Epinephrine Increases Mortality after Brief Asphyxial Cardiac Arrest in an In Vivo Rat Model

In Brief Epinephrine may be detrimental in cardiac arrest. In this laboratory study we sought to characterize the effect of epinephrine and concomitant calcium channel blockade on postresuscitation myocardial performance after brief asphyxial cardiac arrest. Anesthesized rats were disconnected from mechanical ventilation, resulting in cardiac arrest. Resuscitation was attempted after 1 min with mechanical ventilation, oxygen, chest compressions, and IV medication. In experimental series 1 and 2, animals were allocated to 10 or 30 μg/kg epinephrine or 0.9% saline. In series 3, animals received 30 μg/kg of epinephrine and were randomized to 0.1 mg/kg of verapamil or to 0.9% saline. In series 1 and 3, left ventricular function was assessed using transthoracic echocardiography. In series 2, left atrial pressure was measured. Epinephrine was associated with increased mortality (0/8 [0%] in controls, 4/12 [33.3%] in 10 μg/kg animals, and 16/22 [72.8%] in 30 μg/kg animals; P < 0.05), hypertension (P < 0.001), tachycardia (P = 0.004), early transient left atrial hypertension, and dose-related reduction in left ventricular end diastolic diameter (P < 0.05). Verapamil prevented mortality associated with large-dose epinephrine (0% versus 100%) and attenuated early diastolic dysfunction and postresuscitation hypertension (P = 0.001) without systolic dysfunction. Epinephrine appears to be harmful in the setting of brief cardiac arrest after asphyxia. IMPLICATIONS: In a laboratory-based animal experiment, epinephrine administered after brief asphyxial cardiac arrest caused dose-dependent diastolic dysfunction, left atrial hypertension, and increased mortality. These effects were attenuated by cotreatment with calcium channel blockade. If eventually applicable to humans, these data would suggest caution with the use of epinephrine for cardiac arrest due to asphyxia.