Rethinking the role of epinephrine in cardiac arrest: the PARAMEDIC2 trial

Abstract

Epinephrine (adrenaline) is the most commonly used medication in cardiac arrest, and is the only drug recommended by the American Heart Association (AHA) for all arrests regardless of cardiac rhythm (1). The use of epinephrine in cardiac arrest originated from studies in the 1960’s, when epinephrine was found to improve survival in dog models of asphyxia (2). Physiologically, epinephrine produces some effects that may be helpful and others that may be harmful. It is an agonist at both beta- and alpha-adrenergic receptors. The alpha effects cause peripheral vasoconstriction, which in turn leads to increased blood flow in the central circulation, improving perfusion of the heart and brain. These effects are potentially beneficial, and have been hypothesized to increase the likelihood of return of spontaneous circulation (ROSC) among cardiac arrest patients. The beta-adrenergic effects increase cardiac rate, contractility, and automaticity; these effects are potentially deleterious, leading to arrhythmias and increased myocardial oxygen demand.