Epinephrine (EPI) has long been considered the cornerstone of care in cardiac arrest. The use of EPI was first introduced in the 1960s based on studies of asphyxiated dogs[1] in which EPI was used in a standard dose of 1 mg without any weight adjustments or consideration of interspecies variation.[2] The presumed benefits of EPI are mediated by its alpha-adrenergic effects, which include increases in aortic diastolic pressure and coronary blood flow.[3]
Nonrandomized and poorly controlled studies in the 1980s and 1990s did in fact confirm increases in return of spontaneous circulation (ROSC).[3,4,5,6,7,8] Unfortunately, those studies also demonstrated beta-adrenergic-mediated adverse effects associated with cumulative doses including dysrhythmias, increased myocardial oxygen demand, worsened neurologic outcome in survivors, and increased risk for recurrent cardiac arrest.
In spite of these concerns, the use of EPI every 3 to 5 minutes during cardiac arrest has remained in the national and international resuscitation guidelines[9] despite much argument and controversy regarding whether EPI is beneficial or harmful.
A great deal of anticipation and excitement centered on a randomized, prehospital trial of EPI in out-of-hospital cardiac arrest,[3]which would presumably finally, once and for all, answer the question regarding whether the use of EPI in cardiac arrest had an overall beneficial or harmful influence.
