ACLS/BLS Tips: Epinephrine
Quick Info
Indications:
Cardiac Arrest: VF, pVT, Asystole, PEA
Symptomatic Bradycardia: Can be considered after atropine
Severe Hypotension
Anaphylaxis, Severe Allergic Reactions: Combine with large fluid volumes, corticosteroids, antihistamines
Dose:
Cardiac Arrest: VF, pVT, Asystole, PEA
IV/IO Dose: 1mg bolus (in 10 ml - 0.1 mg/ml)
Profound Bradycardia or Hypotension
2-10 mcg/min infusion, titrate to patient response
Caution:
Raising blood pressure and increasing heart rate may cause myocardial ischemia, angina, and increased myocardial oxygen demand.
High doses do not improve survival or neurologic outcome and may contribute to postresuscitation myocardial dysfunction.
Higher doses may be required to treat poison/drug-induced shock
Overview
Epinephrine is a potent sympathomimetic agent used in the treatment of cardiac arrest, profound hypotension, severe allergic reaction, and several other applications. Epinephrine is a common drug used within various advanced cardiac life support (ACLS) algorithms, particularly in cardiac arrest scenarios. As a nonselective adrenergic agonist, it stimulates α₁, β₁, and β₂ receptors, leading to increased heart rate, myocardial contractility, and peripheral vasoconstriction. These effects collectively enhance coronary and cerebral perfusion during resuscitation efforts.
In cardiac arrest management, epinephrine is administered intravenously at a standard dose of 1 mg every 3–5 minutes, regardless of the cardiac rhythm. This means it’s used for ventricular tachycardia (VT), ventricular fibrillation (VF), pulseless electrical activity (PEA), and asystole. Its primary role is to augment aortic diastolic pressure through vasoconstriction, thereby improving blood flow to vital organs. However, clinicians should be vigilant for potential adverse effects, including hypertension, tachycardia, and arrhythmias, which may complicate post-resuscitation care. 
Despite being a common drug within ACLS, recent studies have scrutinized the efficacy of epinephrine in out-of-hospital cardiac arrest (OHCA) cases. While its use has been associated with increased rates of return of spontaneous circulation (ROSC), concerns persist regarding its impact on long-term neurological outcomes. A systematic review and meta-analysis indicated that, although epinephrine improves short-term survival, it does not significantly enhance survival to hospital discharge with favorable neurological status. Excessive alpha- and beta-adrenergic stimulation may contribute to and result in cerebral microvascular insufficiency in patients receiving CPR. Additionally, despite the beta-adrenergic effects increasing cardiac rate, contractility, and automaticity; these effects are also potentially harmful, leading to arrhythmias and increased myocardial oxygen demand.
Given these findings, healthcare providers should adhere to current ACLS guidelines when administering epinephrine during cardiac arrest, balancing its immediate benefits in achieving ROSC against the potential for adverse neurological outcomes. Ongoing research continues to evaluate optimal dosing strategies and the timing of administration to maximize patient survival with good neurological function.
ACLS Tips
Epi is given in cardiac arrest regardless of the cardiac rhythm, so occurring on both sides of the algorithm pathways (pVT/VF vs. PEA/Asystole)
Epi is given every 3-5 min, but when given every 4 min, it works out nicely with being given every other CPR round (each round being 2 min).
The administration of 1 mg Epi in cardiac arrest is given as a push dose bolys, NOT as an infusion.
References:
Heart & Stroke Foundation of Canada. (2020). Advanced Cardiac Life Support. Canada.
Heradstveit, B. E., Sunde., G. A., Asbjørnsen, H., Aalvik, R., Wentzel-Larsen, T., & Heltne, J.-K. (2023). Pharmacokinetics of epinephrine during cardiac arrest: A pilot study. Resuscitation, 193. https://doi.org/10.1016/j.resuscitation.2023.110025
Jung, J., Rice, J., & Bord, S. (2018). Rethinking the role of epinephrine in cardiac arrest: the PARAMEDIC2 trial. Annals of translational medicine, 6(Suppl 2), S129. https://doi.org/10.21037/atm.2018.12.31