Epinephrine, also known as adrenaline, is both a naturally occurring hormone and a powerful drug used in emergency medicine. Produced by the adrenal glands, it triggers the body’s “fight or flight” response via the sympathetic nervous system. In medicine, epinephrine is an indispensable tool for managing cardiac arrest, particularly within Advanced Cardiac Life Support (ACLS) protocols. Its potency requires strict adherence to precise dosing and administration guidelines.
The Standard Cardiac Dose
The standard dose of epinephrine used during the resuscitation of an adult experiencing cardiac arrest is 1 milligram (mg). This dosage is a uniform recommendation within established Advanced Cardiac Life Support guidelines. The drug is typically administered rapidly through an intravenous (IV) line or an intraosseous (IO) access point, which accesses the vascular network within the bone marrow. Following the initial administration, the protocol calls for a repeat dose of 1 mg every three to five minutes for the duration of the resuscitation effort.
This cardiac dose is usually given as a 1:10,000 concentration, meaning 1 milligram of the drug is contained within 10 milliliters of solution. After the medication is pushed into a peripheral vein, a 20-milliliter flush of IV fluid is immediately administered to ensure the drug reaches the central circulation efficiently. Clinicians adhere to this precise regimen because the timing and delivery of the medication are important factors in attempting to restart the heart.
How Epinephrine Affects the Heart
Epinephrine is categorized as a sympathomimetic, meaning it mimics the effects of stimulation on the sympathetic nervous system by interacting with adrenergic receptors throughout the body. In the non-beating heart of a cardiac arrest patient, the drug’s primary benefit comes from its effect on alpha-1 adrenergic receptors, which are located on the smooth muscle of blood vessels. Stimulation of these alpha-receptors causes intense peripheral vasoconstriction, or the narrowing of blood vessels far from the body’s core.
This widespread vasoconstriction forces blood that remains in the body toward the central organs, including the heart and the brain. By shunting blood to these areas, epinephrine increases the coronary perfusion pressure, which is the pressure gradient that drives blood flow to the heart muscle itself. This improved pressure is considered a mechanism that increases the likelihood of achieving Return of Spontaneous Circulation (ROSC) and successfully delivering a life-restoring electrical shock from a defibrillator.
Epinephrine also interacts with beta-1 adrenergic receptors, which are found directly on the heart muscle, leading to an increase in both heart rate and the force of cardiac muscle contraction. While these beta effects can increase the heart’s electrical activity and contractility, the alpha-receptor-mediated vasoconstriction is generally considered the more important mechanism during cardiac arrest. The overall effect of the drug is to create a more favorable environment within the circulatory system for resuscitation efforts to succeed.
Distinguishing Emergency Doses
The cardiac arrest dose of epinephrine is distinctly different from the dosages used for other acute medical emergencies, particularly severe allergic reactions, or anaphylaxis. For anaphylaxis, the dose is significantly smaller, typically 0.3 mg to 0.5 mg, and it is most often administered into the muscle of the outer thigh. This route, known as intramuscular (IM) injection, allows for rapid absorption into the bloodstream to counteract the effects of the allergic reaction.
The difference in concentration between the two formulations is a critical distinction that prevents dangerous medical errors. The epinephrine used for cardiac arrest is a dilute 1:10,000 solution (0.1 mg per milliliter). Conversely, the epinephrine used for anaphylaxis is a much more concentrated 1:1,000 solution (1 mg per milliliter).
Accidentally injecting the highly concentrated 1:1,000 solution intravenously during a cardiac arrest can lead to severe hypertension and dangerous heart rhythms due to the massive overdose. The concentrated anaphylaxis dose is designed for slow absorption from the muscle, while the dilute cardiac dose is formulated for rapid intravenous administration. Understanding these differences is important for appreciating the varied clinical applications of this potent medication.