Epinephrine (adrenaline) is an incredibly versatile catecholamine. It can be administered through intravenous, subcutaneous, intramuscular, and inhalational routes. It treats a myriad of clinical conditions ranging from anaphylaxis and croup to bronchospasm and afterload enhancement in cardiopulmonary arrest. Epinephrine is routinely added to local anesthetics to provide localized vasoconstriction, but literature is also showing that its adrenergic effects are independently conferring a degree of analgesia.
Epinephrine’s mechanism of action is highly dependent on its dose – “beta” agonist effects are seen first followed by “alpha” agonist effects. For this reason, it’s important to understand how the adrenergic system ACTUALLY works rather than thinking “epi increases blood pressure.” I use this medication ALL the time in cardiothoracic anesthesiology and in the ICU for patients with systolic dysfunction (especially in right heart failure). Beta effects allow me to increase a patient’s chronotropy (heart rate) and inotropy (contractility) while simultaneously promoting vasodilation of the vascular smooth muscle (decreased afterload). The net effect? Promoting forward flow!
Some points to think about: epinephrine can create a lactic acidosis even in aerobic conditions due to the accumulation of pyruvate and saturation of the PDH/TCA pathways. Systolic anterior motion (SAM) of the mitral valve misdiagnosed as anaphylaxis and treated with epinephrine can lead to hemodynamic collapse. Patients who are taking beta blockers (especially mixed agents like labetalol) may not manifest the typical hemodynamic responses one would expect with high doses of epinephrine. It’s important to consider how the simultaneous adrenergic agonism/antagonism will present clinically.
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