Epinephrine is the primary drug used in the cardiac arrest algorithm. It is used for its potent vasoconstrictive effects and also for its ability to increase cardiac output. Epinephrine is considered a vasopressor.
Indications for ACLS
- Vasoconstriction effects: epinephrine binds directly to alpha-1 adrenergic receptors of the blood vessels (arteries and veins) causing direct vasoconstriction, thus, improving perfusion pressure to the brain and heart.
- Cardiac Output: epinephrine also binds to beta-1-adrenergic receptors of the heart. This indirectly improves cardiac output by:
- Increasing heart rate
- Increasing heart muscle contractility
- Increasing conductivity through the AV node
- Intravenous Push/IO: 1mg epinephrine IV is given every 3-5 minutes.
- IV infusion for bradycardia: 1mg epinephrine is mixed with 500ml of NS or D5W. The infusion should run at 2-10 micrograms/min (titrated to effect).
- IV infusion for post-cardiac arrest hypotension: The dosing is 2 to 10 micrograms/min.
- Endotracheal Tube: 2-2.5mg epinephrine is diluted in 10cc NS and given directly into the ET tube.
Epinephrine is used in the cardiac arrest algorithm as a direct IV push and also in the bradycardia algorithm as an infusion. See the respective algorithm pages for more information about their use in each.
During ACLS, epinephrine can be given 3 ways: intravenous; intraosseous, and endotracheal tube
Epinephrine should be used with caution in patients suffering from myocardial infarction since epinephrine increases heart rate and raises blood pressure. This increase in HR and BP can increase myocardial oxygen demand and worsen ischemia.
Note: There is no clinical evidence that the use of epinephrine, when used during cardiac arrest, increases rates of survival to discharge from the hospital. However, studies have shown that epinephrine and vasopressin improve rates of ROSC (return of spontaneous circulation).
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