Epinephrine. #CCRN #CMC #CSC in today’s education post.
This drug, produced by the adrenal medulla in times of stress, is referred to as adrenaline. It’s a neurotransmitter that acts on the beta and alpha receptor sites much like the other inotropic medications we’ve discussed so far.
Epinephrine has ACLS-level fame, and is used for the treatment of cardiac arrest. It increases perfusion pressure to the coronary and cerebral blood vessels, as well as increasing blood flow to the skeletal muscle beds.
(Data supporting its use in resuscitation is limited–read about the controversy here.)
Epinephrine has beta-1 and beta-2 adrenergic effects, causing an increase in cardiac output and heart rate, as well as bronchodilation. This makes the medication particularly useful in the treatment of anaphylaxis.
We’ve talked about the beta-2 receptor site, and its vasodilatory properties. So how is epinephrine a treatment for shock states if it activates beta-2 receptors? It also has profound alpha-1 agonist activity, which causes vasoconstriction.
But, wait…doesn’t that mean epi works against itself?
Actually, no, because the concentration (dose) of the catecholamine at the level of the receptor site controls activation. At low doses, say, 2-10 mcg/min (0.02 mcg/kg/min-0.05 mcg/kg/min for weight-based dosing), beta stimulation predominates. At higher doses, the beta-2 stimulation is gradually overwhelmed by alpha-1 agonist activity.
What about the max on epi? Well, there is no true maximum dose of this catecholamine, but at 30 mcgs/min every receptor site accessible to epi is fully covered, so if your patient remains hypotensive adding norepinephrine or phenylephrine (targeting the same alpha-1s) is a futile endeavor. A much better alternative? Vasopressin.
PRIMARY CONSIDERATIONS: Epinephrine is proarrhythmogenic.
Renal flow is greatly reduced even if blood pressure doesn’t change…estimated 2-10 times greater effect on renal circulation when compared to norepinephrine. It also increases renin secretion.
Epinephrine has greater effects on metabolism than any of the other catecholamines we’ve mentioned. It increases blood glucose via glycogenolysis in the liver, lipolysis in adipose tissue, and inhibits insulin secretion. Lactate rises on epinephrine drips, probably due to glycogenolysis in skeletal muscles.
Effects on the gastrointestinal tract include smooth muscle relaxation. In other words, it decreases motility, which can result in nausea, particularly in post-operative patients.
Interestingly, epinephrine increases blood coagulation, possibly due to increased activity of factor V.