Complication of Epi and non-selective beta blocker

1. Non-selective beta blockers
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PGY-5 (CRITICAL CARE)
EPINEPHRINE AND BETA BLOCKERS
RishiApril 7, 2018
12 1 minute read
With the growing usage of β-blocker therapy to control everything from atrial fibrillation
and congestive heart failure to migraine prophylaxis and essential tremor, we need to be
more aware of potential pitfalls due to drug interactions. A classic example is the need for
epinephrine in a patient on a non-selective β-blocker (ie, propranolol).
These non-selective agents block both β1 (inotropy, chronotropy) and β2 receptors
(vasodilation). Yes, I’m disregarding non-cardiovascular implications of blocking β receptors
to highlight the following point. From a pharmacologic standpoint, high doses of

2. epinephrine will potentiate β1, β2, and alpha receptors. With a β-blocker like propranolol on
board, epinephrine will primarily work through the α1 receptor – receptors on the peripheral
vasculature involved with vasoconstriction.
The net effect will be unopposed vasoconstriction leading to significant increases in blood
pressure. This hypertension will, in turn, activate pressure receptors in the carotid sinus to
increase vagal tone on the heart leading to profound decreases in heart rate. Worst case
scenario, the patient will become asystolic. Funny thing because in true asystole, the
treatment is chest compressions and…. you guessed it… epinephrine! �
So why would we need to give epinephrine to these patients anyways? Anaphylaxis is one
example! The mainstay of treatment will be epinephrine to stabilize further mast cell
degranulation and promote bronchodilation, histaminergic blockers, steroids, and
significant intravenous fluid resuscitation. A patient receiving β-blocker therapy may not
mount the typical tachycardic response after receiving epinephrine. One will need to likely

3. escalate their doses rapidly but be mindful of paradoxical bradycardia related to the
mechanism above!
Another option is to give small doses of glucagon (1-3 mg followed by an infusion), but
keep in mind that the evidence supporting the use of glucagon to reverse β-blocker therapy
has only been shown in animal studies. Additionally, patients who receive this much
glucagon invariably become nauseous and can vomit (oh the perils of an unprotected
airway!)
Hopefully this makes sense, but if not, drop me a comment below with questions! �