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Beta blocker poisoning

Fermin Barrueto, Jr, MD, FACEP, FAAEM, FACMT
Section Editor
Stephen J Traub, MD
Deputy Editor
Jonathan Grayzel, MD, FAAEM


Beta adrenergic antagonists (beta blockers) have been in clinical use for more than 30 years, and are employed in the management of a range of disorders, including hypertension, ischemic heart disease, heart failure, arrhythmias, migraine headache, tremor, portal hypertension, and aortic dissection. Although safe for most patients when taken as prescribed, beta blocker toxicity is associated with significant morbidity and mortality. In 2006, there were 9041 single beta blocker exposures reported to poison centers in the United States. Of these, there were 613 moderate or major adverse outcomes and four deaths [1].

Complications following beta blocker overdose are related to excessive beta adrenergic blockade, and occasionally the proarrhythmic (membrane-stabilizing) activity of these agents on cardiac conduction [2]. Ingestion of other cardioactive agents in association with beta blockers increases mortality following overdose [2,3]. Common and potentially dangerous coingestions include calcium channel blockers, cyclic antidepressants, and neuroleptics [2].

An overview of beta blocker intoxication will be presented here. A summary table to facilitate emergent management is provided (table 1). A general approach to an adult patient with possible drug intoxication, and an overview of adverse effects of beta blockade, are discussed separately. (See "General approach to drug poisoning in adults" and "Major side effects of beta blockers".)


Receptor types and general mechanism — There are at least three distinct types of beta receptors:

Beta 1, which are found primarily in heart muscle. Activation of these receptors results in an increase in heart rate, contractility, atrioventricular (AV) conduction, and a decrease in AV node refractoriness.

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Literature review current through: Nov 2017. | This topic last updated: Apr 11, 2017.
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