Thanks to Dr. Gomes for another Morning Report!
Beta-blocker Toxicity
Receptors
- Beta 1- primarily in heart muscle. Activation –> increases HR, contractility and AV conduction. Decreased AV node refractoriness.
- Beta 2- primarily in bronchial and peripheral vascular smooth muscle. Activation –> vasodilation and bronchodilation
- Beta 3- primarily in adipose tissues and heart muscle. Activation –>catecholamine induced thermogenesis
Clinical Presentation:
–symptoms onset usually within 2hrs, always within 6hrs unless delayed-release, then can take up to 24hrs
Beta-blockade
- Decreased cAMP –>
- Decreased myocardial contractility (hypotension), heart rate and conduction velocity through AV node (Beta 1)
- Bronchoconstriction, impaired gluconeogenesis and decreased insulin release
Characteristics that affect toxicity
- Membrane stabilizing activity- inhibit myocardial fast Na channels–> wide QRS and potentiate other dysrhythmias
- Lipophilicity- some are highly lipid soluble –> rapidly cross blood-brain barrier into the CNS –> seizures, delirium
- Intrinsic sympathomimetic activity- some beta-blockers have a partial beta-agonist effect –> less bradycardia and hypotension
Pharmokinetics
- Half life- 2-8hrs
- Sustained release- delayed onset (up to 24hrs) and duration of toxicity
- Hepatic metabolism, Renal elimination
Studies
- EKG- PR prolonagation, bradycardia, QRS and QT prolongation
- Fsg, electrolytes, calcium, BUN, Cr, LFTs
- Tylenol, salicylate, ethanol levels
Management:
- ABCs, IV, O2, monitor, Supportive care as needed
- Atropine
- IVF- boluses
- Hypoglycemia- D50 prn
- Seizures- benzodiazepines
- Charcoal- if within 1-2hrs of ingestion
Hypotension, Bradycardia
- Glucagon- activates adenylate cyclase –> increase cAMP –> increase intracellular Ca –> increase contractility
- Calcium –> increase contractility
- High dose Insulin and glucose- (mechanism of insulin not fully understood). Beta-blockers interfere with myocyte metabolism and inhibit pancreatic insulin release–> decreased glucose availability–> decreased cardiac output. High dose insulin believed to provide substrate for aerobic metabolism within the myocyte –> increased contractility
- Lipid emulsion therapy- works particularly well for the more lipophilic forms
- Last ditch effort
- Vasopressors
- NAHCO3- QRS widening, Magnesium-ventricular dysrhythmias
- Hemodialysis
The views expressed on this blog are the author's own and do not reflect the views of their employer. Please read our full disclaimer here. Any references to clinical cases refer to patients treated at a virtual hospital, Janus General Hospital.
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Jay Khadpe MD
Editor in Chief of "The Original Kings of County"
Assistant Professor of Emergency Medicine
Assistant Residency Director
SUNY Downstate / Kings County Hospital
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