Morning Report: Beta-blocker Toxicity

Thanks to Dr. Gomes for another Morning Report!

Beta-blocker Toxicity

Receptors

1. Beta 1- primarily in heart muscle. Activation –> increases HR, contractility and AV conduction. Decreased AV node refractoriness.
2. Beta 2- primarily in bronchial and peripheral vascular smooth muscle. Activation –> vasodilation and bronchodilation
3. 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

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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

Latest posts by Jay Khadpe MD (see all)

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