- β-Blockers are rapidly absorbed with the onset of symptoms as soon as 30 minutes after ingestion. Cardiovascular manifestations include hypotension, bradycardia, heart block, and heart failure.
- Absorption of β-blockers can be decreased by the administration of activated charcoal.
- Glucagon may reverse the toxic effects of β-blockers.
- Patients who do not respond to glucagon are treated with aggressive fluid resuscitation, vasopressors, and atropine. Refractory cases may require invasive supportive measures.
- A patient who ingested a non–sustained-release β-blocker can be discharged home after 8 hours of observation if they have a normal exam, mental status, vital signs, and EKG.
- A history of sustained-release β-blocker preparation ingestion requires admission to a monitored setting for 24 hours.
β-Adrenergic Blocking Agents
The mortality rate following β-blocker overdose is much than that for calcium channel blockers or digoxin, but in terms of absolute numbers they are the second leading cause of death from cardiovascular medications.1 American Association of Poison Control Centers data from 2006 indicates 18 853 β-blocker exposures. Two thousand eight hundred and twelve of these involved children younger than 6 years and 712 involved 6- to 19-year-olds. β1- and β2-receptor antagonism, intrinsic sympathomimetic activity, and membrane-stabilizing activity are responsible for the clinical effects of these drugs. α-antagonist activity is seen with labetalol and carvedilol.2
The pharmacologic effects of β-blocking drugs are mediated through modulation of intercellular signals and calcium secondary to inhibited adrenergic activation.3 β1-Antagonism causes decreased cardiac contractility and conduction. β2-Antagonism causes increased smooth muscle tone which may manifest as bronchospasm, increased peripheral vascular tone, and increased gut motility. Although many β-blockers are β1-selective at therapeutic doses, these drugs have both β1- and β2-effects in overdose.
Intrinsic sympathomimetic properties of some β-blockers causes agonist–antagonist activity, which may blunt the bradycardic response in some patients.2,4 Drugs with intrinsic sympathomimetic activity include acebutolol, carteolol, oxprenolol, penbutolol, and pindolol. The membrane-stabilizing activity characteristic of some β-blockers is a quinidine-like effect, resulting in inhibition of fast sodium channels, decreased contractility, and ventricular arryhythmias.5 This effect is additive to the β1-toxic effects.
β-Blockers with increased intrinsic sympathomimetic activity and decreased membrane-stabilizing properties demonstrate less toxicity than those with increased membrane-stabilizing properties.5–8 Drugs with significant membrane-stabilizing properties include propranolol, acebutolol, betaxolol, and oxprenolol.9
Sotalol is a β-blocker which has class III antiarrhythmic properties.10 In overdose, it may prolong the QT interval, resulting in ventricular arrhythmias, including torsades de pointes. Each different β-blocker may have only some of the described activities, and the clinical manifestations may vary.
The absorption, distribution, and elimination of β-blockers vary with the preparation. Extended-release formulations of β-blockers can have a marked delay in the onset of ...