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  • β-Blocker and calcium channel blocker poisoning have significant morbidity, and their hallmark is bradycardia and hypotension.

  • If standard Pediatric Advance Life Support (PALS) protocols do not restore adequate cardiovascular function, stepwise administration of glucagon, hyperinsulinemia-euglycemia (HIE) therapy, and lipid emulsion should be considered.

  • Administration of specific anti-digoxin Fab antibody fragments is a highly effective treatment for digoxin poisoning.

  • Consider naloxone if PALS protocols fail to reverse clonidine toxicity.


In 2016, the American Association of Poison Control Centers documented 3076 single substance β-blocker exposures in children younger than 5 years and 832 in 6- to 19-year-olds.1 Those producing the greatest morbidity were metoprolol, atenolol, and propranolol. 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. β-Adrenergic blocking agents account for almost 60% of pediatric emergency department visits due to the ingestion of an adult prescription medication by a child.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 produces decreased cardiac contractility and conduction. β2-Antagonism produces 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 produce 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, and oxprenolol.9

Sotalol is a β-blocker that has class III antiarrhythmic properties.10 In overdose, it may prolong the QT interval, resulting in ventricular arrhythmias, including torsades de pointes. Each 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 drug. Extended-release formulations can have a marked delay of onset of toxic effects. Conversely, standard release β-blockers are rapidly absorbed, with 30% to 90% bioavailability. Only penbutolol and propranolol exhibit high lipid solubility and thus can cross the blood–brain barrier. Protein binding ranges from 10% (timolol) to 98% (carvedilol). Most are metabolized in the liver by the cytochrome P-450 2D6 isoenzyme. The elimination half-life varies ...

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