- In the United States, the American Association of Poison Control Centers at 800-222-1222 is available 24 hours a day to connect callers directly to their region's poison center. They are also available online.
- Initial treatment should immediately address the ABCs – airway, breathing, and circulation.
- Treat hemodynamic instability. Hypertension is first treated with intravenous (IV) isotonic fluid boluses. Symptomatic bradycardia can be managed using atropine.
- Seizures due to beta-blocker toxicity are treated with benzodiazepines.
- If the patient presents acutely after ingestion, gastric lavage or decontamination can be useful.
Beta blockers are competitive antagonists that act on the adrenergic beta-1 (B1), beta-2 (B2), and beta-3 (B3) receptors to block endogenous catecholamine release or dampen catecholamine effects. B1 blockade reduces cardiac chronotropy, dromotropy, inotropy, and lowers blood pressure. Beta blockers are used to treat cardiovascular diseases, tachydysrhythmia, pheochromocytoma, glaucoma, migraine, thyroid disorders, tremors, and anxiety, as well as reduce post-myocardial infarction (MI) mortality.
Nonselective beta blockers act on all types of beta receptors, while selective B1 blockers act on designated receptor sites. Metoprolol and atenolol are selective B1 blockers. Propranolol and timolol are nonselective. Sotalol is a nonselective beta blocker but also affects potassium channels causing higher toxicity. Labetalol is a beta and alpha-1 antagonist.
The most common beta-blocker overdoses involve propranolol, followed by metoprolol. Both are associated with increased cardiovascular complication rates. Beta-blocker overdoses are often an acute one-time ingestion rather than chronic temporal toxicity. Accidental double-dosing may have occurred.
Toxicity occurs within 1-2 hours of overdose, but signs and symptoms may take 6 hours to manifest. The risk of toxicity is highest (up to 20 hours) in sotalol overdose. In cases of true beta-blocker poisoning, patients have high risk of cardiovascular morbidity, but if promptly treated can expect a good prognosis.
Beta-blocker overdose occurs 3 times more often in women than men, with an average age of 30 years. Of these patients, 66% ingested another's medication or were prescribed beta blockers for noncardiac disorders. Simultaneous use of calcium channel blockers, neuroleptics, and tricyclic antidepressants are a common component of higher cardiac adverse events.
Beta blockers that affect sodium channels have membrane stabilizing activity (MSA) that heightens toxicity in overingestion. Beta blockers with MSA have the most effect on adverse cardiovascular events and include propranolol, acebutolol, betaxolol, and oxprenolol. MSA effects are insignificant at therapeutic doses but can cause significant cardiac morbidity in beta-blocker overdose.
Per the Toxic Exposure Surveillance System (TESS) of the American Association of Poison Control (AAPCC) 2015 review, 9.6% of cases of beta-blocker overdose had moderate-to-major outcomes, and 82% of overdoses were unintentional.
