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Beta-adrenergic–blocking agents are widely used for the treatment of hypertension, arrhythmias, angina pectoris, heart failure, migraine headaches, and glaucoma. Beta-blocker poisoning is the most common cause of drug-induced cardiogenic shock in the United States. Many patients with beta-blocker overdose will have underlying cardiovascular diseases or will be taking other cardioactive medications, both of which may aggravate beta-blocker overdose. Of particular concern are combined ingestions with calcium blockers or tricyclic antidepressants. A variety of beta blockers are available, with various pharmacologic effects and clinical uses (Table II–15).



Excessive beta-adrenergic blockade is common to overdose with all drugs in this category. Although beta receptor specificity is seen at low doses, it is lost in overdose.

  1. Propranolol, acebutolol, and other agents with membrane-depressant (quinidine-like) effects further depress myocardial contractility and conduction and may be associated with ventricular tachyarrhythmias. Propranolol is also lipid soluble, which enhances brain penetration and can cause seizures and coma.

  2. Pindolol, acebutolol, and penbutolol, agents with partial beta agonist activity, may cause tachycardia and hypertension.

  3. Sotalol, which also has type III antiarrhythmic activity, prolongs the QT interval in a dose-dependent manner and may cause torsade de pointes (Table I–7) and ventricular fibrillation.

  4. Labetalol and carvedilol have combined nonselective beta- and alpha-adrenergic–blocking actions, and nebivolol is a selective beta1 antagonist with vasodilating properties not mediated by alpha blockade. With these drugs, direct vasodilation can contribute to hypotension in overdose.

  5. Pharmacokinetics. Peak absorption occurs within 1–4 hours but may be much longer with sustained-release preparations. Volumes of distribution are generally large. Elimination of most agents is by hepatic metabolism, although nadolol, atenolol, and carteolol are excreted unchanged in the urine and esmolol is rapidly inactivated by red blood cell esterases (see also Table II–66).

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