Beta-adrenergic receptor blockers are one of the most widely prescribed classes of drug in clinical medicine. Cardiovascular instability presents considerable therapeutic problems in cases of serious poisoning; b rreceptor cardioselectivity is by no means absolute. Receptor blockade leads to a reduction in intracellular cAMP concentration. In the heart, decreased intracellular cAMP inhibits sodium and calcium influx during phase zero of the action potential.

Death in b-blocker poisoning is usually due to pump failure, an effect caused by 'quinidine-like' membrane stabilization, rather than cardiac dysrhythmias. Cardioselectivity is lost in overdose and membrane stabilization becomes a feature common to most b-blockers. Individual response to b-blockers varies considerably and, with the exception of sotalol, blood levels do not correlate well with toxicity; therefore diagnosis should be on clinical grounds. Sotalol levels correlate with the degree of QTc prolongation and the risk of arrhythmias ( 1.994..a.). In addition, toxicity may persist even after the b-blocker is undetectable in the blood; the mechanism underlying this is unknown.

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