Introduction

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 (L.o.ve 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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