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Sodium bicarbonate is a nonspecific antidote effective in the treatment of a variety of poisonings by means of a number of distinct mechanisms (Table A5–1). However, the support for its use in these settings is predominantly based on animal evidence, case reports, and consensus.9 It is most commonly used in the treatment of patients with cyclic antidepressant (CA) and salicylate poisonings. Sodium bicarbonate also has a role in the treatment of phenobarbital, chlorpropamide, and chlorophenoxy herbicide poisonings and wide-complex tachydysrhythmias induced by type IA and IC antidysrhythmics and cocaine. Correcting the life-threatening acidosis generated by methanol and ethylene glycol poisoning and enhancing formate elimination are other important indications for sodium bicarbonate. Use of sodium bicarbonate in the treatment of rhabdomyolysis, metabolic acidosis with elevated lactate, cardiac resuscitation, and diabetic ketoacidosis is controversial and is not addressed in this Antidote in Depth.1,4,15,45,91,92

Table A5–1. Sodium Bicarbonate: Mechanisms, Site of Action, and Uses in Toxicology

Cyclic Antidepressants

The most important role of sodium bicarbonate in toxicology appears to be its ability to reverse potentially fatal cardiotoxic effects of the CAs and other type IA and IC antidysrhythmics. Use of sodium bicarbonate for CA overdose developed as an extension of sodium bicarbonate use in the treatment of patients with other cardiotoxic exposures. Noting similarities in electrocardiographic (ECG) findings between hyperkalemia and quinidine toxicity (ie, QRS widening), investigators in the 1950s began to use sodium lactate (which is rapidly metabolized in the liver to sodium bicarbonate) for the treatment of quinidine toxicity.3,8,95 In a canine model, quinidine-induced ECG changes and hypotension were consistently reversed by infusion of sodium lactate.7 Clinical experience confirmed this benefit.8 Similar efficacy in the treatment of patients with procainamide cardiotoxicity was also reported.95

With the introduction of the CAs during the late 1950s, conduction disturbances, dysrhythmias, and hypotension occurring after overdose were soon reported. Extending the use of sodium lactate from the type I antidysrhythmics to the CAs, uncontrolled observations in the early 1970s showed a decrease in mortality from 15% to less than 3% when sodium lactate was administered to patients with CA poisoning.29 In 1976, the first report of successful ...

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