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Sodium bicarbonate is a nonspecific antidote that is 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.11 It is most commonly used to treat 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 Na+ channel blocking xenobiotics such as type IA and IC antidysrhythmics and cocaine. Correcting the life-threatening acidemia induced by methanol and ethylene glycol metabolism and enhancing formate elimination are other important indications for sodium bicarbonate. The use of sodium bicarbonate in the treatment of rhabdomyolysis, metabolic acidosis with elevated lactate, cardiac resuscitation, and diabetic ketoacidosis is controversial and not addressed in this Antidote in Depth.3,6,17,57,113,114
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Sodium bicarbonate has a molecular weight of 84 Da. It is supplied in solution at approximately pH 8.0 (pH limits range from 7.0 to 8.5). The onset of action of intravenous (IV) sodium bicarbonate is within 15 minutes with a duration of action of 1 to 2 hours. Sodium bicarbonate increases plasma bicarbonate and buffers excess hydrogen ion.32 In normal individuals, the distribution volume for bicarbonate salts is approximately twice the extracellular fluid (ECF) volume.43,105 The apparent bicarbonate space (ABS) proportionally increases in severe acidemia, leading to higher bicarbonate requirements.37 Canine studies demonstrated that this effect is not due to the acidemia per se, but due to the tight correlation of extracellular bicarbonate concentrations with the ABS.1 Whether acidemic or alkalemic, low bicarbonate concentrations increase the apparent space of distribution in a highly dynamic manner.1 Human studies, in which the ABS is described ...