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Metabolic and respiratory acidosis decreases myocardial contractility and inhibits the cardiovascular response to catecholamines.1-3Because of these adverse effects, and because of the relative ease with which the arterial acidemia of cardiac arrest can be reversed with sodium bicarbonate, sodium bicarbonate was quickly incorporated into the pharmacopoeia of resuscitation.4 The study by Kette et al5published in this issue ofThe Journalis an important additional piece of evidence against the routine use of sodium bicarbonate in cardiac arrest. Their findings are important, but not particularly surprising. In 1974, Mattar et al6reported that hyperosmolality occurring as a result of the administration of commercially available preparations of sodium bicarbonate, which contain either 1792 or 2000 mOsm/L, was an independent risk factor for in-hospital death following initially successful resuscitation. The rationale for the use of sodium bicarbonate in cardiac arrest is to correct
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Myron L. Weisfeldt (1991) studied this question.
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