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Myron L. Weisfeldt, MD; Alan D. Guerci, MD

JAMA. 1991;266(15):2129-2130.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Metabolic and respiratory acidosis decreases myocardial contractility and inhibits the cardiovascular response to catecholamines.^1-3 Because 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 al⁵ published in this issue of THE JOURNAL is 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 al⁶ reported 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 . . . [Full Text PDF of this Article]

Author Affiliations
From the Department of Medicine, The Johns Hopkins Hospital/Clayton Heart Center, Baltimore, Md. Dr Weisfeldt is now with the Department of Medicine, Columbia Presbyterian Medical Center, New York, NY.

Footnotes
Reprint requests to Department of Medicine, Columbia Presbyterian Medical Center, 630 W 168th St, New York, NY 10032 (Dr Weisfeldt).

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