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Peter M. Winter, MD; John N. Miller, MB, BS

JAMA. 1976;236(13):1502-1504.

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

ACUTE carbon monoxide poisoning accounts for approximately 3,500 accidental or suicidal deaths per year in the United States. Many are preventable by medical management based on physiologic understanding.

Pathophysiology

Carbon monoxide poisoning and its mechanism have been known since Claude Bernard reported in 1857 that this gas caused death by hypoxia, consequent on its reversible combination with hemoglobin.¹ The equilibrium reactions were well described by Haldane in 1895.² Excellent reviews are available.^3,4

The effects of CO in concentrations encountered clinically are based entirely on its combination with hemoglobin, displacement of oxygen, and consequent disruption of the O₂ transport system. Carbon monoxide competes with O₂ for binding sites on the hemoglobin molecule, and carboxyhemoglobin (COHb) is without practical function as a carrier of O₂. Because affinity of CO for hemoglobin is 230 to 270 times as great as that of O₂, the latter is . . . [Full Text PDF of this Article]

Author Affiliations
From the Department of Anesthesiology, University of Washington School of Medicine, Seattle (Dr Winter), and the Department of Anesthesiology, Duke University School of Medicine, Durham, NC (Dr Miller).

Footnotes
Reprint requests to Department of Anesthesiology, University of Washington School of Medicine RN 10, Seattle, WA 98195 (Dr Winter).

Edited by Samuel Vaisrub, MD, Senior Editor.

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