1976JAMARequires access

Carbon Monoxide Poisoning

P. Winter

Open publisher page 136 citations

Abstract

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.1The equilibrium reactions were well described by Haldane in 1895.2Excellent 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 O2transport system. Carbon monoxide competes with O2for 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

About this research paper

What this paper is about

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.1The equilibrium reactions were well described by Haldane in 1895.2Excellent 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 O2transport system. Carbon monoxide competes with O2for 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

Why it matters

OpenAlex reports 136 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

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.1The equilibrium reactions were well described by Haldane in 1895.2Excellent 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 O2transport system. Carbon monoxide competes with O2for 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

Key concepts: Carboxyhemoglobin, Carbon monoxide poisoning, Carbon monoxide, Medicine, Hemoglobin, CO poisoning, Oxygen, Poison control

Related papers

Back to paper searchBrowse research topicsOriginal source
Carbon Monoxide Poisoning — Research Paper | ScholarLens