What is the pathophysiology of carbon monoxide asphyxiation from smoke inhalation?

Updated: Oct 15, 2021
  • Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS  more...
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Carbon monoxide (CO) is a colorless, odorless gas produced by the incomplete combustion of carbon-containing compounds, such as wood, coal, and gasoline. It is a major component of the smoke produced in open fires.

CO causes tissue hypoxia by decreasing the oxygen-carrying capacity of the blood. Hemoglobin binds CO with an affinity more than 200 times greater than the affinity for oxygen. Other mechanisms contribute, as well. [10] CO causes a left shift in the oxyhemoglobin saturation dissociation curve, which reduces the ability of hemoglobin to unload oxygen.

The heart is particularly affected because CO binds with the heme molecules in myoglobin, decreasing facilitated diffusion of oxygen into muscle. Interaction of CO with myocardial myoglobin results in decreased myocardial contractility.

A classic study demonstrated that dogs breathing 13% CO died within 1 hour after carboxyhemoglobin (CO-Hgb) levels reached 54% to 90%. However, exchange transfusion with blood containing 80% CO-Hgb to otherwise healthy dogs resulted in no toxic effects, despite resultant CO-Hgb levels of 57-64%. This further supports the notion that CO toxicity is not dependent on CO-Hgb formation or, in other words, solely upon a relative anemia. [11]

The literature suggests that hypoxic encephalopathy secondary to CO poisoning results from a reperfusion injury in which the products of lipid peroxidation and free radical formation contribute to morbidity and mortality. The therapeutic effect of hyperbaric oxygen therapy in these patients is attributed to improvement in mitochondrial oxidative metabolism, impairment of adherence of neutrophils to cerebral vasculature (decreases inflammation), and preservation of adenosine triphosphate activity.

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