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Key Points

  • Consider carbon monoxide (CO) poisoning in all patients with headaches, flu-like symptoms, altered mental status, or an unexplained anion gap metabolic acidosis.

  • Immediately administer supplemental O2 to all patients with potential CO poisoning before any confirmatory studies.

  • Pulse oximetry values will be falsely elevated in patients with CO poisoning as a result of the inability of standard oximetry to distinguish between oxyhemoglobin and carboxyhemoglobin.

  • Symptomatology is often more important than the absolute carboxyhemoglobin level when determining treatment and disposition.


Carbon monoxide (CO) is an invisible killer; it is an odorless, colorless, and nonirritating gas. It is generally encountered as a byproduct of the incomplete combustion of carbon-based fuels (eg, coal, gasoline, natural gas). Faulty furnaces and vehicle exhaust fumes are common sources for clinical CO poisoning. Methylene chloride, a substance found in paint stripper and bubbling holiday lights, is metabolized in vivo into CO and may account for cases of delayed poisoning. According to 2010 US Poison Control Center data, more than 13,000 cases of possible CO poisoning were reported. Approximately 5,000 of these cases were treated in medical facilities, and CO is the leading cause of toxin-related fatalities in children less than 5 years of age. In survivors of CO poisoning, it is not uncommon to develop delayed neurologic sequelae, including recurrent headaches, cognitive deficits, and motor disorders.

CO exposure produces toxicity by 3 major pathways. The first of these is an inhibition of systemic O2 delivery. CO binds to hemoglobin (Hb) with an affinity roughly 240 times greater than O2. Systemic O2 delivery plummets as the majority of circulating Hb binding sites are now occupied by CO. In addition, Hb that has bound CO has an increased affinity for concurrently bound O2, resulting in the impaired release of O2 as it reaches the target tissues. This results in a leftward shift and altered shape of the oxyhemoglobin dissociation curve (Figure 58-1).

Figure 58-1.

Carboxyhemoglobin “shift to the left” reshaping of the oxyhemoglobin (HbO2) dissociation curve. Reprinted with permission from Maloney G. Chapter 217. Carbon monoxide. In: Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD, eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill, 2011.

The ability of CO to inhibit normal cellular respiration accounts for its second mechanism of toxicity. CO binds to cytochrome aa3 and inhibits normal transit through the electron transport chain. The resulting shutdown in the oxidative phosphorylation pathway leads to a rapid decimation of stored ATP and secondary cellular death.

The binding of CO to myoglobin accounts for the third mechanism of toxicity. Myoglobin binds to CO with an affinity 40 times that of O2, impairing the adequate delivery of oxygen ...

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