58: Carbon Monoxide Poisoning

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.

Introduction

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).

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 ...