Carbon monoxide (CO) poisoning causes acute symptoms such as headache, nausea, weakness, angina, dyspnea, loss of consciousness, seizures, and coma. Neuropsychiatric symptoms may develop weeks later. Diagnosis is by carboxyhemoglobin levels and ABGs, including measured O₂ saturation. Treatment is with supplemental O₂. Prevention is often possible with household CO detectors.

CO poisoning, one of the most common fatal poisonings, occurs by inhalation. CO is a colorless, odorless gas that results from incomplete combustion of hydrocarbons. Common sources of CO in poisonings include house fires and improperly vented automobiles, gas heaters, furnaces, hot water heaters, wood- or charcoal-burning stoves, and kerosene heaters. CO is produced when natural gas (methane or propane) burns. Inhaling tobacco smoke results in CO in the blood but not enough to cause poisoning.

Pathophysiology

The elimination half-life of CO is about 4.5 h with inhalation of room air, 1.5 h with 100% O₂, and 20 min with 3 atmospheres (pressure) of O₂ (as in a hyperbaric chamber—see Injury During Diving or Work in Compressed Air: Recompression Therapy).

Mechanisms of CO toxicity are not completely understood. They appear to involve

• Displacement of O₂ from Hb (because CO has greater affinity for Hb than does O₂)
• Shifting of the O₂-Hb dissociation curve to the left (decreasing release of O₂ from Hb to tissues—see Fig. 4: Tests of Pulmonary Function (PFT): Oxyhemoglobin dissociation curve.)
• Inhibition of mitochondrial respiration
• Possibly direct toxic effects on brain tissue

Symptoms and Signs

Symptoms tend to correlate well with the patient's peak blood carboxyhemoglobin levels. Many symptoms are nonspecific.

• Headache and nausea can begin when levels are 10 to 20%.
• Levels > 20% commonly cause vague dizziness, generalized weakness, difficulty concentrating, and impaired judgment.
• Levels > 30% commonly cause dyspnea during exertion, chest pain (in patients with coronary artery disease), and confusion.
• Higher levels can cause syncope, seizures, and obtundation.

Hypotension, coma, respiratory failure, and death may occur, usually when levels are > 60%.

Patients may also have many other symptoms, including visual deficits, abdominal pain, and focal neurologic deficits. If poisoning is severe, neuropsychiatric symptoms and signs (eg, dementia, psychosis, parkinsonism, chorea, amnestic syndromes) can develop days to weeks after exposure and become permanent. Because CO poisoning often results from house fires, patients may have concomitant airway injuries (see Sidebar 1: Burns: Smoke Inhalation), which may increase risk of respiratory failure.

Diagnosis

• Diagnosis considered when patients at risk have nonspecific symptoms or metabolic acidosis
• Venous carboxyhemoglobin level

Because symptoms can be vague, nonspecific, and variable, the diagnosis is easily missed. Many cases of mild poisoning with nonspecific symptoms are mistaken for viral syndromes. Physicians must maintain a high level of suspicion. If people from the same dwelling, particularly a heated dwelling, experience nonspecific flu-like symptoms, CO exposure should be considered.

If CO poisoning is suspected, the carboxyhemoglobin level is measured with a CO-oximeter; venous samples can be used because arteriovenous differences are trivial. ABGs are not measured routinely. ABGs and pulse oximetry, alone or combined, are inadequate for diagnosis of CO poisoning because O₂ saturation reported in ABGs represents dissolved O₂ and is thus unaffected by carboxyhemoglobin concentration; furthermore, the pulse oximeter cannot differentiate normal Hb from carboxyhemoglobin and thus provides a falsely elevated oxyhemoglobin reading. Noninvasive CO detectors have not been shown to be accurate or useful in the diagnosis of CO exposure or toxicity. Although elevated carboxyhemoglobin levels are clear evidence of poisoning, levels may be falsely low because they decrease rapidly after CO exposure ends, particularly in patients treated with supplemental O₂ (eg, in an ambulance). Metabolic acidosis can be a clue to the diagnosis. Other tests may help evaluate specific symptoms (eg, ECG for chest pain, CT for neurologic symptoms).

Treatment

• 100% O₂
• Possibly hyperbaric O₂

Patients should be removed from the source of CO and stabilized as necessary. They are given 100% O₂ (by nonrebreather mask) and treated supportively. Although its use is becoming increasingly controversial, hyperbaric O₂ therapy (in a chamber at 2 to 3 atmospheres of 100% O₂) typically should be considered for patients who have any of the following:

• Life-threatening cardiopulmonary complications
• Ongoing chest pain
• Altered consciousness
• Loss of consciousness (no matter how brief)
• A carboxyhemoglobin level > 25%

Hyperbaric O₂ therapy should also be considered for pregnant patients, possibly at lower serum CO levels than in nonpregnant patients.

Hyperbaric O₂ therapy may decrease the incidence of delayed neuropsychiatric symptoms. However, this therapy may cause barotrauma and, because therapy is not available at most hospitals, may require transfer of patients, who may not be stable; also, a chamber may not be available locally. Evidence for the efficacy of hyperbaric O₂ therapy is becoming more controversial, with some studies suggesting harm. In cases where hyperbaric O₂ therapy is considered, consultation with a poison control center or hyperbaric expert is strongly recommended.

Prevention

Prevention involves checking sources of indoor combustion to make sure they are correctly installed and vented to the outdoors. Exhaust pipes should be inspected periodically for leaks. Cars should never be left running in an enclosed garage. CO detectors should be installed because they provide early warning that CO is free in a dwelling's atmosphere. If CO is suspected in a dwelling, windows should be opened, and the dwelling should be evacuated and evaluated for the source of CO.

Key Points

• CO poisoning (eg, caused by house fires, improperly vented automobiles, gas heaters, furnaces, hot water heaters, wood- or charcoal-burning stoves, or kerosene heaters) is one of the most common fatal poisonings.
• Consider toxicity is patients with nonspecific symptoms (eg, flu-like symptoms in winter) or unexplained metabolic acidosis.
• Measure CO level with a CO-oximeter.
• Do not rule out toxicity based on a normal CO level because levels can decrease rapidly, particularly after treatment with supplemental O₂.
• Treat with 100% O₂.
• For severe poisoning, consult an expert or poison control center to discuss treatment with hyperbaric O₂.

Last full review/revision February 2013 by Gerald F. O'Malley, DO; Rika O'Malley, MD

Content last modified March 2013