Carbon Monoxide

How to Cite This Chapter: Perri D, Klimaszyk D, Kołaciński Z, Szajewski J. Carbon Monoxide. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed May 30, 2024.
Last Updated: November 9, 2021
Last Reviewed: November 9, 2021
Chapter Information

Carbon monoxide (CO) is a product of incomplete combustion of organic material such as automobile or other engine exhausts; natural gas, butane, or propane in heaters or gas-powered equipment (such as air compressors); wood or coal in burning stoves; as well as a by-product of cigarette, cigar, and waterpipe (hookah) smoking. Together with other gases, such as cyanides, sulfur oxides, and nitrogen oxides, it is an ingredient of fire smoke. CO binds to hemoglobin with a 200 to 250-fold higher affinity than oxygen. Carboxyhemoglobin (COHb) has no oxygen-carrying capacity, thus causing tissue hypoxia. In addition, CO can bind to cytochrome c oxidase and impair electron transport in the respiratory chain, leading to the production of free radicals and damage to cell membrane structures. CO toxicity can also activate platelet aggregation and stimulate myeloperoxidase release from neutrophils, causing worsening of inflammation and neurologic sequelae. The lethal dose depends on CO concentration in inhaled air, time of exposure, and respiratory activity (toxin uptake). A concentration of 1000 ppm (0.1%) is life threatening, while a concentration of 1500 ppm (0.15%) rapidly leads to death. Although severity does not always correlate with COHb levels, levels >50% are associated with increased risk of death.

Clinical Features and DiagnosisTop

1. Signs and symptoms of acute poisoning: Headache (the most frequent symptom), dizziness, nausea, vomiting, impaired balance, disorientation, weakness, fatigue, tachycardia, arrhythmia, hypotension, impaired mental status up to coma, seizures; features of myocardial ischemia (also in persons with no history of prior coronary artery disease); usually pale, cyanotic skin (cherry-red skin is only seen postmortem or in patients with the most severe poisoning).

2. Diagnostic tests:

1) Pulse oximetry is of limited use, as COHb and oxyhemoglobin have similar optical properties. COHb fraction must be measured by co-oximetry with either venous or arterial blood. Typically, significant COHb values are >5% for nonsmokers and >10% for smokers. Consider the time since removing the patient from the contaminated area and application of oxygen when interpreting COHb levels.

2) Other tests that may help with prognosis or suggest tissue injury:

a) Perform a pregnancy test in females of child-bearing age.

b) Consider checking serum electrolytes, lactate, and blood gases (anion gap metabolic acidosis), BUN, creatinine, and glucose levels.

c) Consider electrocardiographic monitoring for ST segment changes or arrhythmia (measure the concentration of biochemical markers of myocardial injury in patients with features of myocardial ischemia and those with a history of heart disease).

d) Consider chest radiography if the patient has dyspnea or was in housefire.

e) Consider neuropsychologic examination (and electroencephalography [EEG], computed tomography [CT], or magnetic resonance imaging [MRI] as indicated by physical examination and laboratory test results).


1. Stop the exposure and make sure the exposed individuals are safe: Ventilate the room and shut off the gas supply to the burner/heater. Remove the person from the contaminated atmosphere. If the person breathes spontaneously, place them in the recovery position (see Cardiac Arrest) and protect from hypothermia. Intubation may be required.

2. Antidote: Oxygen. Start mild hyperbaric oxygen therapy (irrespective of hemoglobin oxygen saturation in arterial blood [SpO2]) immediately on any suspicion of CO poisoning in a prehospital setting (administration of oxygen through a mask with a reservoir bag [see Oxygen Therapy]) and continue in the hospital with laboratory parameter monitoring (arterial blood gas analysis, serum lactate levels, blood COHb levels). The half-life of COHb is 4 to 6 hours on room air, but it is as short as 40 to 80 minutes on 100% oxygen delivered by nonrebreather mask. In patients with respiratory insufficiency, start mechanical ventilation using 100% oxygen.

Hyperbaric oxygenation (HBO) can reduce the half-life of COHb to as low as 30 minutes, but the clinical data on its use are of low qualityEvidence 1Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to imprecision and heterogeneity). Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. 2011 Apr 13;2011(4):CD002041. doi: 10.1002/14651858.CD002041.pub3. PMID: 21491385; PMCID: PMC7066484. and there is no evidence to suggest routine use of HBO for nonpregnant patients with CO poisoning. Neither the American Academy of Clinical Toxicology nor the American College of Medical Toxicology have published guidelines on the use of HBO for CO poisoning. In patients with severe neurologic or cardiac symptoms, persistent acidosis and no clinical improvement despite normobaric oxygen therapy, consider hyperbaric oxygen therapy (HBOT) provided that transport to a hyperbaric chamber does not pose additional risk to the patient’s life. Thresholds suggested for use in nonpregnant patients range between >25% and 40% while accounting for clinical presentation and availability. Because fetal hemoglobin binds CO with greater affinity, HBOT should be considered for pregnant women with a COHb level >20%. HBOT >24 hours from intoxication is not suggested.

3. Symptomatic treatment: Maintain vital functions and correct abnormalities.

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