Carbon Monoxide Poisoning
Explore 5-Minute Clinical Consult - view these FREE monographs:
-- The first section of this topic is shown below --
- Carbon monoxide (CO) is a leading cause of poisoning death in the US (1). CO is an odorless, tasteless, colorless gas produced by combustion of carbon-containing compounds (wood, charcoal, oil, gas):
- CO inhalation leads to displacement of oxygen from binding sites on hemoglobin.
- Detrimental effects are related to tissue hypoxia from decreased oxygen content and a shift of the oxyhemoglobin dissociation curve to the left.
- CO also binds to mitochondrial cytochrome oxidase, impairing adenosine triphosphate (ATP) production, and to myoglobin, affecting muscle function.
- System(s) affected: Cardiovascular; Musculoskeletal; Nervous
Tissue hypoxia includes the fetus. CO poisoning may cause significant fetal abnormalities, depending on the developmental stage. Adult hemoglobin holds oxygen less tightly than does fetal hemoglobin. Therefore, a pregnant mother potentially may be unaffected while the fetus is affected.
- Roughly 40,000 emergency department visits annually (2)
- 5,000–6,000 deaths annually in the US
- Unintentional CO poisoning likely causes 450 deaths annually.
- Intentional CO poisoning is ~10 times higher.
- Unintended poisoning is most common during winter months in cold climates, but can also occur in warm climates with use of generators, boats, etc.
- Likely markedly underdiagnosed because of vague symptoms.
- Smoke inhalation
- Being in a closed or improperly ventilated space with a faulty furnace or stove or running engine or any fuel-burning device.
- Cigarette smoking
- Extremes of age (3)
- Cardiovascular disease, anemia, chronic respiratory conditions (3)
- Exposure to exhaust (riding in the back of enclosed pickup trucks or swimming near a motor boat)
- Employment in a coal mine, as an auto mechanic, paint stripper, or in the solvent industry
- Appropriate ventilation, especially where there are fuel-burning devices
- Use of CO monitors
- Public education
- Determining the mechanism of exposure is critical in cases of accidental poisoning in order to limit future risk.
- Victims must not be discharged back to a contaminated environment.
- CO is rapidly absorbed in lungs.
- CO has ~220 times the affinity for hemoglobin that oxygen has.
- CO binds to hemoglobin to form carboxyhemoglobin (COHb), resulting in impaired oxygen-carrying capacity, utilization, and delivery:
- Leftward shift of the oxyhemoglobin dissociation curve occurs.
- CO interferes with peripheral oxygen utilization by inactivating cytochrome oxidase.
- Delayed neurologic sequelae, probably due to lipid peroxidation by toxic oxygen species generated by xanthine oxidase.
- The half-life of CO while the patient is breathing room air is ~300 minutes, while breathing 100% oxygen via a tight-fitting, nonrebreathing face mask is ~60 minutes, and with 100% hyperbaric oxygen is ~20 minutes.
- CO exposure also causes inflammation through separate pathways than those that cause cardiac and neurologic sequalae (4).
- CO inhalation
- Inhaled or ingested methylene chloride (from paint remover [dichloromethane]) is metabolized to CO by the liver, causing CO toxicity in the absence of ambient CO.
Commonly Associated Conditions
- CO and cyanide poisoning can occur simultaneously following smoke inhalation (synergistic effect).
- Consider CO poisoning in a burn victim who has been in an enclosed space.