Carbon Monoxide Poisoning
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- Carbon monoxide (CO) is an odorless, tasteless, colorless gas that has the potential to cause sudden illness and death if inhaled.
- CO is 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 (left) shift of the oxyhemoglobin dissociation curve that impairs oxygen unloading from hemoglobin.
- CO binds to mitochondrial cytochrome oxidase, impairing adenosine triphosphate (ATP) production. It also binds to myoglobin, affecting muscle function.
- System(s) affected: cardiovascular, pulmonary, musculoskeletal, nervous
Tissue hypoxia due to CO poisoning may cause significant fetal abnormalities. CO has a greater affinity for (and longer half-life bound to) fetal hemoglobin. A pregnant mother may be unaffected, whereas the fetus is adversely impacted.
Third leading cause of unintentional poisoning deaths in the United States with an average 438 deaths annually
- ~50,000 emergency department visits annually
- Unintentional poisoning is most common during winter months in cold climates.
- Intentional CO poisoning ~10 times higher than unintentional poisonings
- Likely underdiagnosed because some patients may not seek medical attention due to vague symptoms
Etiology and Pathophysiology
- CO is rapidly absorbed in lungs.
- CO has ~240 times the affinity for hemoglobin compared to oxygen.
- CO binds to hemoglobin to form carboxyhemoglobin (COHb), resulting in impaired oxygen-carrying capacity, utilization, and delivery:
- CO interferes with peripheral oxygen utilization by inactivating cytochrome oxidase.
- Delayed neurologic sequelae, related to lipid peroxidation by toxic oxygen species generated by xanthine oxidase
- The half-life of CO on room air is ~320 minutes, whereas breathing 100% oxygen via a tight-fitting, nonrebreathing face mask decreases to ~74 minutes. With 100% hyperbaric oxygen, T1\2 is ~30 minutes (1).
- CO can promote nitric oxide release causing profound hypotension.
- CO affects L-type myocardial calcium channels causing myocardial depression.
- Inhaled or ingested methylene chloride (from paint remover [dichloromethane]) is metabolized to CO by the liver, potentially resulting in acute CO toxicity.
- Alcohol use; smoking
- Elderly and infants at higher risk if exposed
- Closed or improperly ventilated space with faulty furnace, stove, engine, or other fuel-burning device
- Cigarette smoking
- Use of generators during power outages and storms
- Underlying cardiovascular disease, anemia, chronic respiratory conditions
- Exposure to exhaust (e.g., riding in the back of enclosed pickup trucks or swimming near a motor boat) in precatalytic converter era automobiles
- Employment in a coal mine, as an auto mechanic, paint stripper, or in the solvent industry
- Increased endogenous production in patients with hemolytic anemia
- Appropriate ventilation, especially around fuel-burning devices
- Use of CO monitors
- Determining the mechanism of exposure is critical in cases of accidental poisoning helps limit future risk.
- Victims must not return to contaminated environment.
- Regular building maintenance to ensure safe environment and adequate ventilation
- Public policy to ensure building code safety
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.