Clinical meaning
Carbon monoxide (CO) is a colorless, odorless, tasteless gas produced by the incomplete combustion of carbon-containing fuels (natural gas, gasoline, wood, charcoal, propane). CO exerts its toxic effects through multiple cellular mechanisms that impair oxygen delivery and utilization at the tissue level. The primary mechanism involves CO binding to hemoglobin with an affinity approximately 200-250 times greater than oxygen, forming carboxyhemoglobin (COHb). This binding occurs at the same site on the hemoglobin molecule where oxygen normally attaches (the iron center of the heme group). When CO occupies one or more of the four heme binding sites, it causes a conformational change in the hemoglobin molecule that increases the affinity of the remaining heme groups for oxygen. This is known as the left shift of the oxyhemoglobin dissociation curve, meaning that hemoglobin holds onto oxygen more tightly and releases it less readily to the tissues. The result is a dual insult: reduced oxygen-carrying capacity (because CO-occupied sites cannot carry oxygen) and impaired oxygen release at the cellular level (because the remaining oxygen is bound too tightly). CO also binds to myoglobin in cardiac and skeletal muscle with high affinity, directly impairing muscle oxygen storage and contributing to cardiac dysfunction and rhabdomyolysis. At the mitochondrial level, CO binds to cytochrome c oxidase (Complex IV of the electron transport chain), disrupting oxidative phosphorylation and ATP production. This causes a shift to anaerobic metabolism, resulting in lactic acid accumulation and metabolic acidosis. CO also triggers inflammatory cascades by activating neutrophils and promoting lipid peroxidation in the brain, which contributes to delayed neurological sequelae (DNS) that can appear days to weeks after apparent recovery. Carboxyhemoglobin levels correlate roughly with severity: non-smokers have baseline COHb of less than 3%, smokers up to 10%; symptoms typically begin at 10-20% (headache, dizziness), moderate toxicity at 20-40% (confusion, syncope, tachycardia), severe toxicity at 40-60% (seizures, coma, cardiac arrhythmias), and levels above 60% are often fatal. Standard pulse oximetry is UNRELIABLE in CO poisoning because the device cannot differentiate between oxyhemoglobin and carboxyhemoglobin, often displaying falsely normal SpO2 readings. CO-oximetry, which uses multiple wavelengths of light, is required for accurate measurement.