Clinical meaning
Carbon monoxide (CO) binds hemoglobin with 200-250x greater affinity than oxygen, forming carboxyhemoglobin (COHb). This displaces oxygen from heme binding sites and causes a left shift of the oxyhemoglobin dissociation curve, impairing oxygen release to tissues. CO also binds myoglobin (causing cardiac dysfunction) and mitochondrial cytochrome c oxidase (blocking oxidative phosphorylation). The resulting cellular hypoxia triggers anaerobic metabolism with lactic acidosis. Inflammatory cascades from CO-induced oxidative stress cause lipid peroxidation in the CNS, contributing to delayed neurological sequelae (DNS) appearing 2-40 days post-exposure.
Diagnosis & workup
Diagnostics & workup: - CO-oximetry (gold standard): measures COHb directly; venous sample acceptable; normal non-smoker <3%, smoker <10% - ABG: PaO2 is often NORMAL (measures dissolved O2, not Hb-bound); evaluate for metabolic acidosis and elevated lactate - Serum lactate: elevated from anaerobic metabolism; disproportionately high lactate suggests concurrent cyanide toxicity - Troponin and 12-lead ECG: assess for myocardial injury; CO causes direct cardiac toxicity with ST changes and arrhythmias - Standard pulse oximetry is UNRELIABLE: cannot distinguish COHb from oxyhemoglobin; will read falsely normal - Neuropsychological testing: baseline and follow-up at 1 and 6 months to detect delayed neurological sequelae