Carbon monoxide (CO) poisoning
Carbon monoxide is a colourless, odourless gas produced by incomplete combustion of hydrocarbon fuels (vehicle exhausts, poorly ventilated boilers, cooking appliances, portable generators, some industrial chemicals). In the UK there are several dozen accidental CO deaths each year with additional morbidity from acute and delayed neurological injury (Department of Health / UKHSA).
Mechanism and kinetics
CO binds haem‑containing proteins (haemoglobin, myoglobin, cytochromes), forming carboxyhaemoglobin (COHb). Its affinity for haemoglobin is very high (≈245× that of O2), causing a left shift of the oxygen-haemoglobin dissociation curve and impaired oxygen delivery. CO also interferes with cellular respiration via binding to myoglobin and mitochondrial cytochromes.
Elimination half‑lives (approximate) inform therapy:
- Room air: ≈320 minutes
- 100% oxygen (normobaric): ≈80 minutes
- Hyperbaric oxygen (typical treatment pressures): ≈20-30 minutes (≈23 min reported)
These kinetics underpin immediate high‑flow oxygen and the theoretical rationale for hyperbaric oxygen therapy (HBOT) in selected cases (UKHSA).
Clinical features
Presentation ranges from nonspecific symptoms to life‑threatening organ failure. Mild, early or chronic exposure commonly causes headache, nausea or vomiting, dizziness or vertigo, malaise, weakness and confusion. Severe poisoning can produce syncope, seizures, arrhythmia or myocardial ischaemia, focal neurological signs, coma and death.
Delayed neuropsychiatric sequelae (DNS) may develop days to weeks after apparent recovery. Pregnancy carries higher fetal risk because fetal haemoglobin and placental transfer prolong fetal exposure.