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Carbon Monoxide Toxicity in Anesthesia — Cooximetry, HBO Indications
TEXTCrisis Management · 6 min read
Volatile anesthetic + desiccated CO₂ absorbent produces carbon monoxide — the Monday-morning first case is the classic setup. SpO₂ reads falsely normal, the patient is poisoned.
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2 min read6 sectionsSources of CO in the anesthesia environment
Worst offender: desflurane > enflurane > isoflurane >> sevoflurane (which preferentially makes Compound A instead). 'Monday-morning first case' classic — fresh-gas flow left on over weekend desiccates the absorbent canister, first case of week induces with desflurane CO production peaks.
- smoke inhalation (house fire victim, industrial exposure)
- faulty heating
- methylene chloride (paint stripper, metabolized to CO endogenously)
- suicide attempts
Pathophysiology
Worse: COHb left-shifts the dissociation curve of remaining normal Hb, so the unaffected fraction releases LESS O₂ to tissues at any given PaO₂.
CO also binds cytochrome a3 in mitochondria, directly inhibiting cellular respiration.
CNS + cardiac most vulnerable (highest O₂ demand).
Normal COHb: <2% non-smoker, up to 10% heavy smoker.
- 15-25% mild (headache, nausea)
- 25-40% moderate (confusion, dyspnea)
- >40% severe (seizures, coma, death)
SpO₂ trap + cooximetry
Mechanism: COHb and O₂Hb have similar absorbance at 660 nm (the red channel), so the pulse ox cannot distinguish them.
A patient with 30% COHb + 70% O₂Hb may show SpO₂ 100%.
Co-oximetry on a blood gas separately measures O₂Hb, deoxyHb, COHb, and MetHb at four wavelengths — this is the diagnostic test.
Newer pulse ox devices (Masimo Rad-57 with multiple wavelengths) measure SpCO non-invasively but are not standard on every machine.
Clinical recognition
Cardiac: ischemia even in patients without CAD (demand-supply mismatch).
Pregnancy: fetal Hb has higher CO affinity than adult Hb — fetal toxicity at lower maternal levels.
Delayed neurological sequelae (cognitive impairment, parkinsonism, demyelination) appear days-weeks after exposure in ~30% of severe cases.
Treatment — 100% O₂ + hyperbaric indications
- 4-6 hours on room air
- 60-90 minutes on 100% normobaric O₂
- 20-30 minutes on hyperbaric O₂ at 2.5-3 atm
Continue normobaric O₂ until COHb <5% AND symptoms resolved.
Hyperbaric O₂ indications (HBO consensus): loss of consciousness at any point, neurological deficit (cognitive, focal), cardiac ischemia/arrhythmia, COHb >25% (>20% in pregnancy or any level with fetal distress), persistent symptoms despite normobaric O₂, age >36 with longer exposure.
HBO protocol: 2.5-3 ATA × 90 minutes, often repeated.
Hyperbaric O₂ reduces delayed neurological sequelae (Weaver NEJM 2002).
Prevention in the OR
If the canister has been bypassed/dry for unknown duration, replace before the next case.
Modern absorbents (Amsorb Plus, Drägersorb 800+, lithium hydroxide-based) lack the strong bases (NaOH/KOH) needed for CO production + are color-changing when desiccated.
Switching from baralyme (now off-market for this reason) to modern hydrophilic absorbents has nearly eliminated machine-generated CO.
Sevoflurane Compound A risk still warrants fresh gas flows >2 L/min for long sevo cases per FDA labeling.
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