Carbon Monoxide Poisoning: Why the Pulse Oximeter Lies

Carbon monoxide is colourless, odourless and non-irritant, which is exactly why it kills whole families overnight. In examinations it is a favourite because a single physiological fact — its affinity for haemoglobin — explains almost every feature.

At a glance

Mechanism

Carbon monoxide binds haemoglobin to form carboxyhaemoglobin, reducing the oxygen-carrying capacity of blood. Worse, it shifts the oxyhaemoglobin dissociation curve to the left, so the oxygen that is still bound is released less readily to tissues. It also binds myoglobin, impairing cardiac and skeletal muscle function, and inhibits cytochrome c oxidase, producing histotoxic hypoxia that persists after carboxyhaemoglobin has cleared.

Clinical features

• Mild: headache (the earliest and commonest), nausea, dizziness, fatigue — frequently misdiagnosed as viral illness or food poisoning. A clue is that several people in one household are ill at once, and that symptoms improve when they leave the building.
• Moderate: confusion, ataxia, visual disturbance, chest pain, breathlessness.
• Severe: syncope, seizures, coma, myocardial ischaemia, lactic acidosis, rhabdomyolysis, death.
• Delayed neuropsychiatric sequelae appear from 2 to 40 days after apparent recovery: memory impairment, personality change, parkinsonism, incontinence. Basal ganglia — especially the globus pallidus — are characteristically affected.

Cherry-red discolouration of skin and mucosae is the classical answer, but in life it is uncommon and unreliable; it is far more consistently seen at autopsy, where it is a genuinely useful finding along with cherry-red hypostasis.

Diagnosis

Standard pulse oximetry is falsely normal or high, because it cannot distinguish carboxyhaemoglobin from oxyhaemoglobin. Arterial blood gas PaO₂ is also normal, since dissolved oxygen is unaffected. You need CO-oximetry to measure carboxyhaemoglobin directly. Interpret the level alongside symptoms and time since removal from exposure — a low level in a patient who has been on oxygen for an hour does not exclude serious poisoning.

Management

1. Remove from the source; ensure rescuer safety.
2. 100% oxygen by tight non-rebreather mask, or via the ventilator if intubated, continued until symptoms resolve and the level normalises. The elimination half-life of carboxyhaemoglobin falls from roughly 4–5 hours on room air to about an hour on high-flow oxygen, and to around 20–30 minutes under hyperbaric conditions.
3. Consider hyperbaric oxygen for loss of consciousness, neurological signs, cardiac ischaemia, severe metabolic acidosis, a markedly raised carboxyhaemoglobin level, or pregnancy. The evidence for reducing delayed neuropsychiatric sequelae is debated, but these are the accepted indications.
4. Pregnancy deserves a lower threshold: fetal haemoglobin binds carbon monoxide more avidly and clears it more slowly than maternal blood.
5. Follow up for delayed neuropsychiatric effects and arrange formal cognitive assessment where indicated.

Last-minute checklist

• Pulse oximetry is useless; use CO-oximetry.
• Leftward shift means tissues get less oxygen than the numbers suggest.
• Headache first; whole household affected is the giveaway.
• Cherry-red is an autopsy sign, not a bedside one.
• Delayed sequelae up to six weeks later.

Frequently asked questions

Why does the pulse oximeter read normal in carbon monoxide poisoning?

Conventional two-wavelength oximeters cannot distinguish carboxyhaemoglobin from oxyhaemoglobin because the two absorb light similarly at the wavelengths used, so the device reports a falsely reassuring saturation.

Why is a leftward shift of the dissociation curve harmful here?

It increases haemoglobin’s affinity for the oxygen it is still carrying, so less is unloaded at the tissues. The patient suffers a double hit: less oxygen carried, and less of it delivered.

Why does pregnancy lower the threshold for treatment?

Fetal haemoglobin binds carbon monoxide with greater affinity and eliminates it more slowly, so fetal levels lag behind and remain elevated after the mother’s have fallen.

References

• Harrison’s Principles of Internal Medicine — carbon monoxide poisoning.
• Reddy KSN. The Essentials of Forensic Medicine and Toxicology.
• Guyton & Hall, Textbook of Medical Physiology — oxygen transport.