Carbon Monoxide: The Silent Asphyxiant

Where the gas comes from

Carbon monoxide is the product of incomplete combustion — burning fuel without enough oxygen. Whenever a carbon-based fuel burns cleanly it makes carbon dioxide; when it burns starved of air, it makes carbon monoxide instead. That is why the classic sources are faulty or unventilated appliances — gas boilers and water heaters with blocked flues, paraffin and charcoal stoves used indoors, and portable generators run in enclosed spaces. Add house fires (smoke is thick with it), car exhaust in a closed garage, and, in some countries, water heaters vented into bathrooms. One more source hides in plain sight in the toxicology curriculum: methylene chloride (dichloromethane), a paint stripper solvent, is absorbed and then metabolised by the liver into carbon monoxide, producing a delayed, prolonged poisoning hours after the exposure. It is, worldwide, the single commonest cause of fatal poisoning — and much of that toll is unintentional and preventable.

The mechanism: a triple assault on oxygen

Carbon monoxide poisons oxygen delivery at three points at once, which is why so little of it does so much harm. First and most importantly, it competes with oxygen for the same binding sites on haemoglobin — but it binds with roughly 250 times the affinity of oxygen. So even tiny concentrations of the gas capture a large share of the haemoglobin, forming carboxyhaemoglobin (COHb), which can no longer carry oxygen. That alone reduces the blood's oxygen-carrying capacity. But it does something subtler and nastier: where carbon monoxide binds one of haemoglobin's four sites, it distorts the molecule so that the remaining oxygen-loaded sites cling to their oxygen more tightly. This shifts the oxygen dissociation curve to the left — the very curve taught in the Haematology section — meaning the oxygen that is still on board is not released to the tissues where it is needed. Reduced carrying capacity plus impaired offloading is a far deadlier combination than either alone: an equivalent degree of anaemia would be much better tolerated. Finally, carbon monoxide does not stop at the blood. It diffuses into cells and binds myoglobin in cardiac and skeletal muscle (weakening the heart) and cytochrome c oxidase in the mitochondria, stalling the electron transport chain. The result is cellular hypoxia — the tissues cannot get oxygen, and cannot use what little arrives.

The clinical picture: the great mimic

The symptoms are notoriously non-specific, and the organs that suffer first are the ones most greedy for oxygen: the brain and the heart. Early poisoning looks exactly like a viral illness — headache (often the first and most consistent symptom), nausea, malaise, dizziness and poor concentration. This is why carbon monoxide is one of the most under-diagnosed poisonings in medicine: it is mistaken for flu, migraine, food poisoning or simple fatigue. As levels climb, confusion, drowsiness, breathlessness on exertion, chest pain and blurred vision appear, progressing to syncope, seizures, cardiac arrhythmia, myocardial ischaemia, coma and death. Two clues cut through the fog. First, the epidemiological pattern: several people in the same building falling ill together, symptoms that worsen at home and ease when they go outside, and a seasonal spike in cold weather when heating is on and windows are shut — even pets can be affected. Second, and worth stating plainly because exams love to test the myth: the classic "cherry-red" skin is rare, unreliable and usually a late or post-mortem finding — never wait for it, and never exclude the diagnosis by its absence. Most poisoned patients simply look pale or normal.

The diagnostic trap: why your monitors lie

This is the single most important — and most tested — point about carbon monoxide. A standard pulse oximeter shines light through the finger and estimates saturation from how much red light the blood absorbs. The catch is that carboxyhaemoglobin absorbs light almost identically to oxyhaemoglobin — so the oximeter cannot tell them apart and counts the COHb as though it were fully oxygenated haemoglobin. The reading comes back falsely normal, or even high, in a patient who is profoundly poisoned. The arterial blood gas is just as treacherous: it measures the oxygen dissolved in plasma (the PaO2), which is entirely normal, because the problem is not how much oxygen reaches the plasma — it is that the haemoglobin cannot carry or release it. A normal SpO2 and a normal PaO2 in a symptomatic patient are exactly what you would expect in carbon monoxide poisoning, and they are the trap that sends poisoned families home. The only way to see the truth is to measure the carboxyhaemoglobin level directly with a co-oximeter (on a blood gas sample) or a specialised pulse CO-oximeter. This sits alongside two sibling poisonings from the same corner of the curriculum: cyanide (which poisons cytochrome oxidase) and methaemoglobinaemia (which oxidises the iron in haemoglobin) — all three share the paradox of a normal PaO2 with genuine tissue hypoxia, and all three are covered in their own chapters. Note that COHb levels correlate only loosely with severity; treat the patient and the clinical picture, not the number alone.

Management: oxygen is the antidote

The principles are simple and the priorities are fixed. Remove the patient from the source (and protect rescuers — a room that poisoned one person will poison the next). Secure the airway and support breathing and circulation as always. Then give high-flow 100% oxygen through a non-rebreather mask, or via the ventilator in the unconscious patient, and continue it — this is the oxygen therapy principle developed in the Respiratory section, applied at maximum. The debated question is when to escalate to hyperbaric oxygen. The accepted indications, though the evidence is genuinely contested, are the markers of severe poisoning: any loss of consciousness, neurological signs or confusion, evidence of cardiac ischaemia or arrhythmia, a very high COHb level (often quoted around >25%, or lower in specific groups), and pregnancy. Hyperbaric therapy clears carbon monoxide fastest and, in several trials, reduces the rate of delayed neuropsychiatric sequelae — the reason it is offered despite the controversy — but it is logistically demanding and not available everywhere, so high-flow normobaric oxygen remains the universal backbone. Alongside oxygen, correct acidosis cautiously, treat seizures and arrhythmias, and monitor cardiac enzymes and the ECG, because the heart is a frequent silent casualty.