Carbon monoxide poisoning and the left shift
Carbon monoxide makes tissues hypoxic (short of oxygen) because haemoglobin holds on to its oxygen, despite a normal arterial oxygen tension (the pressure of oxygen dissolved in arterial blood).
Remember
Carbon monoxide blocks the part of haemoglobin it binds and makes the rest of the molecule hold oxygen more tightly, so oxygen is poorly released at the tissues despite a normal PaO2 (the pressure of oxygen dissolved in arterial blood).
Memory aid
Carbon monoxide clings on to haemoglobin, and the oxygen left on the molecule clings on too.
Carbon monoxide clings on to haemoglobin and the oxygen left on the molecule clings on too, so oxygen is poorly released at the tissues.
Carbon monoxide (CO) is a colourless, odourless gas produced by incomplete burning. House fires are a classic source, and faulty gas heaters produce it too.
CO binds to the same sites on haemoglobin as oxygen does, but about 200 to 250 times more tightly, forming carboxyhaemoglobin (haemoglobin carrying carbon monoxide). A subunit holding CO is blocked, so it cannot carry oxygen.
The effect does not stop there. Haemoglobin is cooperative, which means its four subunits influence one another. Once one subunit holds CO, the unoccupied subunits bind oxygen more tightly and hold on to it. The oxygen dissociation curve of haemoglobin (how saturated haemoglobin is with oxygen at each oxygen pressure) therefore shifts to the left. This shows an increased affinity for oxygen (oxygen is bound more tightly) and a reduced P50 (the oxygen pressure at which haemoglobin is half saturated). Oxygen is poorly released at the tissues, so they become hypoxic, and typical features are dizziness, tiredness and, when severe, unconsciousness.
Arterial oxygen tension (PaO2) reflects the oxygen dissolved in plasma, which is only about 1.5% of the oxygen in blood, and CO does not change it. So PaO2 can be entirely normal while the tissues are starved of oxygen. A standard pulse oximeter (the probe that reads oxygen saturation) also cannot tell carboxyhaemoglobin from oxyhaemoglobin, so its reading may be falsely reassuring and blood co-oximetry (a blood test that can tell the two apart) is needed to make the diagnosis. Early high-flow oxygen is essential.
Key facts
- Binding
- carbon monoxide takes the same sites on haemoglobin as oxygen, about 200 to 250 times more tightly, forming carboxyhaemoglobin
- Blocked sites
- a subunit holding carbon monoxide cannot carry oxygen
- Cooperativity
- the remaining subunits shift to a high-affinity form and hold on to oxygen
- Curve
- the oxygen dissociation curve shifts to the left and the P50 falls, so oxygen is poorly released at the tissues
- Dissolved oxygen
- it is unchanged, so the measured arterial oxygen value can look normal while the patient is severely hypoxic
- Detection
- a standard pulse oximeter cannot tell carboxyhaemoglobin from oxyhaemoglobin, so blood co-oximetry is needed
- Severity
- how ill someone is correlates poorly with the carboxyhaemoglobin level
Exam traps
- Carbon monoxide does not stop haemoglobin being made, because it changes how existing haemoglobin behaves, so the total haemoglobin concentration is normal at first.
- Competing with oxygen for the same binding sites does not make the oxygen dissociation curve shift to the right, because carbon monoxide shifts it to the left by raising the affinity of the remaining subunits.
- Poor diffusion of oxygen across the lung membrane would lower the arterial oxygen partial pressure, which is normal or near normal in carbon monoxide poisoning, because carbon monoxide acts on haemoglobin in the blood rather than on the lung membrane.
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