What is the pathophysiology of CO poisoning?
CO is absorbed via the lungs and binds with haemoglobin; it binds 200-300 times more than oxygen.
The presence of COHb leads to a left shift in the oxygen dissociation curve, resulting in tissue hypoxia and therefore increasing serum lactate levels.
It is also hypothesised that CO has some direct negative effects on cells within the body; impairing the respiratory function of cells due to the binding of CO to hemeproteins. This leads to permanent mitochondrial damage, especially in cells of the heart and central nervous system.
CO also binds to cardiac myoglobin causes depression of the cardiovascular system.
Normal CO levels are anywhere between 0-3%, however it is often elevated within smokers to up to 10%.
Regarding the clinical significance of CO within the blood, it becomes difficult to use this marker to predict clinical picture as this is often dependent of the length of exposure and the amount of CO which has permeated into the tissues. Physiological reserve, amount of Hb and length of exposure are likely to contribute to severity of presentation. However, general consensus is that COHb of over 25% and/or features such as altered consciousness dictate severe poisoning.
Often when patients first present, they may have been receiving high flow oxygen which will decrease the percentage of Carboxyhemoglobin in their blood with time.