Acute exogenous poisoning with carbon monoxide
CO is most commonly from car exhausts, faulty heaters, fires and industrial accidents. CO binds to haemoglobin at the oxygen binding sites with greater affinity, to form carboxyhemoglobin (COHb). Its affinity is such that even at very low concentrations there can be severe affect. The main route of toxicity is through the lungs, where it is also excreted .
As CO binds to the haemoglobin it reduces the oxygen carrying capacity of the blood leading to tissue hypoxia when compensatory mechanisms fail. CO also inhibits mitochondrial cytochrome oxidase, thereby directly inhibiting aerobic metabolism (similar to cyanide). The most heavily affected organs are the heart and the brain, and this is where the primary symptoms present. Clinical effects being at COHb concentrations <40%, with tachycardia, headache, breathlessness, confusion, weakness, nausea and vomiting at low levels. As the COHb % increases, symptoms such as CNS (coma, convulsions) and cardiac (arrhythmias, angina) develop. When concentrations exceed 70%, death is likely.
On initial examination the best method for assessment of toxicity is the symptoms (as COHb takes time to get back from the lab), if the patient was found unconscious you can assume >50% COHb. Always look for ischaemic damage of tissues (ECG, neurological exam, troponin and lactate).
Management is 100% oxygen ASAP, performs for 4-6 hours and this will remove over 90% of the CO. Treat acidosis if severe, but not routinely, it should sort itself as you sort out the % of COHb. Treat any ischemic changes to the organs (e.g. cardiac ischaemia).