Carbon monoxide, a colorless and odorless gas, can be potentially fatal after exposure if not properly diagnosed and treated. Carbon monoxide poisoning is associated with:
Carbon monoxide has several pathophysiological consequences on oxygen transport and utilization:
In addition to a history consistent with CO exposure, patients with mild CO poisoning present with:
Patients severely exposed to carbon monoxide typically present with:
Physical exam signs of carbon monoxide toxicity may include:
The diagnosis of carbon monoxide poisoning is dependent upon:
Following the diagnosis of carbon monoxide poisoning, an electrocardiogram is recommended to detect for ischemia as myocardial infarction is a common complication.
Carboxyhemoglobin shifts the oxygen dissociation curve to the left, impairing the ability of heme to unload oxygen at the tissue level. This results in tissue hypoxia. The kidney responds to tissue hypoxia by producing more erythropoietin (EPO). EPO stimulates the bone marrow to differentiate more red blood cells. Chronic CO toxicity is a cause of secondary polycythemia.
Chronic tobacco smokers may have up to 15% carboxyhemoglobin at baseline.
Carbon monoxide saturation levels above 40% is considered to be severe exposure, whereas levels above 55% can potentially be fatal.
The management of carbon monoxide poisoning includes: