The cornerstone of treatment for CO poisoning is supplemental oxygen that should be initiated as soon as possible and continued throughout treatment. CT of the head is not required however, CO poisoning can manifest as globus pallidus hemorrhage, therefore, it may be useful. Chest radiographs should be ordered as well. New ischemia on ECG is indicative of severe CO poisoning. Other assessments such as a complete blood count (CBC), electrolytes, BUN, creatinine level, and baseline troponin should be assessed. ECG should be checked for any signs of ischemia. ![]() The take-home point is to treat the patient, not the number. It is agreed that levels greater than 20 in adults indicate a significant poisoning, and levels greater than 15 in children are considered significant. COHb levels above 3% to 4% in non-smokers and 10% in smokers are typically considered outside of normal limits. This number should not be the foundation upon which the treatment plan is built however because COHgB levels are loosely associated with symptoms, and there is no direct correlation between COHgb levels and the severity of the symptoms or the risk of mortality and morbidity. The carboxyhemoglobin level is reported in this analysis. Typically, an arterial blood gas sample with a co-oximetry analysis is the most useful initial step. It is important to note that standard peripheral pulse oximeter devices cannot differentiate COHb from oxyhemoglobin and hence oxygen saturation (SpO2) will not show any abnormalities on the monitor. Supplemental oxygen is the cornerstone of treatment. The standard ABCs (airway, breathing, and circulation) apply to CO-poisoned patients as well. ![]() The overall cause of death for most animals poisoned by CO is combined hypoxia and ischemia during the acute event. There is evidence that myocardial impairment begins at the relatively low level of COHgb of 20%. Ventricular arrhythmias are implicated as the cause of death most often in CO poisoning. Cardiac effects, especially ventricular arrhythmias occur. If exposure continues, central respiratory depression develops which may result from cerebral hypoxia. As carboxyhemoglobin (COHgb) levels rise, the cerebral blood vessels dilate, and both coronary blood flow and capillary density increase. The CO causes capillary leakage of macromolecules from the lungs and systemic vasculature, and this can occur in humans who have been exposed to relatively low concentrations of CO for prolonged periods. Elsewhere in the body, CO is delivered by hemoglobin. ![]() Direct interactions may damage the lung parenchyma without the need for delivery of blood-borne hemoglobin.
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