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Carbon Monoxide

Carbon monoxide (CO) poisoning is the most common form of unintentional poisoning. CO induces toxic effects by tightly binding to hemoglobin to form carboxyhemoglobin (COHb) and reducing the oxygen carrying capacity of red blood cells. It also interferes with cellular respiration by binding to mitochondrial cytochrome oxidase. CO poisoning may be misdiagnosed as an acute self-limited illness because its early symptoms are nonspecific (headache, dizziness, weakness, and confusion). The diagnosis is confirmed by detecting increased COHb % saturation in either venous or arterial blood.

Endogenous heme catabolism in the absence of environmental exposure results in COHb levels below 1%. Most nonsmoking urban dwellers have COHb saturations of <3%, whereas most smokers have chronic saturations of 3 to 10%. COHb levels >3% in a nonsmoker suggest exogenous CO exposure or cryptic smoking. COHb levels >10% in urban smokers should be investigated for other potential sources of CO exposure. The clinical severity of CO poisoning correlates poorly with CO saturation and is determined by four factors: concentration of CO in the environment, duration of exposure, activity level of the exposed, and interval between exposure and clinical assessment. A brief intense exposure may give COHb levels >50% with minimal symptoms, while other patients may become comatose with COHb levels of 20%.In general, exposure to CO concentrations of 105 to 205 ppm for 1 to 2 hours produces COHb levels of 10 to 20%. The elimination half-life of COHb is approximately 4 hours when breathing room air and decreases to 1 hour after giving 100% oxygen.

Arterial Blood Gas instruments were upgraded to new models in June 2004. The reference range for carboxyhemoglobin (CoHb) changed from 0 – 1.5% to 0 – 2%.

Specimen requirement is one green top (lithium heparin), lavender top (EDTA) tube of blood or a heparinized blood gas syringe. Venous or arterial blood is acceptable.

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