Published on 07/02/2015 by admin
Filed under Anesthesiology
Last modified 07/02/2015
This article have been viewed 903 times
John M. VanErdewyk, MD
Carbon monoxide (CO) is a colorless, odorless, tasteless, and nonirritating gas produced by the incomplete combustion of materials containing carbon. Its effects on the O2-carrying capacity of blood are profound: CO is responsible for approximately 3500 accidental and suicide deaths each year in the United States and is the major cause of death in patients exposed to smoke inhalation from fires. Many additional people are exposed to concentrations of CO that produce major morbidity.
CO is emitted from almost any flame or combustion device. A 3% to 7% concentration is present in the exhaust of internal combustion engines. Much higher concentrations can be generated during the burning of most illuminating and heating gases. Both CO and O2 compete for binding with hemoglobin; however, the affinity of hemoglobin for CO is 200 times greater than that for O2. CO binding results in carboxyhemoglobin (HbCO), which is incapable of off loading significant quantities of O2 in tissues. A HbCO level of approximately 25% is a critical level at which the central nervous system is profoundly affected. The HbCO level depends on the CO concentration in the air and on the duration of exposure. Besides decreasing O2-carrying capacity, HbCO also interferes with the release of O2 from oxyhemoglobin (i.e., a leftward shift in the oxyhemoglobin dissociation curve), further reducing the amount of O2 available to the tissues, which is the cause of tissue anoxia in CO-poisoned patients.
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