Published on 07/02/2015 by admin
Filed under Anesthesiology
Last modified 22/04/2025
This article have been viewed 1441 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.
Small amounts of CO are present in all individuals because CO is a byproduct of erythrocyte destruction, resulting in an HbCO concentration of approximately 1%. Cigarette smokers often have HbCO levels exceeding 5%.
Signs and symptoms of HbCO poisoning vary, depending on the concentration of HbCO present, the tissue O2 demands, and the hemoglobin concentration. Small amounts of HbCO in the blood may manifest as irritability, headache, nausea or vomiting, confusion, dizziness, visual disturbances, and dyspnea. Increasing concentrations of HbCO may produce respiratory failure, agitation, seizures, coma, or death (when HbCO concentrations reach 50%).The classic cherry-red color of the skin is usually a sign of high CO concentrations in the blood; however, cyanosis may be seen in patients with severe CO poisoning.
Significant hypoxemia can be present despite apparently normal oximeter readings. Conventional pulse oximetry (most oximeters emit only two wavelengths of light—660 nm and 940 nm) overestimates the true SpO2 because HbCO competes with oxyhemoglobin in the absorption spectrum. Independent of the true oxyhemoglobin concentration, the pulse oximeter will display a reading of no less than 84% to 86% even with a HbCO of 50% and an oxyhemoglobin of 50%. The concentration of HbCO can be accurately measured with a co-oximeter that is based on fractional oximetry (in which the oximeter emits five wavelengths of light to detect all hemoglobin species).
The first step in treatment is to remove the patient from the environment containing CO to prevent further exposure. The next is to administer 100% O2. Because the binding of CO to hemoglobin is competitive with O2, increasing the inspired concentration of O2 to 100% will cause more O2 to displace CO from the hemoglobin molecule, shortening the elimination half-life. Thus, the half-life of CO elimination can be shortened from 4 h to 40 min by ventilation of the lungs with 100% O2. The administration of 100% O2 will also partially relieve tissue hypoxia by increasing the amount of O2 dissolved in the plasma. Tracheal intubation and mechanical ventilation may be necessary. Hyperbaric O2 therapy is indicated for the treatment of severe CO poisoning; the use of hyperbaric O2 therapy can decrease the HbCO elimination half-life to 15 to 30 min. Transfusion of red blood cells (thereby increasing O2-carrying capacity) may also be helpful. The use of diuretics, steroids, or both may be indicated if the patient develops cerebral edema.
CO may be produced when any currently used inhalation anesthetic (desflurane > isoflurane >>> sevoflurane) reacts with a desiccated CO2 absorber containing strong bases (KOH > NaOH). For further details, see Chapter 8, Carbon Dioxide Absorption.
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