Carbon monoxide (CO) is the leading cause of death resulting from poisoning (458,459). CO is a tasteless, odorless, colorless, and nonirritant gas that is produced by the incomplete combustion of carbon-containing substances (460-468). During combustion, if the availability of oxygen (O2) is high and the temperature below 710°C (1310°F), carbon dioxide (CO2) production is favored, but in O2-deficient environments at higher temperatures, CO formation occurs (see Chapter 4, Heading 2. and ref. 469). Common sources of CO include tobacco smoking, automobile exhaust, industrial processes, unvented or faulty heating units, and fires (460,462,464,466-468,470-472). An uncommon source of CO is dichloromethane (methylene chloride), used in paint remover, aerosol propellants, and degreasers (460-462,465,466,468,469). A combination of formic acid and sulfuric acid produces CO (473).
CO binds reversibly to hemoglobin to form carboxyhemoglobin (COHb; refs. 461 and 474). Because CO affinity for hemoglobin is 200 to 250 times greater than O2, blood O2-carrying capacity is reduced (461,462,464-466,468,471,474-476). Hypoxic effects are enhanced because CO binding to hemoglobin modifies remaining O2 binding sites, increasing hemoglobin affinity for O2 and displacing the O2 dissociation curve to the left, thereby decreasing O2 release to cells (461,462,465-468,471,472,475, 477-480). Decreased tissue O2 delivery stimulates breathing, increasing CO uptake and causing respiratory alkalosis, further shifting the oxyhemoglobin dissociation curve to the left (481). About 10 to 15% of absorbed CO binds reversibly to other heme proteins, myoglobin, and the mitochondrial cytochrome oxidase (cytochrome a3) system essential in the production of ATP (462,466,467,471,475,478,481-485). CO may reduce muscle function (475,481). Other harmful mechanisms of tissue damage (e.g., brain-lipid peroxidation) have been described (461,467,472,475,481).
Endogenous production of CO yields a baseline COHb saturation of 0.4 to 0.7% (461,462,465,479). An abnormal COHb level depends on the atmospheric concentration of CO, duration of CO exposure, and the ventilatory rate and depth (461-463,465-471, 474,480,486).
The normal atmospheric concentration of CO is usually less than 0.001% (10 ppm [461,463,468]). The atmospheric concentration can exceed 0.01% (100 ppm) in heavy urban traffic and during periods of atmospheric stagnation (460,463,466). COHb averages 1 to 2% in urban nonsmokers (461-463,465,468). Heavy smokers can have a COHb saturation approaching 10% and cigar smokers up to 20% (460,462,466,480, 487). An atmospheric CO concentration of 1% (10,000 ppm) can equilibrate to about 95% COHb (462,466).
At rest (pulmonary ventilation about 6 L/min), COHb saturation = 3 X % CO in environment X time of exposure (min). For light activity (ventilation about 9-10 L/min), COHb saturation = 5 X % CO X time of exposure (470). High concentrations of CO (>1% or 10,000 ppm), such as in suicidal inhalation and fire deaths, lead to unconsciousness and death, without prodromal symptoms, within a short time (462,466,
Symptoms Related to COHb Concentrations
History of heart disease
Up to 1G% Asymptomatic
Headache; dyspnea with exertion.
Throbbing headache; nausea; abnormal manual dexterity; fatigue; dimming of vision.
Severe headache; nausea and vomiting; visual disturbance; mental confusion; weakness (35% potentially lethal).
Syncope; tachycardia; tachypnea.
Coma; seizure (life-threatening).
Compromised cardiorespiratory function; death.
Less exertion needed to cause chest pain in individuals with angina pectoris. Potentially lethal (arrhythmia).
Adapted from refs. 462, 465, 466, 471, 482, 488, 491, and 498-500.
488-491). An active person, breathing air containing 5% CO, has a COHb level of about 10% in about 10 s, and about 40% in 30 s (492). Lethal levels of COHb are achieved within 10 min in a closed garage (CO 0.5-1.0%) (468,470,493). A CO concentration of 0.2 to 0.3% (2000-3000 ppm) can lead to death within 1 to 2 h (465,469,491,494). CO uptake is enhanced when ventilation is increased by CO2 emission from automobile exhaust, stimulating the central respiratory control center (491). Household pets, because of their smaller size and greater metabolic rate, succumb before human occupants in a dwelling (471,472,481,495).
Because of the fixed oxygen needs of the cardiovascular system and CNS, related symptoms are common with prolonged (subacute) exposure to relatively low CO concentrations (0.02-0.12% [200-1200 ppm]; see Table 4 and refs. 461, 467, 468, 470, 477, 479, 496, and 497).
Patients admitted to a burn unit with COHb levels above or equal to 10% have shown electrocardiographic and biochemical evidence of cardiac injury (501). Low levels of CO worsen myocardial ischemia in physically active individuals with angina (502). Patients with coronary artery disease cannot increase coronary blood flow when COHb saturation is raised acutely (<10% saturation [470,485]). Other medical and constitutional factors predispose individuals to the toxic effects of CO (462,465,466,468,474,481,491,503,504). Infants, individuals with anemia or lung disease, and the elderly are more susceptible. Fetal death has been observed in cases of nonlethal maternal CO poisoning (463,472). CO binds more avidly to fetal hemoglobin than to maternal hemoglobin (hemoglobin A).
The half-life of COHb in resting adults at sea level is 4 to 5 h. CO is eliminated essentially unchanged from the lungs (462,465,468,479). Resuscitation decreases COHb. The administration of pure O2 reduces the half-life to 80 min, and to 24 min when hyperbaric O2 is used (460,462,463,465,466). Low levels are also encountered if the clinical presentation is delayed, or there has been a period of survival (463,464,472, 475,480).
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