INTRODUCTION

Carbon monoxide (CO) is the single leading cause of toxin-related death in the United States. From 1979 to 1988, 56,133 death certificates filed in the United States contained codes implicating CO as a contributing cause of death. The incidence of nonlethal CO poisoning is not established. CO is a colorless, odorless, nonirritating gas. Its specific gravity is 0.97 relative to air, so it does not stratify. CO has a high affinity for hemoglobin. It reversibly displaces oxygen from hemoglobin to produce carboxyhemoglobin (COHb), resulting in tissue hypoxia.

The symptoms of CO poisoning are protean and vague, resulting in a high rate of misdiagnosis. Correct treatment requires aggressive oxygen therapy and the select use of hyperbaric oxygen (HBO).

SOURCES

Carbon monoxide is endogenously produced during the metabolism of heme pigments. When protoporphyrin is converted into bilirubin, CO is released. This generates 75 percent of the endogenous production of CO, producing a serum COHb level of 0.4 to 0.7 percent. This level increases slightly during the menstrual cycle and pregnancy. Higher levels (4 to 6 percent) are seen with acute hemolytic anemia due to the accelerated metabolism of hemoglobin. CO is eliminated primarily unchanged during pulmonary respiration, though a small amount is metabolized to CO₂.

Exogenous CO is produced by the incomplete combustion of organic fuels. Gas-powered engines produce significant amounts of CO. Other sources include furnaces, home water heaters, gas heaters, pool heaters, wood stoves, kerosene heaters, indoor charcoal fires, and Sterno fuel. Industrial sources include steel foundries, pulp paper mills, and plants producing formaldehyde and coke. Exposures have resulted from wildland firefighting, airplane crashes, military ship explosions, propane-fueled forklifts, smoke-filled bingo halls, selfimmolation, ice skating rink zambonis, and indoor tractor pulls. Fire fighters are at high risk, and most immediate deaths from building fires are due to CO poisoning. All patients from a fire scene must, therefore, be evaluated for CO toxicity.

Tobacco smoke is a significant source of CO. Serum COHb levels in smokers often approach 9 percent but may reach 20 percent. These levels can compromise patients with preexisting cardiopulmonary disease. Furthermore, CO toxicity from cigarette smoking has been implicated as a major factor in atherogenesis. It is also known to be a precipitating factor in angina, myocardial infarction, and cardiac arrhythmias. Smoke released from the tip of the cigarette contains 2.5 times more CO than the inhaled smoke. Cigarette smoking in poorly ventilated rooms can cause CO toxicity in the exposed nonsmoker.

Methylene chloride is found in many paint removers and its vapors are readily absorbed through the lungs. In the liver it is converted into CO. Since methylene chloride is stored in tissues and gradually released, the CO elimination half-life in patients exposed to this substance is about twice that of inhaled CO.

PATHOPHYSIOLOGY

The pathophysiology of CO poisoning is not completely understood. Nevertheless, five mechanisms explaining the toxic effects of CO have been proposed: (1) direct binding of CO to hemoglobin; (2) shifting of the oxygen-hemoglobin dissociation curve; (3) CO binding to myoglobin; (4) inhibition of cellular respiration; and (5) brain lipid peroxidation.

Tissue Hypoxia

Carbon monoxide readily crosses the pulmonary alveolar membrane. It acts as a competitive inhibitor of oxygen binding by reversibly coupling with hemoglobin. The affinity of CO for hemoglobin is 210 to 270 times greater than the affinity of oxygen for hemoglobin. This results in high serum COHb levels from exposures to environments with relatively low partial pressures of CO. When inhaled air contains 0.01% CO, the resulting serum COHb level is 10 percent. The net effect of COHb production is a reduction of the oxygen-carrying capacity in the blood. This produces tissue hypoxia, the predominant toxicologic property of CO.

Shifting the Oxygen-Hemoglobin Curve

The tissue hypoxia caused by the formation of COHb does not adequately explain the toxic effects of CO. Hemoglobin has four binding sites for oxygen. When CO binds to one of these sites, the hemoglobin molecule is altered in such a way that the remaining three oxygen molecules are held more tightly. This shifts the oxygen-hemoglobin curve to the left, further reducing the amount of oxygen available at the cellular level

Myoglobin Binding

Carbon monoxide has a high affinity for myoglobin, especially cardiac myoglobin. Carbon monoxide impairs cardiac performance because cardiac carboxymyoglobin reduces the oxygen available to myocardial tissue. Cardiac ischemia and arrhythmias can also be caused by CO. Since carboxymyoglobin dissociates more slowly than COHb, a rebound increase of the serum COHb level may occur after treatment. After oxygen therapy causes the serum COHb to decrease, the myoglobin releases its bound CO, causing an increase in the serum COHb concentration.

Inhibition of Cellular Respiration

Carbon monoxide also binds to cytochromes A₃ and P-450. By reversibly binding to the cytochrome oxidase system, CO may cause inhibition of cellular (mitochondrial) respiration. The affinity of cytochrome oxidase for oxygen is much greater than the affinity of cytochrome for CO. Therefore, an environment with a low oxygen tension (hypoxia) is required for significant CO-cytochrome binding to occur. The exact impact that the inhibition of cellular respiration produces in CO poisoning remains unclear.

Brain Lipid Peroxidation

A recent theory suggests that the neurologic findings associated with CO poisoning may result from brain lipid peroxidation. Carbon monoxide converts xanthine dehydrogenase into xanthine oxidase. Xanthine oxidase reacts with hypoxanthine, eventually producing superoxide, a free-radical reduction product of oxygen. Superoxide reacts with the body's iron stores and ultimately causes cell membrane lipid peroxidation, which results in neuronal damage. This strongly suggests that CO-mediated brain injury is similar to postischemic reperfusion phenomena.

CLINICAL PRESENTATION

The manifestations of CO poisoning are often vague, leading to frequent misdiagnoses with subsequent delays in therapy. Initial symptoms commonly include headache, dizziness, weakness, and nausea. Other symptoms include difficulty in thinking, chest pain, palpitations, visual disturbances, and abdominal pain. CO poisoning is often misdiagnosed as flu, gastroenteritis, and psychiatric disorders.

Routine CO screening of emergency patients during the winter months revealed a 2.8 percent incidence of elevated CO levels. With patients complaining of headache during colder months, a similar incidence was found. In addition, physicians were unable to predict elevated COHb levels in patients.

At the scene of the exposure, COHb levels correlate fairly well to symptoms (Table -1). When patients are removed from CO or have been breathing 100% oxygen, there is a poor correlation between COHb levels and the clinical manifestations. Despite nontoxic COHb levels after treatment, patients may still demonstrate signs of severe poisoning. Patients may lapse into coma and die without intermediary symptoms when exposed to high levels of CO. Low-level exposures over a long period of time may be more harmful than high-level exposures over a brief time, though COHb levels may be similar. It is therefore important that a serum sample be drawn by emergency medical personnel at the scene. The field specimen COHb level will correlate best with the clinical presentation.

SYSTEMIC MANIFESTATIONS

Cardiac

Although CO poisoning affects every organ system (Table -2), the brain and heart, having the highest metabolic requirements, are most susceptible to CO toxicity. When coronary artery disease is present, a low serum COHb level can produce myocardial ischemia and infarction. In fact, ischemia and infarction can occur in the absence of coronary artery disease. In a study of burn victims, 5 of 18 patients (28 percent) with COHb levels greater than 10 percent sustained myocardial infarctions. Decreased exercise tolerance also results from CO poisoning.

Myocardial ischemia is most prominent in the subendocardial and subepicardial regions of the ventricles. This may produce papillary muscle dysfunction, abnormal ventricular wall motion, and mitral valve prolapse. The electrocardiogram often reflects ischemia, showing ST-segment and T-wave abnormalities. Atrial flutter, atrial fibrillation, premature ventricular tachycardia, and conduction system disturbances are also seen. The ventricular fibrillation threshold is lowered in cases of severe CO poisoning. However, in patients with existing cardiac arrhythmias, mild elevations of COHb (up to 5 percent) are not reported to increase the frequency of single or multiple ventricular ectopic beats during rest or exercise.

Ophthalmologic

Visual disturbances are frequent and correlate with the duration of exposure. Funduscopic examination may reveal flame-shaped retinal hemorrhages. They are caused by hypoxia and may be unilateral. The hemorrhages often resolve without visual deficit. A sensitive indicator of CO toxicity is the presence of bright red retinal veins. These may be seen before the mucous membranes become erythematous and appear at lower COHb levels. Blindness is infrequent and is usually temporary.

Dermatologic

The classic cherry-red skin of CO poisoning is rarely seen; more often, victims are pale or cyanotic. Dermal necrosis with bullae formation may occur anywhere but especially at pressure point areas in the comatose patient and over areas of myonecrosis. Myonecrosis from pressure or prolonged tissue hypoxia may cause rhabdomyolysis, a potential cause of renal failure. Other dermal changes include sweat gland necrosis, alopecia, edema, and erythematous patches.

Other

Other physiologic effects of CO poisoning include noncardiogenic pulmonary edema, bowel ischemia, hepatic failure, vestibular dysfunction, hearing loss, disseminated intravascular coagulation, and thrombotic thrombocytopenic purpura. Even low COHb levels can significantly diminish exercise tolerance in patients with chronic destructive pulmonary disease.

Fetal

Up to 10 percent of patients receiving HBO are pregnant. In pregnancy, the fetus is particularly susceptible, as CO readily crosses the placenta. During exposure, fetal COHb levels lag behind the maternal level, achieving equilibration after 14 to 24 h. After equilibration with maternal blood, fetal COHb levels are 10 to 15 percent higher than maternal levels. In addition, because the fetal oxygen-hemoglobin dissociation curve is shifted to the left , small amounts of COHb can markedly decrease the fetal oxygen tension and content. Fetal elimination of CO is prolonged, resulting in a fetal CO elimination half-life that is three and a half times longer than that of the mother. Pregnant women should receive more aggressive and prolonged oxygen therapy. Longo suggests that the mother should receive oxygen for a period five times longer than the time period needed to complete just the maternal course of therapy . For example, if 4 h is required to completely treat the mother, an additional 20 h of oxygen treatment is required. Fetal heart tones should be obtained, and cardiotachodynomanometry instituted at 20 weeks’ gestation or greater. Up to 60 percent of children born to women surviving CO poisoning have neurologic sequelae. In addition, CO is teratogenic and causes lower-birth-weight infants. Fetal death has occurred in cases of nonlethal maternal poisoning. Fetal demise may be seen immediately or be delayed. Fetal outcome roughly correlates to maternal symptoms at the time of CO exposure; however, there may be no relationship between fetal death and maternal COHb levels.

Pediatric

Children make up 37 percent of patients receiving HBO therapy; children less than 5 years old account for 25 percent of victims receiving HBO. Among acutely exposed children, as many as 17 percent die and 48 percent require cardiopulmonary resuscitation (CPR). Most childhood deaths from CO poisoning are fire-related. Newborns are more susceptible to the effects of CO poisoning due to a higher fetal hemoglobin concentration which shifts the oxygen-hemoglobin curve to the left.

In children, in whom nausea is a common complaint, CO toxicity is frequently misdiagnosed as acute gastroenteritis; in young infants it can be confused with colic. Carbon monoxide toxicity has been implicated as a cause for some cases of sudden infant death syndrome.

Children are frequently affected by riding in vehicles with faulty exhaust systems, especially in the back seats of cars or in the enclosed backs of pickup trucks. In one study of 68 children requiring HBO therapy, 20 (29 percent) were exposed from riding in pickup trucks. Children riding in the same vehicle can have different symptoms with the same COHb levels or have markedly different COHb levels from the same exposure.

The treatment of CO toxicity for children is similar to that for adults; however, myringotomy is more commonly performed in children undergoing HBO therapy.

Neurologic

Neurologic Since the brain has a high oxygen requirement, most acute symptoms are related to the central nervous system (CNS). In a mass exposure of 184 victims, the most common complaints were headache (90 percent dizziness (82 percent), and weakness (53 percent). Carbon monoxide poisoning has been suggested as an occult cause of syncope. Of CO-poisoned patients, 35 percent complained of spells which mimicked near-syncope. The prevalence of CO poisoning among patients presenting with seizures may be 5 to 7 percent.

The most significant pathologic changes of the brain seen with CO poisoning are white matter lesions. These include white matter demyelination, edema, focal and laminar necrosis, and petechiae. Lesions of the hippocampus are reported in half of the cases. Gray matter lesions also occur in the watershed area between the anterior and middle cerebral arteries. The characteristic pathologic injury of CO poisoning is bilateral lesions of the globus pallidus. These lesions are seen with other hypoxic-ischemic insults and may be unilateral or asymmetric. The globus pallidus lesions are most likely the result of hypoxia with concomitant ischemia. This area has relatively low oxygen requirements, protecting it from pure hypoxia, but it has a poor blood supply, making it vulnerable to hypoperfusion. Low-density lesions of the globus pallidus demonstrated on CT scan or magnetic resonance imaging (MRI) are associated with a high incidence of neurologic sequelae.

Neurologic abnormalities are frequent in acute poisoning (Table -2). The most common neurologic complaints are headache, dizziness, agitation, stupor, seizures, and coma. Other aberrations include behavioral disorders, decreased cognitive ability, gait disturbance, memory deficits, emotional lability, parkinsonism, mutism, tic disorders, and impairment of parietal lobe functions. Long-term psychiatric and neurologic sequelae are grossly apparent in 11 percent of survivors. Memory impairment occurs in up to 43 percent. The most common personality change, affective incontinence, is characterized by emotional lability and may be a consequence of damage to the hippocampus. Resolution of the neurologic sequelae, when it occurs, may take 2 years. These deficits may be permanent.

A syndrome of delayed neurologic sequelae has been described. Delayed sequelae usually occur after coma from a prolonged exposure. The patient recovers, has a symptom-free interval, then undergoes rapid neurologic deterioration. In 10 to 30 percent of poisonings, neuropsychiatric symptoms will appear within 2 to 3 weeks after exposure. The common symptoms are mental deterioration, urinary and fecal incontinence, and gait disturbance. Complete recovery occurs in two-thirds. Older patients are at greater risk for developing delayed sequelae. Diffuse demyelinization of white matter is associated with delayed deterioration. More aggressive oxygen therapy may reduce the incidence of sequelae.

CLINICAL EVALUATION AND LABORATORY STUDIES

History

The diagnosis of CO poisoning is most often suggested by the circumstances in which the patient is found. Victims of a house fire who are comatose pose little diagnostic difficulty. In patients with vague symptoms who have been chronically exposed to low CO levels (e.g., smokers), reaching the diagnosis may be difficult. In the absence of a reliable history of CO exposure, alternative diagnoses include viral illness, food poisoning, depression, functional illness, encephalitis, and toxin-induced encephalopathy.

The physician should continually suspect CO poisoning during the colder months. Common complaints associated with CO poisoning include headache, nausea, weakness, fatigue, difficulty in thinking, dizziness, paresthesias, chest pain, palpitations, visual disturbances, diarrhea, and abdominal pain. In addition, CO poisoning has been confused with psychogenic hyperventilation and polycythemia.

One feature in the medical history which is suggestive of CO poisoning is when another person in the same dwelling also experiences similar symptoms. The appropriate agency should then be notified to measure ambient CO levels at the suspected site. The physician should further ask about the source of home heating and the condition of the exhaust system on the patient's car.

Physical Examination

The physical examination is of limited use in establishing the diagnosis of CO poisoning. Nevertheless, once the diagnosis is established, the physical examination does help define the severity of the poisoning. Vital sign abnormalities reflect the severity of the intoxication. The presence of singed nasal hairs, carbonaceous sputum, and thermal injury to the oral mucosa suggests thermal airway injury and severe CO poisoning. Auscultation may reveal wheezing from the exacerbation of preexisting pulmonary disease or from bronchospasm that results from irritation due to inhalation injury. Rales can be heard from the development of noncardiogenic pulmonary edema.

Laboratory Evaluation

The diagnostic evaluation of the CO poisoning victim must be guided by the situation. For example, the fire victim should be evaluated for cyanide toxicity. When evaluating those attempting suicide, a routine drug screen and measurement of ethanol, phenobarbital, salicylate, and acetaminophen levels may be required. Asymptomatic individuals with minor exposure do not require extensive evaluations.

A COHb level should be obtained in all cases. This should not delay the administration of 100% oxygen. Levels should be obtained by a modified spectrophotometric blood gas analyzer or, less accurately, by measuring expired CO concentration with a hand-held breath analyzer. A high expired CO concentration or serum COHb level confirms CO poisoning, but a low level does not exclude the diagnosis. If a patient has been removed from the CO-containing environment and has been given 100% oxygen, the COHb level may be deceptively normal.

An arterial blood gas measurement calculates the reported oxygen tension from the amount of oxygen that is dissolved in the blood, not from the amount of oxygen that is bound to hemoglobin. The amount of oxygen that is dissolved in the blood is essentially unaffected by CO. In addition, pulse oximetry units mistakenly measure COHb as oxyhemoglobin. Therefore, the oxygen saturation as reported by most arterial blood gas measurements and pulse oximeters will be falsely elevated. The difference between the oxygen saturation that is accurately measured and the false elevated oximetry reading is called the saturation gap. This saturation gap is characteristic of CO poisoning and correlates with the COHb level. For example, if the oximeter reads 93 percent and the arterial blood gas directly measures (not calculates) the saturation to be 88 percent, the COHb is about 5 percent. Likewise, if the pulse oximeter is 95 percent and the measured COHb is 5 percent, the true oxygen saturation is only 90 percent.

An ECG should be performed on patients with cardiac symptoms, coronary artery disease, altered mental status, or a COHb level greater than 10 percent. The ECG is often abnormal. Sinus tachycardia and ST-segment changes are the most frequently seen aberrations, although almost any abnormality may be present.

Fire victims must have a chest radiograph taken. Though frequently normal acutely, it serves as a valuable baseline study. Cyanide levels can be obtained but are of limited value. Assays for other toxic inhalants, such as acrolein, phosgene, or gaseous hydrogen chloride, are unavailable. Spirometry and fiberoptic bronchoscopy may be required.

Serial creatine phosphokinase (CPK) and lactic dehydrogenase (LDH) levels assist in determining myocardial damage. The CPK is frequently elevated. Isoenzymes, especially of the CPK, differentiate habdomyolysis from cardiac necrosis or infarction. In addition, a urinalysis may reveal myoglobinuria.

Alcohol is frequently consumed with both suicidal and accidental CO poisoning, sometimes making a rapid diagnosis difficult. Therefore, a blood alcohol level should be measured. If a suicide attempt is suspected, a drug screen may be sent for analysis. In addition, quantitative aspirin, phenobarbital, and acetaminophen levels should be obtained.

Other laboratory tests assist in confirming CO poisoning. A routine complete blood count (CBC) may show a leukocytosis. Determination of arterial blood gas and electrolyte levels may demonstrate an anion gap acidosis. The acidosis results from lactic acid production. Abnormalities are commonly seen with measurements of the blood glucose, amylase, and transaminases. These findings, however, are of limited clinical significance.

Brain CT is used to define focal or otherwise unexplainable neurologic symptoms as well as to assess for cerebral edema. MRI is a more sensitive neuroimaging modality for detecting CO-induced CNS lesions. MRI can demonstrate cerebral findings associated with CO poisoning, which include necrosis of the globus pallidus, demyelinated lesions of the white matter, and necrotic lesions of the hippocampus. MRI has also defined lesions in the anterior thalami in a CO-poisoned child.

Psychometric testing is performed on CO-poisoned patients at some hospitals. The Carbon Monoxide Screening Battery has been developed to detect patients with subtle cognitive deficit resulting from CO exposure. The battery includes: the general orientation, digit spans, trail-making, digit symbols, aphasia screening, and block design. This battery is used to assess the need for HBO treatment. After HBO treatment, the patient is tested again to determine the effectiveness of therapy.

TREATMENT

Initial Approach

In treating CO-poisoned patients, one should remove the victims from the CO-containing atmosphere, keep them at rest to minimize oxygen requirements, immediately administer 100% oxygen, and institute cardiac monitoring. Pulse oximetry will not adequately measure oxygen status. A simple mask which allows for mixture with room air is inadequate. A tight-fitting mask with a bag reservoir is required to deliver a high FIO₂. The serum elimination half-life of COHb when breathing room air is 240 to 320 min, compared to 50 to 80 min when breathing 100% oxygen. Oxygen therapy should not be discontinued until the patient is asymptomatic and the COHb level is less than 10 percent. In patients with angina, 100% oxygen should be applied until the COHb is below 2 percent or the patient is pain free.

Hyperbaric Oxygen Therapy

HBO use is empiric but is recommended for severe cases of CO toxicity. HBO is delivered in monoplace or multiplace chambers. The multiplace chamber permits treatment of multiple patients simultaneously and provides room for staff and accessory equipment, e.g., ventilators. Most treatment regimens have been empirically developed; they usually involve 100% oxygen at pressures of 2 to 3 atm for 46 to 120 min. A second treatment is given in 6 to 8 h if symptoms persist. With HBO therapy, the elimination half-life of CO is reduced to 23 min. When HBO is used to treat methylene chloride–induced CO toxicity, the CO half-life changes from 13.0 h at room air to 5.8 h.

With HBO therapy at 3 atm pressure, the amount of oxygen dissolved in the blood is increased to 6.6 vol percent. This amount is sufficient to meet the demands of cerebral metabolism independent of the COHb concentration. HBO therapy may also reduce the amount of cerebral edema. HBO therapy has been shown to prevent CO-mediated lipid peroxidation in the brain.

HBO use remains somewhat empiric since no well-designed prospective study has adequately defined the benefits of HBO. Nevertheless, the growing weight of scientific evidence suggests an advantage of HBO in severe poisoning or in cases with protracted symptoms. The prompt application of HBO may reduce mortality. In one study, patients treated within 6 h of CO exposure had a mortality rate of 13.5 percent; of those treated after 6 h, 30.1 percent died. Reports have demonstrated a dramatic reduction in the incidence of neuropsychiatric sequelae when HBO is used.

As many as 10 percent of patients requiring HBO therapy are pregnant. Animal studies have raised concerns regarding the potential adverse effects of high partial pressures of oxygen on the fetus, but the pressures and durations used were greater than those used in humans. The Russians have the largest experience with HBO in pregnancy. They found a decrease in perinatal complications and mortality. A Canadian study involving pregnant women exposed to CO had five cases of severe poisoning. Of the three patients treated with high-flow (non-HBO) oxygen, two had stillbirths; the child of the third patient had cerebral palsy. The two patients treated with HBO had normal outcomes. The greatest advantage of HBO over 100% normobaric oxygen is that it reduces the time required to decrease fetal COHb. Given the safety of HBO and the danger of CO toxicity to the fetus, many recommend liberal use of HBO in pregnant women.

When HBO therapy is required, it should be started promptly. Nevertheless, delays of 7 to 20 h have still resulted in favorable outcomes. Treatment guidelines have been developed to assist in defining those patients needing HBO therapy (Table -3). However, assigning patients into different treatment plans based on the clinical presentation and the COHb level is imprecise. In addition, HBO should be used more readily in cases of pregnancy, age extremes, cardiovascular or neurologic impairment, and metabolic acidosis.

The potential benefits of HBO are based upon sound physiologic principles; the risks of treatment are minimal. During HBO treatment patients may develop otalgia and sinus discomfort. Myringotomy can be performed to ease otic pressure. Tympanic membrane rupture and epistaxis are rare. Of patients with severe CO poisoning who undergo HBO, 5 percent will have a seizure and 6 percent will vomit. The cause of these adverse reactions (CO toxicity versus HBO treatment) is unclear.

Patients with significant neurologic abnormalities, cardiovascular abnormalities, or symptomatic pregnant patients require prompt HBO treatment. Such patients should be stabilized and prepared for transfer to the nearest HBO chamber. The indications for transfer and HBO therapy may be unclear, or the patient's condition may remain unstable. Therefore, the patient's transfer and interim treatment should be discussed with the HBO chamber physician. The role of nitrites with mixed cyanide and CO exposures is not clearly defined and is theoretically harmful. The nitrites given to treat cyanide toxicity cause methemoglobinemia. This shifts the oxygen-hemoglobin dissociation curve further to the left, exacerbating tissue hypoxia. If the patient has been removed from the source and presents to the emergency department alive, sodium thiosulfate, 12.5 g intravenously, should detoxify the cyanide.

Cerebral edema should be treated with mannitol and by elevation of the head of the bed. Hyperventilation should be used in severe cases. The efficacy of glucocorticoids is debated.

Correcting the metabolic acidosis may be harmful; a mild acidosis is often a normal compensatory response. A low pH shifts the oxygen-hemoglobin dissociation curve to the right, increasing oxygen unloading to the tissue. Alkalinization will shift the oxygen-hemoglobin curve to the left, further reducing tissue availability of oxygen and exacerbating the toxic effect of CO. Nevertheless, if the pH is less than 7.20, cardiovascular performance is compromised, and judicious alkalinization is required.

PROGNOSIS

Many variables, such as age, smoking habit, existing cardiopulmonary disease, severity of exposure, prior state of health, and form of therapy, influence outcome. Coma, cardiac arrest, metabolic acidosis, and high COHb levels have been associated with poor neurologic outcome. These factors, however, are inconsistent predictors of outcome and therefore are of limited value. Abnormal CT findings are associated with neurologic sequelae, which will often persist.

TABLE 1

Signs and Symptoms at Various Carboxyhemoglobin Concentrations

TABLE 2

Reported Complications of Carbon Monoxide Poisoning

TABLE 3

Treatment Guidelines Based on Severity of CO Poisoning