Carbon Monoxide Poisoning,Treatment,Epidemiology,Pathology

 Carbon monoxide poisoning is an asphyxiant gas capable of producing disease and death in man as a result of its ready capacity to induce severe hypoxia. The most vulnerable organs are the brain and the heart. The danger of this gas derives from its affinity for the hemoglobin of human red blood cells, which is 300 times that of oxygen: further­more, the hemoglobin dissociation curve is shifted to the left so that tissue oxygen tensions must fall too much lower levels before the oxyhemo­globin that remains can give up it? oxygen. The hazard to the body of exposure to carbon mon­oxide is compounded by the fastidiousness with which high concentrations of carboxyhemoglobin can be attained without ringing the physiologic alarm bell of dyspnea. Consciousness course, is dulled by anoxia.

When carbon monoxide is breathed, the absorp­tion of the gas is rapid until an equilibrium is reached, provided an immediately fatal concen­tration is not inhaled. The reaction is reversible upon removal from exposure, the gas being ex­creted unchanged through the expired air in a matter of hours. The reversal is expedited by breathing oxygen-carbon dioxide mixtures or pure oxygen, still more if the Oxygen is under pressure. Ledingham reports 100 per cent recovery in 32 patients created with oxygen at two atmo­spheres of pre. are (absolute). There is danger in exceeding two atmospheres of pressure. Recovery of consciousness can be expected within 30 to 90 minutes with this regimen.

Facts You Must Know About Carbon Monoxide Poisoning, And Its Treatment


Carbon monoxide is colorless, odorless, and slightly lighter than air. It is pro­duced whenever incomplete combustion of carbon or carbon-containing compounds occurs. Poison­ing may occur by accident, at home or at work, or by suicidal intent. Rarely, carbon monoxide has been a homicidal weapon. Natural gas, predomi­nantly methane and free of carbon monoxide, has largely replaced manufactured gas (20 to 40 per cent CO) in the United States. With this change a significant decline has occurred in accidental deaths from illuminating gas. Nonetheless, faulty gas refrigerators and heaters fueled by gas, coal, oil, or kerosene continue to cause accidental poison­ing and death in houses and in trailer homes.

The combination of incomplete combustion and in­adequate venting provides the exposure. Picnic grilles brought indoors and the use of gasoline powered machinery inside the home are often unsuspected hazards. The exhaust from gasoline internal combustion engines contains, on the average, 7 per cent carbon monoxide. It is gen­erally held that so long as the carbon monoxide content of inhaled air does not exceed 0.01 per cent (100 ppm), it can be breathed for eight hours without ill effects. An air concentration of 1 per cent (10,000 ppm) produces a 50 per cent satura­tion of the hemoglobin in 15 minutes. Haldane extrapolated the rise in saturation in 23 minutes to be 80 per cent at this concentration in the air; this is a fatal level of carboxyhemoglobin. The blood of heavy cigarette smokers may contain as much as 10 per cent carboxyhemoglobin. A blood saturation of 20 per cent is a fair bench mark beyond which symptoms can be expected.

A running automobile engine in an enclosed garage is an increasingly common cause of death by accident and suicide. In. 1967 in the United States, 1,417 deaths caused by accidental carbon monoxide poisoning were recorded, whereas 2,191 deaths were attributed to suicide resulting predominantly from exposure to motor vehicle exhaust gas.In industry, sources of poisoning are charcoal ovens, kilns, blast furnaces, blasting with high explosives, mine explosions, – and combustion engines. Much carbon monoxide is produced during fires, a hazard recognized by professional firemen.



The skin of victims of carbon monoxide poisoning may be pink; in addition there may be areas of trophic erythema, blister forma­tion, and dubious ulcers. The blood may be cherry red, as may the viscera. A variety of lesions are encountered, all attributed to anoxia. They are usually seen when unconsciousness has been prolonged or death delayed. The brain is often the Site of hyperaemia, edema, hemorrhage, and local or defuse degeneration. Symmetrical softening in the lenticular nucleus in the globus pallidus is regarded as the most typical pathologic change. The heart may show necrosis of the papillary muscles or gross myocardial infarction, and the kidney may exhibit tubular degeneration.


Clinical Manifestations

The disease is best described as an acute poisoning with all degrees of severity. Chronic exposure does not produce chronic poisoning but. rather, repeated episodes of mild acute poisoning. Intermittent day-to-day exposures are not cumulative in effect. However, the higher morbidity and mortality from coronary heart disease among cigarette smokers has prompted some epidemiologists to suggest an association with chronic exposure to carbon monoxide in the air stream of cigarette smoke, which is considerably higher than community pollution by carbon monoxide.

In general, symptoms occur more acutely with higher air concentrations of carbon monoxide. Severity is increased by exercise and in the presence of anemia. With concentrations in the air higher than 1.5 per cent, unconsciousness, apnea, and death will occur in several minutes. However, protracted exposures to lower concen­trations can be ultimately disastrous. Symptoms develop with a progression that roughly parallels the rise in concentration of carboxyhemoglobin. Victims become unconscious at about 60 per cent saturation, and fatal cases show saturations in the range of 60 to 80 per cent. Haldane, using himself as an experimental subject, displayed such in coordination and confusion at 40 per cent saturation as to be incapable of driving an auto­mobile.

Meigs and Hughes analyzed the records of 105 patients admitted to the Yale-New Haven Hos­pital. In declining order of frequency, they re­corded the following findings: abnormal mental state, neurologic abnormalities, abnormal skin color, suffused mucous membranes, abnormal chest signs, vomiting, headache, skin lesions, excessive sweating, palpable liver, localized pains in the chest or extremities, localized edema, evi­dence of bleeding and “pseudo recovery. The pulse, respiratory rate, and temperature may be elevated and there may be protein, sugar, casts, and eryth­rocytes in the urine. Leukocytosis with increase in neutrophils and decrease in lymphocytes and eosinophils, when present, is of serious prog­nostic import, as are temperature elevations above 102° F., neurologic abnormalities, relapse after the second day, irregularities of cardiac rhythm, tachycardia, and the presence of skin lesions.

Recovery without permanent sequelae is usual in nonfatal cases, and recovery of consciousness usually occurs over a period of several hours. However, unconsciousness may persist for days after relief of anoxia and may be followed by parkinsonism, peripheral neuritis, or a confusional psychosis. Recovery from psychosis may occur up to two years from onset. Cerebral hemorrhage has been observed some days after apparent recovery. Increasingly, electrocardiographic abnormalities, some  reversible, and acute myocardial infarction have been reported, even in the absence of coma.


Identification and quantization of carboxyhemoglobin is decisive in diagnosis but it is not a requisite for the institution of treatment Blood should be collected early if it is to the degree of saturation.


Removal of the patient from the contaminated atmosphere is the first and obvious indication. In mild cases without loss of consciousness, fresh air and absolute rest for four  hours will probably suffice. The patient should not be allowed to go home without an escort. Treatment in a hospital is indicated when there has. even transient loss of consciousness, fresh air is found unconscious, emergency treatment is ­called for. If respiration has ceased, artificial respiration is instituted at once along with administration of 100 per cent oxygen.

Since the concentration of carboxyhemoglobin is halved in about 40 minutes under conditions of adequate ventilator exchange with pure oxygen, two to three hours of continuous oxygen therapy should suffice for the control of anoxic. Most police emergencies  squads are trained to use a positive pressure face mask respirator with an automatic cycling valve. The British Medical Research Council recommends use of 95 per cent oxygen and 5 percent carbon dioxide.

Rapid recovery from profound coma by treatment  in a pressure chamber with oxygen ur.mer two atmospheres of pressure has been reported Persistent coma, after anoxia has cleared, calls for the usual treatment of the comatose patient. In the presence of temperature elevation over 102 f.Or serious neurologic disorder appearing on  first day, induction of hypothermia should be considered.

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