The clinical presentation of acute CO poisoning is variable, but in general, the severity of the observed symptoms correlates roughly with the observed level of COHb (Table 1); however, in terms of diagnostic value, the nonspecificity of these presenting symptoms makes definitive diagnosis difficult. Therefore, in circumstances such as these, careful attention to the history of the patient is of great import.

The most revealing of facts is in the case where multiple individuals have a common symptomatology and environmental exposure. Another telling fact is the occurrence of illness in household pets concurrent with or just preceding the onset of a patients own illness. Due to their smaller size and in general higher metabolic rates, pets may be more obviously and more severely affected by CO intoxication than their owners. In cases of individual exposure, a history of exposure to known sources of CO should suggest at least the possibility of CO intoxication. A great many of these cases are occupationally related.

The most important effect of CO is tissue hypoxia. This effect is most significant in areas of high blood flow and oxygen demand. For this reason, it is not surprising that neurologic and cardiovascular manifes­tations are common and that these are the tissues at greatest risk in CO intoxication.
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The most common symptoms include fatigue, head­aches, dizziness, difficulty in thinking, nausea, dysp­nea, weakness, and confusion. Diarrhea, abdominal pain, visual disturbances, and chest pain are found less frequently. In light of these symptoms, one can see why the diagnosis of viral influenza is often made, particularly when the history also reveals that another member of the family is similarly affected. In addition, the incidence of CO poisoning tends to rise during the winter months due to the increased use of home heating appliances rising in step with the number of cases of true viral influenza.

Table 1—Symptoms Commonly Found with Different CO Levels

Blood Level

of COHb,




Usually none in healthy individuals; reduced exer­

cise tolerance in patients with pulmonary dis­

ease; decreased threshold for angina in patients

with coronary heart disease


Headache; dyspnea on mild exertion; angina in

patients with coronary heart disease; dilation of

cutaneous vessels


Throbbing headache; nausea or vomiting (or both);

easy fatigability and irritability; difficulty with



Severe headache; dizziness; fatigue and weakness;

syncope on exertion; impaired thought proc­



Tachypnea; tachycardia; syncope; confusion


Respiratory failure; collapse; intermittent convul­

sions or seizures; coma


Respiratory failure; severe hypotension; coma, fre­

quently fatal


Coma, rapidly fatal

Physical findings, like symptoms, are of little help in establishing a diagnosis. Marked tachycardia and tachypnea are common as the cardiovascular and pulmonary systems try to compensate for the reduced peripheral oxygen delivery. Mild hypertension is found in some patients, while others may actually be hypotensive as a result of hypoxic myocardium; how­ever, in otherwise healthy individuals, increases in blood flow due to compensatory dilatation of the coronary vessels are sufficient to meet the increased cardiac needs. Patients with a history of atheroscle­rotic heart disease may not be able to meet these increased oxygen requirements, and in them, arrhyth­mias may be noted.

Neurologic findings include audiovestibular abnor­malities. Tinnitus and neurosensory hearing losses may be found. Nystagmus and ataxia are also seen. In extremely severe poisonings, cerebral edema is pres­ent. Computer tomographic scans and MRI have shown white matter to be particularly sensitive to cerebral hypoxia brought about by CO intoxication. Although gray matter has greater metabolic oxygen needs, the more restricted vascular supply of the white matter limits its tolerance for reduced oxygen tensions and thus increases its susceptibility to damage during hypoxic events. Late sequelae in up to 45 percent of the patients may develop gradually from three days to three weeks after initial exposure and therapy for acute poisoning. The development of delayed se­quelae can be predicted by the appearance of delete­rious neurologic changes as observed by CT within the first 24 hours after admission. The resulting neuropsychiatry problems may include intellectual deterioration, memory impairment, and personality changes manifested by increased irritability, aggres­siveness, violence, and moodiness. The occurrence of these delayed sequelae is more common in patients with decreased levels of consciousness at the time of admission. If the proper therapies are instituted at the time of initial treatment, most, if not all, of these sequelae can be prevented. Those patients not re­ceiving aggressive therapy are more likely to develop permanent neurologic deficits.

Cherry-red discoloration of the skin, long thought to be typical in CO poisoning, is rarely found. Retinal hemorrhages are not common but, when discovered, may suggest the diagnosis. Findings of smoke inhalation such as singed nasal hairs, carbona­ceous mucus discharge, or injured mucous membranes should raise concern, since patients in whom these are found are more than likely to have suffered severe CO poisoiilng.
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The measurement of COHb levels is, at present, the most useful laboratory method for ascertaining the severity of exposure to CO. Care must be taken in interpreting the results of these tests, since they may not reflect the initial severity of exposure due to elapsed time or treatment begun since removal of the patient from the vicinity of the source. Additional complicating factors include the smoking history of patients and the fact that individuals with high levels of COHb may be totally asymptomatic.

Arterial blood gas levels are of little use, since these values measure oxygenation of the plasma and are not affected by hemoglobin saturation. As such, they are not a very sensitive indicator of tissue oxygenation in the periphery. Elevated hemoglobin concentrations and hematocrits due to an absolute elevation in red blood cell mass have been found with chronic expo­sures to CO. The elevation in red blood cell mass is caused by increased erythrocyte production due to hypoxic stimulation.