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Abstract
While it appears that normal individuals may compensate for decreased oxygen availability resulting from 10% to 15% car- boxyhemoglobin, the patient with heart disease may be unable to compensate. An experimental study was undertaken to test this hypothesis. Normal monkeys and monkeys with induced myocardial infarction were continuously exposed to 100 ppm (115 mg/cu m) carbon monoxide for 24 weeks (23 hr/day) and the physiologic effects on the cardiovascular system were evaluated. Significant and persistent characteristic elevations in the hematocrit, hemoglobin, and red blood cell were observed after three weeks of exposure in both nonínfarcted and infarcted animals. The electrocardiograms of infarcted and nonínfarcted animals inhaling the carbon monoxide displayed increased P wave amplitudes. The incidence of T wave inversion was higher in infarcted than in noninfarct- ed animals, indicating a greater degree of myocardial ischemia in the infarcted animals breathing carbon monoxide.