Transmural Myocardial Infarction after Exposure to Carbon Monoxide in Coronary-Artery Disease

Abstract

CARBON monoxide poisoning leads to tissue hypoxia primarily by binding to hemoglobin to form carboxyhemoglobin, which cannot deliver oxygen to the tissues. Carbon monoxide poisoning with 50 per cent or more of the circulating hemoglobin in the form of carboxyhemoglobin can lead to patchy myocardial necrosis in man and laboratory animals.^{1 2 3 4} More moderate (10 to 25 per cent carboxyhemoglobin) intoxication leads to a shift toward anaerobic metabolism⁵ in the heart. Carbon monoxide intoxication causes coronary-artery vasodilatation and an increase in coronary blood flow that is linearly related to the reduction in arterial oxygen content^{5 6 7} and is ordinarily sufficient to maintain . . .