Myocardial findings in fatal carbon monoxide poisoning: a human and experimental morphometric study

Abstract

The aim of this study was to define the status of the myocardium in selected human cases of acute, fatal carbon monoxide intoxication and the myocardial changes in rats exposed to carbon monoxide in relation to the type of cardiac arrest and the effects of reoxygenation following pre-fatal CO intoxication. The human study consisted of 26 cases (17 accidental and 9 suicide) of acute, fatal CO intoxication, without evidence of obstructive coronary atherosclerosis or history of ischemic heart disease which were compared with 45 cases of fatal head trauma in subjects who died instantaneously (26 cases) or within 1–12 h (19 cases). Inhalation of a lethal dose of CO in rats was compared with sub-lethal doses plus reoxygenation with and without pre-treatment by a betablocker. In all human and experimental histological sections, changes were normalised per mm² area. In the human cases the myocardium did not show any ischemic types of changes or other lesions. Only in “three accidental” cases a few, small foci of coagulative myocytolysis were detected. In the case of spontaneous death in 31 rats following CO intoxication, no pathological myocardial changes were seen. Of the 15 “reoxygenated” rats, 2 of the 7 spontaneous deaths presented coagulative myocytolysis with 15 ± 6 foci and 381 ± 255 necrotic myocells. All the eight rats sacrificed at 3 h had coagulative myocytolysis with 5 ± 4 foci and ¶60 ± 47 myocells. Of the 24 reoxygenated rats pre-treated with a betablocker, 5 died spontaneously after a short survival and 2 of these showed 11 ± 9 foci and 21 ± 20 myocells. The 19 rats sacrificed after 3 h all presented coagulative myocytolysis with figures of 75 ± 43 and ¶356 ± 301 with 0.5 mg/kg of propranolol hydrochloride and 55 ± 45 and 253 ± 216 with 2 mg/kg, respectively.