International Journal of Medical Toxicology & Legal Medicine
  • Year: 2011
  • Volume: 14
  • Issue: 2

Acute carbon monoxide-induced cardiotoxicity: clinical study

  • Author:
  • Mohamed AM Khalaf1, Nevin A El-Desouky2, Ghada MA El-Galad2, Ahmed H. Abbas1
  • Total Page Count: 9
  • Page Number: 28 to 36

1Dept. of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Al-Minya Universities

2Dept. of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Cairo Universities

Online published on 12 June, 2014.

Abstract

Carbon monoxide poisoning is a serious health problem that represents the 6th most frequent toxic exposure in Egypt. Cardiotoxicity may be one of the commonest causes of morbidity and mortality of such cases.

This study aimed at studying the commonest presentation of CO poisoning regarding the electrical and biochemical changes in relation to the carboxyhemoglobin level (COHb)

Eighty sex patients of both sexes were admitted at Al-Minya PCC with acute CO exposure during the period from 1st of October 2007 to 30th of April 2010. Diagnosis was confirmed by COHb blood level on admission. Two persons died on arrival and the study was carried out on the remaining 84 persons. They were classified into 4 different groups according to the COHb level: group I (control group): consists of 20 apparently healthy persons; group II (Mild toxicity); COHb% is 10–20% (No. =34); group III (Moderate toxicity); COHb% is 20–40% (No. = 36), and group IV (severe toxicity); COHb% is > 40% (No. = 14). All subjects were investigated for electrical changes by continuous electrocardiogram monitoring and measuring the cardiac Biomarkers (ALT, AST, LDH, CK-MB, and cTnT).

Regarding to pulse, there was no significant difference between the 3 intoxicated groups. Estimation of blood pressure revealed that most patients were normotensive or hypotensive, while hypertension was infrequent. In group II; 16 persons presented with tachycardia, and 6 with bradycardia. In group III; 22 persons presented with tachycardia, 5 with bradycardia. In group IV; 11 persons presented with tachycardia, 3 with bradycardia. There was a significant difference between groups II, IV and III, IV according to palpitation and dysrhythmias but not between groups II, III. One person of group III and 3 in group IV developed myocardial ischemia with a significant difference between groups II, IV and groups III, IV, but there was no significant difference at all between groups II, III. Interpretation of ECGs showed that: in group II; only one showed a depressed ST segment, 2 showed elevated ST segment, and the resting (31/34) had normal ECG, in group III; (27/36) had normal ECG and (9/36) showed abnormalities; depressed ST segment (2), elevated ST segment (2), inverted T-wave (1), paroxysmal ventricular contractions (PVCs) (2) and prolonged Q-T interval (2), in group IV; (6/14) had normal ECG and (8/14) showed abnormality; depressed ST segment (2), elevated ST segment (2), inverted T-wave (1), PVCs (2) and prolonged Q-T interval (1). There was a significant increase between group II, IV and III, IV when compared to each other regarding the ECG changes. There was no significant difference in ALT and AST levels in patient groups when compared together or to control. There was a significant increase of LDH in group IV when compared to group II, and a significant increase in LDH in all intoxicated groups when compared to control. There was a significant increase of CPK-MB and cTnT levels in groups III and IV when compared to group II or to control. There was a positive correlation of the severity of the cardiovascular manifestations and the electrical and biochemical changes to the blood level of COHb.

CO poisoning can induce serious cardiotoxic effects which are directly proportional to the blood level of COHb.

Keywords

Carbon monoxide, Cardiotoxicity, Electrocardiogram, Cardiac enzymes, Cardiac biomarkers