Early Detection of Cardiac Affection in Acute Carbon Monoxide Intoxicated Patients

Background and Objective: Cardiovascular sequelae of Carbon monoxide (CO) poisoning may be clinically occult and remains undiagnosed due to lack of overt symptoms as acute chest pain and ischemic changes in the ECG. The advent of more sensitive and specific markers capable of detecting minor degree of cardiac damage may enable the clinicians to detect patients suffering from acute CO cardiotoxicity. The main objective of this study is to detect the cardiac effects of carbon monoxide toxicity through the estimation of cardiac biomarkers.

Subjects and Methods: An observational prospective study design was used in the data collection process. Cardiovascular system examination and Electrocardiography (ECG) were performed for eighty CO poisoned patients who reported to Poison Control Center (PCC), Ain Shams university Hospital, Egypt over six months. Patients with coronary artery disease or other known heart disease, patients with renal failure as well as smoker subjects were excluded. Carboxyhemoglobin level (COHb), serial cardiac markers (serum of aspartate aminotransferase (AST), creatine kinase-MB (CPK-MB), lactate dehydrogenase (LDH), and cardiac troponin-I (cTnI) quantitative determination) have been assessed.

Results: ECG changes were present in 67.7% of patients. cTnI was 100% sensitive and 73.2% specific, CPK-MB was 79.5% sensitive and 92.7% specific, LDH was 69.2% sensitive and 92.6% specific while AST was 71.8% sensitive and 73.2% specific. cTnI was found elevated in 43 out of 80 cases. There was no statistical significant difference between cardiac markers in patients with normal and changed ECG. There was no statistical significant difference between COHb in patients with normal and elevated cTnI.

Conclusion: Although CO poisoned patients may present to the PCC, fully conscious, with low COHb level, even with free ECG recordings, yet the possibility of cardiac affection should not be excluded. This highlights the importance of cTnI detection in the serum of CO poisoned patients even those with normal ECG recordings to detect any minute cardiac injury.