Non-infarctual ST elevation and acute cardiopulmonary failure in carbon monoxide poisoning: a case report

Y. Longhitano, M. Candelli, H.A. Muir, A. Audo, S. Meda, P. Dennet Lumb, J. Marshall Berger, G. Pignataro, S. Cicchinelli, C. Zanza, F. Franceschi

Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA. lon.yaro@gmail.com

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• Cardiology

OBJECTIVE: Carbon monoxide is produced by the incomplete combustion of organic fuel. In the United States, it is responsible for about 500 deaths annually. Increased carboxyhemoglobin concentration and hypoxia disrupt cardiac myocyte integrity and cause dysrhythmias, acute cardiac failure and coronary artery disease. We described a case of a patient with CO-poisoning and ST elevation at ECG precordial leads who developed severe transient heart failure.

CASE PRESENTATION: A 57-year-old man was admitted to the emergency department for acute carbon monoxide poisoning that led to respiratory and cardiac failure. The electrocardiogram showed ST elevation in precordial leads, but the coronary angiography was normal. The patient was successfully treated and discharged. Three days later he was readmitted for similar symptoms and subsequently died. We hypothesize that the ECG findings were related to transient coronary vasospasm due to CO poisoning and that acute respiratory and cardiac failure related to carbon monoxide toxicity caused death.

CONCLUSIONS: The management of patients poisoned by carbon monoxide requires early identification and intensive treatment and a careful evaluation of the home environment prior to discharge. ST elevation in such patients may be related to coronary vasospasm.

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