Pathophysiology, clinics, diagnosis and treatment of heart involvement in carbon monoxide poisoning

Abstract

The toxicity of carbon monoxide has been recognized for long throughout history and is unquestionably the leading cause of unintentional poisoning deaths in the Western countries. The severity of poisoning is dependent upon environmental and human factor. The leading pathophysiological mechanism resides in the ability of carbon monoxide to bind to hemoglobin molecules with high affinity, displacing oxygen and generating carboxyhemoglobin, which is virtually ineffective to deliver oxygen to the tissues. The organs with the highest demand for oxygen such as the brain and the heart are more vulnerable to injury. Myocardial involvement is commonplace in moderate to severe carbon monoxide poisoning and is associated with a substantially higher risk of mortality. Besides hypoxic damage, carbon monoxide produces myocardium injuries with cardiospecific mechanisms, mostly attributable to direct damage at cellular or subcellular level. The clinical spectrum of heart involvement is broad and encompasses cardiomyopathy, angina attack, myocardial infarction, arrhythmias and heart failure up to myocardial stunning, cardiogenic shock and sudden death. Patients with underlying cardiac disease, especially coronary heart disease, are at greater risk of infarction and arrhythmias. Single photon emission computed tomography (SPECT) is the technique of choice for diagnosing cardiac involvement, whereas the recent introduction of the highly sensitive troponin immunoassays seems promising for the early triage of patients. No specific treatment other than oxygen delivery can be advocated for cardiac toxicity at present, and 100% oxygen therapy should be continued until the patient is asymptomatic and carboxyhemoglobin levels decrease below 5-10%.