Hemodynamic response to carbon monoxide.

Abstract

Historically, and at present, carbon monoxide is a major gaseous poison responsible for widespread morbidity and mortality. From threshold to maximal nonlethal levels, a variety of cardiovascular changes occur, both immediately and in the long term, whose homeostatic function it is to renormalize tissue oxygen delivery. However, notwithstanding numerous studies over the past century, the literature remains equivocal regarding the hemodynamic responses in animals and humans, although CO hypoxia is clearly different in several respects from hypoxic hypoxia. Factors complicating interpretation of experimental findings include species, CO dose level and rate, route of CO delivery, duration, level of exertion, state of consciousness, and anesthetic agent used. For example, tachycardia is commonly observed, although bradycardia also can result from myocardial and/or central nervous system (CNS) hypoxemia at high carboxyhemoglobin (COHb) saturations, as can electrocardiographic abnormalities. Augmented cardiac output usually observed with moderate COHb may be compromised in more severe poisoning for the same reasons, such that regional or global ischemia result. The hypotension usually seen in most animal studies is thought to be a primary cause of CNS damage resulting from acute CO poisoning, yet the exact mechanism(s) remains unproven in both animals and humans, as does the way in which CO produces hypotension. This review briefly summarizes the literature relevant to the short- and long-term hemodynamic responses reported in animals and humans. It concludes by presenting an overview using data from a single species in which the most complete work has been done to date.

Carbon monoxide poisoning

“…Early cardiovascular effects of CO poisoning are manifested as a response to hypoxia [103]. More significant exposures result in hypotension, dysrhythmia, ischemia, infarction, and, in extreme cases, cardiac arrest.…”

“…Chronic CO exposure may accelerate atherosclerosis, although other risk factors, such as smoking, confound the picture [105]. In addition, chronic CO exposure has been associated with polycythemia and cardiomegaly, likely secondary to chronic hypoxia [103].…”

A Case of Carbon Monoxide Poisoning Presenting with Supraventricular Tachycardia

“…Therefore, patients admitted to the hospital with CO poisoning should have examinations for baseline ECG and serial cardiac enzymes. The severity and duration of myocardial injury depend on the duration and amount of CO exposure (6).…”

“…Myocardial injury in CO poisoning can be demonstrated by elevated cardiac injury biomarkers, e.g., troponin, brainnatriuretic peptide, creatinine kinase, and creatinine kinase-MB and ischemic ECG changes (2,6). Decreased left ventricular ejection fraction and right ventricular dysfunction also can be observed in CO-poisoned patients (2, 7-9).…”

Uncommon MRI and Echocardiographic Findings in a Patient of Carbon Monoxide Poisoning

“…The cardiovascular effects of CO poisoning are manifested initially by tachycardia in response to hypoxia [8] but more significant exposures may result in hypotension, arrhythmias, ischemia, infarction and even cardiac arrest. Most cases of deaths after CO exposure have been reported to be due to cardiac arrhythmias [9].…”