Carboxyhemoglobin levels in medical intensive care patients

Abstract

We read with interest the study by Fazekas and colleagues demonstrating that lower levels of carboxyhemoglobin are associated with increased mortality in critically ill patients [1]. Th is observation is of interest since prior studies have shown that carbon monoxide (CO), the silent killer, may actually have therapeutic applications. CO suppresses infl ammation and apoptosis, reduces pulmonary hypertension and potentially protects against multiple organ injury in animal models [2]. Th e fact that average carboxyhemoglobin levels are slightly lower in ICU nonsurvivors compared with survivors (1.5% vs. 1.6%, P = 0.003) supports the fi ndings of animal studies. However, an important confounding factor deserves consideration. ICU nonsurvivors are sicker and therefore likely to receive a higher FiO 2 than ICU survivors. Most hospitals supply oxygen from liquid oxygen, whereas medical air is supplied by compressing fi ltered environmental air. Previous work at Pittsburgh has shown that nitric oxide (NO) contamination of compression medical air resulted in a clinically detectable diff erence in NO levels that directly altered oxygenation [3]. Th e air in most major cities is also contaminated with CO [4] consequent to fossil fuel combustion. Medical air thus contains varying amounts of CO, as well as other pollutants. Patients receiving a higher FiO 2 receive less medical air, and are therefore exposed to less occult CO. Th is reduction in medical air might explain the small diff erences in carboxyhemoglobin seen in the present study, just as it explained the lower NO levels. Until this confounding infl uence is accounted for, the prior observations may merely refl ect this CO washout phenomenon.