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Arterial carboxyhemoglobin level and outcome in critically ill patients*

Melley, Daniel D. MBBS; Finney, Simon J. PhD; Elia, Androula MSc; Lagan, Anna L. PhD; Quinlan, Gregory J. PhD; Evans, Timothy W. PhD, MD

doi: 10.1097/01.CCM.0000275268.94404.43
Clinical Investigations
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Objective: Arterial carboxyhemoglobin is elevated in patients with critical illness. It is an indicator of the endogenous production of carbon monoxide by the enzyme heme oxygenase, which modulates the response to oxidant stress. The objective was to explore the hypothesis that arterial carboxyhemoglobin level is associated with inflammation and survival in patients requiring cardiothoracic intensive care.

Design: Prospective, observational study.

Setting: A cardiothoracic intensive care unit.

Patients: All patients admitted over a 15-month period.

Interventions: None.

Measurements and Main Results: Arterial carboxyhemoglobin, bilirubin, and standard biochemical, hematologic, and physiologic markers of inflammation were measured in 1,267 patients. Associations were sought between levels of arterial carboxyhemoglobin, markers of the inflammatory response, and clinical outcome. Intensive care unit mortality was associated with lower minimum and greater maximal carboxyhemoglobin levels (p < .0001 and p < .001, respectively). After adjustment for age, gender, illness severity, and other relevant variables, a lower minimum arterial carboxyhemoglobin was associated with an increased risk of death from all causes (odds risk of death, 0.391; 95% confidence interval, 0.190–0.807; p = .011). Arterial carboxyhemoglobin correlated with markers of the inflammatory response.

Conclusions: Both low minimum and high maximum levels of arterial carboxyhemoglobin were associated with increased intensive care mortality. Although the heme oxygenase system is protective, excessive induction may be deleterious. This suggests that there may be an optimal range for heme oxygenase-1 induction.

From the Department of Critical Care Medicine, Imperial College School of Medicine, Royal Brompton Hospital, London, UK.

Supported, in part, by the Garfield Weston Trust (DDM), the British Heart Foundation (TWE, GJQ, ALL), and the Dunhill Medical Trust (TWE, GJQ).

Professor Evans has been (2005–2007) a member of the scientific advisory board for the Gemi Fund (Linde Gas Therapeutics, Lidingö, Sweden), which provides awards for investigation relating to the therapeutic use of inhaled gases. The remaining authors have not disclosed any potential conflicts of interest.

For information regarding this article, E-mail: t.evans@rbht.nhs.uk

© 2007 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins