Citation

Hess DR. Respir. Care 2017; 62(10): 1333-1342.

Affiliation

Massachusetts General Hospital and Harvard Medical School. dhess@aarc.org.

Copyright

(Copyright © 2017, American Association for Respiratory Therapy, Publisher Daedalus Enterprises)

DOI

10.4187/respcare.05781

PMID

28807985

Abstract

Carbon monoxide (CO) is usually recognized as a toxic gas that can be used to assess lung function in the pulmonary function laboratory. The toxicity of CO relates to its high affinity for hemoglobin and other heme molecules, producing carboxyhemoglobin (HbCO). Despite that blood HbCO levels are commonly measured in patients with CO poisoning, the clinical presentation often does not correlate with the HbCO level, and clinical improvement in the patient's condition does not correlate with HbCO clearance. In patients with CO poisoning, administration of 100% O2 is standard practice. If available, hyperbaric O2 can be used, although this is controversial. Measurement of exhaled CO might be useful to estimate HbCO, such as in smoking cessation programs, but assessment of HbCO using pulse oximetry can be misleading. Endogenous CO is generated as the result of heme oxygenase activity. It is becoming increasingly recognized that the results of heme oxygenase activity, specifically CO production, might have important physiologic functions. These include effects on vascular function, inflammation, apoptosis, cell proliferation, and signaling pathways. Given the abundance of basic science supporting a therapeutic role for CO, clinical trials are exploring this potential.

Copyright © 2017 by Daedalus Enterprises.

Language: en

Keywords

carbon monoxide; carbon monoxide poisoning; carboxyhemoglobin; heme oxygenase