© 2005 American Thoracic Society
Blood Carbon Monoxide Will Increase from a Decline in Pulmonary Function AloneTo the Editor:Yasuda and colleagues recently reported increased levels of carboxyhemoglobin (HbCO) in patients with COPD and suggested that the increase resulted from increased endogenous production of CO caused by "lung and systemic inflammation and production of reactive oxygen species" (1). No consideration was given to the effect of the major alterations of gas exchange in COPD on the HbCO level that would be expected without any change in the endogenous production in COPD. Yet, we know from the classical work of Coburn, Forster, and Kane (2) that a decrease in alveolar ventilation, a decrease in the carbon monoxide diffusing capacity (DLCO), or a decrease in the capillary oxygen tension would cause an increase in HbCO with no change in production. The patients in the current study had a significant increase in the arterial PCO2 (53.5 compared with 40.5 mm Hg in controls), compatible with a decrease in alveolar ventilation, and a significant decrease in arterial PO2 (64.4 compared with 90.2 mm Hg), compatible with a decrease in capillary O2 tension. DLCO measurements were not reported, but it is highly likely that DLCO would have been reduced in the patients studied. Thus, the patients of the present study would have had elevated HbCO levels as a result of the abnormal pulmonary function alone. It should be apparent that without actual measurements of the endogenous production, we cannot learn any more about inflammation from an increase in HbCO than we could about endogenous CO2 production from an increase in arterial PCO2. Either could become elevated without a change in endogenous production from a decrease in alveolar ventilation alone. There are methods to measure the endogenous production of CO (3), and it has been reported that increased endogenous CO production occurs in patients with severe sepsis (4); but these methods were not applied in the current study. The authors used the arteriovenous HbCO concentration differences in an attempt to gain insight into CO production, but it is highly unlikely that these differences reflect endogenous production. The affinity of CO for hemoglobin is so great that there is a negligible arteriovenous difference (5). The apparent arteriovenous difference found in the current study is likely the result of a dependence of the spectrophotometrically measured HbCO on the difference in the oxygen tension between venous and arterial blood (6).
Johns Hopkins University, Baltimore, Maryland FOOTNOTES Conflict of Interest Statement: Neither of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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