Anesth Analg 2005;100:896
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000146646.02457.55
LETTER TO THE EDITOR
Exhaled CO After Surgery: A Consequence of Postoperative Narcotics?
Marshall B. Dunning, III, PhD, MS, and
Harvey J. Woehlck, MD
Division of Pulmonary/Critical Care Medicine; Medical College of Wisconsin; mdunning{at}mcw.edu (Dunning)
Department of Anesthesiology; Medical College of Wisconsin; Milwaukee, WI (Woehlck)
To the Editor:
Hayashi et al. (1) attribute increased exhaled carbon monoxide (CO) or carboxyhemoglobin (COHb) concentrations after surgery and anesthesia to increased production from stress-induced activation of heme oxidase. Many factors may confound this relationship. Oxygen at 4.0 L/min was administered postoperatively, but the resulting inspired oxygen concentrations (Fio2) during gas sampling were not reported. Because exhaled CO concentrations vary with Fio2 at the same COHb (2–4), errors of attribution may result. Intraoperatively, increased Fio2 may speed CO elimination and reduce COHb, introducing additional errors of attribution. Second, at the same endogenous production rate and Fio2, alveolar ventilation is inversely related to COHb once a new steady state is achieved. The half-life of CO averages 4 h, but ranges from 23 min to 11 h with extremes of ventilatory parameters (2). If mechanical ventilation increased alveolar ventilation, CO and COHb may decrease from increased elimination. If narcotics depressed spontaneous ventilation intraoperatively or postoperatively, CO and COHb may increase, rendering them poor markers of endogenous CO production. Third, regardless of minute ventilation, rebreathing during low flow anesthesia may increase CO and COHb via impaired elimination (3–5). The authors do not provide necessary data to calculate rebreathing, nor was rebreathing controlled during the study. Fourth, there was no control group. The observed changes may result from systematic pharmacokinetic alterations, requiring a nonoperative control group. Alternatively, since the CO production rate = elimination rate + accumulation, the production rate can be calculated from timed expiratory gas collections and COHb measurements. The authors must demonstrate that their results transcend mere pharmacokinetic effects of Fio2, rebreathing, and alveolar ventilation. Finally, one should determine whether metabolism of extravasated blood or transfused, senescent red cells could account for any actual increased CO production.
References
- Hayashi M, Talahashi T, Morimatsu H, et al. Increased carbon monoxide concentration in exhaled air after surgery and anesthesia. Anesth Analg 2004;99:444–8.[Abstract/Free Full Text]
- Pearce AC, Jones RM. Smoking and anesthesia: preoperative abstinence and perioperative morbidity. Anesthesiology 1984;61:576–84.[ISI][Medline]
- Coburn RF, Forster RE, Kane PB. Considerations of the physiological variables that determine the blood carboxyhemoglobin concentration in man. J Clin Invest 1965;44:1899–910.
- Peterson JE, Stewart RD. Predicting the carboxyhemoglobin levels resulting from carbon monoxide exposures. J Applied Physiol 1975;39:633–8.[Abstract/Free Full Text]
- Woehlck HJ, Mei D, Dunning MB III, Ruiz F. Mathematical modeling of carbon monoxide exposures from anesthetic breakdown. Anesthesiology 2001;94:457–60.[Medline]
