Measuring End-Tidal CO2 During Intentional Rebreathing

To the Editor: I read with interest the recent article by Chassard et al. 1, which reported that increasing ETCO2 does not increase lower esophageal sphincter tone in pigs. The investigators used a rebreathing method for increasing the ETCO (2), but, as described, this methodology poses some potential problems. The authors' protocol only measured ETCO2, which may or may not be representative of PaCO (2) in their experimental design. The "40 cm of dead space" added to the Y-piece on the breathing system increased the total dead space ventilation by its contribution to the apparatus dead space. This maneuver typically does not increase the end-tidal to arterial PCO2 gradient that is characteristic of increases in alveolar dead space. However, a different bias is introduced if the sampling site remains at the Y-piece (as opposed to the endotracheal tube connector), as ETCO2 values can be falsely decreased by a diluent effect of the fresh gas flow 2. The authors do not report where sampling took place. Additionally, the volume (not the length) of the extra apparatus dead space is the meaningful variable. When the tidal volume to apparatus dead space ratio is low, ETCO2 sampling can be an unreliable reflection of alveolar and arterial PCO22. While measuring ETCO2 is noninvasive, convenient, and relatively inexpensive compared with measuring PaCO2, one must remember that it is an approximation of PaCO2. Equating these two variables requires that several conditions hold true. Thus, an arterial sample should be measured at least once to document the end-tidal to arterial gradient and justify the use of ETCO2 as a surrogate measurement. Jerome M. Klafta, MD Department of Anesthesia and Critical Care The University of Chicago Hospitals Chicago, IL 60637