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Department of Anesthesiology, University Clinics UCL of Mont-Godinne, Yvoir, Belgium
To The Editor:
We read with interest the article by Berkenbosch et al. (1), who compared the accuracy of end-tidal CO2 (ETCO2) and transcutaneous CO2 (TCCO2) monitoring in >4-yr-old patients suffering from respiratory failure. This article is particularly interesting in that it defends the use of TCCO2monitoring, which remains an underused monitoring tool for most of us.
The authors discussed the efficiency of ETCO2 monitoring, arguing that it tends to underestimate PaCO2 levels because of a failure to document alveolar ventilation, and that these discrepancies started to occur at a PaO2/PaO2 ratio <0.3. This manner of presentation could mislead readers who are not familiar with the subtleties of ETCO2 monitoring. It is important to remember that the sample of exhaled gases that is used to measure ETCO2 is an image of the total mixture emptied from the lungs, except from West Zone 3 (nonventilated and perfused territories) (2). Yet among the alveoli that have been ventilated, some have participated in gas exchanges, and the product of their exhalation is therefore charged in CO2, corresponding to West Zone 2 (ventilated and perfused territories), whereas others have not, true to the definition of West Zone 1 (ventilated and nonperfused territories). It is specifically the presence of the latter which causes the dilution of gases exhaled from West Zone 2, which contains CO2 proportionally to PaCO2, by gases containing no CO2. It is therefore here that the PaCO2/ETCO2 gradient originates, in proportion to the size of West zone 1, still known as alveolar dead space.
This phenomenon therefore has nothing to do with a PaO2/PaO2 ratio, which is mainly linked to the presence of West Zone 3, corresponding truly to the notion of shunt.
Establishing an amalgam between these two phenomena, although they may be associated to varying degrees in numerous clinical diseases, is a shortcut that is not conducive to a clear understanding of the mechanisms involved.
References
Child Health, Pediatric Critical Care, University of Missouri–Columbia, Columbia, MO
In Response:
We would like to thank Dr. Broka for his comments regarding the use of the PaO2/PaO2 ratio referred to in our recent article (1). As our intent in this paper was primarily to draw attention to the accuracy of transcutaneous CO2 monitoring in the older pediatric patient, our discussion regarding the limitations of end-tidal (ETCO2) monitoring in this population was somewhat less detailed that it could have been, and we thank the respondent for his expansion upon this.
What we attempted to point out in the paper and what the respondent has clarified is the principle that the ETCO2 (PACO2) to PaCO2 gradient increases with increasing dead space ventilation. This is what we referred to as the failure to achieve and therefore document alveolar ventilation. As the respondent points out, a major reason for this is dilution of CO2-rich gas from lung regions conforming to West Zone 2 conditions (ventilated and perfused) by CO2-poor gas from lung regions conforming to West Zone 1 conditions (ventilated but not perfused). The respondent’s conclusion, therefore, is that the increase in West Zone 1 conditions (alveolar dead space) often seen in the critical care environment accounts for the increased ETCO2 to PaCO2 gradient we reported.
However, this conclusion assumes unimpeded delivery of the CO2-poor alveolar gas from these West Zone 1 regions to the ETCO2 detector. This may not always be the case, such as in patients with severe status asthmaticus. Under these conditions, regions of the lung may very well conform to West Zone 2 conditions but be so severely obstructed that delivery of their CO2-rich alveolar gas to the ETCO2 detector does not occur; this is the phenomenon referred to as air trapping. Under these conditions, the ETCO2 to PaCO2 gradient is also increased but the predominant mechanism is the persistent ventilation of more proximal airways, representing an increase in anatomical, rather than alveolar, dead space (2). It is interesting that the greatest increases in the ETCO2 to PaCO2 gradient we found were in the patients with status asthmaticus and that clinical resolution of disease correlated nicely with a decrease in the ETCO2 to PaCO2 difference.
Therefore, while increases in the ETCO2 to PaCO2 difference certainly do derive from increases in alveolar dead space, particularly in the critical care environment, contributions may also occur from increases of anatomic dead space, with the relative contribution of each being dependent on the pathophysiologic process present.
References
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