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We completely agree with the assertion that methods to improve minute ventilation (MV) in stable hypercapnic chronic obstructive pulmonary disease (COPD) patients are of clinical relevance and we appreciate Esquinas and Petroianni highlighting factors that might facilitate a clinical extrapolation of our findings.
We agree with the fact that improvements in clinically-relevant parameters during noninvasive ventilation (NIV) are dependent on different factors such as inspiratory muscle unloading (Citation1), decreasing lung hyperinflation (Citation2), or simply increasing MV. However, to the best of our knowledge there is no conclusive evidence directly linking NIV with a decrease in lung hyperinflation in COPD patients; several studies showed no change in total lung capacity after a period of effective ventilation (Citation3–5). Although Esquinas and Petroianni pointed out that residual volume and total lung capacity in our study increased over time, it is also important to note that these changes were not even close to being statistically significant (p = 0.95 and p = 0.52, respectively).
From a pathophysiological point of view, Esquinas and Petroianni are correct in assuming that differences in respiratory rate between obese and non-obese COPD patients might be due to the higher levels of ventilatory drive required to maintain normocapnia in obese patients. However, in our study respiratory rate during spontaneous breathing was lower in obese compared with non-obese patients. Therefore, whether or not the detection of lower MV during iVAPS in non-obese versus obese COPD patients can be explained by trigger problems in non-obese patients due to greater hyperinflation or, as Esquinas and Petroianni stated, due to the restrictive component in obese COPD patients, needs to be investigated in future trials.
Regarding PaCO2 values before starting high-intensity NPPV (HI-NPPV) and their proportionality with the achieved results, we would like to point out that the studies cited by the correspondents (Citation6–8) did not use HI-NPPV strictly according to the definition (Citation3,4). Furthermore, we did not show that non-obese COPD patients failed to achieve a good reduction in PaCO2 because PaCO2 values were not addressed in our study. It is highly likely that the lower respiratory rate and, therefore also MV, might result in higher values of PaCO2 but, again, this was not shown in our study.
We do agree with Esquinas and Petroianni that results obtained using daytime measurements are not directly transferable to night-time ventilation, and highlighted this as part of the discussion of study limitations in the paper. Finally, we would like to thank Esquinas and Petroianni for their meaningful comments regarding our manuscript.
Declaration of Interest
The study was supported by an unrestricted research grant from ResMed Germany Inc., Martinsried, Germany. The authors state that the sponsor had no input into the study design, results or interpretation, or manuscript preparation. English language editing assistance was provided by Nicola Ryan. This assistance was funded by Resmed.
The authors’ state that neither the study design, the results, the interpretation of the findings, nor any other subject discussed in the submitted manuscript was dependent on support.
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