the risk of muscular exhaustion leading to rapid shallow breathing and hypercarbia, while avoiding the risk of additional lung injury, self-inflicted by high transpulmonary pressure and VT. Noninvasive respiratory support that grants lungand diaphragmprotective ventilation should then be considered as ideal (3, 4). The authors should be commended for providing a complete set of physiological data that could enhance our understanding of the effects of different noninvasive support in patients with AHRF. Overall, helmet NIV dramatically decreased the inspiratory effort compared with HFNC. Thus, helmet NIV could be highly efficient in decreasing the diaphragm workload to a desired physiological level, able to protect it from myotrauma and failure (3). On the lung protection side, the authors measured transpulmonary pressure swings (ΔPL) as a surrogate of dynamic lung stress during both study phases, reporting nonsignificant differences between HFNC and helmet NIV (Figure 2 of Reference 1, right upper panel; P= 0.11) (1). The reduction in inspiratory effort during helmet NIV might have been due to two different mechanisms: the improvement in respiratory mechanics because of higher positive end-expiratory pressure effect and/or the muscles unloading owing to pressure support. For a given VT, with the first mechanism, the decrease in inspiratory effort (DPES) would be associated with a decrease in ΔPL (5); on the opposite side, pressure support could decrease DPES with unchanged (if mechanics remain stable) or even increased ΔPL (in the presence of overdistension). Thus, identifying which mechanism is predominant in each patient might help individualize the type of support and NIV settings more than looking at average global values. As an example, it could be interesting to investigate whether the changes in DPES and ΔPL between HFNC and helmet NIV were correlated with end-expiratory transpulmonary pressure during HFNC (6), with subjects with highly negative values experiencing unchanged or even decreased ΔPL. If this correlation does exist, helmet NIV would be preferred to HFNC in patients with very low end-expiratory transpulmonary pressure. The finding that patients with lower DPES during HFNC increased ΔPL more during helmet NIV could further corroborate this hypothesis: indeed, there was no correlation between DPES and oxygenation during HFNC, suggesting that the major determinant of respiratory effort is not altered gas exchange, but rather worse respiratory mechanics and inflammation (4). The authors also describe that higher ΔPL during helmet NIV was associated with the need for intubation and with mortality. The latter is undoubtedly an exploratory analysis, but it is interesting to note that seven out of eight patients who ultimately required intubation were clinically supported by helmet NIV for a certain number of hours. It would be interesting to explore whether this might have led to higher lung stress and additional lung injury. Additional explorative analyses could include comparing gas exchange during the study protocol and the last one measured before intubation to check whether lung edema worsened or if derangements of pH and PaCO2 were the main determinants of intubation. Already, looking at the results, it seems that the ability to limit lung stress by helmet NIV might be lower than during HFNC. Helmet NIV could be considered as step-up support before intubation only in selected patients or if monitoring confirms lung-protective conditions. n Author disclosures are available with the text of this letter at www.atsjournals.org.
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