One of the objectives of our study was to describe alterations in VD alv induced by PP. ARDS is characterized by a heterogeneous lung with the existence of a slow compartment [18, 20] , defined as areas available for, but partially or totally excluded from, ventilation due in part to a bronchiolar collapse [12, 21] . In a previous study, we reported that PP may induce recruitment of this slow compartment, as suggested by its ability to counteract intrinsic PEEP and to decrease the expiratory time constant [12] . In the same study, we also reported that PP leads to a decrease in PaCO 2 , suggesting diminution of VD alv (alveolar dead space) [12] . Our present study demonstrates that PP may induce a decrease in VD alv . It occurred from the third hour and was maintained throughout the PP session. VD alv may be the consequence of nonperfused or poorly perfused lung areas in ventilated anterior areas, but also of a slow compartment partially excluded from ventilation. Our results suggest that PP induces functional lung recruitment, especially since decreases in VD alv related to PP were associated with a decrease in Pplat and strongly correlated with improvement in compliance. did not report a decrease in Pplat in PP, as we found, but after returning patients to the supine position [22] . This could be explained by the fact that they used roll under the upper part of the chest wall, leading to a significant impairment in chest wall compliance [22] , whereas we did not. The most beneficial reported effect of PP is oxygenation improvement [24, 25] . However, this better oxygenation can be due to (1) lung recruitment related to restoration of functional residual capacity [7] and improvement of the diaphragmatic movement in the posterior part [26] [27] [28] or (2) simply to an improvement in the ventilation/perfusion ratio due to a decreased hydrostatic gradient between the anterior and posterior parts of the lung [26, 29] . Whereas the first mechanism is crucial, one can say that the second mechanism is less important. This is why the second objective of our study was to test whether the response to PP in terms of PaCO 2 was physiologically more relevant than in terms of PaO 2 /FiO 2 ratio. Gattinoni et al. [10] reported that an increase in PaO 2 /FiO 2 ratio > 20 mmHg after six hours of PP is not predictive of the patient's prognosis, whereas a decline in PaCO 2 ≥1 mmHg is. In our present study, 7 of 13 patients were PaO 2 responders (increased PaO 2 /FiO 2 ratio > 20 mmHg after 15 hours of PP). However, changes in Pplat, PaCO 2 and VD alv did not differ between PaO 2 responders and PaO 2 nonresponders. On the other hand, 7 of 13 patients were PaCO 2 responders (decreased PaCO 2 > 2 mmHg after 15 hours of PP). PaCO 2 responders had a significant decrease in Pplat and VD alv , as well as a significant increase in oxygenation and compliance, compared with nonresponders. Our results are in accordance with a recent study of 32 ARDS patients [23] , in which the investigators reported that PaCO 2 variation induced by PP, and not PaO 2 /FiO 2 variation, is associated with lung recruitability. Interestingly, in our study, changes in VD alv were not correlated with changes in oxygenation but were strongly correlated with changes in compliance of the respiratory system.