The second objective of our study was to validate a recently proposed method to evaluate the VD physiol /V T ratio [14] . The method is based on CO 2 production calculated from the Harris-Benedict equation [19] and on the expired minute ventilation. Siddiki et al. [14] reported that it was associated with mortality in acute lung injury patients in a dose-response manner and proposed its routine use to estimate VD physiol /V T . However, they did not report any comparison with measured VD physiol /V T . In the present study, we have demonstrated that this method significantly underestimates VD physiol /V T , rendering it not accurate enough to assess the degree of lung injury. Interestingly, changes in estimated VD physiol /V T during PP appeared better correlated with changes in measured VD physiol /V T and could be proposed in the future in this field. Siddiki et al. [14] proposed the method in the context of a much larger series than ours and in patients with less severe ARDS, rendering it difficult to draw any definitive conclusions. Our work is limited by the small number of patients included. This is a consequence of our routine protocol, which strictly restricts PP to patients with the most severe ARDS, that is, those with a PaO 2 /FiO 2 ratio < 100 mmHg after 48 hours of ventilation. This also explains why it is not possible to link our results to outcomes. However, despite this limitation, we consider our results relevant from a physiological point of view.