In patients with acute respiratory distress syndrome (ARDS), ventilatory support is aimed at re-establishing lung aeration in order to provide adequate arterial oxyenation and CO2 elimination. Tidal inflation provides inspiratory lung recruitment and renewal of alveolar gas whereas positive end-expiratory pressure (PEEP) prevents expiratory derecruitment. Hypotheses and concepts proposed to explain the loss of aeration characterizing the injured lung directly impact the optimization of the ventilatory strategy aimed at re-establishing adequate gas exchange and avoiding ventilator-induced lung injury (VILI). One of the major advances in the understanding of the mechanisms of aeration loss has been the possibility of directly measuring lung volumes of gas and tissue and the distribution of lung aeration using lung computed tomography (CT) [1]. The current and well-accepted view of the ARDS lung relies on the 'sponge theory' where alveolar collapse plays a pivotal role: the injured lung collapses under his own weight according to gravity [2] and 'opening' pressures of the lung increase from the sternum to the diaphragm in the supine position [3]. The respiratory effects of mechanical ventilation are thought to act according to the 'opening and collapse hypothesis': tidal volume (Vt) participates in 'lung reopening' if insufficient PEEP does not prevent end-expiratory lung collapse by counteracting entirely the 'superimposed pressure' resulting from the increased lung weight. Lung barotrauma appears as the direct result of repetitive opening and collapse of lung units as demonstrated experimentally; the high local pressure stress applied to collapsed lung units induces bronchiolar lesions [4] and the systemic release of inflammatory cytokines that participates in multiorgan failure and death [5, 6]. As a consequence, the logical ventilatory strategy is to 'keep the lung fully open' by increasing PEEP [7] and reducing Vt to avoid 'lung volutrauma', another form of VILI [8].

This theory that views the ARDS lung mainly as a 'collapsed' lung, is largely invalidated by recent experimental data [9, 10], is far from supported by CT data obtained in the whole lung, and is difficult to reconcile with the pathophysiology of ARDS [11] and the theoretical concepts governing alveolar inflation and collapse [12]. In addition, it does not fit experimental and clinical studies showing that VILI is made for a good part ofbronchiolar and alveolar distension [13,14]. Last but not least, the reappraisal of mechanisms of aeration loss and VILI directly impacts the ventilatory strategy and questions the concept of keeping the lung fully open at end-expiration.

The aim of the present chapter is to review how the mechanisms and the distribution of aeration loss in ARDS (lung morphology) impact ventilatory strategy and the prevention of VILI.

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