© 2007 American Thoracic Society
Ventilator-induced Lung Injury Distribution: The Key to Understanding Injury MechanismsTo the Editor:Unfortunately, there are few studies about the regional distribution of ventilator-induced lung injury (VILI), but, in a recent article, Tsuchida and colleagues (1) demonstrated that in previously injured rat lungs, injury does not occur in atelectatic regions but occurs instead in remote nondependent and nonatelectatic regions. We published a study with similar results in previously normal rat lungs (2). However, both studies are in an apparent conflict with two other studies (3, 4). Broccard and coworkers studied the regional distribution of histologic damage in mechanically ventilated dogs with lungs previously injured by oleic acid. In the supine position, the dependent region showed more intense histologic damage (3). Similarly, Takeuchi and coworkers demonstrated in sheep with lungs previously injured by saline lavage that histologic damage and induction of proinflammatory mediators were higher in the dependent region (4). The contradictory results of the injury distribution can be explained by the different ventilatory settings. In the animal groups of the studies that showed injury predominance in dependent regions, animals were ventilated with positive end-expiratory pressure (PEEP) around 17 (4) or 11 cm H2O (3). In animal groups of the studies that showed injury predominance in nondependent regions, animals were ventilated with PEEP between 4 and 7 cm H2O (1) or zero (2). It is evident that in the studies that showed nondependent predominance of lung injury and induction of proinflammatory mediators, a lower PEEP was used. We can hypothesize that, in these studies, tidal volume was shifted by dependent atelectasis toward nondependent regions. The same hypothesis was offered by Tsuchida and coworkers in their discussion. In contrast, in the studies where animals showed dependent predominance of lung injury and induction of proinflammatory mediators, a higher PEEP was used. This higher PEEP may have lessened atelectasis at dependent regions and overdistended nondependent regions due to the higher transpulmonary pressure present, causing predominant ventilation in the dependent regions. There is no fixed dependent or nondependent predominance of VILI. However, the sites of greater injury depend on ventilatory settings. As lung injury occurs in the more ventilated regions, considering the studies that showed injury predominance in the nondependent region, it is clear that cyclic alveolar overdistention and not cyclic small airway reopening is the main mechanism of VILI. This hypothesis was previously suggested by an in vitro study that showed higher alveolar epithelial death with cyclic large-amplitude deformations (5). Tsuchida and coworkers' study corroborates this hypothesis.
Pulmonary Division—University of São Paulo and Centro de Tratamento e Pesquisa do Hospital do Câncer São Paulo, Brazil FOOTNOTES Conflict of Interest Statement: P.C. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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