© 2007 American Thoracic Society
Ventilator-induced Lung Injury Distribution: The Key to Understanding Injury MechanismsFrom the Authors:We thank Dr. Mitzner for his kind comments on our article (1), and agree with his concerns about the pressure–volume (PV) curves in this model. The "baby lung concept" was proposed by Dr. Gattinoni and colleagues, who examined the amount of aerated lung tissue at three different positive end-expiratory pressure (PEEP) levels, and measured the PV curve in patients with acute respiratory distress syndrome (ARDS) (2). Those data, among others, suggested that the PV curve in ARDS reflects better the residual aerated regions and is a poor estimate of the atelectatic regions. Although the current PV curves were constructed on the edematous lungs of very small animals, potentially causing an experimental or analytic artifact as Dr. Mitzner pointed out, edematous lungs can certainly exhibit unusual PV curves (3). In the current study, we directly measured the volume of aerated lung tissue at end-expiration, and constructed PV curves in both the "lavaged noninjurious" and "lavaged injurious" groups (1). The PV curves mirrored the FRC in each group, allowing us to confirm the above concept. In fact, the inherent limitation of standard PV curves is such that the atelectatic regions are not estimated and that information on the regional lung mechanics is not available at all. We used stereologic techniques to compare the mean alveolar volume between dependent and nondependent regions because we thought that the "absolute alveolar volume" would directly reflect the regional differences in alveolar recruitment. Although we know that the mean alveolar volume conveys only an aspect of regional alveolar recruitment—as described in our article (1)—it provided us with a new insight into the relationship between the regional atelectasis and lung injury. Ideally, in the future we would like to see the "regional PV curve," as proposed by Dr. Hubmayr and colleagues (3, 4), in more widespread use. As for the regional distribution of lung injury, we totally agree with Dr. Caruso's comments. Dr. Takeuchi and colleagues demonstrated that lung injury was more predominant in dependent versus nondependent regions, although the bronchoalveolar lavage cytology did not parallel the histology (5). The contradictory distribution of lung injury can be explained by the different ventilatory settings, especially different PEEP levels. In fact, we failed to show a regional difference in lung injury when we adopted higher PEEP (= 9 cm H2O) in our pilot study. Of the greatest importance herein is not the simple distribution of lung injury but the regional relationship between atelectasis and lung injury. To date, it is unclear whether repetitive opening and closing of distal airways actually takes place in the atelectatic regions and that such a cyclic phenomenon is a direct cause of lung injury. For the comprehensive demonstration of that hypothesis, it would be necessary to show that the cyclic phenomenon occurs exclusively in the atelectatic regions and that distal airway injury develops in the same areas.
The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada FOOTNOTES Conflict of Interest Statement: Neither author has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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