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Protective ventilation strategies are central to the conventional management of patients with the acute respiratory distress syndrome (ARDS). Experimental studies (1) suggest two main mechanisms of ventilator-induced lung injury: volutrauma, injury from excess distension; and atelectrauma, local shear injury from tidal opening and closing. Lung distension and tidal opening result from a balance of recruitment and tidal volume, but the contribution of each is unpredictable. Thus, while sound principles exist for population-based recommendations-avoid excess lung stretch-the specifics remain polemic.
In this issue of the Journal, Bellani and coworkers (pp. 1193- 1199) report that, in patients with ARDS, the metabolic activity- likely reflecting inflammation-in aerated lung regions was correlated with the tidal volume delivered to those regions, as well as to the overall plateau pressure (2). The data, determined using cross-registration of lung computerized tomography and positron emission tomography (PET) imaging of [18F]fluoro-2- deoxy-glucose, support the notion that overdistension is injurious to aerated lung.
These are the first such data from patients with ARDS and, unsurprisingly, questions remain. Although the metabolic signal is presumed to come from activated neutrophils, we do not know this for sure. It could be a signal from alveolar Type II cells; after all, stretch is known to activate such cells and initiate a myriad of signaling cascades (3), and such activation could be injurious or could reflect beneficial processes such as surfactant synthesis or active alveolar fluid clearance. Even if the source of the signal was neutophils, we do not know whether it reflects stretch or preexisting inflammation.
The data on lung distension (2) are consistent with previous reports that lowering tidal volume reduces both lung inflammation (4) and mortality (5), but also provide important additional insight. When plateau pressures exceeded 26-27 cm H2O, a level lower than what many clinicians consider a safe limit, an "injury" signal was apparent (2). This pressure level is similar to that in the lower tidal volume group in the ARDS Network trial (5) and supports the prediction that tidal volume reduction could confer additional benefit even at lower plateau pressure (6). Thus, "excess" distension of normally aerated lung regions is adverse, and the associated injury may be rapid and may occur at lower pressures than previously suspected.
There is, however, an important "flip side"...