© 2007 American Thoracic Society doi: 10.1164/rccm.200610-1564ED
Tidal Recruitment and Overinflation in Acute Respiratory Distress SyndromeYin and YangPitié-Salpêtrière Hospital and University Pierre et Marie Curie, Paris-6, France
Henri Mondor Hospital and University Paris-12, Paris, France In this issue of the AJRCCM (pp. 160–166), Terragni and coworkers provide compelling evidence in patients with the acute respiratory distress syndrome (ARDS) that low tidal volume ventilation can be associated with cyclic hyperinflation of lung areas normally aerated at end-expiration (1). Using computed tomography of the whole lung, the authors demonstrate that around 80% of the tidal volume is directed toward aerated lung regions, whereas the remaining part of the tidal volume ensures the cyclic recruitment of nonaerated lung regions. In the majority of patients, tidal recruitment is associated with inflation of lung regions normally aerated at end-expiration. In one-third of the patients, however, hyperinflation largely predominates over recruitment, bringing into question the protection against ventilator-induced lung injury expected from the ARDSnet (Acute Respiratory Distress Syndrome Network) ventilatory strategy. Interestingly, the pulmonary inflammatory response, assessed as the concentrations of different proinflammatory cytokines in the bronchoalveolar lavage, is significantly greater in patients in whom tidal hyperinflation predominates over recruitment. These results confirm previous findings on the ambivalent effects of high levels of positive end-expiratory pressure (PEEP) in increasing plateau pressure (2–4) and may significantly impact the selection of the "right" ventilatory strategy in patients with ARDS. The classical view of ventilator-induced lung injury is based on concepts initially proposed in the 1990s. Lung edema and inflammation increase lung weight and, in the supine position, dependent lung regions are compressed (5). Ventilator-induced lung injury is postulated to be caused by cyclic "opening" and "closing" of collapsed airways during tidal ventilation and by end-inspiratory distension of the lungs, with the respective contribution of each component being debated (5, 6). The large shear stress required to reopen collapsed airways and alveoli damages the bronchial epithelium and induces a lung inflammatory reaction (so-called biotrauma) (6), which may aggravate multiorgan failure and precipitate death (7). PEEP, by counterbalancing superimposed external pressure leading to airway collapse, prevents this problem during expiration, and reduces ventilator-induced lung injury and biotrauma (5, 7). As a consequence of this reasoning, "injurious" ventilation in which there is repetitive opening/closing of lung units should be avoided (6), and high PEEP administered to keep the lung open (8). These concepts about injurious ventilation have been seriously challenged by a series of experimental and clinical investigations. In experimental models of high-permeability pulmonary edema, the lung is not collapsed but filled with liquid and its overall volume is preserved (9). Although the increase in lung tissue edema predominates in upper lobes, the loss of lung volume primarily involves the lower lobes, suggesting that the heart and the abdominal content are the predominant compressive factors in patients lying in the supine position (10). A large randomized trial in humans has failed to demonstrate that high PEEP reduces mortality and duration of mechanical ventilation (11). Terragni and coworkers provide additional evidence against the "opening and closing" theory of lung injury. In their study (1), an increased production of lung cytokines was associated with overinflation of previously aerated lung regions: in patients exposed to tidal volume–induced hyperinflation, ventilation-associated recruitment/derecruitment represented 13% of the change in lung volume versus 23% in patients not exposed to tidal hyperinflation. For the first time, this study clearly demonstrates that the pulmonary inflammatory response is associated with overinflation of previously aerated lung regions more than recruitment/derecruitment of poorly or nonaerated lung regions. The results of this study may have direct implications in defining a "noninjurious" ventilatory strategy. Experimental studies demonstrated that PEEP was protective against ventilator-induced lung injury, provided it did not further increase end-inspiratory lung volume and plateau airway pressure (12). Several clinical studies have shown that PEEP-induced recruitment was frequently associated with end-expiratory overinflation in patients with those forms of ARDS characterized by focal loss of aeration, predominating in lower lobes (2–4, 13). Terragni and coworkers provide evidence that a ventilatory strategy expected to be noninjurious and protective, using a PEEP setting based on oxygenation and reduction of tidal volume to 6 ml/kg, may, nevertheless, overinflate lung areas normally aerated at end-expiration, and expose some parts of the pulmonary parenchyma to ventilator-induced lung injury. Their study was not designed for assessing the contributions of PEEP and tidal volume to overinflation, nor for identifying predisposing factors to overinflation. It is highly likely, however, that lung recruitability and initial lung morphology (i.e., regional distribution of loss of lung aeration before PEEP implementation) are major determinants of tidal hyperinflation, as demonstrated for PEEP-induced overinflation (4). As previously recommended (14, 15), a reasonable ventilatory approach involves limiting PEEP to values of 10 cm H2O or less, tidal volume to 6 ml/kg or less, and plateau pressure to 25 cm H2O or less in patients with a focal loss of lung aeration present before PEEP administration. At the bedside, the presence of radiologic densities predominating in the lower lung quadrants and sparing the upper lobes at PEEP levels of 5 cm H2O or less is an easy way to identify such patients (15). Deciding that the lung should be "fully recruited," whatever the pressure required, appears to be a high price to pay, since it ignores the risk of lung overinflation and of regional and systemic inflammation. What other practical considerations can we infer from these results? First, individual titration of our ventilatory approach seems highly desirable, particularly in assessing the relative contributions of tidal hyperinflation and distension. The study by Terragni and colleagues shows correlations between tidal hyperinflation and markers of inflammation. Although it does not explore the mechanism for such associations, it does suggest that such markers could be used in the future to indicate the need to lower the ventilatory stress imposed on the lung. Second, the relationship between plateau pressure and tidal hyperinflation, if anything, suggests that a plateau strictly lower than 28 cm H2O may be of value. The small number of patients and the absence of outcome data in this study preclude any stronger conclusions. Chinese thought is based on the interaction of opposites. One of the maxims proposed by Lao Tzu in his classical book Tao Tö King ("The Book of the Way and the Virtue"), written in China during the fifth century B.C., states, "Between Yes and No, the frontier is thin. Good and Evil are mixed" (16). This quotation highlights the difficult issue of mechanical ventilation applied to injured lungs. The safe approach should follow "The Way of Wisdom and Compromise": in each individual, the physician should select intrathoracic pressures and tidal volumes that provide the best compromise between recruitment (yin) and overinflation (yang). FOOTNOTES Conflict of Interest Statement: None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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