© 2004 American Thoracic Society doi: 10.1164/rccm.2409001
Optimizing Lung Aeration in Positive End-Expiratory PressureRéanimation Chirurgicale Pierre Viars La Pitié-Salpétrière University School of Medicine University Pierre et Marie Curie Paris, France In this issue of the AJRCCM, Albaiceta and coworkers (pp. 1066–1072) provide computed tomographic (CT) evidence in patients with acute respiratory distress syndrome (ARDS) that lung reexpansion resulting from positive end-expiratory pressure (PEEP) is markedly influenced by the pressure applied to the respiratory system immediately before PEEP implementation. Lung aeration is greater at the same level of PEEP reached by decreasing airway pressure along the deflation limb of the static pressure–volume curve, as compared with achievement of the same level of PEEP by increasing pressure along the inflation limb (1). These results are in accordance with theoretical predictions (2) and confirm previous experimental studies (3–6). They have an important pathophysiologic implication: the reaeration pressures of the injured lung are always higher than the pressures at which lung aeration vanishes. According to these results, optimizing lung aeration at the bedside is best accomplished by setting the PEEP either using the deflation limb of the static pressure–volume curve or immediately after a recruitment maneuver. The different pressure thresholds for lung expansion at inflation and deflation are likely to depend on complex mechanisms associated with the loss of functional lung volumes that characterizes ARDS. Such mechanisms include: external compression of dependent distal bronchioles causing alveolar collapse, the filling of alveoli and alveolar ducts by edema fluid or inflammatory cells, and alteration of surfactant properties. In the supine position, compression of dependent bronchioles, the widely accepted explanation for "lung collapse," may result from excessive lung weight, as well as cardiac and abdominal compression. Although the edematous ARDS lung was initially considered to collapse under its own increased weight (7), this theory has been recently challenged (8, 9), in that cardiac and abdominal compressions appear to be the predominant factors causing lung collapse (9–11). However, if body position remains unchanged, cardiac and abdominal compression of the lungs do not provide a plausible explanation for the differences in opening and closing pressures associated with lung recruitment. A more plausible explanation is that reaeration of fluid-filled alveoli may require different pressures at inflation and deflation.
Reaeration of the injured lung is basically an inspiratory phenomenon. Increases in airway pressure displace the gas–liquid interface from alveolar ducts to alveolar spaces and increase the hydrostatic pressure gradient between the alveolar space and pulmonary interstitium (12). Under these conditions, liquid is rapidly removed from the alveolar space, thereby increasing alveolar compliance (12), decreasing the threshold aeration pressure, and increasing alveolar aeration. Inactivation of surfactant is a hallmark of ARDS. In addition to being inactivated by direct injury to the lung related to inflammation, infection, or aspiration, surfactant may also be inactivated by the loss of end-expiratory lung volume (13). By preserving inspiratory recruitment and reestablishing end-expiratory lung volume, PEEP has been shown to prevent surfactant loss in the airways and avoid surface film collapse (13). As a consequence, alveolar compliance increases and the pressure required for alveolar expansion decreases. It has been shown that the time scale for alveolar recruitment and derecruitment is within a few seconds (4), whereas the time required for fluid transfer from the alveolar space to the pulmonary interstitium is in the range of a few minutes (12). In Albaiceta's study (1), as in most studies on recruitment maneuvers (3), the entire study procedure lasted several minutes. In the time interval when static inflation and deflation pressure–volume curves were measured, peak inspiratory airway pressures were maintained Albaiceta and coworkers did not find any differences in terms of lung recruitment between ARDS due to pulmonary or extrapulmonary etiologies (1). This result contradicts the hypothesis of Gattinoni and coworkers (7) that the lung behaves differently depending on the initial mechanism of ARDS, and confirms several recent human studies (9, 14). It also suggests that whatever the initial insult to the lung, the responses leading to extensive lung injury are similar, as are the mechanisms for positive pressure–induced lung reaeration. Surprisingly, the authors did not find any evidence of lung overdistension even though static airway pressures as high as 35 cm H2O were applied to the injured lungs. In patients and experimental animals with acute lung injury, recruitment resulting from PEEP is frequently associated with overinflation of previously aerated areas in the lung (3, 9, 12, 14–16). Two reasons might explain why overinflation was not detected in the study by Albaiceta and colleagues. Some patients probably had diffuse loss of aeration, a condition known to be "protective" against high airway pressure–induced lung overinflation (9, 14, 15). Focal losses of aeration, with some lung regions remaining normally aerated at zero end-expiratory pressure, were likely present in other patients, a condition that leads to increased risk of overinflation. In the study by Albaiceta and coworkers, at each static pressure level, a single high spatial resolution CT section was performed 2 cm below the carina. In patients with ARDS lying supine, lung overinflation resulting from mechanical ventilation with PEEP is primarily located in nondependent lung regions, predominantly involving caudal parts of middle lobes (9, 15, 16). In a recent study where 40% of patients with ARDS had CT evidence of lung overinflation at PEEP 15 cm H2O, less than 1% of the CT section located 2 cm below the carina was overinflated, whereas more than 10% was overinflated at the level of the diaphragmatic cupola (16). Therefore, it is very likely that overinflation existing in more caudal lung areas was missed in the study by Albaiceta and colleagues (1). As pointed out by the authors, their study does not give any guidance in selecting the PEEP level that will provide optimal lung recruitment while avoiding risks of overinflation (14, 15). What they have convincingly demonstrated is that once the "right" PEEP is selected, that PEEP level should be reached along the deflation limb of a prolonged recruitment maneuver, rather than simply increasing PEEP levels from low baseline values. FOOTNOTES
Conflict of Interest Statement: J.-J.R. was the French Coordinator of the multicenter study on the administration of exogenous surfactant in ARDS patients sponsored by Leo Pharma and received REFERENCES
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30 cm H2O for 6 minutes, whereas PEEP was interrupted only for a few seconds immediately before performing the deflation pressure–volume curve. It can be reasonably assumed that decreasing end-expiratory pressure to zero for a few seconds was long enough to derecruit the lung but too short to eliminate the beneficial effects on surfactant function and alveolar clearance that resulted from maintaining high PEEP and high inspiratory pressures for 6 minutes. Further studies are required to confirm these pathophysiologic hypotheses. Direct visualization of the behavior of juxtapleural injured alveoli using in vivo video microscopy will be of particular interest in resolving these issues (
6000 that were entirely transferred to the Association pour la Recherche Clinique et Experimentale en Anesthesie-Reanimation (ARCEAR). The Experimental Intensive Care Unit, of which J.-J.R. is the Scientific Director, has some of the research protocols financed by GlaxoSmithKline and Pulsion.