Watching What PEEP Really Does

Laurent Brochard

Service de Réanimation Médicale, Hôpital Henri Mondor, Créteil, France

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In this issue of the American Journal of Respiratory and Critical Care Medicine, Malbouisson and coworkers (pp. 1444-1450) describe a new method to compute the amount of alveolar recruitment induced by positive end-expiratory pressure (PEEP) in patients with the acute respiratory distress syndrome (ARDS), using computer tomography (CT) (1). CT has already been employed as a research technique by Gattinoni and his group for more than a decade (2, 3), but new developments in technology and a more global approach to the effects of recruitment have allowed Rouby's group to propose a new gold standard for this measurement.

A better understanding of the effects of PEEP in ARDS is of central importance for several reasons. The lack of a randomized trial demonstrating a benefit of PEEP on clinical outcome has led to a battle between opponents and proponents of PEEP. "Prophylactic," "super," or "minimal" PEEP have all been proposed as the more suitable strategy. The "best" method for selecting and titrating PEEP at the bedside has been a subject of ongoing debate. One factor provoking debate is the difficulty in clearly demonstrating the major goal of PEEP, that is, alveolar recruitment. Indeed, measuring an increase in lung volume resulting from PEEP is a simple application of basic laws of physics, and does not per se indicate recruitment. Katz and coworkers first showed in patients that the net increase in volume induced by PEEP was greater than that predicted from the pressure-volume (P-V) relationship at a lower PEEP (4). This suggested that, for the same pressure, more aerated lung volume was available for ventilation. This corresponded to the definition later used by Ranieri and coworkers to estimate alveolar recruitment using P-V curves traced from different PEEP levels (5). Gattinoni and coworkers (2, 3) were the first to show the morphological changes induced by PEEP and the reality of alveolar recruitment. It took much longer to visualize alveolar recruitment than to show the deleterious effects of PEEP on cardiovascular function, even showing that such deterioration could mediate apparent improvement in oxygenation without evidence of lung recruitment (6). A more recent debate concerns the ability of PEEP to protect against ventilator-induced lung injury (VILI). PEEP-induced alveolar recruitment potentially protects against VILI (7), but PEEP-induced overdistension might increase the risk of VILIthe existence of the latter has now been definitely demonstrated. Lastly, although it may be possible to estimate alveolar recruitment at the bedside with the P-V curve technique (8), it is uncertain whether changes in surface tension caused by alveolar surfactant could explain part of the PEEP-induced shift in the P-V curve. Randomized clinical trials cannot provide all the answers, as they usually compare two specific settings or two different strategies. It is impossible to determine whether a third or a fourth setting might have been better; moreover, it may be impossible to extract from the overall strategy the setting that might be optimal in each situation. Mechanistic studies become even more important than ever in this era of evidence-based medicine.

Gattinoni and coworkers demonstrated and quantified alveolar recruitment induced by PEEP, and stressed the importance of inflation in opening the lung, and of PEEP in avoiding derecruitment. Several limitations of the methods used by Gattinoni and coworkers are discussed by Malbouisson and coworkers (1). Gattinoni and coworkers performed only one to three cuts, which could miss the effects of positive pressure because of the inhomogeneous nature of lungs in ARDS. For instance, Gatttinoni and coworkers demonstrated a vertical gradient in lung densities, characterizing the "sponge" model. Using the fast helicoidal CT technique, Rouby's group was able to show the coexistence of a cephalocaudal gradient as well as a direct effect of the heart, which could not be observed with the previous technique (9). Also, poorly aerated zones of the lung were not considered in the computation of recruitment.

Malbouisson and coworkers used the new CT technology to determine nonaerated and poorly aerated zones at ZEEP, to delineate these zones, and to subsequently compute the amount of aeration in these zones with application of PEEP. This created the possibility of quantifying, as best possible, the entire recruited lung. This was made possible by the numerous cuts allowed by the new CT, and by including poorly aerated zones in the computation. Strictly speaking, the authors' definition of recruitment identifies the quantity of air introduced in the diseased lung. It thus demonstrates what is desirable with PEEPtransforming abnormal lung into normal lung. Concomitantly, hyperinflation computed from a distribution toward the most negative densities may help determine overdistension. Not surprisingly, the results of the new technique were only poorly correlated with Gattinoni's technique. In addition, only the new technique correlated well with oxygenation.

The new CT technique, necessitating a complex procedure, has a number of limitations of differing consequence. Acquiring the cuts over 15 s with 100% oxygen may promote atelectasis or regional redistribution; new, faster, CT scans may solve this problem. Another limitation, discussed by the authors, is that one pixel is not one alveolus. Therefore, condensed areas could include aerated alveoli, and normal zones could result from the combination of overinflated and condensed alveoli. Given the pathology of ARDS, this is unlikely to be a major problem; nevertheless, relative homogeneity of alveolar filling within each pixel is an assumption that underlies the technique. Delineation may not be possible in certain forms of ARDS, about 15% of cases according to the authors' estimates, and vascular structures may introduce uncertainties. Despite these limits, this appears to be the best available research tool for quantifying lung recruitment.

Quantification of overdistension may be more questionable. It is based on an absolute threshold of density defined in normal volunteers (10). In normal subjects, overdistension results from an excess of air in normal lung. In an edematous lung, the same amount of overdistension may have a different density because of a concomitant excess in extravascular lung water. Overdistension may thus be underestimated and another definition may be necessary (11).

This new technique may help solve several important issues, such as individual responses to PEEP, the influence of the chest wall, and the responses in pulmonary and extrapulmonary ARDS. This technique is reserved for clinical investigation. By undertaking the proper comparison, however, it may provide important information regarding the accuracy of the P-V curve in measuring recruitment. Indeed, the P-V technique has the enormous advantage of being applicable at the bedside, and validation of the P-V curve by CT scan may open new horizons for the clinician.

	References

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