© 2007 American Thoracic Society
Plateau Pressures in the ARDSnet Protocol: Cause of Injury or Indication of Disease?To the Editor:In their recent article, Terragni and colleagues (1) ascribed poor outcome in acute respiratory distress syndrome (ARDS) to "tidal hyperinflation," after dividing patients into two subpopulations based on lung density measured in computed tomography scans at FRC and end-inflation. In the "less protected" group, hyperlucent, low-density areas were relatively extensive at FRC and accounted for most of the tidal increase in lung volume, whereas in the "more protected" group, normally lucent regions were more extensive at FRC and accounted for most of the tidal increase in volume. The tidal increase in hyperlucent lung regions was termed "tidal hyperinflation," implying regional overexpansion of the lung parenchyma. The authors concluded that the less protected subpopulation was at risk, noting somewhat higher mortality and higher levels of inflammatory cytokines, which are indications of lung injury correlated with mortality (2). The authors attributed greater hyperinflation in the less protected group to higher end-inspiratory plateau pressures (25–26 vs. 28–30 cm H2O), and recommended that "plateau pressure should be limited to 28 cm H2O to guarantee lung protection." This analysis and recommendation neglect the relationship between plateau pressure and severity of disease. In the less protected group, the PaO2:FIO2 was lower, indicating more abnormal gas exchange. Because these patients were ventilated according to the ARDSnet protocol (3), higher levels of positive end-expiratory pressure (PEEP) were prescribed for greater degrees of hypoxemia (i.e., for greater lung injury). Indeed, the higher PEEP in the less protected group (12.6 vs. 9.3 cm H2O) is an indication of greater disease. Higher PEEP, given a fixed tidal volume, causes higher plateau pressure, and, in addition, greater lung injury in the less protected group reduces compliance, raising the plateau pressure further. Thus, higher plateau pressure in the less protected group is an expected result of raising PEEP to meet oxygenation demands in sicker patients. That the sicker population had more inflammatory cytokines and lower survival is also expected. In recommending a safe level of plateau pressure, it is not sufficient to demonstrate that a given level is associated with a better outcome, especially when the PEEP level is specified by protocol to be higher with greater lung injury. Moreover, plateau pressure may not accurately reflect the peak pressure inflating the lungs (4). We suggest that the higher plateau pressures and hyperinflation in the less protected subpopulation are less a cause of lung injury than a manifestation of what Hippocrates called the "extreme treatment" fitting the "extreme disease" of the sickest patients.
Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 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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