We thank Dr. Perel for his interest in our article.1He raises the issue of the influence of sepsis on positive end-expiratory pressure (PEEP) response in terms of oxygenation in patients with adult respiratory distress syndrome. Based on his own studies published in the late 1970s,2,3he indicates that their result supports the concept that the cause of adult respiratory distress syndrome, or at least the presence of sepsis, influences the effectiveness of PEEP. He also suggests that the effect of PEEP on oxygenation may be part of a diagnostic test to determine whether adult respiratory distress syndrome is septic.

In our study, we did not directly address the points raised and try to reproduce these effects, for several reasons. First, Dr. Perel used small levels of PEEP with no standardization, making it difficult to reproduce these results. Second, we do not have systematic measurements of oxygenation at every level tested or assessment of the precise criteria for defining “sepsis” exactly at the time when the curves were performed. We do not think, however, that this is the right approach for at least two reasons. Based on the last 15 yr literature on PEEP, it has become clear that if PEEP is important, it is not because of its effects on oxygenation, but mainly because of its effects on lung recruitment and by making ventilation more homogeneously distributed.4Arterial oxygenation has many drawbacks as a pure indicator of recruitment,5,6and we have focused our more recent research on recruitment rather than oxygenation, mainly for this reason. The differences Dr. Perel described many years ago could be entirely explained by hemodynamic reasons independent of recruitment and could thus be misleading for clinicians. In addition, what we have shown is that there is no a priori  difference in terms of PEEP-induced recruitment whatever the origin of adult respiratory distress syndrome.1In other words, the clinician has to look for the individual effect of PEEP and not base the administered therapy on a priori  criteria. We think this is an important message for today’s clinicians.

*Henri Mondor Hospital, University of Paris XII, Créteil, France. arnaud.thille@wanadoo.fr

Thille AW, Richard JC, Maggiore SM, Ranieri VM, Brochard L: Alveolar recruitment in pulmonary and extrapulmonary acute respiratory distress syndrome: Comparison using pressure-volume curve or static compliance. Anesthesiology 2007; 106:212–7
Cotev S, Perel A, Katzenelson R, Eimerl D: The effect of PEEP on oxygenating capacity in acute respiratory failure with sepsis. Crit Care Med 1976; 4:186–92
Perel A, Olshwang D, Eimerl D, Katzenelson R, Cotev S: The variable effect of PEEP in acute respiratory failure associated with multiple trauma. J Trauma 1978; 18:218–21
Grasso S, Fanelli V, Cafarelli A, Anaclerio R, Amabile M, Ancona G, Fiore T: Effects of high versus  low positive end-expiratory pressures in acute respiratory distress syndrome. Am J Respir Crit Care Med 2005; 171:1002–8
Aboab J, Louis B, Jonson B, Brochard L: Relation between PaO2/FIO2ratio and FIO2: A mathematical description. Intensive Care Med 2006; 32:1494–7
Takala J: Hypoxemia due to increased venous admixture: Influence of cardiac output on oxygenation. Intensive Care Med 2007; 33:908–11