First, Pes measures a local value of pressure, while Pw is not uniform ( 13), and therefore, relating overall lung volume and P l to a local value of Pw may be misleading ( 13). According to the German philosopher Immanuel Kant ( 12), “actions are acceptable only if everyone could do or could receive it.” Under these circumstances, several steps need to be taken to make measurement of Pes acceptable according to Immanuel Kant’s view. However, because clinicians tend to adopt innovations very slowly, to introduce Pes in the clinical practice, the scientific community still needs “to move to sort through ambiguous evidence, proceed to collaboration within a community of observers, and finally move to consensus for action” ( 11). Years ago, the clinical use of Pes was proposed by clinical physiologists ( 9) that Berwick would define as “visionary innovators” ( 10). Despite the intrinsic limitations of a retrospective, post hoc, not prespecified analysis, and the fact that the APACHE score does include variables not directly related to organ failure, these data seem to suggest that measurements of Pes may allow replacing Prs with P l as a tool to set ventilator settings and that targeting an end-expiratory P l nearer 0 cm H 2O might enhance lung protection. The relevance of the observation that, independent of treatment group or multiorgan dysfunction severity, mortality was lowest when PEEP titration achieved end-expiratory P l near 0 cm H 2O should not escape our notice ( 8). By contrast, in patients with vasopressor-dependent shock at baseline, Pes-guided PEEP was associated with fewer shock- and ventilator-free days. Moreover, in patients without shock or hypotension at baseline, Pes-guided PEEP was associated with more days free of shock and of ventilator support. The authors found that Pes-guided PEEP was associated with lower mortality among patients with lower Acute Physiology and Chronic Health Evaluation-II (APACHE-II), having the opposite effect in patients with higher APACHE-II. 1153–1163) present a post hoc analysis of the latter trial ( 8). In this issue of the Journal, Sarge and colleagues (pp. The primary outcome, a ranked composite score incorporating death and ventilator-free days among survivors through Day 28, was not different between groups ( 7). The second multicenter trial enrolled 200 patients. The first single-center trial enrolled 61 patients and found that the ratio of the partial pressure of arterial oxygen to the F i O2 at 72 hours was 88 mm Hg higher in the Pes-guided group than in the control group (95% confidence interval, 78.1–98.3 P = 0.002) ( 6). Central in this hypothesis is the assumption that the absolute value of Pes would provide an estimate of Pw accurate enough to allow a clinically relevant assessment of P l. Recent clinical trials tested the hypothesis that alveolar collapse and hypoxemia may be determined by negative values of P l caused by high Pw and that, therefore, setting PEEP to maintain a positive P l might optimize alveolar recruitment, minimizing the risk of hyperinflation and of hemodynamic impairment ( 6, 7). Grasso and colleagues suggested that positive end-expiratory pressure (PEEP) should be titrated to reach a maximal value of 20 cm H 2O of P l instead of a maximal value of 30 cm H 2O of Prs ( 4). Recent studies highlight the potential clinical relevance of using measurements of Pes to estimate P l. The most used method to provide an indirect determination of Pw uses an air-containing latex balloon sealed over a catheter placed in the esophagus and transmitting balloon pressure to a transducer (esophageal pressure ) ( 1). Several studies confirmed these observations ( 4, 5), leading to the suggestion that assessment of P l instead of Prs should be considered to optimize protective ventilatory strategies ( 2). However, Talmor and colleagues found that only 24% of the variance in P l was explained by Prs, whereas 52% was due to variation in chest wall pressure (Pw) ( 3). On the basis of the assumption that the pressure across the respiratory system (Prs) closely approaches P l, protective ventilatory settings are obtained, limiting Prs to a maximal value of 30 cm H 2O ( 2). We learned that ventilatory strategies minimizing the pressure applied to the lung (i.e., transpulmonary pressure ) can decrease mortality ( 2).
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