As the kinase inhibitor 17-DMAG use of sedation in the intensive care unit (ICU) has decreased over the past few years, this situation is rarely encountered, except in cases such as severe respiratory failure (such as acute respiratory distress syndrome (ARDS)) requiring perfect patient-ventilator interactions. Of note, fluid responsiveness prediction is crucial in patients with ARDS because of increased alveolar-capillary membrane permeability [5], and avoiding unnecessary fluid loading has been shown to have a positive effect on patient outcome [6].Nevertheless, cardiopulmonary interactions are complex in case of ARDS, particularly when lung-protective mechanical ventilation (low tidal volume) is performed as recommended nowadays [5], and several limitations may downplay the usefulness of ��RESPPP.

First, the magnitude of the insufflated tidal volume (Vt) affects the magnitude of ��RESPPP (or other indices derived from respiratory changes in stroke volume) in non-ARDS or mixed ARDS and non-ARDS patients [7-9]. Thus, the performance of ��RESPPP becomes poor when the Vt is settled below 8 ml/kg [10,11]. Second, ARDS patients exhibit a marked decrease in lung and sometimes chest wall compliance [5]. Consequently, airway driving pressure (plateau pressure (Pplat) minus total positive end-expiratory pressure (PEEPt)) for a given Vt is greater in ARDS than in healthy lungs [12]. Therefore, it has been hypothesized that, despite a reduced Vt, cyclic swings in airway pressure are still high enough to maintain ��RESPPP predictive ability in ARDS patients [13]. However, one may question this assumption.

Indeed, ��RESPPP results of swings in right atrial pressure which are close to pericardial and pleural pressure swings. Rather than airway driving pressure, the main determinants of respiratory changes in pleural, pericardial and atrial pressure are Vt magnitude and chest wall compliance (both of which determine the compression of the anatomic structures in the cardiac fossa) [14,15]. Decreased lung compliance during ARDS may therefore have little effect on ��RESPPP [12]. Last, to avoid respiratory acidosis, reduced Vt is frequently combined with an increased respiratory rate (RR), which may also downplay the performance of ��RESPPP [16].Thus, ��RESPPP may be of interest to guide fluid therapy during ARDS, but Drug_discovery several physiological mechanisms may limit its validity. The current literature about its performance in ARDS is scarce, and opposite conclusions have been drawn [10,17]. We aimed to assess the performance of ��RESPPP to predict fluid responsiveness in a large population of patients with ARDS.Materials and methodsARDS patients from another study were studied [3] and are being partly shared with another study [18].