3). ECMO is an efficient treatment for refractory ARDS [22]. No studies selleck chemicals have assessed the usual dynamic parameters of preload reserve on ECMO-assisted patients, probably because of the complex interactions between the protective mechanical ventilation and ECMO system on heart-lung interaction. As previously shown in the context of ARDS without ECMO support, neither ��respPP nor ��PLRPP predicts fluid responsiveness [8-10,12]. In two prospective studies, the poor predictive performance of ��respPP has been attributed to insufficient changes in transpulmonary and pleural pressure [10,12], which are related to protective ventilation and altered pulmonary compliance. In addition, ��respPP could reflect postload variation on right ventricular dysfunction and cannot be used as a predictor even in the presence of hypovolaemia [8,9,11].

Such clinical situations are frequent in the treatment of ECMO-assisted patients, which limit the use of such indices. ECMO patients with late ARDS were ventilated with ‘ultraprotective’ ventilation because of altered compliance and a high incidence of acute cor pulmonale (Table (Table1).1). As ��resp indices must be avoided because they fail to predict fluid responsiveness and fluid overload, fluid management may rely on a reversible and safe fluid challenge. Thus, we assessed predictive values of ��PLR indices.Figure 3Passive leg raising (PLR)-induced stroke volume (SV) increase in responders and nonresponders. ��SV, stroke volume increase between baseline and PLR expressed as a percentage.

��PLRPP cannot predict fluid responsiveness, even among patients with a minimal increase in CVP of 2 mmHg. On the basis of physiological knowledge, the use of Dacomitinib PP as a substitute for SV would assume constant arterial compliance. By increasing intrathoracic blood volume, PLR may also induce sympathetic activation; however, our patients were deeply sedated, and their HRs remained unchanged during PLR. In clinical practice, SV, PP and vascular tone can vary with the patient’s haemodynamic conditions and can be altered by PLR [28], which may have been the case in our present study.In this context, echocardiographic measurement of ��PLRSV and ��PLRCO may predict fluid responsiveness. The best threshold was 5% for ��PLRSV, with 92% sensitivity (CI95: 64 to 100) and 83% specificity (CI95: 52 to 98), and 5% for ��PLRCO, with 85% sensitivity (CI95: 46 to 95) and 83% specificity (CI95: 52 to 98) (Table (Table4).4). The lower sensitivity of ��PLRCO may be explained by the fact that CO is the product of SV and HR. In some responders, the VE-induced SV increase was associated with decreased HR (nonsignificantly). Whereas sensitivity differed, the ��PLRCO and ��PLRSV AUCs were not statistically different.