During acute respiratory distress syndrome (ARDS) the application of positive end-expiratory pressure (PEEP) prevents expiratory alveolar collapse. However, it can induce a predominant recruitment effect or, on the contrary, alveolar overdistension. The recruitment/overdistension ratio can be easily assessed using R/I ratio (or recruitment-to-inflation ratio). However, PEEP is likely to lower cardiac output and contribute to the cardiovascular failure that often occurs in patients with ARDS. Among its hemodynamic effects, PEEP is likely to increase pulmonary vascular resistance and, thus, right ventricular afterload. In theory, this effect should only occur if PEEP over-distends the lung volume, compressing the extra-alveolar vessels and increasing their resistance. However, this different effect of PEEP on pulmonary vascular resistance depending on the degree of recruitment or overdistension has never been demonstrated during ARDS in humans.~We retrospectively studied data collected from patients with ARDS, monitored by pulmonary artery catheter (PAC), to eventually find a correlation between the high PEEP-induced PVR increase and recruitement/overdistension profile.
The corner stone of the treatment of ARDS is mechanical ventilation with high levels of positive end-expiratory pressure, also called PEEP. A high level of PEEP is recommended and frequently used. But PEEP can lower cardiac output and contribute to circulatory failure during mechanical ventilation. Nevertheless, in theory, the PEEP-induced pulmonary vascular resistance (PVR) increase could depend on the level of alveolar recruitment, but it has never been proven. Thus, the aim of this study is to determine the relation between the high-PEEP induced PVR and the alveolar recruitment or overdistension.