 Over the past few decades, highly significant progress has been made in understanding the pathophysiology of the acute respiratory distress syndrome ARDS. Recognition of ventilation-induced lung injuries VILI has led to the radical modification of the ventilatory management of these patients. The landmark trial by the ARDSnet trial group demonstrated in 2000 that ventilating ARDS patients with a low tidal volume VT of 6 mlkg calculated from predicted body weight, and with a maximum end-inspiratory plateau pressure Pplat of 30 cmH2O decreased mortality from 39.8 in the conventional arm treated with a VT of 12 mlkg PBW to 31 . However, recent studies have shown that lung hyperinflation still occurs in approximately 30 of ARDS patients even though they are being ventilated using the ARDSNet strategy. Additionally, Hager and coworkers found that mortality decreased as Pplat declined from high to low levels at all levels of Pplat on the data collected by the ARDSNet trial group. Their analysis suggested a beneficial effect of VT reduction even for patients who already had Pplat30 cm H2O before VT reduction.Similar observation was also recently reported by Needham et al on a cohort of 485 patients with ARDS. Because VT reduction to 6 mlkg to achieve very low Pplat may induce severe hypercapnia and may cause elevated intracranial pressure, pulmonary hypertension, decreased myocardial contractility, decreased renal blood flow, and the release of endogenous catecholamines, this strategy using ultraprotective MV settings is not possible for most patients on conventional mechanical ventilation for moderate to severe ARDS. 