Protective mechanical ventilation (MV) involves the use of low tidal volumes (Vt) in order to reduce transpulmonary pressure levels to avoid damage induced by MV. That clinical practice has demonstrated to improve survival in patients with respiratory distress syndrome (ARDS). 1,2 However, an undesirable consequence of protective MV is hypoventilation and hypercapnia, 3 acute pulmonary hypertension, diminished myocardial contractility, reduced renal blood flow, and release of endogenous catecholamins. 4 Hypercapnic acidosis associates to increase hospital mortality, prolonged hospital stay, and a reduction in survival with PaCO 2 greater than 65 mmHg. 5 Molecular studies had shown a close association between hypercapnia and alveolar cell membrane repair disorders, alveolar clearance, and local immune response. 6 Gattinoni 1986 designed the first device that separated the ventilatory support from oxygen supply, which made possible to optimize lung protection during VM. 7 That was the first published ECCO 2 R system, which allowed the removal of CO 2 from the blood through a gas exchange membrane, without oxygenating the blood in a meaningful way. 2