Permissive hypercapnia (PHY) represents an interesting approach in critically ill ventilated patients, because it allows to ensure adequate gas exchange while avoiding the adverse effects related to excessive airway pressures. Its objective is to improve oxygenation while reducing the risk of barotrauma and circulatory impairment. This concept is all the more important when considering that in majority of lung diseases for which MV is applied, lung involvement is highly inhomogeneous, meaning that the functionally normal or near normal areas are the most exposed to the deleterious effects of overdistension. Undesired physiological effects of non massive respiratory acidosis (PaCO2 < or = 80 mmHg, arterial pH > or = 7.15) are reversible and mostly minor. This good tolerance legitimizes two strategies: firstly to accept hypercapnia in conditions such as acute severe asthma for which enforced normalization of PaCO2 would imply potentially lethal complications, and secondly to deliberately induce respiratory acidosis while using very low airway pressures and alveolar ventilation to limit or prevent overdistension lung damage in injured as well as in normal areas. When the cerebral vasodilation induced by CO2 might aggravate a preexisting intracranial disorder, PHY is obviously contraindicated.