Alveolar permeability and stretch: too far, too fast.

M echanical ventilation is the most widely used therapy in intensive care units and the cornerstone treatment for patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) [1]. Although essential for successful management of respiratory failure, mechanical ventilation can also exacerbate or even directly injure the lungs [2, 3]. This damage, commonly referred to as ventilatorinduced lung injury (VILI), is characterised by increased permeability of the alveolar epithelium to fluids and macromolecules [4]. Mechanisms leading to such increase include direct mechanical damage caused by excessive stretch of the lungs (barotrauma and volutrauma) or by repetitive opening and closing of recruitable alveolar units (atelectrauma) [3]. In addition, mechanical stretch alone can trigger mechanotransduction pathways that may lead to local [5] and systemic inflammatory responses (biotrauma) [6].