Figure 1

Potential mechanisms of ventilator-induced lung injury. Mechanical ventilation induces tensile strain and shear forces in the lung. These forces result in increased permeability and disruption of the alveolar–capillary barrier. Mechanical forces also induce an increase in the concentrations of proinflammatory mediators (including IL-1β, tumor necrosis factor alpha, IL-8 and IL-6) in the distal airspaces of the lung. The loss of compartmentalization in the lung results in the release of these mediators into the systemic circulation where they may play a role in end organ dysfunction. Mechanical strain also reduces the active sodium transport-dependent clearance of edema fluid from the airspaces. This potentially contributes to increased edema formation, ongoing lung volume loss, and greater ventilator-associated lung injury.