| Background: Acute respiratory distress syndrome (ARDS) is still a critical illness syndrome with high mortality. It is character of severe hypoxemia. Mechanical ventilation is a critical component of the treatment of patients with ARDS. However, recent experimental and clinical research have demonstrated that conventional ventilatory strategy has no benefit to ARDS patients and has not decreased the mortality rate of ARDS. Injurious ventilation not only may exacerbate or create lung injury, but also initiate or propagate a systemic inflammatory response leading to local and systemic tissue injury and promote the release of cytokine into the blood, thus could play a role in the development of MODS.Ventilator induced lung injury (VILI) means that mechanical ventilation may create injury to normal lung or worsen injured lung. Many experimental and clinical studies have indicated that VILI is the main reason of ARDS with high mortality. The mechanisms of VILI have been attributed to stress and strain either by lung overstretching at high tidal volume/pressure ventilation or excessive shear stress due to collapse and tidal recruitment of alveoli. Overstretch and excessive shear stress lead to deformation of alveolar epithelial cell. Deformation of the epithelium is a stimulus for surfactant secretion, which would reduce surface tension at the air liquid interface. It may also result in stress failure of the plasma membrane, disruption alveolar epithelial and endothelial cells, denudation capillary basement membrane. It also can activate local inflammatory cells and augment the inflammatory reaction substantially and induce or worsen lung injury.Dynamic ventilatory factors such as the inspiratory flow profile, the inspiratory flow rate and respiratory rate may also alter lung strain to VILI. Inspiratory flow rate is an important determinant of stress in the lung. High inspiratory flow increases shear stress to the surface of the... |
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