Ventilator-Induced Lung Injury

An acute lung injury represents a continuum of injury that may arise from a number of primary insults. When it is present, it may progress due to the trauma from mechanical ventilation, a finding that has led to an intense debate over the optimal ventilator management. Moreover, it has been demonstrated that mechanical ventilation per se, even in the absence of a preexisting lung injury, may lead to the development of ventilator-induced lung injury (VILI). The association between positive pressure mechanical ventilation and lung injury has fostered the concepts of barotrauma, volutrauma, atelectrauma, and biotrauma and led to the clinical development of “lung-protective ventilation,” which has led to a significant improvement in outcomes. Several theories have attempted to explain the mechanistic basis of VILI. The stretched-pore hypothesis suggested that vascular distention may open the endothelial intercellular junctions, thus increasing fluid and protein leak and leading to a compromised lung function. The stress failure hypothesis proposes that pressure-induced tensile failure of capillary endothelium and basement membrane may result in hemorrhage and fluid leak. The stretch-recoil hypothesis introduced the concept that active cellular components are involved in the development of VILI. In the current chapter, ventilator-induced lung injury is examined as it relates to the pathophysiological changes beyond direct airway trauma. The role of lung-related factors such as stress, strain, and lung inhomogeneity will be examined, as well as extra-parenchymal factors and factors more directly related to mechanical ventilation (such as tidal volume, driving pressure, respiratory rate, inspiratory-to-expiratory ratio and flow). The recently proposed, unifying theory of mechanical power will also be presented and discussed.