![]() This pattern over time caused progressive RV failure, presumably due to repetitive microvascular injury from cycles of absent/excessive vascular flow (vascular shear stress). Similar effects of ventilation have been observed in a computational study, and interruption of pulmonary blood flow due to cyclic changes in afterload has been reported in patients with ARDS. During expiration the reverse occurs, and the pulmonary artery flow and pressure increase, briefly exceeding normal values. This in turn interrupts pulmonary artery flow and pressure, and therefore pulmonary capillary pressure becomes very low.Īt this point the lung enters West zone I condition (ventilation, no perfusion) however, this is because of cyclic inspiratory interruption of RV preload, rather than excessive alveolar pressure. During high V T ventilation, at peak inspiration the pleural pressure exceeds the pressure in large veins and right atrium, resulting in their collapse, abolition of venous return, and absent right ventricular filling. This cyclic pattern of altered perfusion was not due to microvascular compression at peak inspiration (from very high alveolar pressure) instead, it was due to abolition of right ventricular preload in inspiration and (compensatory) greater ventricular filling in expiration. 1 see animated figure in online supplement). ![]() Recent observations advance this interpretation, because the (same) combination of high V T and zero PEEP caused cycles of obliteration of perfusion during inspiration and increased perfusion during expiration (Fig. On the basis of these experiments it was discovered that increased microvascular permeability and hydrostatic pressure were responsible for the associated edema. ![]() The classic experiments of Webb and Tierney demonstrated that high V T and zero PEEP caused overwhelming lung injury this in vivo experiment largely prompted a generation of work on VILI that ultimately changed practice. Endothelial disruption will increase pulmonary vascular resistance, and may cause right ventricle (RV) strain, which in clinical ARDS is associated with worse outcome. Less recognized is vascular shear stress produced by turbulent (or rapidly changing) blood flow this can cause endothelial dysfunction and injury and induce inflammation and vascular leak, as demonstrated during reperfusion following ischemia. While modest changes in airway pressure can amplify focal force in the lung parenchyma via tissue interdependence and induce cell stress failure, increases in transmural pressure (across the vessel walls) could fracture capillaries and cause hemorrhagic pulmonary edema. Endothelial dysfunction impairs transcytotic and paracytotic transport and increases permeability, leading to alveolar flooding indeed, increased microvascular permeability is universal in experimental VILI, and is presumed in the current ARDS definition. In parallel, lung overventilation triggers endothelial Ca 2+ signaling which in turn increases vascular permeability and inflammatory responses. Lung overventilation (signaling due to mechanical stress) initiates pro-inflammatory events on lung microvascular endothelial cells (e.g., expression of adhesion molecules, deposition of leukocyte/platelet-binding proteins). First, in a classic model of VILI, disruption of the endothelium occurs before epithelial injury. epithelium) may be responsible for initiation or propagation of injury. Several findings suggest that the endothelium (vs. ![]()
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