Critical care medicine
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Critical care medicine · Apr 2003
ReviewPhysiologic rationale for ventilator setting in acute lung injury/acute respiratory distress syndrome patients.
To review the physiologic approach to setting mechanical ventilation in acute lung injury/acute respiratory distress syndrome. ⋯ The majority of physiologic, experimental, and clinical trial data converge on one simple concept: treat the lung gently.
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Critical care medicine · Apr 2003
ReviewCoagulation, fibrinolysis, and fibrin deposition in acute lung injury.
To review: a) the role of extravascular fibrin deposition in the pathogenesis of acute lung injury; b) the abnormalities in the coagulation and fibrinolysis pathways that promote fibrin deposition in the acutely injured lung; and c) the pathways that contribute to the regulation of the fibrinolytic system via the lung epithelium, including newly recognized posttranscriptional and urokinase-dependent pathways. Another objective was to determine how novel anticoagulant or fibrinolytic strategies may be used to protect against acute inflammation or accelerated fibrosis in acute lung injury. ⋯ Disordered coagulation and fibrinolysis promote extravascular fibrin deposition in acute lung injury. It is this deposition that characterizes acute lung injury and repair. Expression of uPA, uPAR, and PAI-1 by the lung epithelium, as well as the ability of uPA to induce other components of the fibrinolytic system, involves posttranscriptional regulation. These pathways may contribute to disordered fibrin turnover in the injured lung. The success of anticoagulant or fibrinolytic strategies designed to reverse the abnormalities of local fibrin turnover in acute lung injury supports the inference that abnormalities of coagulation, fibrinolysis, and fibrin deposition have a critical role in the pathogenesis of acute lung injury.
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Critical care medicine · Apr 2003
ReviewLung recruitment maneuvers in acute respiratory distress syndrome and facilitating resolution.
To summarize the possible ways that acute respiratory distress syndrome (ARDS) lungs can be recruited and to present the experimental and clinical results of these maneuvers, along with the possible effects on patient outcome. ⋯ High airway pressures can open collapsed ARDS lungs and partially open edematous ARDS lungs. High PEEP levels and low tidal volume ventilation decrease bronchoalveolar and plasma inflammatory mediators and improve survival compared with low PEEP/high tidal volume ventilation. In the near future, thoracic computed tomography associated with high-performance monitoring of regional ventilation (electrical impedance tomography) may be used at the bedside to determine the optimal mechanical ventilation of ARDS patients.
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To review recent advances in the field of endothelial cell heterogeneity, and to apply this knowledge to an understanding of site-specific vasculopathy, including acute lung injury. ⋯ The structure and function of endothelial cells are differentially regulated in space and time. Far from being a giant monopoly of homogeneous cells, the endothelium represents a consortium of smaller enterprises of cells located within blood vessels of different tissues. Although united in certain functions, each enterprise is uniquely adapted to meet the demands of the underlying tissue. The endothelium may also vary in its response to pathophysiologic stimuli and therefore contribute to the focal nature of vasculopathic disease states. In acute lung injury, the unique properties of the endothelium may conspire with systemic imbalances to localize pathology to the pulmonary vasculature.
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Critical care medicine · Apr 2003
ReviewTransforming growth factor-beta: a mediator of cell regulation in acute respiratory distress syndrome.
To review recent advances in the use of transforming growth factor (TGF)-beta in acute lung injury and to apply this knowledge to understanding the pathophysiology of this syndrome. ⋯ These studies suggest that TGF-beta not only participates in the late phase of acute lung injury, but also might be active early in acute lung injury and potentially could contribute to the development of pulmonary edema. Integrin-mediated local activation of TGF-beta is critical to the development of pulmonary edema in ARDS, and blocking TGF-beta or its activation could be an effective treatment for this disorder.