Abstract
Acute respiratory distress syndrome (ARDS) is characterized by diffuse pulmonary infiltrates, severe hypoxemia at high breathing oxygen concentrations, the presence of a precipitating underlying disease, acute onset, and absence of left ventricular failure. The pathophysiology of ARDS includes increased membrane permeability, decreased oncotic pressure, and augmented transvascular hydrostatic pressure gradients that cause non-cardiogenic pulmonary edema, atelectasis and loss of lung volume. As a result of these alterations, ventilation/perfusion (V/Q) heterogeneity and intrapulmonary shunt increase, and oxygenation is severely impaired. Although acute lung injury (ALI) does not have a unilateral distribution, some degree of in-homogeneity generally exits. In clinical practice, lobar or one lung pneumonia or atelectasis, and lung contusion are common findings. In this scenario, application of positive intrathoracic pressure may over-inflate the uninvolved more compliant lung and divert pulmonary blood flow to the injured lung, thereby worsening V/Q mismatch and decreasing oxygenation [1–7].
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Blanch, L., Murias, G., Nahum, A. (2002). Lung Recruitment in Localized Lung Injury. In: Vincent, JL. (eds) Intensive Care Medicine. Springer, New York, NY. https://doi.org/10.1007/978-1-4757-5551-0_29
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DOI: https://doi.org/10.1007/978-1-4757-5551-0_29
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