Mechanisms include regional alveolar over distention, repetitive alveolar collapse with shearing (atelectrauma), and oxygen toxicity ( 2, 3, 6).Įxperimental data suggest that atelectrauma is prominent in ARDS. In patients with ARDS, massive alveolar collapse and cyclic lung reopening and over distention during mechanical ventilation may perpetuate alveolar injury ( 5). The level of oxygen in the blood can stay dangerously low, even if the person receives ventilation support. The lungs of the afflicted individuals show severe pulmonary edema, distributed cellular destruction, diffuse alveolar damage with alveolar flooding by proteinaceous fluid, neutrophil influx into the alveolar space, patchy alveolar collapse, loss of alveolar epithelial cells, deposition of hyaline membranes on the denuded basement membrane, formation of microthrombi and disordered repair ( 1, 3, 4). ![]() ![]() ARSD diagnostic criteria include acute respiratory distress, bilateral radiographic pulmonary infiltrates, hypoxemia, and the Pao2 to Fio2 (P/F) ratio is less than 200, in the absence of heart failure (pulmonary artery occlusion pressure (PAOP) less than 18 mm Hg) ( 1, 3).ĪRDS is a severe lung syndrome caused by a variety of direct and indirect issues therefore, its pathophysiology is so complex. Regardless of the severe lung injury, pulmonary function in most survivors returns nearly normal within 6 to 12 months ( 1). Its mortality remains between 30-50%, despite early aggressive intervention ( 2). It is a devastating injury to the lungs, characterized by diffuse pulmonary inflammation, hypoxemia, and respiratory distress ( 1). ![]() Acute respiratory distress syndrome (ARDS) is a serious life-threatening lung reaction to various forms of injuries that cause hypoxia.
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