• J Mancebo.
• Servicio de Medicina Intensiva. Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. jmancebo@hsp.santpau.es
• Rev Esp Anestesiol Reanim. 2001 Dec 1; 48 (10): 465-70.

AbstractThe pathophysiology of acute respiratory distress syndrome (ARDS) is characterized by pulmonary edema due to extravasation from capillary lesions in the endothelium. A clinical diagnosis is made when there is a predisposing cause (sepsis and pneumonia being the most common) that gives rise to acute respiratory insufficiency (PaO2/FiO2 ratio (3/4) 200 mmHg, bilateral infiltrates visible on a chest film and hemodynamic or other clinical signs of left cardiac insufficiency). Most patients require invasive support ventilation at a high FiO2 and positive end-expiratory pressure (PEEP). The only therapeutic approach available at this time associated with a highly significant decrease in mortality in patients with ARDS is ventilation at low flow volumes (6 ml/kg) and moderate levels of PEEP (approximately 10 cmH2O).

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