The Role of the Contact System in the Pathophysiology of ARDS

The development of the adult respiratory distress syndrome (ARDS) follows disruption of the alveolar basement membrane. This damage causes a “permeability” pulmonary edema which is manifest as respiratory insufficiency in the presence of a normal capillary wedge pressure and a normal plasma protein content. The clinical consequences are those of severe dyspnea, cyanosis, hypoxia, decreased pulmonary compliance and bilateral diffuse alveolar infiltrates on the chest roentgenogram, with a normal pulmonary capillary wedge pressure [1].