In ARDS, all are seen except :

Acute respiratory distress syndrome Aetiology and pathogenesis Acute respiratory distress syndrome (ARDS) is a diffuse neutrophilic alveolitis caused by a range of conditions and characterised by bilateral radiographic infiltrates and hypoxaemia. Activated neutrophils are sequestered into the lungs and capillary permeability is increased, with damage to cells within the alveoli. The pathophysiology is part of the inflammatory spectrum, and the triggers are similar: infective and non-infective inflammatory processes. These processes result in exudation and accumulation of protein-rich cellular fluid within alveoli and the formation of characteristic ‘hyaline membranes’. Local release of cytokines and chemokines by activated macrophages and neutrophils results in progressive recruitment of inflammatory cells. Secondary effects include loss of surfactant and impaired surfactant production. The net effect is alveolar collapse and reduced lung compliance, most marked in dependent regions of the lung (mainly dorsal in supine patients).  The affected airspaces become fluid-filled and can no longer contribute to ventilation, resulting in hypoxaemia (due to increased pulmonary shunt) and hypercapnia (due to inadequate ventilation in some areas of the lung): that is, ventilation–perfusion mismatch. Reference: : Davidson P R I N C I P L E S   and Practice O F M E D I C I N E 23rd edition page no  198