Pathophysiology of acute respiratory distress syndrome

The acute respiratory distress syndrome (ARDS) has a high mortality rate and is often diagnosed too seldom and too late. Key characteristics are acute onset, a precipitating disease, bilateral pulmonary infiltrates, reduced compliance of the respiratory system, intrapulmonary shunt, and oxygen-refractory hypoxaemia. Dominant pathophysiological factors are a protein-rich oedema due to increased permeability of the alveolo-capillary barrier with reduced synthesis of surfactant as well as damage of lung parenchyma by neutrophil granulocytes and their products. Mediators can cause extrapulmonary inflammation and organ dysfunction. Characteristic radiological findings in the acute phase are pulmonary atelectasis and ground glass opacities of lobar, patchy or diffuse distribution. Densities typically show a gravity-dependent gradient from ventral to dorsal in supine patients. Biomarkers are relevant only in accordance with clinical parameters. The most relevant therapeutic approach is lung protective ventilation with a low tidal volume and limited airway pressure together with adequate PEEP, positioning and restrictive fluid-volume management.