[Acute respiratory distress syndrome. Pathogenesis and therapy of acute pulmonary failure]

Adult respiratory distress syndrome (ARDS) is the pulmonary response to systemic inflammation precipitated by local or systemic tissue hypoxia, or ischaemia and reperfusion. ARDS is a dynamic, pathological process with a multifactorial etiology. The main clinical manifestations of ARDS are dyspnoea, non-cardiogenic pulmonary oedema, and hypoxia due to increased pulmonary capillary permeability, pulmonary vasoconstriction and diminished pulmonary vascular reactivity. Eventually this pulmonary pathology results in first, oedema, pulmonary hypertension, and increased ventilation-perfusion inequality and later, pulmonary remodelling and irreversible pulmonary hypertension. The inflammatory mechanisms involved in acute lung injury are complex and include activation of polymorphonuclear neutrophils, endothelial cells, and synthesis of free radicals, predominantly derived from oxygen. Cytokines synthesized by macrophages maintain and regulate the inflammatory host response. Immune-modulating therapy in ARDS is yet experimental. Accordingly, treatment in ARDS is supportive, directed towards pulmonary oedema, pulmonary hypertension and hypoxaemia. The use of low tidal volumes and low inspiratory pressures in mechanical ventilation is established therapy. The goal in haemodynamic monitoring by applying a Swan-Ganz catheter is to obtain a low pulmonary capillary wedge pressure (< 12-15 mmHg) without compromising adequate delivery of oxygen to vital organs. For treatment of pulmonary hypertension nitric oxide is useful. Change of position and inhalation with beta2-agonists are therapeutic possibilities. Steroids may be of benefit in the late proliferative phase of ARDS.