• M Max, U Kaisers, and R Rossaint.
• Klinik für Anästhesiologie und operative Intensivmedizin, Virchow-Klinikum der Medizinischen Fakultät der Humboldt-Universität zu Berlin.
• Swiss Med Wkly. 1997 Jun 14;127(24):1030-8.

AbstractDespite more than 25 years of extensive research, the mortality of ARDS patients remains high. The inflammatory process within the lung and the associated gas exchange disturbances require an aggressive ventilatory regimen, which itself may harm the lung. Therapeutic measures which are used to reduce iatrogenic damage to the lung are pressure controlled mechanical ventilation in combination with PEEP and permissive hypercapnia, dehydration and extracorporeal gas exchange. At present, new strategies such as intratracheal instillation of surfactant, partial liquid ventilation and inhalation of nitric oxide (NO) are being evaluated. Surfactant reduces the surface tension, forming a monomolecular layer at the air/tissue interface. It thereby decreases the forces necessary to expand the alveoli and prevents alveoli with small diameter from collapsing. In ARDS, a disturbance of surfactant synthesis, function and re-uptake is the rationale for treatment with exogenous surfactant. Initial clinical results suggest a limited positive effect independently of the surfactant preparation used, the dose and the application mode. Experience with partial liquid ventilation with perfluorocarbons in ARDS has also been reported. Perfluorocarbons are liquids with a high binding capacity for oxygen and carbon dioxide. During normal mechanical ventilation with gas, repetitive doses of perfluorocarbons are instilled into the lungs up to a volume equal to the functional residual capacity. The liquid is pushed into collapsed alveoli and keeps them open by reducing the surface tension. First clinical studies have demonstrated the possible improvement in pulmonary gas exchange. In ARDS, inhalation of NO may cause a predominantly selective vasodilation in blood vessels of ventilated lung regions, resulting in an increase in PaO2 and a decrease in pulmonary artery pressure. The effect of NO on the pulmonary vasculature also induces a reduction in right ventricular afterload and also in pulmonary capillary pressure, which may lead to a faster resolution of pulmonary edema. However, in spite of the promising results of these new strategies, further studies are needed to evaluate their influence on morbidity and mortality.

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