Strategies to improve oxygenation in experimental acute lung injury

One of the most important clinical syndromes, in which failure of oxygen uptake in the lung leads to severe hypoxia, is the so-called acute respiratory distress syndrome (ARDS). ARDS is a complex of clinical signs and symptoms which occur following diverse pulmonary or systemic insults, including sepsis. shock, pneumonia. trauma, liquid aspiration. hematological disorders, smoke inhalation, and many others, In ARDS, the treatments available are still inadequate and morbidity, mortality, and costs remain unacceptably high. The failure of the lung as a gas exchange organ results in peripheral tissue hypoxia, which appears to be related to the development of multiple organ failure (MOF). Since MOF is the predominant cause of death in ARDS, therapeutic efforts are aimed at improving oxygen delivery to the tissues. Available treatments include mechanical ventilation with positive end-expiratory pressure (PEEP) and high inspiratory oxygen concentration. However, despite extensive research on new ventilation modes, mortality has 110t changed much and remains 30-70%, as high as when first rcported by Ashbaugh et al. in 1967. It should be realized that mechanical ventilation is only a supportive strategy and that some ventilatory strategies even contribute to lung injury. That is why ARDS may, in part. be a product of our therapy - rather than the progression of the underlying disease. Several strategies for ARDS, such as exogenous surfactant therapy, ventilation according to the "Open Lung Concept" and partial liquid ventilation are currently under evaluation. In this chapter, we describe the central role of pulmonary surfactant in the pathophysiology of ARDS, and discuss the impact of these new strategies on surfactant function.

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