Abstract
Advances in our understanding of the pathogenesis of acute respiratory distress syndrome (ARDS) and sepsis have shown the two to be intimately related. Al-though ARDS may develop from local lung injury, it is commonly part of the systemic inflammatory response to severe sepsis, and tissue damage in the lungs is the result of the same inflammatory mediators involved in other organ damage. Inflammatory injury to the lung microvessels is an early pathogenetic event in ARDS, and leukocytes in particular are implicated. The sequestration of neutrophils in the lungs and their activation by inflammatory mediators leads to the release of toxic substances such as lipid mediators and reactive oxygen metabolites. The result is an increase in pulmonary endothelial and epithelial permeability, and an accumulation of fluid in the pulmonary interstitial and alveolar spaces. This causes a reduced ventilated lung volume and impaired gas exchange. Hence, the same inflammatory response mechanisms take place in the lungs as in other organs leading to organ failure. Although cardiac output is normal or high and thus systemic oxygen delivery (D02) is well preserved, distant tissue hypoxia may thus arise. Most patients with ARDS, however, do not have tissue hypoxia, this only occurring if there is also acute circulatory failure. Poor tissue oxygenation may play a role in the development of organ failure which is often fatal. Mortality in ARDS patients is more often due to multiple organ failure than to refractory hypoxemia [1,2], and recognition of these abnormalities is therefore vitally important.
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Vincent, J.L., De Backer, D. (1998). Systemic Circulatory Function and Peripheral Oxygen Delivery in ALI and ARDS. In: Marini, J.J., Evans, T.W. (eds) Acute Lung Injury. Update in Intensive Care and Emergency Medicine, vol 30. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60733-2_11
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