Abstract
The acute respiratory distress syndrome (ARDS) characterizes different states of acute impairment of pulmonary gas exchange. Underlying noxious events may directly affect lung parenchyma from the alveolar side (e.g. gastric acid aspiration), or — more classically — the lung vasculature may be the primary target site of circulating humoral or cellular mediators activated under conditions of systemic inflammatory events such as sepsis or severe polytrauma [1]. Key pathophysiological features of the initial “exudative” phase of ARDS include:
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1.
increased capillary endothelial and alveolar epithelial permeability.
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2.
leakage of protein rich edema fluid into interstitial and alveolar spaces.
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3.
increased pulmonary vascular resistance with maldistribution of pulmonary perfusion.
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4.
alveolar instability with formation of atelectases and ventilatory inhomogenities.
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5.
severe disturbances of gas exchange characterized by ventilation-perfusion mismatch and extensive shunt flow.
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Keywords
- Acute Respiratory Distress Syndrome
- Adult Respiratory Distress Syndrome
- Acute Respiratory Distress Syndrome Patient
- Alveolar Space
- Surfactant Replacement
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Seeger, W., Günther, A., Walmrath, H.D. (1998). Alveolar Surfactant 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_6
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