Abstract
Normal water homeostasis in the lung is based on a balance among the so-called “Starling” forces: a vascular-to-extravascular hydrostatic pressure gradient, a similar but directionally opposite oncotic pressure gradient, and the “leakiness” or “permeability” of the alveolo-capillary endothelial membrane to protein [1,2]. This paradigm leads to a natural and clinically relevant distinction: Pulmonary edema can be either “cardiogenic”(i.e. due to increased hydrostatic pressures) or “non-cardiogenic” (i.e. due to increased vascular permeability). The prototypical example of non-cardiogenic pulmonary edema is the acute respiratory distress syndrome (ARDS).
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Schuster, D.P. (1998). Quantifying Lung Injury in 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_12
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DOI: https://doi.org/10.1007/978-3-642-60733-2_12
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