Abstract
Pulmonary edema, both in its lesional as well as hydrostatic version, is a frequent cause of acute respiratory failure. From the pathophysiological point of view, the most important advance is undoubtedly the knowledge that the reabsorption process of pulmonary edema is an active process with energy consumption. This concept has revolutionized this field due to the possibility of finding substances or factors that stimulate or inhibit this reabsorption. Furthermore, in the monitoring field, significant advances have also been experimented due to the possibility of quantifying the edema in a simple and reliable way with transpulmonary thermodilution.
MeSH terms
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Acute Lung Injury / complications
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Acute Lung Injury / physiopathology
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Adrenergic beta-Agonists / therapeutic use
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Alveolar Epithelial Cells / metabolism
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Biological Transport, Active
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Diagnostic Imaging / methods
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Diuretics / therapeutic use
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Extracellular Fluid / metabolism
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Humans
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Hydrostatic Pressure
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Hypoxia / etiology
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Indicators and Reagents / pharmacokinetics
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Models, Cardiovascular
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Pulmonary Atelectasis / etiology
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Pulmonary Atelectasis / physiopathology
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Pulmonary Edema / classification
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Pulmonary Edema / diagnosis
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Pulmonary Edema / drug therapy
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Pulmonary Edema / etiology
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Pulmonary Edema / physiopathology*
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Pulmonary Gas Exchange
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Respiratory Distress Syndrome / etiology
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Respiratory Distress Syndrome / prevention & control
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Sodium-Potassium-Exchanging ATPase / physiology
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Thermodilution
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Vasodilator Agents / therapeutic use
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Ventilation-Perfusion Ratio
Substances
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Adrenergic beta-Agonists
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Diuretics
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Indicators and Reagents
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Vasodilator Agents
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Sodium-Potassium-Exchanging ATPase