About: Pathophysiology of acute respiratory distress syndrome

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The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. Additional common findings in ARDS include partial collapse of the lungs (atelectasis) and low levels of oxygen in the blood (hypoxemia). The clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage (DAD). Of these, the pathology most commonly associated with ARDS is

Attributes	Values
rdfs:label	Pathophysiology of acute respiratory distress syndrome (en)
rdfs:comment	The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. Additional common findings in ARDS include partial collapse of the lungs (atelectasis) and low levels of oxygen in the blood (hypoxemia). The clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage (DAD). Of these, the pathology most commonly associated with ARDS is (en)
name	Pathophysiology of acute respiratory distress syndrome (en)
foaf:depiction
dcterms:subject	Respiratory diseases
Wikipage page ID	58114194 (xsd:integer)
Wikipage revision ID	995864353 (xsd:integer)
Link from a Wikipage to another Wikipage	Capillaries Pulmonary alveolus Pulmonary edema Endothelium Eosinophilic pneumonia Epithelium Barotrauma Hypoxemia Patent foramen ovale Cytokine Compliance (physiology) Mechanical ventilation Endothelial cell Gradient Cryptogenic organizing pneumonia Shock (circulatory) Tidal volume Micrograph Bronchioles H&E stain Lobe (anatomy) Airway Respiratory diseases Diffuse alveolar damage Hyaline Respiratory burst Permissive hypercapnia Atelectasis Fibrosis Endotracheal intubation National Institutes of Health Shear stress Multiple organ dysfunction syndrome Systemic inflammatory response syndrome Kilopascal Transpulmonary pressure Respiratory acidosis MmHg Right-to-left shunt Neutrophils Type II pneumocyte Perfusion pressure Ventilator associated lung injury T-lymphocytes
sameAs	Pathophysiology of acute respiratory distress syndrome Pathophysiology of acute respiratory distress syndrome
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thumbnail	wiki-commons:Special:FilePath/Hyaline_membranes_-_intermed_mag.jpg?width=300
caption	Micrograph of diffuse alveolar damage, the histologic correlate of ARDS. H&E stain. (en)
has abstract	The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. Additional common findings in ARDS include partial collapse of the lungs (atelectasis) and low levels of oxygen in the blood (hypoxemia). The clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage (DAD). Of these, the pathology most commonly associated with ARDS is DAD, which is characterized by a diffuse inflammation of lung tissue. The triggering insult to the tissue usually results in an initial release of chemical signals and other inflammatory mediators secreted by local epithelial and endothelial cells. Neutrophils and some T-lymphocytes quickly migrate into the inflamed lung tissue and contribute in the amplification of the phenomenon. Typical histological presentation involves diffuse alveolar damage and hyaline membrane formation in alveolar walls. Although the triggering mechanisms are not completely understood, recent research has examined the role of inflammation and mechanical stress. (en)
biological system	respiratory system (en)
prov:wasDerivedFrom	wikipedia-en:Pathophysiology_of_acute_respiratory_distress_syndrome?oldid=995864353&ns=0
page length (characters) of wiki page	12248 (xsd:nonNegativeInteger)
foaf:isPrimaryTopicOf	wikipedia-en:Pathophysiology_of_acute_respiratory_distress_syndrome
is Link from a Wikipage to another Wikipage of	Acute respiratory distress syndrome
is foaf:primaryTopic of	wikipedia-en:Pathophysiology_of_acute_respiratory_distress_syndrome

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