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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. [1]
Pulmonary edema (British English: oedema), also known as pulmonary congestion, is excessive fluid accumulation in the tissue or air spaces (usually alveoli) of the lungs. [1] This leads to impaired gas exchange , most often leading to shortness of breath ( dyspnea ) which can progress to hypoxemia and respiratory failure .
High-altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft). [2] HAPE is a severe presentation of altitude sickness. Cases have also been reported between 1,500–2,500 metres or 4,900–8,200 feet in people who ...
The edema contributes to the deposition of a hyaline membrane (composed of dead cells, surfactant, and proteins) along the alveolar walls. Hyaline membranes are characteristic of DAD. The edema interferes with the naturally occurring surfactant, which is critical for reducing surface tension and allowing alveoli to remain open and allow air in ...
NPPE develops as a result of significant negative pressure generated in the chest cavity by inspiration against an upper airway obstruction. These negative pressures in the chest lead to increase venous supply to the right side of the heart while simultaneously creating more resistance for the left side of the heart to supply blood to the rest of the body (). [4]
Diagram of a pulmonary artery catheter in position. The pulmonary wedge pressure (PWP) (also called pulmonary arterial wedge pressure (PAWP), pulmonary capillary wedge pressure (PCWP), pulmonary artery occlusion pressure (PAOP), or cross-sectional pressure) is the pressure measured by wedging a pulmonary artery catheter with an inflated balloon into a small pulmonary arterial branch. [1]
They are suggestive for the diagnosis of congestive heart failure, but are also seen in various non-cardiac conditions such as pulmonary fibrosis, interstitial deposition of heavy metal particles or carcinomatosis of the lung. Chronic Kerley B lines may be caused by fibrosis or hemosiderin deposition caused by recurrent pulmonary edema.
Later, the capillary vasculature is overwhelmed by increased pressure and fluid backs up into the alveolar sac, resulting in pulmonary edema and decreased oxygenation capability. [2] Additionally, increased pressure demands on capillary vasculature result in increases in vascular tone to include remodeling of pre-capillary vessels such as ...