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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]
Swimming induced pulmonary edema also known as immersion pulmonary edema [23] [24] [25] Transfusion associated Acute Lung Injury is a specific type of blood-product transfusion injury that occurs when the donors plasma contained antibodies against the recipient, such as anti-HLA or anti-neutrophil antibodies.
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 ...
This can be done with electrocardiogram, echocardiogram, measurement of cardiac enzymes, etc. Other causes of pulmonary edema that require rapid intervention and should be considered first include fluid overload, brain injury, and anaphylaxis. If when considering these differentials, there is no evidence for administration of excessive fluids ...
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 ...
On the other hand, gravity causes a gradient in blood pressure between the top and bottom of the lung of 20 mmHg in the erect position (roughly half of that in the supine position). Overall, mean pulmonary venous pressure is ~5 mmHg. Local venous pressure falls to -5 at the apexes and rises to +15 mmHg at the bases, again for the erect lung.
Patients in shock often experience respiratory distress due to pulmonary edema (e.g., in cardiogenic shock). Lactic acidosis and anemia can also result in type 4 respiratory failure. [ 1 ] However, type 1 and 2 are the most widely accepted.
Pneumonia and sepsis are the most common triggers, and pneumonia is present in up to 60% of patients and may be either causes or complications of ARDS. Alcohol excess appears to increase the risk of ARDS. [47] Diabetes was originally thought to decrease the risk of ARDS, but this has shown to be due to an increase in the risk of pulmonary edema.