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Oncotic pressure, or colloid osmotic-pressure, is a type of osmotic pressure induced by the plasma proteins, notably albumin, [1] in a blood vessel's plasma (or any other body fluid such as blood and lymph) that causes a pull on fluid back into the capillary.
As the pulmonary venous pressure rises, these pressures overwhelm the barriers and fluid enters the alveoli when the pressure is above 25 mmHg. [14] Depending on whether the cause is acute or chronic determines how fast pulmonary edema develops and the severity of symptoms. [12] Some of the common causes of cardiogenic pulmonary edema include:
The most common causes of pathologic transudate include conditions that: [citation needed] Increase hydrostatic pressure in vessels: left ventricular heart failure, Decrease oncotic pressure in blood vessels: Cirrhosis (Cirrhosis leads to hypoalbuminemia and decreasing of colloid oncotic pressure in plasma that causes edema)
The osmotic pressure of the plasma affects the mechanics of the circulation in several ways. An alteration of the osmotic pressure difference across the membrane of a blood cell causes a shift of water and a change of cell volume. The changes in shape and flexibility affect the mechanical properties of whole blood.
Pulmonary capillary pressures in this level cause an imbalance between the hydrostatic pressure and the oncotic pressure, leading to extravasation of fluid from the vascular tree and pooling of fluid in the lungs (congestive heart failure causing pulmonary edema). [citation needed]
A fall in osmotic pressure occurs in nephrotic syndrome and liver failure. [8] Causes of edema that are generalized to the whole body can cause edema in multiple organs and peripherally. For example, severe heart failure can cause pulmonary edema, pleural effusions, ascites and peripheral edema. Such severe systemic edema is called anasarca.