cardiovascular disorders
Edema
Pathophysiology of Edema
Edema results from increased movement of fluid from the intravascular to the interstitial space or decreased movement of water from the interstitium into the capillaries or lymphatic vessels. The mechanism involves one or more of the following: Increased capillary hydrostatic pressure Decreased plasma oncotic pressure Increased capillary permeability Obstruction of the lymphatic system (ADH) system, resulting in renal sodium retention. By increasing osmolality, renal sodium retention triggers water retention by the kidneys and helps maintain plasma volume. Increased renal sodium retention also may be a primary cause of Volume Overload and hence edema. Excessive exogenous sodium intake may also contribute. Less often, edema results from decreased movement of fluid out of the interstitial space into the capillaries due to lack of adequate plasma oncotic pressure as in nephrotic syndrome, protein-losing enteropathy, liver failure, or starvation. Increased capilliary permeability occurs in infections or as the result of toxin or inflammatory damage to the capillary walls. In Angioedema , mediators, including mast cell–derived mediators (eg, histamine, leukotrienes, prostaglandins) and bradykinin and complement-derived mediators, cause focal edema. The lymphatic system is responsible for removing protein and white blood cells (along with some water) from the interstitium. Lymphatic obstruction allows these substances to accumulate in the interstitium. 