Dan edem free#

Plasma volume contraction is reflected in increased hematocrit values. Hematologic effects: Plasma volume contraction may develop, with risk of rapid onset hypovolemic shock, if hemorrhage occurs. Cardiovascular effects: Elevated blood pressure is seen as the result of potential vasoconstriction as well as an increase in cardiac output. These five mechanisms, in any combination or permutation, are thought to contribute to the following common pathophysiologic changes seen in patients with preeclampsia: 1. Decreased antioxidant levels are also noted.

Dan edem free#

Lipid peroxide, free radicals, and antioxidant release: Lipid peroxides and free radicals have been implicated in vascular injury and are increased in pregnancies complicated by preeclampsia. Changes in endothelium-derived factors: Nitric oxide, a potent vasodilator, is decreased in patients with preeclampsia and may explain the evolution of vasoconstriction in these patients.

Because of this imbalance, vessel constriction occurs. In patients who develop preeclampsia, the balance shifts to favor TXA2.ДЄgain, PGI2 functions to promote vasodilatation and decrease platelet aggregation, and TXA2 promotes vasoconstriction and platelet aggregation. Changes in prostanoids: Prostacyclin (PGI2) and thromboxane (TXA2) are increased during pregnancy, with the balance in favor of PGI2. Endothelial damage is then thought to promote further vasospasm. Low antithrombin III levels are permissive for microthrombi development. Endothelial fibronectin levels are increased and antithrombin III and пѓЎ2-antiplasmin levels are decreased, reflecting endothelial damage. Hemostatic changes: Increased platelet activation with increased consumption in the microvasculature is noted during the course of preeclampsia. Endothelial damage is also noted within the vessels. Vascular changes: Instead of noting the physiologic trophoblast-mediated vascular changes in the uterine vessels (decreased musculature in the spiral arterioles leads to the development of a low-resistance, lowpressure, high-flow system), inadequate maternal vascular response is seen in cases of preeclampsia and/or intrauterine fetal growth restriction. Several potential causes for maternal vasospasm have been postulated: 1. The predominant pathophysiologic finding in preeclampsia and gestational hypertension is maternal vasospasm. Given the characteristic multisystem effects, it is clear that several pathophysiologic mechanisms are involved (Fig. PATHOPHYSIOLOGY Hypertension in pregnancy affects the mother and newborn to varying degrees. The intensity of acidosis relates to the amount of lactic acid produced and the rate at which carbon dioxide is exhaled. Following an eclamptic convulsion, the serum pH and bicarbonate concentration are lowered due to lactic acidosis and compensatory respiratory loss of carbon dioxide. This may not be the case if there has been vigorous diuretic therapy, sodium restriction, or administration of free water with sufficient oxytocin to produce antidiuresis. Electrolyte concentrations do not differ appreciably in women with preeclampsia compared with those of normal pregnant women. This reduction creates a filtration imbalance and further displaces intravascular fluid into the surrounding interstitium. In addition to generalized edema and proteinuria, these women have reduced plasma oncotic pressure. The mechanism responsible for pathological fluid retention is thought to be endothelial injury. Mengapa tangan, kaki dan mukanya edem ?ДЇluid and Electrolyte Changes In women with severe preeclampsia, the volume of extracellular fluid, manifest as edema, is usually much greater than that of normal pregnant women.