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Heparin inhibits reactions that lead to the clotting of blood and the formation of fibrin clots both in vitro and in vivo. Heparin acts at multiple sites in the normal coagulation system. Small amounts of heparin in combination with antithrombin III (heparin cofactor) can inhibit thrombosis by inactivating activated Factor X and inhibiting the conversion of prothrombin to thrombin. Once active thrombosis has developed, larger amounts of heparin can inhibit further coagulation by inactivating thrombin and preventing the conversion of fibrinogen to fibrin. Heparin also prevents the formation of a stable fibrin clot in inhibiting the activation of the fibrin stabilizing factor.
Bleeding time is usually unaffected by heparin. Clotting time is prolonged by full therapeutic doses of heparin; in most cases, it is not measurably affected by low doses of heparin.
Peak plasma levels of heparin are achieved 2 to 4 hours following subcutaneous administration, although there are considerable individual variations. Loglinear plots of heparin plasma concentrations with time for a wide range of dose levels are linear which suggests the absence of zero order processes. Liver and the reticuloendothelial system are the site of biotransformation. The biphasic elimination curve, a rapidly declining alpha phase (t½) and after the age of 40 a slower beta phase, indicates uptake in organs. The absence of a relationship between anticoagulant half-life and concentration of half-life may reflect factors such as protein binding of heparin.
Heparin does not have fibrinolytic activity; therefore, it will not lyse existing clots.
Heparin Lock Flush Solution does not induce systemic anticoagulant action at single doses of 10 or 100 USP units per mL when used for maintenance of potency of intravenous injection devices. It may interfere with laboratory tests on blood samples withdrawn from such devices, unless the volume of in situ heparin saline, equal to that of the priming volume of the catheter, is aspirated and discarded before such samples are taken.
Isotonic concentrations of sodium chloride are suitable for parenteral replacement of chloride losses that exceed or equal the sodium loss. Hypotonic concentrations of sodium chloride are suited for parenteral maintenance of water requirements when only small quantities of salt are desired.
Sodium chloride in water dissociates to provide sodium (Na+) and chloride (Cl-) ions. Sodium (Na+) is the principal cation of the extracellular fluid and plays a large party in the therapy of fluid and electrolyte disturbances. Chloride (Cl-) has an integral role in buffering action when oxygen and carbon dioxide exchange occurs in the red blood cells. The distribution and excretion of sodium (Na+) are largely under the control of the kidney which maintains a balance between intake and output.
The small volume of fluid and amount of sodium chloride provided by Heparin Lock Flush Solution, USP, when used only as a vehicle for maintaining potency of an intravenous injection device, is unlikely to exert a significant effect on fluid and electrolyte balance except possibly in very small infants.
Last reviewed on RxList: 1/10/2004
This monograph has been modified to include the generic and brand name in many instances.
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