Comparative Pharmacology
Head-to-head clinical analysis: HEPARIN SODIUM 20 000 UNITS IN DEXTROSE 5 versus LIQUAEMIN LOCK FLUSH.
Peer-Reviewed Evidence
Head-to-head clinical analysis: HEPARIN SODIUM 20 000 UNITS IN DEXTROSE 5 versus LIQUAEMIN LOCK FLUSH.
HEPARIN SODIUM 20,000 UNITS IN DEXTROSE 5% vs LIQUAEMIN LOCK FLUSH
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Heparin sodium binds to antithrombin III, causing a conformational change that accelerates the inactivation of thrombin and factor Xa, and to a lesser extent factors IXa, XIa, and XIIa, thereby inhibiting coagulation. It also inhibits platelet aggregation and prolongs clotting times.
Heparin potentiates the activity of antithrombin III, thereby inactivating thrombin (factor IIa) and activated factor X (Xa), and preventing fibrin clot formation. It also inhibits factors IXa, XIa, and XIIa.
Adults: Initial IV bolus 80 units/kg, then continuous IV infusion at 18 units/kg/hour. For therapeutic anticoagulation, adjust to target aPTT 1.5-2.5 times control. Dosing per institutional nomogram.
10-100 units/mL solution; flush intermittent intravenous catheters after each use with 1-5 mL; for central venous catheters, use 2-3 mL of 10 units/mL solution; for peripheral catheters, use 1-2 mL of 10 units/mL solution.
None Documented
None Documented
Terminal half-life 1.5 hours (range 1-3 hours) for therapeutic doses; dose-dependent, with higher doses prolonging half-life; half-life prolonged in hepatic or renal impairment.
1-2 hours (dose-dependent; prolonged with higher doses, renal impairment, or in elderly).
Renal: 50-60% as unchanged drug via glomerular filtration; hepatic metabolism (desulfation) accounts for minor clearance; fecal elimination negligible (<1%).
Renal (predominantly via reticuloendothelial system and liver metabolism; unchanged drug excreted in urine).
Category A/B
Category C
Anticoagulant
Anticoagulant