A glycosaminoglycan of varying molecular weights and polysaccharide units.

Naturally occurring biological agent derived from porcine mucosa.

Induces a conformational change in ant thrombin an endogenous inhibitor of several enzymes participating in the coagulation cascade.

Heparin is negatively charged, sulfated glycosaminoglycan polysaccharide polymer isolated from porcine intestine, where it is stored in mast cell granules.

Strong negatively charged heparin molecules bind to many proteins including: platelet factor 4, lipoproteins, von Willebrand factor, factor eight, and fibrinogen, as well as monocytes, endothelial cells, growth factors, and non-endothelial surfaces, including intravenous tubing and extracorporeal circuit components.

Unfractionated heparin is a mixture of polymers with chain lengths ranging from 3000 to 30,000 daltons, whereas low molecular weight heparin purified from unfractionated heparin, has a more uniform polymer size and the molecular weight of 3500 to 5000 daltons.

Heparin polymers bind to anti-thrombin and accelerate the interaction between anti-thrombin and thrombin or anti-thrombin and factor Xa, either of which results in the inhibition of prothrombin activity.
Low molecular weight heparin can inhibit thrombin,it, however, preferentially inhibits factor Xa.

Unfractionated heparin containing 18 or more polysaccharide units are required to inhibit thrombin.

Can be administered intravenously or by subcutaneous injection.

Unfractionated heparin has a short half-life and rapid reversibility with the administration of protamine making it the anticoagulant choice when careful control of anticoagulation is needed, such as in critically ill patients or in conjunction with extracorporeal circuits used in patients undergoing cardiopulmonary bypass or extracorporeal membrane oxygenation.

Uses: DVT, pulmonary embolism treatment and prophylaxis, acute coronary syndromes, percutaneous coronary intervention, thromboembolism disorders, arterial embolization: treatment and prophylaxis, atrial fibrillation, vascular and cardiac surgery, cardiopulmonary bypass surgery, arterial and venous catheters and pulmonary artery catheters.

Cleared rapidly by internalization of heparin by endothelial cells and macrophages and a slower process of renal clearance.

Binds to histidine-rich glycoprotein, platelet factor 4, vitronectin and von Willebrand factor.

Heparin can bind to platelets to transiently decrease platelets accounts after platelet transfusions.

The administration of unfractionated heparin can activate platelets and release platelet factors 4 a known heparin binding protein.

Heparin can trigger antibody formation and cause heparin induced thrombocytopenia.

Used for prevention and treatment of arterial and venous thromboembolism, unstable angina, acute myocardial infarction, cardiac and vascular surgery, coronary stents and angioplasty and with thrombolytic agents.

Anticoagulant of choice during pregnancy because it does not cross the placental barrier.

60-70% effective associated a prophylactic agent for venous and pulmonary embolism.

In a trial of dalteparin vs unfractionated heparin randomly assigned in 3764 patients, and given subcutaneoulsy 5000 u daily or 5000 u bi, respectively in ICU patients: among critically ill patients dalteparin was not superior to unfractionated heparin in decreasing the incidence of proximal deep vein thrombosis (PROTECT Investigators).

In pulmonary embolus should not be discontinued until warfarin treatment has reached a therapeutic INR for at least 2 days.

Its anticoagulant effect is by activating antithrombin III and thereby inhibits thrombin.

Reduces ischemic events beyond the use of aspirin alone in acute coronary artery syndrome.

Long term use of greater than 1 month may cause osteoporosis.

Can decrease plasma aldosterone levels and increase potassium levels (heparin induced hyperkalemia).

Unfractionated heparin possesses a number of limitations including continuous intravenous infusion which can interfere with procedures such as MRI, diagnostic testing, requires anticoagulation monitoring, infusion adjustments, or additional bolus treatment.

Functional assays used to monitor heparin anticoagulation measure how quickly clot formation occurs in vitro and the most commonly used test is the plasma based activated partial thromboplastin time (aPTT).




The whole blood based activating clotting time, is widely used for point of care monitoring in interventional procedures, such as percutaneous coronary interventions and extracorporeal circulation.

Use of unfractionated heparin in hospitalized patients associated with more than half of patients requiring 2 or more interruptions of their anticoagulation due to other medical procedures and only 7% had a therapeutic activated partial thromboplastin time on each day of a 4 day evaluation period (Hylek).

Heparin resistance is defined by the need for higher heparin dosage to achieve a targeted level of anticoagulation.

There is a lack of consensus to define heparin resistance, but it’s suggested as the need for more than 35,000 units per day to achieve anticoagulation.

Deficiency of antithrombin resulting from acquired causes is commonly implicated as a cause of heparin resistance.

Many disease states are associated with reduced anti-thrombin levels including: liver disease, sepsis, DIC, asparaginase use,and the use of extracorporeal circuits in cardiopulmonary bypass or ECMO.


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