Unfractionated Heparin
Heparin doesn't dissolve clots — it prevents them from growing. Knowing why changes how you understand every indication and dosing decision.
Core Concept
Heparin is an indirect anticoagulant that works by binding to antithrombin III (AT-III), dramatically accelerating AT-III's ability to inactivate thrombin (factor IIa) and factor Xa — roughly 1,000-fold faster than AT-III alone. Without adequate AT-III, heparin cannot work. Unfractionated heparin (UFH) inhibits both thrombin and factor Xa, while low-molecular-weight heparins (LMWHs like enoxaparin) preferentially inhibit factor Xa. UFH is given IV or subcutaneously; its short half-life (~60-90 minutes IV) and reversibility with protamine sulfate make it the choice when rapid on-off control is needed — acute PE, MI, during cardiac bypass, or bridging to warfarin. LMWH is given subcutaneously with more predictable pharmacokinetics, making it preferred for DVT prophylaxis and treatment, especially outpatient. Key indications: DVT/PE treatment and prevention, acute coronary syndromes, atrial fibrillation bridging, and maintaining patency of IV lines (heparin flushes at low doses). Heparin does NOT lyse existing clots — the body's fibrinolytic system does that. Heparin prevents propagation while the clot resolves.
Watch Out For
Don't confuse anticoagulation with thrombolysis — heparin prevents clot extension, it doesn't break clots down (that's alteplase). Students mix up UFH and LMWH: therapeutic UFH is typically given as continuous IV infusion with aPTT monitoring, while LMWH (enoxaparin) is fixed-dose subcutaneous and generally doesn't require routine lab monitoring. Protamine reverses UFH completely but only partially reverses LMWH.
Clinical Pearl
Heparin is the bodyguard, not the assassin — it stops the clot from recruiting reinforcements while the body's own cleanup crew dissolves it.
Test Your Knowledge
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