BBioBody OSCardiovascular atlas ↗

CARDIOVASCULAR / HEMOSTASIS

Seal the injury.
Constrain the seal.

Hemostasis is a coupled repair system, not two independent cascades. Vessel responses, platelets, tissue factor, thrombin, fibrin, natural anticoagulants, and fibrinolysis act in space and time to limit bleeding without blocking healthy circulation.

Play the narrated clot flow ▶See plaque disruption

14-STAGE REPAIR MAP

Initiation, amplification,
shutdown, removal.

The classic intrinsic/extrinsic laboratory scheme is useful for tests, while living hemostasis is cell-surface based and highly integrated. Arterial and venous thrombi arise in different flow and disease contexts.

01VESSEL & PLATELET RESPONSE
01

Vessel injury is exposed

Endothelial disruption reveals subendothelial matrix and tissue-factor-bearing surfaces.

02

Local vasoconstriction

Neural and local mediators transiently reduce flow at the injury site.

03

Platelets tether and adhere

von Willebrand factor and platelet receptors support capture and adhesion, especially under high shear.

04

Platelets activate

Shape change, granule release, thromboxane, ADP, and receptor activation recruit additional platelets.

05

Platelets aggregate

Activated integrin αIIbβ3 binds fibrinogen and related ligands to bridge platelets into an initial plug.

02THROMBIN & FIBRIN AMPLIFICATION
06

Tissue factor initiates

Tissue factor with factor VIIa begins protease activation and produces an initial thrombin signal.

07

Platelet surfaces amplify

Activated platelets localize enzyme complexes that accelerate factor X activation and thrombin generation.

08

Thrombin integrates the response

Thrombin activates platelets and cofactors while converting fibrinogen to fibrin.

09

Fibrin stabilizes the plug

Polymerized, cross-linked fibrin strengthens the platelet mass and traps cells.

10

Clot retracts

Platelet cytoskeletal force compacts the clot and may draw wound edges together.

03LOCALIZATION & FIBRINOLYSIS
11

Antithrombin restrains proteases

Antithrombin limits thrombin and other activated coagulation factors; endothelial glycosaminoglycans support this control.

12

Protein C pathway switches down

Thrombin bound to thrombomodulin supports activated protein C, which inactivates cofactors Va and VIIIa with protein S.

13

Plasmin is generated

Tissue plasminogen activator promotes plasmin generation on fibrin, while inhibitors constrain premature or systemic lysis.

14

Fibrin is removed

Plasmin degrades fibrin as repair progresses; breakdown products are cleared and the vessel remodels.

THERAPEUTIC TARGETS

Platelet drugs and
anticoagulants are not synonyms.

Every antithrombotic choice trades lower thrombosis probability against more bleeding. Indication, dose, timing, kidney/liver function, interactions, procedures, age, and prior bleeding all matter.

COX-1

Aspirin

Irreversibly reduces platelet thromboxane production; benefits and bleeding differ sharply between prevention settings.

P2Y12

P2Y12 inhibitors

Reduce ADP-mediated platelet activation; agents differ in onset, potency, metabolism, reversibility, and indications.

THROMBIN / XA

Direct oral anticoagulants

Target thrombin or factor Xa for selected indications; dosing and eligibility vary.

VITAMIN K

Warfarin

Reduces synthesis of vitamin-K-dependent factors; monitoring, food/drug interactions, and indication-specific targets matter.

HEPARIN PATHWAY

Heparins

Potentiate antithrombin with class-specific effects and uses, often in acute or procedural settings.

FIBRINOLYSIS

Thrombolytic medicines

Promote clot breakdown in tightly selected emergencies; time and major bleeding risk are central.

Core sources: NCBI Bookshelf: Coagulation Pathways ↗ · 2025 Acute Coronary Syndromes Guideline ↗

Do not start, stop, or combine antiplatelet, anticoagulant, or thrombolytic medicines from this map. Active major bleeding or suspected stroke/heart attack requires emergency assessment.