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Anaes TopicsApplied cardiovascular & respiratory physiology

Anaes · Applied cardiovascular & respiratory physiology

Haematology & coagulation cascade physiology

Also known as Coagulation cascade · Haemostasis · Clotting factors · Fibrinolysis · Anticoagulants · Platelet function

Haemostasis is a precisely balanced process of clot formation (primary platelet plug, secondary coagulation cascade) and clot dissolution (fibrinolysis), and the anaesthetist intervenes in it with anticoagulants, antiplatelets, transfusion and neuraxial technique. The framework rests on five exam-critical ideas: primary haemostasis is the platelet plug (von Willebrand factor mediates platelet adhesion, then activation releases agonists, and aggregation forms the plug); the coagulation cascade amplifies via the intrinsic (contact) pathway (Factor XII through IX, monitored by the APTT) and the extrinsic (tissue factor) pathway (Factor VII, monitored by the PT and INR), converging on the common pathway (Factor X to thrombin to fibrin, cross-linked by Factor XIII); natural anticoagulants (antithrombin, protein C and S, tissue factor pathway inhibitor) prevent runaway clotting; fibrinolysis (plasmin from plasminogen via tPA) dissolves the clot, producing D-dimer; and the anticoagulant drugs (heparin via antithrombin, warfarin via vitamin K antagonism, DOACs by direct factor inhibition) act at specific points and are monitored by specific tests. Built on the contact-pathway COVID-coagulopathy study (Capecchi 2025), the Factor V deficiency review (Stoj 2026), the SERPINB2-fibrinolysis study (Zhu 2026), the fibrinolytic-DIC review (Iba 2026), the tPA-coagulopathy study (Takenaka 2026), and the paediatric DOAC perioperative-management review (Furman 2024).

high6 referencesUpdated 26 July 202611 min readVerification in progress

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Red flags

  • The APTT monitors the INTRINSIC pathway (and heparin); the PT and INR monitor the EXTRINSIC pathway (and warfarin) — an isolated abnormality in one test localises the defect to that pathway.
  • Heparin potentiates antithrombin (inhibiting thrombin and Factor Xa); warfarin inhibits vitamin-K-dependent Factor synthesis (II, VII, IX, X, and proteins C and S); DOACs directly inhibit thrombin (dabigatran) or Factor Xa (rivaroxaban, apixaban).
  • Protein C and S have the shortest half-lives of the vitamin-K-dependent factors, so warfarin initially causes a transient PROCOAGULANT state (because C and S fall first) — the rationale for heparin bridging when starting warfarin.
  • Neuraxial anaesthesia (spinal, epidural) in the anticoagulated patient risks an epidural haematoma that can compress the spinal cord — anticoagulant timing before and after neuraxial insertion or catheter removal is a critical safety protocol.
  • Fibrinolytic shutdown (impaired plasminogen activation, as in sepsis and trauma) leads to microvascular thrombosis and organ dysfunction — redefining DIC as a disorder of BOTH coagulation activation AND fibrinolytic failure.
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Your progress

Saved on this device.

Practise this topic8 MCQs with explanations

Target exams

ANZCAFRCAABAEDAICFCAIFCA_SA

Red flags

  • The APTT monitors the INTRINSIC pathway (and heparin); the PT and INR monitor the EXTRINSIC pathway (and warfarin) — an isolated abnormality in one test localises the defect to that pathway.
  • Heparin potentiates antithrombin (inhibiting thrombin and Factor Xa); warfarin inhibits vitamin-K-dependent Factor synthesis (II, VII, IX, X, and proteins C and S); DOACs directly inhibit thrombin (dabigatran) or Factor Xa (rivaroxaban, apixaban).
  • Protein C and S have the shortest half-lives of the vitamin-K-dependent factors, so warfarin initially causes a transient PROCOAGULANT state (because C and S fall first) — the rationale for heparin bridging when starting warfarin.
  • Neuraxial anaesthesia (spinal, epidural) in the anticoagulated patient risks an epidural haematoma that can compress the spinal cord — anticoagulant timing before and after neuraxial insertion or catheter removal is a critical safety protocol.
  • Fibrinolytic shutdown (impaired plasminogen activation, as in sepsis and trauma) leads to microvascular thrombosis and organ dysfunction — redefining DIC as a disorder of BOTH coagulation activation AND fibrinolytic failure.
The one-line answer

Haemostasis is a balance of clot formation and clot dissolution, and the anaesthetist intervenes at every step. Primary haemostasis is the platelet plug (von Willebrand factor mediates adhesion, activation releases agonists, aggregation seals the breach); secondary haemostasis is the coagulation cascade — intrinsic (APTT) and extrinsic (PT and INR) converging on the common pathway to thrombin and cross-linked fibrin (cascade orchestration: XII→XI→IX→X intrinsic, tissue-factor→VII extrinsic, prothrombinase of calcium/phospholipid/Va/Xa converting prothrombin to thrombin [2]). Natural anticoagulants and fibrinolysis keep it bounded; heparin, warfarin, the DOACs and antiplatelets hit defined targets; and the APTT watches heparin while the PT and INR watch warfarin. Contact-pathway activation dominates over extrinsic in COVID-19 coagulopathy, proportional to severity (n-111) [1]; DOAC perioperative management balances thrombotic against bleeding risk (paediatric-review scope) [6].[1][2][6]

Meet the patient

A trauma patient arrives in haemorrhagic shock, cold, acidotic, and bleeding from every cannula site. His prothrombin time is prolonged, his fibrinogen is low, and the viscoelastic trace shows a fibrinolysis phenotype. He needs a clot, not a textbook. (Teaching vignette; sepsis-DIC fibrinolytic-insufficiency phenotype — high D-dimers, elevated PAI-1, reduced plasmin generation, low viscoelastic activity — reviewed in [4].)[4]

That patient is the whole topic at the bedside: primary plug, thrombin burst, fibrin, natural inhibitors, fibrinolysis — and the moment one fails you see it in the blood. Hold the four-part map — plug, cascade, inhibitors, lysis — and every test and drug below slots into place. (Cascade orchestration [2].)[2]

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References6ShowHide
  1. [1]Capecchi M, et al. Involvement of the contact pathway in COVID-19 coagulopathy Intern Emerg Med, 2025.PMID 41206422
  2. [2]Stoj KM, et al. Factor V Deficiency StatPearls [Internet], 2025.PMID 35593819
  3. [3]Zhu Y, et al. Epithelial SERPINB2 Overexpression Contributes to Impaired Fibrinolysis in Chronic Rhinosinusitis With Nasal Polyps via tPA Downregulation Front Biosci (Landmark Ed), 2026.PMID 42216541
  4. [4]Iba T, et al. Redefining Fibrinolytic Insufficiency in Sepsis-Associated DIC Semin Thromb Hemost, 2026.PMID 41956121
  5. [5]Takenaka R, et al. Prolonged low-dose tPA ameliorates coagulopathy and organ injury in an LPS-induced rat DIC model Int J Hematol, 2026.PMID 41801558
  6. [6]Furman K, et al. A review of the perioperative management of direct oral anticoagulants for pediatric anesthesiologists Paediatr Anaesth, 2024.PMID 39244715

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