Past Papers · SAQ

Viscoelastic Assays: Platelets, Heparin & Hyperfibrinolysis

Current · V5 (2025) → N3.i 1 exam appearance

2026A Q18

Exam question

With respect to viscoelastic assays, describe the expected alterations and the underlying mechanisms resulting from the following:
a) platelet dysfunction (40% of marks),
b) therapeutic heparin use (40% of marks),
c) hyperfibrinolysis (20% of marks). Either TEG or ROTEM is acceptable for your answer.

CICMWrecks answer

Master answer

TEG / ROTEM parameter key

Process TEG ROTEM
Clot initiation R time CT
Rate of clot formation K time, α angle CFT, α angle
Maximum clot strength / firmness MA MCF
Clot lysis LY30 = % amplitude reduction 30 min after MA LI30 = % clot firmness remaining 30 min after CT; ML = maximum % lysis

Terminology note: TEG and ROTEM use different names for analogous properties: R ≈ CT, K ≈ CFT, and MA ≈ MCF.

Educational diagram comparing ROTEM and TEG mechanics and key viscoelastic parameters, including R or CT, K or CFT, alpha angle, MA or MCF, LY30, LI30 and maximum lysis.
CICMWrecks original (2026)

a) Platelet dysfunction (40%)

TEG / ROTEM feature Expected change Mechanism
R / CT Usually unchanged Initial fibrin generation is largely preserved because coagulation factor activity is intact.
K / CFT Prolonged Impaired platelet–fibrin interaction slows development of a firm clot.
α angle Reduced Slower increase in clot strength.
MA / MCF Reduced Platelets are a major determinant of maximal clot strength; dysfunction reduces clot firmness.
LY30 / LI30 / ML Usually no primary fibrinolytic abnormality Primary abnormality is clot strength, not fibrinolysis.

b) Therapeutic heparin (40%)

Mechanism: heparin potentiates antithrombin, inhibiting thrombin and factor Xa (and other activated serine proteases) → slower fibrin generation and clot propagation.

TEG / ROTEM feature Expected change Mechanism
R / CT Prolonged Delayed thrombin generation → delayed clot initiation.
K / CFT Prolonged Slower fibrin formation delays development of adequate clot strength.
α angle Reduced Rate of clot formation is reduced.
MA / MCF Reduced Reduced thrombin/fibrin generation produces a less firm clot.
LY30 / LI30 / ML Usually no primary fibrinolytic abnormality Heparin impairs coagulation rather than directly accelerating fibrinolysis.

Useful confirmation: correction of the abnormal trace in a heparinase channel supports heparin as the cause.

c) Hyperfibrinolysis (20%)

TEG / ROTEM feature Expected change Mechanism
R / CT Often initially normal Clot initiation may be preserved.
K / CFT Often initially near normal Early clot formation may still occur.
α angle Often initially near normal Initial clot propagation may be preserved.
MA / MCF Initially preserved, then falls The formed clot is progressively degraded.
LY30 Increased Greater percentage fall in amplitude measured 30 minutes after MA because fibrinolysis is accelerated.
LI30 Decreased Lower percentage of clot firmness remains 30 minutes after CT because fibrin is being broken down.
ML Increased Greater overall maximum clot lysis.
Trace appearance Rapid narrowing after peak amplitude Accelerated plasmin-mediated fibrin breakdown.

One-line comparison

Quick reference

Summary

StateKey TEG / ROTEM pattern
Platelet dysfunctionR/CT preserved; K/CFT prolonged / α reduced; MA/MCF reduced
HeparinR/CT prolonged; K/CFT prolonged; α reduced; MA/MCF reduced; heparinase correction supports diagnosis
HyperfibrinolysisClot may form initially, then ↑ LY30 (30 min after MA), ↓ LI30 (30 min after CT) and ↑ ML

Past papers

Exam appearances

1 appearance
Exam Exact exam wording Candidate success
2026A Q18 With respect to viscoelastic assays, describe the expected alterations and the underlying mechanisms resulting from the following: a) platelet dysfunction (40% of marks), b) therapeutic heparin use (40% of marks), c) hyperfibrinolysis (20% of marks). Either TEG or ROTEM is acceptable for your answer. 29%