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Module 2

Basic Clinician Training. Module 2. Review of the Hemostatic Process Hemostasis Monitoring with the TEG Analyzer How the TEG Analyzer Monitors Hemostasis Parameters Tracings Blood Sample Types and Preparation Test Your Knowledge. TEG ® Technology. Hemostatic Process. Endothelial Cells.

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Module 2

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  1. Basic Clinician Training Module 2 Review of the Hemostatic Process Hemostasis Monitoring with the TEG Analyzer How the TEG Analyzer Monitors Hemostasis Parameters Tracings Blood Sample Types and Preparation Test Your Knowledge TEG® Technology

  2. Hemostatic Process Endothelial Cells Change in Platelet Shape Area of Injury Endothelium damaged Collagen Platelet AA ADP Platelet plug formed (white clot) CoagulationCascade Thrombin generated on platelet surface Platelet-fibrin plug formed (red clot) tPA Fibrin Strands Fibrinolysis Plasminogen Plasmin Degradation Products Clot lysis

  3. Routine Coagulation Tests: PT, aPTT, Platelet Counts • Based on cascade model of coagulation • Measure protein interaction in plasma (thromboplastin) • Exclude cellular contributions (platelets, monocytes, etc.) • Determine adequacy of coagulation factor levels • Use static endpoints • Ignore altered thrombin generation • Ignore cellular elements • Ignore overall clot structure

  4. Hemostasis Monitoring:TEG Hemostasis System • Whole blood test • Measures hemostasis • Clot initiation through clot lysis • Net effect of components • TEG system • Laboratory based • Point of care • Remote, can be networked • Flexible to institution needs

  5. The TEG Analyzer:Description • Reflects balance of the hemostatic system • Measures the contributions and interactions of hemostatic components during the clotting process • Uses activated blood to maximize thrombin generation and platelet activation in an in vitro environment • Measures the hemostatic potential of the blood at a given point in time under conditions of maximum thrombin generation

  6. TEG Technology The TEG Analyzer How It Works

  7. TEG Technology:How It Works • Cup oscillates • Pin is attached to a torsion wire • Clot binds pin to cup • Degree of pin movement is a function of clot kinetics • Magnitude of pin motion is a function of the mechanical properties of the clot • System generates a hemostasis profile • From initial formation to lysis

  8. Utility of TEG Analysis • Demonstrates all phases of hemostasis • Initial fibrin formation • Fibrin-platelet plug construction • Clot lysis • Identifies imbalances in the hemostatic system • Risk of bleeding • Risk of thrombotic event

  9. What TEG Analysis Captures Amplitude of pin oscillation Time

  10. Basic Clinician Training TEG Parameters Identification Definition

  11. Thrombin Formation (Clotting Time)The R Parameter: Identified Amplitude of pin oscillation Time • Reaction time • Fibrin creates a connection between cup and pin Initial fibrin formation Intrinsic,extrinsic,commonpathways Pin is engaged Pin is stationary Cup oscillates, pin remains stationary Pin starts to oscillate with cup 

  12. Thrombin FormationThe R Parameter: Defined • Time until formation of critical mass of thrombin • Expression of enzymatic reaction function (i.e. the ability to generate thrombin and fibrin) Initial fibrin formation Intrinsic,extrinsic,commonpathways Pin is engaged Pin is stationary Cup oscillates, pin remains stationary Pin starts to oscillate with cup 

  13. Thrombin Formation AbnormalitiesThe R Parameter: Elongated R • Possible causes of imbalance: • Slow enzymatic reaction • Possible etiologies: • Factor deficiency/ dysfunction • Residual heparin • Common treatments: • FFP • Protamine Initial fibrin formation Initial fibrin formation Pin is stationary Pin is engaged

  14. Thrombin Formation AbnormalitiesThe R Parameter: Short R • Possible causes of imbalance: • Over-stimulated enzymatic reaction • Fast fibrin formation • Possible etiologies: • Enzymatic hypercoagulability • Common treatments: • Anticoagulant Initial fibrin formation Pin is engaged Pin is stationary

  15. FibrinogenThe α (Angle) Parameter: Identified • Rate of increase in pin oscillation amplitude as fibrin is generated and cross-links are formed Fibrin increases Baseline Pin is engaged

  16. FibrinogenThe α (Angle) Parameter: Defined • Kinetics of clot formation • Rate of thrombin generation • Conversion of Fibrinogen  fibrin • Interactions among fibrinogen, fibrin, and platelets • Cellular contributions Fibrin increases Baseline Pin is engaged

  17. Fibrinogen AbnormalitiesThe α (Angle) Parameter: Low a • Possible causes of imbalance: • Slow rate of fibrin formation • Possible etiologies: • Low fibrinogen levels or function • Insufficient rate/amount of thrombin generation • Platelet deficiency/dysfunction • Common treatments: • FFP • Cryoprecipitate Fibrin increases Baseline Pin is engaged

  18. Fibrinogen AbnormalitiesThe α (Angle) Parameter: High a • Possible causes of imbalance: • Fast rate of fibrin formation • Possible etiologies: • Platelet hypercoagulability • Fast rate of thrombin generation • Common treatments: • None Fibrin increases Baseline Pin is engaged

  19. Platelet FunctionThe MA Parameter: Defined • Maximum amplitude • Clot strength = 80% platelets + 20% fibrinogen • Platelet function influences thrombin generation and fibrin formation  relationship between R, α, and MA Maximum amplitude (MA) of pin oscillation Amplitude of pin oscillation

  20. Platelet Function AbnormalitiesThe MA Parameter: Low MA Maximum amplitude (MA) of pin oscillation • Possible causes: • Insufficient platelet- fibrin clot formation • Possible etiologies: • Poor platelet function • Low platelet count • Low fibrinogen levels or function • Common treatments: • Platelet transfusion Amplitude of pin oscillation

  21. Platelet Function AbnormalitiesThe MA Parameter: High MA Maximum amplitude (MA) of pin oscillation • Possible causes: • Excessive platelet activity • Possible etiologies: • Platelet hypercoagulability • Common treatments: • Antiplatelet agents • Note: Should be monitored for efficacy and/or resistance (See Module 6: Platelet Mapping) Amplitude of pin oscillation

  22. Coagulation IndexThe CI Parameter: Defined • Global index of hemostatic status • Linear combination of kinetic parameters of clot development and strength (R, K, angle, MA) • CI > +3.0: hypercoagulable • CI < -3.0: hypocoagulable

  23. Fibrinolysis: LY30 and EPLLY30 and EPL Parameters: Identified • LY30 is the percent decrease in amplitude of pin oscillation 30 minutes after MA is reached • Estimated percent lysis (EPL) is the estimated rate of change in amplitude after MA is reached MA 30 min

  24. Fibrinolysis: LY30 and EPLLY30 and EPL Parameters: Defined • Reduction in amplitude of pin oscillation is a function of clot strength, which depends on extent of fibrinolysis MA 30 min

  25. Fibrinolytic AbnormalitiesLY30 Parameter: Primary Fibrinolysis • Possible causes: • Excessive rate of fibrinolysis • Possible etiologies: • High levels of tPA • Common treatments: • Antifibrinolytic agent

  26. Fibrinolytic AbnormalitiesLY30 Parameter: Secondary Fibrinolysis • Possible causes: • Rapid rate of clot formation/break- down • Possible etiologies: • Microvascular hypercoagulability (i.e. DIC) DIC = disseminated intravascular coagulation

  27. Fibrinolytic AbnormalitiesLY30 Parameter: Secondary Fibrinolysis • Possible causes: • Rapid rate of clot formation/break- down • Possible etiologies: • Microvascular hypercoagulability (i.e. DIC) • Common treatments: • Anticoagulant DIC = disseminated intravascular coagulation

  28. Clot Strength:The G Parameter • Representation of clot strength and overall platelet function • G = shear elastic modulus strength (dyn/cm2) • G = (5000*MA)/(100-MA) • Relationship between clot strength and platelet function • MA = linear relationship between clot strength and platelet function • G = exponential relationship between clot strength and platelet function • More sensitive to changes in platelet function

  29. MA vs. G(Kaolin Activated Sample) Normal MA range (Kaolin activated) Hyperactive platelet function G(dynes/cm2) x 1000 Normal platelet function Hypoactive platelet function

  30. TEG Parameter Summary:Definitions

  31. TEG Parameter Summary Platelet function Clot strength (G) Clotting time Clot kinetics Clot stability Clot breakdown

  32. Basic Clinician Training TEG Results Tracings Data Decision Tree

  33. Components of the TEG TracingExample: R Amplitude of pin oscillation Time Actual value Normal range ParameterUnitsValueNormal range

  34. “Normal” TEG Tracing 30 min

  35. Hemorrhagic TEG Tracing 30 min

  36. Prothrombotic TEG Tracing 30 min

  37. Fibrinolytic TEG Tracing 30 min

  38. TEG Decision TreeQualitative

  39. TEG Decision TreeQuantitative Hemorrhagic Fibrinolytic Thrombotic US Patent 6,787,363

  40. TEG TracingExample: Hemorrhagic

  41. TEG TracingExample: Prothrombotic

  42. TEG TracingExample: Fibrinolytic

  43. Basic Clinician Training TEG Blood Sampling

  44. TEG Blood Sampling • Blood samples • Arterial or venous • Samples should be consistent

  45. TEG Blood SamplingNative • Non-modified blood samples • Assayed 4 minutes • TEG software based upon assay at 4 minutes

  46. TEG Blood Sampling Modified • Activator • Reduces variability • Reduces running time • Maximizes thrombin generation • Kaolin • Activates intrinsic pathway • Used for normal TEG analysis • Tissue factor • Specifically activates extrinsic pathway

  47. TEG Blood SamplingHeparin • Heparinase • Neutralizes heparin • Embedded in specialized (blue) cups and pins

  48. TEG Blood SamplingCitrated • Citrated tubes are used • Recalcified before analysis • Standardize time between blood draw and running test • Specific platelet activators are required to demonstrate effect of antiplatelet agents

  49. Sample Type Designations Whole blood + kaolin

  50. Summary • The TEG technology measures the complex balance between hemorrhagic and thrombotic systems. • The decision tree is a tool to identify coagulopathies and guide therapy in a standardized way.

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