test 5 Flashcards
Clot strength
- Platelets 80%-90%
* Fibrin 10%-20%
Component Measurements:
PT/INR:
PTT:
- PT/INR: measures extrinsic clotting (VIIa, Xa, IIa)
- PTT: measures intrinsic clotting (XIIa, XIa, IXa, IIa)
- Fibrinogen concentration
- Platelet Count (doesn’t tell you function of platelets)
What is thromboeleastography (TEG)
- A whole blood hemostasis analyzer
* Point of care test
How does TEG work
- Cup oscillates • Pin is attached to torsion wire
- Clot binds pin to cup
- Degree and magnitude of pin motion are functions of the clot kinetics and mechanical properties
- System generates a hemostasis profile
TEG parameters: R
Likely variable
- Reaction time (time to clot formation)
- Likely variable: Coagulation factors
TEG parameters: Alpha
- Speed of fibrin accumulation
- Likely variable: Fibrinogen
TEG parameters: K
- Time elapsed until clot reaches a fixed strength
- Likely variable: Fibrinogen
TEG parameters: MA
- Highest vertical amplitude of TEG tracing
- Likely variable: Platelets
TEG parameters: LY30
- % of amplitude reduction 30 minutes after its maximum
- Likely variable: fibrinolysis
Elongated R - Thrombin formation abnormalities 1. Possible cause of imbalance? 2. Possible Etiologies? 3. Common Treatments?
Possible cause of
imbalance:
• Slow enzymatic reaction
Possible Etiologies
• Factor deficiency/dysfunction
• Residual heparin
Common Treatments:
• FFP
• ProtamineLow alpha angle - Fibrinogen abnormalities 1. Possible cause of imbalance? 2. Possible Etiologies? 3. Common Treatments?
Possible cause 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
Low MA - Platelet function abnormalities 1. Possible cause of imbalance? 2. Possible Etiologies? 3. Common Treatments?
Possible causes:
• Insufficient platelet-clot formation
Possible etiologies
• Poor platelet function
• Low platelet count
• Low fibrinogen levels or function
Common treatments:
• PlateletsHigh MA - Platelet function abnormalities 1. Possible cause of imbalance? 2. Possible Etiologies? 3. Common Treatments?
Possible causes:
• Excessive platelet activity
Possible etiologies
• Platelet hypercoagulability
Common Treatments
• Antiplatelet agentsPictures of possible tracings
- Look at them
TEG assays - Standard (kaolin)
- Use normal parameters
TEG assays - Rapid TEG
- Uses tissue factor and kaolin to activate extrinsic and intrinsic pathways
- R-value is replaced by TEG-ACT value
- Other parameters the same
- Increased speed can save valuable time
TEG assays - Heparinase
• Used on bypass or post bypass alongside a standard TEG
TEG assays - Platelet Mapping
- Determines to what degree platelet function is inhibited due to pharmacological inhibition of either the arachidonic acid (AA) or adenosine diphosphate (ADP) pathways
* AA: Aspirin
* ADP: Clopidogrel
* Run alongside a standard TEG and a TEG with added AA or ADP.
* Calculates the percentage of inhibition relative to the patient’s maximum platelet function
What drugs are monitored during platelet mapping
- Antiplatelet Drugs
* ADP receptor inhibitors
* Examples: clopidogrel, ticlopidine
* Arachidonic acid pathway inhibitors
* Example: aspirin
* GPIIb/IIIa inhibitors
* Examples: abciximab, tirofiban, eptifibatide
Why platelet mapping
- Individual response to antiplatelet drugs determines clinical outcome
- Knowing percent of platelet inhibition is insufficient to determine therapeutic efficacy
- Knowledge of maximum platelet function is also required as a reference point
Rotational Elastometry (ROTEM)
- STATIONARY CUP, ROTATING SPINDLE
- Clot impedes rotation of the pin
- Additional tests available
Sonoclot
• Viscoelastic detection system
• Provides information on the entire hemostatic process
• Generates a qualitative graph and quantitative results
- Tells you
-coagulation, formation of the fibrin network, clot retraction, and the breakdown of the clot
- helps determine if it’s a coagulation issue or if there is a bleeder
• Tubular probe oscillates up and down within a blood sample
• Senses resistance to motion that the probe encounters through various stages of hemostasis
- slightly faster than other 2
- fibrinolysis takes longer to be determined
Sonoclot graph
- Clot evolution saved as a graph
* Clot signal value versus time
Sonoclot Liquid Phase
• Ends when the viscosity of the sample begins to increase with thrombin generation and the resulting initial fibrin formation
Sonoclot fibrin gel formation
- Once thrombin forms, the fibrinogen converts to fibrin
* Fibrin spontaneously polymerizes into a fibrin gel
Sonoclot clot retraction
- Occurs when platelets function normally
- Platelets adhere to nodes of the fibrin gel and cause the gel to collapse together or retract
- As the clot retracts, it tightens
Sonoclot time to peak
- The faster the time to peak, the greater the platelet function
- Sharp, well defined peaks infication strong retraction
- Dull, poorly defined peaks indicate weak retraction
