TEG Flashcards
Hemostasis: tightly regulated process by
- Activation
* Clot formation • Clot lysis
Clot: platelet-fibrin network
• Platelets form plug • Clotting factors reinforce platelets • Fibrin acts as a glue • Clot strength
platelets percentage of platelet- fibrin network
80%-90%
fibrin percentage of platelet fibrin network
10%-20%
Component Measurements • PT/INR:
measures extrinsic clotting (VIIa, Xa, IIa)
Component Measurements PTT:
measures intrinsic clotting (XIIa, Xia, IXa, IIa)
other two component measurement tests
• Fibrinogen concentration • Platelet Count
Measurement of component interactions • TEG
Shows net effect “whole picture” of hemostasis
what is TEG
A whole blood hemostasis analyzer • Point of care test
how does TEG machine 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
coagulation parameters of TEG graph
enzymatic(R) Fibrinogen (K, alpha)
enzymatic(R) what it measures
clotting time, coag. factors
Fibrinogen (K, alpha) what it measures
clot kinetics
fibrinolysis parameters of TEG graph
thrombolysins (Ly30, EPL)
thrombolysins (Ly30, EPL) what it measure
clot stability and clot breakdown
thrombolysins (Ly30, EPL) what it measure
clot stability and clot breakdown
formal definition of TEG parameters (R)
latency from time blood was placed in TEG until initial fibrin formation
formal definition of TEG parameters (ALPHA)
rapidity (kinetics) of fibrin building and cross linking
formal definition of TEG parameters (K)
measure of rapidity to reach a certain clot strength
formal definition of TEG parameters (MA)
Max amplitude is a direct function of the max dynamic properties of fibrin and platelet bonding via GPIIB/IIIA and represents ultimate strength of fibrin clot
formal definition of TEG parameters (Cl)
coagulation index is a linear combo of above parameters
formal definition of TEG parameters (LY30)
measures the rate of amplitude reduction 30 minutes after MA. Gives indication of stability of clot
formal definition of TEG parameters (LY30)
measures the rate of amplitude reduction 30 minutes after MA. Gives indication of stability of clot
or more simply (R)
Reaction time (time to clot formation). Likely variable is Coagulation Factors
or more simply (α)
Speed of fibrin accumulation. likely variable is
Fibrinogen
or more simply (K)
Time elapsed until clot reaches a fixed strength
likely variable isFibrinogen
or more simply (MA)
Highest vertical amplitude of TEG tracing
likely variable isPlatelets
or more simply (LY30)
% of amplitude reduction 30 minutes after its maximum
likely variable is Fibrinolysis
TEG assays Standard (kaolin)
uses parameters listed above
TEG assays Rapid TEG
Uses tissue factor in place of kaolin to speed up the reaction R-value is replaced by TEG-ACT value Other parameters the same
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 platelet inhibition as a percentage
elongated ( R) thrombin formation abnormalities Possible cause of imbalance:
Slow enzymatic
reaction
elongated ( R) thrombin formation abnormalities Possible Etiologies
Factor deficiency/dysfunction • FFP • Protamine
elongated ( R) thrombin formation abnormalities
Common Treatments:
• FFP • Protamine
LOW (α) angle fibrinogen abnormalities. Possible cause of imbalance
• Slow rate of fibrin formation
LOW (α) angle fibrinogen abnormalities. Possible etiologies.
• Low fibrinogen levels or function • Insufficient rate/amount of thrombin generation • Platelet deficiency/dysfunction
LOW (α) angle fibrinogen abnormalities
Common Treatments
FFP • Cryoprecipitate
LOW (α) angle fibrinogen abnormalities. Possible etiologies.
• Low fibrinogen levels or function • Insufficient rate/amount of thrombin generation • Platelet deficiency/dysfunction
LOW (α) angle fibrinogen abnormalities
Common Treatments
FFP • Cryoprecipitate
Low MA platelet function abnormalities. Possible causes: •
Insufficient platelet-clot
formation
Low MA platelet function abnormalities, Possible etiologies
Poor platelet function • Low platelet count • Low fibrinogen levels or
function
Low MA platelet function abnormalities. Common treatments:
• Platelets
High MA platelet function abnormalities. possible causes:
Excessive platelet activity
High MA platelet function abnormalities. Possible etiologies
• Platelet hypercoagulability
High MA platelet function abnormalities. Common Treatments
Antiplatelet agents
R between 7-10 min
slight decrease in clotting factors. give x 1FFP or 4 ml/kg
R between 11-14 min
moderate decrease in clotting factors. give x 2FFP or 8 ml/kg
R between >14 min
significant decrease in clotting factors. give x 4FFP or 16 ml/kg
MA between 49-54 mm
slight decrease in platelet function. .3 mcg/kg DDAVP
MA between 41-48 mm
moderate decrease in platelet function. x5 platelet units
MA
significant decrease in platelet function. x 10 platelet units
(α) angle less than 45 degress
moderate decrease in fibrinogen levels. .06 u/kg cryoprecipitate
(α) angle less than 45 degress
moderate decrease in fibrinogen levels. .06 u/kg cryoprecipitate
LY30 AT 7.5% or greater with C.I. less than 3
primary fibrinolysis. antifibrinolytic of choice
LY30 AT 7.5% or greater with C.I. greater than 3
secondary fibrinolysis. anticoagulant of choice
LY30 LESS THAN 7.5% or greater with C.I. greater than 3
prothrombotic state. anticoagulant of choice
platelet mapping measures
Measures the effect of antiplatelet agents on platelet function • Measures the patient’s maximum platelet function as a
reference point
• Measures the percentage of inhibition relative to the patient’s reference point
platelet mapping antiplatelet drugs, ADP receptor inhibitors
Examples: clopidogrel, ticlopidine
platelet mapping antiplatelet drugs, Arachidonic acid pathway inhibitors
• Example: aspirin
platelet mapping antiplatelet drugs, 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
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
INTEM
contains phospholipid and ellagic acid as activators amd provides info. similar to that of the APTT
EXTEM
contains tissue factor as an activator and provides info. similar to that of the PT
HEPTEM
contains lyophilised heparinase for neutralizing heparin
APTEM
contains aprotinin for inhibiting fibrinolysis
FIBTEM
utilises cytochalasin D, a platelet inhibitor which blocks platelet contribution to clot formation. this allows qualitative analysis of the functional fibrinogen component
ECATEM
contains ecarin so it is similar to ecarin clotting time. this makes it sensitive to presence of direct thrombin inhiitors