14. TEG- Exam 3 Flashcards
Hemostasis is a tightly regulated process. What are the steps?
- Activation
- Clot formation
- Clot lysis
Clot is a platelet-fibrin network. What are the steps
- Platelets form plug
- Clotting factors reinforce platelets
- Fibrin acts as a glue
- Clot strength
clot strength for platelets?
80-90%
clot strength for fibrin?
10-20%
PT/INR measures?
extrinsic clotting (VIIa, Xa, IIa) --longer: takes 35 min
PTT measures?
intrinsic clotting (XIIa, Xia, IXa, IIa)
TEG=
- A whole blood hemostasis analyzer
* Point of care test
how does the TEG work? 5 steps
- 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
R=
reaction time (time of clot formation) -Likely variable= coagulation factors
alpha=
speed of fibrin accumulation
-Likely variable= fibrinogen
K=
time elapsed until clot reaches full strength
-Likely variable= fibrinogen
MA=
maximum amplitude= highest vertical amplitude of TEG tracing
-Likely variable= platelets
Cl=
coagulation index= linear combination of R, alpha, K, and MA
LY30=
% of amplitude reduction 30 min after the max
-Likely variable= fibrinolysis
TEG Assays: Standard (kaolin)=
30-40 min
Uses parameters listed above???? ASK GASPAR
TEG Assays: Rapid TEG=
20 min or less
•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=
type of cuvette
Used on CPB or post CPB 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
•Run alongside a standard TEG and a TEG with added AA or ADP.
•Calculates platelet inhibition as a percentage
arachidonic acid (AA)=
aspirin
adenosine diphosphate (ADP)=
Clopidogrel
elongated R- Thrombin formation abnormalities:
Possible cause of imbalance=
Slow enzymatic reaction
elongated R- Thrombin formation abnormalities:
Possible Etiologies=
- Factor deficiency/dysfunction
* Residual heparin
elongated R- Thrombin formation abnormalities:
Common Treatments:
- FFP
* Protamine
low alpha angle - fibrinogen abnormalities:
Possible cause of imbalance=
Slow rate of fibrin formation
low alpha angle - fibrinogen abnormalities:
Possible etiologies=
- Low fibrinogen levels or function
- Insufficient rate/amount of thrombin generation
- Platelet deficiency/dysfunction
low alpha angle - fibrinogen abnormalities:
Common Treatments=
- FFP
* Cryoprecipitate
low MA - platelet funciton abnormalities:
Possible causes:
•Insufficient platelet-clot formation
low MA - platelet funciton abnormalities:
Possible etiologies=
- Poor platelet function
- Low platelet count
- Low fibrinogen levels or function
low MA - platelet funciton abnormalities:
Common treatments=
Platelets
high MA - platelet funciton abnormalities:
Possible causes:
Excessive platelet activity
high MA - platelet funciton abnormalities:
Possible etiologies=
Platelet hypercoagulability
high MA - platelet funciton abnormalities:
Common treatments=
Antiplatelet agents
R between 7-10min
Clinical cause?
Treatment?
Clinical cause: small decrease in clotting factors
Treatment: x1 FFP or 4 ml/kg
R between 11-14min
Clinical cause?
Treatment?
Clinical cause: medium decrease in clotting factors
Treatment: x2 FFP or 8 ml/kg
R greater than 14min
Clinical cause?
Treatment?
Clinical cause: large decrease in clotting factors
Treatment: x4 FFP or 16 ml/kg
MA between 49-54 mm
Clinical cause?
Treatment?
Clinical cause: small decrease in platelet function
Treatment: 0.3 mcg/kg DDAVP
MA between 41-48 mm
Clinical cause?
Treatment?
Clinical cause: medium decrease in platelet function
Treatment: x5 platelet units
MA less than 40mm
Clinical cause?
Treatment?
Clinical cause: large decrease in platelet function
Treatment: x10 platelet units
CI less than 45 degrees
Clinical cause?
Treatment?
Clinical cause: medium decrease in fibrinogen levels
Treatment: .03 u/kg cryo
LY30 at 7.5% or greater and a CI less than 3.0
Clinical cause?
Treatment?
Clinical cause: primary fibrinolysis
Treatment: anticoagulant of choice
LY30 at 7.5% or greater and a CI greater than 3.0
Clinical cause?
Treatment?
Clinical cause: secondary fibrinolysis
Treatment: anticoagulant of choice
LY30 at 7.5% or less and a CI greater than 3.0
Clinical cause?
Treatment?
Clinical cause: prothrombic state
Treatment: anticoagulant of choice
LY30 at 7.5% or less and a CI greater than 3.0
Clinical cause?
Treatment?
Clinical cause: prothrombic state
Treatment: anticoagulant of choice
what 3 things does platelet mapping measure
- Effect of antiplatelet agents on platelet function
- Patient’s maximum platelet function as a reference point
- Percentage of inhibition relative to the patient’s reference point
ADP receptor inhibitors=
clopidogrel, ticlopidine
Arachidonic acid pathway inhibitors=
aspirin
GPIIb/IIIa inhibitors=
abciximab, tirofiban, eptifibatide
why should we use platelet mapping
- Individual response to antiplatelet drugs determines clinical outcome
2, 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
