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Perf Tech 3 > 14. TEG- Exam 3 > Flashcards

14. TEG- Exam 3 Flashcards

(49 cards)

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1
Q

Hemostasis is a tightly regulated process. What are the steps?

A
  • Activation
  • Clot formation
  • Clot lysis
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2
Q

Clot is a platelet-fibrin network. What are the steps

A
  • Platelets form plug
  • Clotting factors reinforce platelets
  • Fibrin acts as a glue
  • Clot strength
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3
Q

clot strength for platelets?

A

80-90%

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4
Q

clot strength for fibrin?

A

10-20%

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5
Q

PT/INR measures?

A 
extrinsic clotting (VIIa, Xa, IIa)
--longer: takes 35 min
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6
Q

PTT measures?

A

intrinsic clotting (XIIa, Xia, IXa, IIa)

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7
Q

TEG=

A
  • A whole blood hemostasis analyzer

* Point of care test

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8
Q

how does the TEG work? 5 steps

A
  • 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
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9
Q

R=

A 
reaction time (time of clot formation)
-Likely variable= coagulation factors
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10
Q

alpha=

A

speed of fibrin accumulation

-Likely variable= fibrinogen

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11
Q

K=

A

time elapsed until clot reaches full strength

-Likely variable= fibrinogen

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12
Q

MA=

A

maximum amplitude= highest vertical amplitude of TEG tracing

-Likely variable= platelets

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13
Q

Cl=

A

coagulation index= linear combination of R, alpha, K, and MA

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14
Q

LY30=

A

% of amplitude reduction 30 min after the max

-Likely variable= fibrinolysis

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15
Q

TEG Assays: Standard (kaolin)=

A

30-40 min

Uses parameters listed above???? ASK GASPAR

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16
Q

TEG Assays: Rapid TEG=

A

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

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17
Q

TEG Assays: Heparinase=

A

type of cuvette

Used on CPB or post CPB alongside a standard TEG

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18
Q

TEG Assays: Platelet Mapping=

A

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

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19
Q

arachidonic acid (AA)=

A

aspirin

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20
Q

adenosine diphosphate (ADP)=

21
Q

elongated R- Thrombin formation abnormalities:

Possible cause of imbalance=

Study These Flashcards
A

Slow enzymatic reaction

22
Q

elongated R- Thrombin formation abnormalities:

Possible Etiologies=

Study These Flashcards
A
  • Factor deficiency/dysfunction

* Residual heparin

23
Q

elongated R- Thrombin formation abnormalities:

Common Treatments:

Study These Flashcards
A
  • FFP

* Protamine

24
Q

low alpha angle - fibrinogen abnormalities:

Possible cause of imbalance=

Study These Flashcards
A

Slow rate of fibrin formation

25
low alpha angle - fibrinogen abnormalities: | Possible etiologies=
* Low fibrinogen levels or function * Insufficient rate/amount of thrombin generation * Platelet deficiency/dysfunction
26
low alpha angle - fibrinogen abnormalities: | Common Treatments=
* FFP | * Cryoprecipitate
27
low MA - platelet funciton abnormalities: | Possible causes:
•Insufficient platelet-clot formation
28
low MA - platelet funciton abnormalities: | Possible etiologies=
* Poor platelet function * Low platelet count * Low fibrinogen levels or function
29
low MA - platelet funciton abnormalities: | Common treatments=
Platelets
30
high MA - platelet funciton abnormalities: | Possible causes:
Excessive platelet activity
31
high MA - platelet funciton abnormalities: | Possible etiologies=
Platelet hypercoagulability
32
high MA - platelet funciton abnormalities: | Common treatments=
Antiplatelet agents
33
R between 7-10min Clinical cause? Treatment?
Clinical cause: small decrease in clotting factors | Treatment: x1 FFP or 4 ml/kg
34
R between 11-14min Clinical cause? Treatment?
Clinical cause: medium decrease in clotting factors | Treatment: x2 FFP or 8 ml/kg
35
R greater than 14min Clinical cause? Treatment?
Clinical cause: large decrease in clotting factors | Treatment: x4 FFP or 16 ml/kg
36
MA between 49-54 mm Clinical cause? Treatment?
Clinical cause: small decrease in platelet function | Treatment: 0.3 mcg/kg DDAVP
37
MA between 41-48 mm Clinical cause? Treatment?
Clinical cause: medium decrease in platelet function | Treatment: x5 platelet units
38
MA less than 40mm Clinical cause? Treatment?
Clinical cause: large decrease in platelet function | Treatment: x10 platelet units
39
CI less than 45 degrees Clinical cause? Treatment?
Clinical cause: medium decrease in fibrinogen levels | Treatment: .03 u/kg cryo
40
LY30 at 7.5% or greater and a CI less than 3.0 Clinical cause? Treatment?
Clinical cause: primary fibrinolysis | Treatment: anticoagulant of choice
41
LY30 at 7.5% or greater and a CI greater than 3.0 Clinical cause? Treatment?
Clinical cause: secondary fibrinolysis | Treatment: anticoagulant of choice
42
LY30 at 7.5% or less and a CI greater than 3.0 Clinical cause? Treatment?
Clinical cause: prothrombic state | Treatment: anticoagulant of choice
43
LY30 at 7.5% or less and a CI greater than 3.0 Clinical cause? Treatment?
Clinical cause: prothrombic state | Treatment: anticoagulant of choice
44
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
45
ADP receptor inhibitors=
clopidogrel, ticlopidine
46
Arachidonic acid pathway inhibitors=
aspirin
47
GPIIb/IIIa inhibitors=
abciximab, tirofiban, eptifibatide
48
why should we use platelet mapping
1. Individual response to antiplatelet drugs determines clinical outcome 2, Knowing percent of platelet inhibition is insufficient to determine therapeutic efficacy 3. Knowledge of maximum platelet function is also required as a reference point
49
Rotational Elastometry (ROTEM)
* Stationary cup, rotating spindle * Clot impedes rotation of the pin * Additional tests available

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