APP 1 final Flashcards
TEG R Time
- latency until clot formation begins as defined by an amplitude of 2 mm- Normal 3-9 mins
TEG K Time
time from the end of R until the clot reaches 20mm – reflects speed of initial clot formation (Normal .5 to 3 mins)
Normal R Time-TEG
3-9 mins
Normal K-Time-TEG
.5-3 mins
α - alpha angle - TEG
the angle tangent to the curve at K
MA - maximum amplitude
reflects total clot strength
Lysis time (LY30)
% lysis after 30 min - reflects the fibrinolysis stage of clot development
TEG- Increased R Time
FFP
TEG- Decreased alpha angle
Cryo
TEG- Decreased MA
Platelets/ DDAVP
Fibrinolysis
TXA or aminocaproic acid
TEG- Platelet Blockers
MA Decreased
TEG- Fibrinolysis
MA Decreased
LY30 Markedly increased
TEG- Hypercoagulable state
*α angle increased
*MA increased
TEG- Early DIC
*α angle increased
*MA increased
LY 30 increased
TEG- Late DIC
R Prolonged
*α angle increased
*MA increased
Normal Platelet count
150-450k
Thrombocytopenia Goals for Neuraxial, Major surgery, Central Line placement
Neuraxial- 70k
Major Surgery- 50K
Central Line 20k
PCC (Prothrombin Complex Concentrates)/ KCentra
Contains the 4 vitamin K dependent clotting factors
II, VII, IX, X
Vitamin-K Dependent Factors
II, VII, IX, X
Indications for PCC
Hemophilia
Immediate reversal of Vitamin K antagonists (Warfarin)
PCC Vs Vitamin K for reversal of warfarin
Compared to vitamin K, PCC is faster and requires less redosing (IV vitamin K corrects INR over 12-24 hours
PCC vs FFP For reversal of Warfarin
Compared to FFP, reversal with PCC is faster (no thawing) and has less infection risk
Desmopressin
synthetic analog for the endogenous antidiuretic hormone, vasopressin
acts at the V2 receptor found in the nephron and within endothelial cells
causes the release of FVIII and vWF from within vascular endothelial cells, thereby improving platelet function