Perf Tech Test 10 Flashcards
Heparin Directly Activates
platelets, factor XII, complement, neutrophils, monocytes (aka: immune, inflammatory, complement systems)
HIT
heparin-induced thrombocytopenia and thrombosis
heparin binds to PF4 and makes IgG antibodies= decrease platelets by 50%
On Bypass and quick exposure of blood to ECC
-plasma protein adsorption to ECC surface
-contact activation of blood (coag/complement/cell signaling stimulation-XII, C3, platelets)
-emboli formation 1)surgery (wound debris) 2)blood activation 3) homologous bld (if not filtered) 4) crystalloid solution 5) roller/spallation
-increased interstitial fluid/edema
=====Whole body inflammation and Temp organ dysfunction
Inflation Response Spectrum
(varies patient to patient) 1- mild= fever and leukocytosis 2- significant= tachycardia, high CO/O2 consumption/perm, low SVR 3- Organ dysfunction 4- multiple organ dysfunction 5- death
Key Players: 5 Protein Systems
Contact Activation, Intrinsic , Extrinsic Coag, Fibrinolysis, Complement
Heparin Directly Effects/Stimulates
platelets, factor XII, complement, neutrophils, monocytes
Protein on Tubing Stimulates
platelets, factor XII, complement
Contact Activation Stimulates
complement, coagulation
Plasma Contact Activations Involves 4 Proteins
factor XII, prekallikrein, HMWK, factor XI
Intrinsic Coagulation Initiated by
plasma contact activation with ECC because of Factor XII (along with HMWK and kallikrein)
(inside vessels)
Extrinsic Coagulation Initiated by
Tissue Factor exposure- converse IX and X to IXa and Xa
outside vascular
Thrombin Actions
produces fibrin, activates platelets, stimulates tPA
fibrinolysis extrinsic: tPA, fibrin/ intrinsic: XIIa, HMWK, kallikrein
Complement System
innate system
classical (antigen-antibody complex)
alternative (C3b, terminal pathway feedback, contact, plasmin)
terminal (C3 convertase)
–end product prevent/limit damage from antigen
Complement End Products
- opsonization and phagocytosis (C3b, C4b)
- lysis= MAC (C5b, 6-9)
- agglutination= antigens adhere to each other
- neutrolize virus
- chemotaxis (C5a- call neutrophil and macrophages)
- activates mast and basophils (C3a, C4a, C5a)
- inflammation= increase perm/dilation, decrease CO
C Factors= anaphylactic
C3a, C4a, C5a (dilates, mast/basophils, inflammation)
C Factors= chemotaxis neutrophil, monocytes, endothelial cells
C5a
C Factors= opsonization
C3b, C4b
neutrophil and macrophages come eat!
Key Players: 5 Cells
platelets, neutrophils, monocytes, lymphocytes, endothelial cell
(please not my little eel)
Platelet: early, late activation and response
early activation- EEC contact, heparin, thrombin!
late activation- C5b-9, hypothermia, hemodilution, sheer force, cytokines
response to activation (change in shape)= express GPIIb/IIIa (fibrin), secrete P-selectin receptor (mono and neutrophils)
Neutrophils
C5a, kallikrein, XIIa, heparin, MAC
- express MAC and L-selectins (rolling)
- MAJOR role in reperfusion injury
Monocyte
C5a, thrombin, bradykinin at wound or injury
- takes longer than neutrophils
Lymphocytes response
decrease numbers after CPB= increase chance for infections
Endothelial Cell Activates
(C5a, thrombin, cytokines)
-extrinsic coag, vasodilator, fibrinolysis, inflammatory, perm
How can we control Blood-Surface interface
1) surface bound heparin
2) surface modifications
3) blood modifications (colloid prime, corticosteroids, TXA, platelets, NO)
4) pump modifications (cent vs roller, mini circuit, ultrafiltration)
