Exam 10 - Blood Surface Interactions Flashcards
1
Q
Heparin activates
A
- platelets
- factor 12
- compliment
- monocytes
- neutrophils
2
Q
HIT mechanism
A
- Heparin binds to PF4 and induces IgG
- Heparin/PF4/IgG complex activates platelets
- 40-50% decrease in platelets = HIT
- platelet decrease AND thrombosis = HITT
3
Q
Protein adsorption onto ECC
A
- fast
- impossible to predict
Depends on: - [protein]
- surface chemistry
- electrical properties
- hydrophobic/hydrophilic ratio
- receptor site distribution
- wettability
4
Q
Contact activation and ECC
A
- exposes factor 12 / C3 / platelets Stimulates: - coagulation cascade - complement system - alters cell signaling
5
Q
Emboli formation and ECC
A
- most emboli from surgery….not pump
- plaque debris
- air emboli
- blood activation emboli
- whole blood IF NOT filtered….we need to filter
- emboli from crystalloid
- emboli from roller pump
6
Q
Emboli material
A
- fibrin
- fat
- protein
- platelet aggregates
- red cell debris
- air
- spallation
7
Q
ECC and body reactions
A
- ECC stimulates rxns all over body
- change in blood composition triggers inflammation
- inflammation all over body
- temporary organ dysfunction
8
Q
Mild inflammatory response
A
- fever
- leukocytosis
9
Q
Severe inflammatory response
A
- tachycardia
- increase CO
- decrease PVR
- increase O2 consumption
10
Q
5 protein systems
A
- contact activation system
- intrinsic coagulation
- extrinsic coagulation
- fibrinolysis
- complement activation
- C I E F C
11
Q
CIEFC
A
Creates an Imperfect Excessive Feuding Concoction
12
Q
Heparin effects
A
- platelets
- factor 12
- complements
- neutrophils
- monocytes
13
Q
ECC tubing stimulates
A
- factor 12
- compliment
- platelets
14
Q
Contact activation stimulates
A
- coagulation
- complement
15
Q
Factor 12
A
- intrinsic pathway
- adsorbed onto ECC
- need HMWK and prekallikrein
- changes shape and becomes XIIa
16
Q
XIIa
A
- cleaves prekallikrein to kallikrein (neutrophil agonist)
- kallikrein cleaves HMWK to bradykinin (vasodilator)
- cleaves XI to XIa ( intrinsic coagulation cascade)
17
Q
Intrinsic pathway
A
- initiated by contact activation
- factor XII
18
Q
Extrinsic coagulation
A
- initiated by TF + VII
- TF can be cell bound (not pericardium) or in plasma
- TF + VIIa activates 9 and 10
19
Q
Thrombin actions
A
- turns fibrinogen into fibrin
- cross linking
- activates platelets
- stimulates t-PA….fibrinolysis
20
Q
Extrinsic fibrinolysis activation
A
- t-PA / urokinase / fibrin
21
Q
Intrinsic fibrinolysis activation
A
- XIIa / HMWK / kallikrein
22
Q
Complement system
A
- coats antigens
- innate
- primary mechanism antibodies use to kill
23
Q
Classical complement activation
A
- antigen-antibody complex
24
Q
Alternative complement activation
A
- starts with C3b (product of classical)
- continuous
- positive feedback loop for amplification
25
Terminal complement pathway
- classical and alternative merge at C3 convertase
26
C3b
- opsonization
27
Functions of complement end products
- opsonization (C3b)
- lysis (MAC)
- agglutination
- neutralization
- chemotaxis (C5a)
- activation of mast cells / basophils (C3a/C4a/C5a)
- inflammation
28
Classical activation
- contact of factor 12
- heparin-protamine complex at end of CPB
- ischemia reperfusion
- blood-air interface
29
Alternative activation
- contact with foreign surface
- activated suction blood
- ischemia reperfusion
30
Granulocytes
- neutrophils: 60-70% / phagocytosis
- Eosinophils: 2-4% / antigen-antibody rxns
- basophils: 1% / histamine and heparin
31
Agranulocytes
- monocytes: become macrophage in tissue
| - lymphocytes: specific / B and T
32
Platelets: early activation initiators
- contact w/ ECC
- heparin
- circulating thrombin
- PAF
33
Platelets: late activators
- C5b-C9
- Plasmin
- Hypothermia
- IL- 6
- Serotonin
- Epi
34
Platelets response to activation
- get sticky and angry
- bind to monocytes and neutrophils
- P selectin: rolling of monocytes/neutrophils...platelets stick together
- express GPIIb/IIIa and GPIb....lose after CPB
35
Neutrophil activation
- strong and fast
- agonists: kallikrein / C5a.....also XIIa/heparin/MAC
- release granules
- express MAC and selectin receptors
- ischemia reperfusion injury and inflammation on CPB
36
Monocytes activation
- slow activation
- agonists: c%a / thrombin / bradykinin
- at wound and circuit
- express TF
- release cytokines / ILs
- during/post: 6 and 8
- post: 1, 2, 4, 6 and 8
37
Lymphocyte response
- drops in # post CPB
- patient susceptible to infection
- septic shock / endocarditis / infection
38
Endothelial cell response
- activated by: thrombin / C5a / cytokines / TNF
- synthesize TF to make thrombin (clot and fibrinolysis)
- t-PA / PAi-1 for fibrinolysis
- acute inflammatory response
- edema
39
Non platelet bleeding post CPB
- fibrinolysis
- heparin excess
- hypothermia
- Protamine excess
40
Platelet related bleeding post CPB
- thrombocytopenia
- aspirin
- platelet dysfunction
41
Control of blood surface interface on CPB
- good biomaterial tubing
- prevent blood activation
- limit blood activation
42
Terumo X Coating
- no heparin
- less adhesion
- on all types of material
- tie-bond everything
- PMEA
43
Medtronic Carmeda
- gold standard
- YES heparin
- less blood loss / less given
- shorter LOS and ventilator
- non-leaching
- reduces blood activation
- covalent
44
Medtronic Trillium
- Heparin based
- non-leaching
- mimics endothelium
- negative charge
- covalent
45
Medtronic Balance
- No heparin
- same as trillium
- can use on HIT
46
Maquet Bioline
- Heparin
- Albumin
- mimics endothelium
47
Maquet Softline
- NO heparin
| - mimics endothelium
48
Sorin Phisio
- No heparin
- phosphorylcholine
- stable and durable
- improves platelet preservation
- decreases blood activation
49
Blood modifications
- corticosteroids
- colloid prime (albumin...prevents edema)
- antifibrinolytic agents
- ACA...Amicar / TA - blocks plasminogen to plasmin
- Aprotonin - inhibits plasmin directly
- platelet anesthesia (NO)
- complement inhibitors
50
Pump mods
- centrifugal pump
- pulse flow
- mini circuits
- off pump
- ultrafiltration
- leukodepletion
- shed blood management
