Cardiopulmonary Bypass Flashcards
(42 cards)
When is CO2 extracted from blood?
At the same time that O2 is added back
Process of blood going through CPB stuff
Venous Reservoir
Oxygenator/Heat exchanger (CO2 is extracted from the blood while adding O2 back)
Main pump
Arterial filter (removes fat, thrombi, calcium, and tissue debris)
Patient
Roller vs centrifugal pump:
Roller: non pulsatile flow, constant regardless of pressure generated.
Centrifugal: pressure dependent, less traumatic to RBCS
Which perfusion pressure is recommended to maintain systemic organ function?
50-80 mmHg
Why do we use heparin to anticoagulant patients for CPB?
Consistent in its dose and achievement of adequate AC
Rapid onset time
Easy to monitor
Adequate therapeutic window.
We want it because we don’t want thrombosis to occur in CPB circuit.
How does ACT work? Normal pre-heparin ACT? What do surgeons want before starting? Normal heparin dose?
small aliquot of blood added to a medium which stimulates thrombosis. In a normal, pre-heparinized state, the ACT is 90-150 seconds. Following administration of heparin, 300-400 U/kg, ACT is repeated after 2 minutes. Most surgeons want ACT >400, others want >480
Why is CPB so harmful to the system?
It destroys RBCs, Activates and destructs platelets, stimulates inflammatory and complement system leading to further stimulation of coagulation system after reversal of heparin
How does heparin work?
It enhances the activity of anti-thrombin 3 leading to an enhanced destruction of thrombin and thereby making it difficult to form clots
What situations would make a person be exposed to heparin thereby increasing their chances of having HIIT?
previous MI or STEMI, This could cause decreased levels of heparin and/or decreased activity of antithrombin 3 leading to an inability to reach adequate ACT values
What can you give to patents who have less AT3, or aren’t responding to heparin?
you could give ATIII via 1-2 units of FFP
What makes CPB worse for a person’s system?
Length of time on CPB. So longer surgeries with more parts to it=more time on CPB, and more time for issues of destruction of RBCs, and platelets.
One thing that can affect patients undergoing cardiac surgery as far as getting back to normal after CPB is:
Temperature! if you’re having a problem with coagulation after CPB. Consider their temperature.
How does protamine work? What are 3 potential reactions that can happen with administration of protamine? How do you treat these?
It binds to heparin to form a stable salt
3 reactions: Anaphylactic (profound vasodilation and CV collapse), this can happen in its who have been exposed to protamine before (previous exposure, diabetics using insulin NPH) since protamine is used to prolong effects. Men who have had vasectomies or episodes of orchitis.
tx: support of CV system, admin of diphenhydramine or epinephrine to block histamines and stop degranulation of leukocytes
2. Fulminate pulmonary vasoconstriction-can happen in its with elevated pulmonary pressures. Tx: stop admin of protamine and support CV system. Methylene blue could help counteract increase in pulmonary pressures
3. Giving it too rapidly could cause decrease in intravascular calcium and stimulate release of histamine leading to drop in SVR and hypotension. Rec that no more than 50 mg of protamine be given in a 10 min period.
Tell me about the type 1 HIT:
what happens? why do they think this? what is heparin binding to? What does this binding facilitate?
Heparin induced thrombocytopenia Type 1:
Results in a decrease in the number and function of platelets following admin of heparin-thought to be due to an aggregation of platelets. Heparin binds to the surface of platelets as well as to Platelet factor 4. This binding facilitates platelets clumping together and these aggregates are removed from circulation by the RES
Type 2 HIT: Usually happens in which patient population? What decreases (like in HIT 1), and what else happens? Tell me more about that additional thing and what it leads to. Complications?
Seen in those who have been treated with heparin for a more prolonged time 5-10 years. Decrease in platelet levels due to aggregation and removal from circulation however, there is an additional antibody mediated effect. Antibodies are generated and bind to heparin platelet factor 4 complex-this leads to activation of inflammatory system as well as activation of complement cascade. Thrombotic complications are a thing with HIT 2
So, for type 2 HIT: can you get antibody levels afterwards? Does repeated exposure to heparin always reproduce the HIT type 2 reaction?
Antibody levels in patients who survive a HIT type 2 reaction become undetectable several weeks after cessation of heparin. Repeated exposure does not always reproduce this.
What can you use for AC during CPB in a patient who has a hx of HIT? How does it work? how is it eliminated? half life? is there a reversal agent? how must you administer it for CPB? How to measure its clotting?
Bivalirudin:
Acts by binding to active site on thrombin, preventing its ability to cleave fibrinogen to fibrin. It is itself cleaved by thrombin leading to elimination in the plasma and is not dependent on an organ for removal. Half life of 24 minutes. No reversal agent. You must give a bolus and then an infusion for CPB.
Coagulation system tends to favor___ until ___.
How do endothelial cells play a role in prevention of platelet activation, aggregation, and generation of fibrin clotting? They contain ___, they release ____, they display ____.
Tends to favor AC until endothelial damage occurs
They contain heparin sulphate (which inhibits clotting factors)
Endothelial cells are also responsible for releasing prostacyclin, a molecule that leads to vasodilation, and stabilizes platelet cells preventing their activation and formation of a platelet plug
-endothelial cells, except those present in the cerebral circulation, synthesize and display thrombomodulin on their cell surface. Thrombomodulin greatly decreases activation of clotting cascade .
Once endothelial cells become damaged, ____ becomes expased, and there is activation of _____
Thrombosis occurs when _____.
First phase of clotting: Happens after? decrease in ___ resulting in___
Then what forms?
Following that-what becomes exposed? What is released with that?
sub endothelial matrix becomes exposed and there is an activation of the clotting pathway.
Thromobosis occurs when platelets and fibrin become intertwined, filling area of endothelial damage
First phase (after endothelial damage), occurs with a decrease in prostacyclin and an increase in thromboxane-this results in vasoconstriction
Then-platelet plug forms at area of endothelial damage and this coupled with vasoconstriction limits bleeding, and provides a place where clotting can form
Following platelet plug, Tissue factor becomes exposed when endothelial cells are damaged and is the primary initiator of clotting cascade. From this point, both pro and anti coagulation stuff is released in order to prevent balance from tipping too far in the other direction.
Starting with factor 5, Tell me how we get to fibrin
Factor V turns into Va, which is responsible for transforming prothrombin (2) into thrombin (2a). Thrombin turns fibrinogen into fibrin.
___ is the main initiator of clotting:
Thrombin
The clotting cascade activates which system?
The fibrinolytic system whose role is to remodel and degrade clot formation-allowing for endothelial cell repair
CPB stimulates which two systems?
Fibrinolytic and clotting system
What are the 3 main anti-fibrinolytic drugs used to decrease blood loss and decrease the amount of blood transfusions?
Epsilon aminocaproic acid (amir)
TXA
Aprotinin
