Extracorporeal Circulation Flashcards
Name at least 10 complications of CPB
Protamine reaction, Thrombosis during CPB, Aortic dissection, Dislodgment of cannula, Rupture of arterial connection, Gas embolism, Massive systemic gas embolism, Electrical power failure, Pump failure, Heater-cooler problems, Replace oxygenator during CPB, Other oxygenator problems, Urgent re-setup after takedown, Early unplanned cessation of CPB
How much does cerebral metabolism drop during hypothermia
Metabolism is halved for every 10C drop in temperature from 37C
What does Heparin do?
Catalyzes the reaction of antithrombin III
What are the advantages of unfractionated Heparin?
Parenteral use, immediate onset of action, rapid reversal by protamine or recombinant platelet factor 4
What is heparin resistance and how is it treated?
Heparin resistance occurs when a dose of heparin does not achieve the ACT desired. Treatment is 1. another dose of heparin and recheck the ACT 2. FFP or ATIII if ACT still below goal
What is heparin rebound?
Heparin rebound is a delayed anticoagulant effect after protamine neutralization because of the rapid metabolism of protamine and delayed seepage of heparin into the circulation from lymphatic tissues or other deposits.
What are safe alternatives for heparin for CPB in HIT?
Argatroban, bivalirudin, recombinant hirudin, LMWH (long half life 4-8 hours)
What is heparin associated thrombocytopenia (HAT)?
A benign non-immune 5-15% decrease in platelet count that occurs within a few hours to 3 days after heparin exposure
What is HIT and HITT?
An autoimmune condition whereby Heparin binds to platelets causing PF4 release which binds to heparin forming Heparin-PF4 complexes. In some individuals, this is antigenic and causes an IgG autoimmune reaction. IgG and Heparin-PF4 complexes combine to form HIT complexes which can activate platelets to release more PF4 which is a catalyst for more HIT complexes. This platelet activation can release several pro-coagulatory proteins thus generating thrombin and thrombosis
What is the clinical presentation of HIT?
A decrease in platelet count by 50% or more in a patient who has had exposure to heparin within 5-15 days
When do you suspect post-operative HIT and what do you do?
If platelet count is <80,000, all heparin should be stopped, daily platelet counts should be obtained and the patient should be examined for DVT, ischemia, stroke MI or evidence of thrombosis. Any evidence of thrombosis should prompt a HIT screen.
What is the management for HIT/HITT?
Do not give heparin nor platelet transfusions. Start anticoagulation with recombinant hirudin, argatroban or bivalirudin to prevent further thrombosis.
What is the therapeutic level of hirudin in CPB?
3.5-4.5ug/mL. Bolus dose 0.25mg/kg IV and 0.2 mg/kg in the priming volume and infusion of 0.5mg/min until 15 min before stopping CPB. At that time add 5mg of hirudin to the perfusate.
What are the components of the inflammatory response to CPB?
C3a,C4a,C5a, Neutrophils, Monocytes, Macrophages, Platelets, Lipopolysaccharides, Matrix Metalloproteinases Il-1B, TNF-a, IL-10 (anti-inflammatory)
What are strategies to minimize microemboli?
Membrane oxygenator and centrifugal arterial pump, cardiotomy reservoir filter, arterial line filter/bubble trap, keep temperature differentials <8-10C, prime with carbon dioxide flush and recirculate with saline and filter, prevent air entry into circuit, snug purse string sutures, 3 way stop-cocks on all sampling ports, meticulous syringe management, adequate cardiotomy reservoir volume, avoid excessive suction on vents, one-way valved purge lines for bubble traps, TEE to locate trapped intracardiac air, de-airing thoroughly, wash blood aspirated from the surgical field, adequate anticoagulation, avoid atherosclerotic aorta during cannulation with epiaortic ultrasound, cannulate distal aorta or axillary artery, special aortic cannulas with baffles/screens, reduce # of applications of aortic clamps
