11-25-20 - CPB and circulatory arrest - Dr. Julie Wise

11-25-20 - CPB and circulatory arrest - Dr. Julie Wise

Transcript

1. Cardiopulmonary Bypass and Circulatory Arrest
2. Objectives O Discuss the basic principles of CPB and components of the circuit O Review CPB related anesthetic goals O Discuss circulatory arrest and its consequences O Highlight high yield topics likely to show up on exams
3. History O 1940s: start of cardiac surgery O 1950s: Need for heart-lung machine became apparent O 1953: First successful operation using heart- lung machine (ASD closure) O Patient still alive 50 years later
8. Circuits O Components O Cannulae O Oxygenator O Pump O Heat Exchanger O Blood Filters O Cardioplegia delivery system O Vents, Cardiotomy suction, and cell saver
11. Cannulae O Venous - Drains venous blood from the patient to the CPB circuit - Single RA cannula vs. Bicaval cannula - Drains passively O Arterial - Returns oxygenated blood back to the patient - Aorta, femoral, axillary, or innominate arteries
12. Oxygenator O Modern membrane oxygenators greatly improved from previous bubble oxygenators O Use bundles of fibers contained within a plastic housing
13. Pumps O Centrifugal and Roller pumps both used in clinical practice today O Centrifugal: magnetically controlled impeller rotate to provide flow O Roller: simplest and earliest type - Works by alternating tube compression and release 180 degrees apart
14. Pumps O Roller
15. Pumps O Centrifugal
16. Roller vs. Centrifugal ADVANTAGES DISADVANTAGES O Roller - Simple and easy design O Centrifugal - Less blood trauma - Lower line pressures - Less cavitation - Lower risk of massive air emboli - Elimination of tubing wear and spallation O Roller - Destruction of blood elements - Spallation - Complications from inflow and outflow occlusion of the pump O Centrifugal - More expensive - More complex design - Flow dependent on preload and afterload
17. Pumps O Neither centrifugal or roller pumps provide physiologically significant pulsatile flow. O Lack of pulsatile flow has been linked to renal dysfunction and production of ischemic metabolic by-products O Increased survival seen in high risk patients with the use of pulsatile flow on CPB
18. Heat Exchanger O Counter current device - Heated or cooled water circulates around a conducting material - Conducting material needs to have close contact with the patient’s blood
19. Prime O Prime is the fluid contained within the CPB tubing O Crystalloid solution with additives - Mannitol - Albumin - Heparin - Calcium O Average prime volume ~ 1500 ml O RAP: patient blood partially primes CPB tubing
20. Anticoagulation O Contact between blood and CPB circuit  activates coagulation cascade O Preventing thrombosis requires anticoagulation prior to cannulae insertion O Heparin = AC of choice O What is the dose? O How is it monitored?
21. Heparin O Potentiates activity of AT III O Binding to AT III alters its configuration and increases its thrombin inhibitory potency > 1,000 fold O Inhibiting thrombin prevents formation of fibrin clot O Higher doses required in patient’s on heparin preoperatively or in those with AT deficiencies
22. Monitoring O ACT O gold standard for monitoring anticoagulation with heparin O ACT > 480 acceptable for initiating CPB O Blood- Heparin concentrations
23. O What to do when the ACT won’t reach therapeutic levels - First step: O try giving additional dose of heparin and recheck - Next step: O Give FFP (contains AT III) - Finally: O Administer exogenous AT III
24. HIT and Heparin Allergies O Two types of HIT 1. Mild form: associated with transient decrease in platelet count 2. More severe form: autoimmune mediated decrease in platelet count 2/2 formation of anti- PF4  Platelet clumping and microvascular thrombosis O What to do with these patients: O Type 1, if possible wait until platelet number recovers before proceeding to surgery O Type 2, heparin alternatives should be used  Defibrinogenating agents: Hirudin, Bivalrudin, and Factor Xa inhibitors
25. Protamine O Polycationic protein from salmon sperm O Mild anticoagulant effect of its own O Forms complexes with sulfate groups of heparin  neutralizes its effect O Dose= 1 mg protamine/ 100 units heparin
26. Protamine Reactions O Type I: Hypotension O Type II O IIA: Anaphylaxis O IIB: Immediate anaphylactoid O IIC: Delayed anaphylactoid O Type III: Severe unrelenting pulmonary vasoconstriction
27. Blood Conservation O High risk of bleeding in cardiac surgery - Nature of the surgery itself - Reoperation (higher blood loss) - Use of anticoagulants or antiplatelet agents - Platelet dysfunction and coagulopathy due to CPB
28. Blood Conservation O Methods: - Intraoperative autologous hemodilution - Scavenging of shed blood O cell saver - Use of antifibrinolytics O Aminocaproic acid and TXA - Retrograde autologous Prime - Ultrafiltration O Contraindications to autologous hemodilution: - Preoperative anemia - Unstable angina - High grade coronary stenosis (LM disease) - AS
29. Blood Conservation O Cell Salvage - Hematocrits up to 70% - Reinfusion can worsen coagulopathy - Contraindications include: O infection O malignancy O use of topical hemostatic agents
30. Blood Conservation O Antifibrinolytics - Aminocaproic Acid and Tranexamic Acid O Lysine analogs O Bind plasminogen and block its ability to bind lysine residues on fibrinogen  prevents lysis of fibrin clots - Aprotinin O Naturally occurring fibrinolytic O inhibits kallikrein, preserves platelet glycoprotein receptors, inhibits proinflammatory cytokine release, and inhibits plasmin and protein C O No longer in use in US
31. Blood Conservation O Retrograde Autologous Prime - Crystalloid prime is partially replaced by patient’s blood drained retrograde via arterial cannula - Reduces hemodilution and decrease in SVR when initiating CPB - Must watch for acute hypovolemic hypotension! O Ultrafiltration - AKA hemoconcentration - Done by perfusionist on CPB - Reduces free water, Increases HCT, preserves hemostasis, and decreases circulating inflammatory mediators
32. Myocardial Protection O Systemic Hypothermia - Provide both myocardial and neuro protection - Benefits: O reduction in metabolic rate and O2 consumption O preservation of high-energy phosphate substrates O reduction in excitatory neurotransmitters - Can be active or passive (most cardiac surgeries involve active cooling to 32°C)
33. Myocardial Protection O Cold Cardioplegia - Cold solution (10-15°C) of blood or crystalloid with high potassium concentration injected into coronary arteries or veins  induces diastolic electrical arrest - Antegrade O injected via aortic root following cross clamping and into native coronary arteries O follows normal flow of blood - Retrograde O used in patients with severe CAD and/or AI O Coronary sinus catheter
34. Physiologic consequences of CPB O Cellular trauma - High flow rates cause trauma to hematologic elements O Hemodilution O Complement activation - Rewarming O Impaired immune function
35. Physiologic consequences of CPB O Platelet Dysfunction O AKI O Cerebral Injury O Systemic Inflammatory Response O Vasoplegia - TX: Vasopressors, IVF, and methylene blue
36. Thromboelastography
37. Acid Base Management Alpha Stat PH Stat O pH not corrected O PaCO2 falls with decrease in temperature O Blood gases are uncorrected at 37°C O Limits microemboli O Maintains constant pH and CO2 O CO2 is added O Increases cerebral blood flow O Increases risk of microemboli
38. Deep Hypothermic Circulatory Arrest O Indications: - Severe aortic atherosclerosis - Type A aortic dissections - Complex aortic arch repairs - Resection of IVC tumors O Temperature Control: - Cool to 18- 20 °C - Pack the head and heart with ice
39. DHCA O Neuroprotection - 1 gram IV methyprednisolone (~ 20mg/kg) - High dose steroids have been shown to attenuate cerebral response to ischemia - Cerebral oximetry monitoring - Antegrade and retrograde cerebral perfusion can extend acceptable period of DHCA O Physiologic Consequences - Extensive cooling and rewarming associated with significant coagulopathy - High risk of ischemic cerebral injury - Impaired glucose metabolism
40. References 1. Kaplan’s Cardiac Anesthesia. Joel A Kaplan. 2. Clinical Anesthesia. Paul G. Barash, et al. 3. Evolution of Cardiopulmonary Bypass. William Stoney. Historical Perspectives in Cardiology. 2009.