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8.myocardial protection during cpb

.myocardial protection during cpb

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8.myocardial protection during cpb

  2. 2. PATHOPHYSIOLOGY OF SURGICAL ISCHEMIA  Myocardial injury in surgical setting occurs 1. Pre cpb 2. During cpb 3. After cpb(post ishemic reperfusion)
  3. 3. Determinants of ishemic injury  Accumilation of tissue metabolites(lactate,co2 and hydrogen ions)  Duration of ishemia  Baseline health of tissue  Distinction b/w Global and regional ishemia
  4. 4. Mechanisms of myocardial ischemic injury  Depletion of high energy phosphates  Intracellular acidosis.  Alteration in intracellular calcium.  Direct myocellular injury from ischemia.  Oxygen derived free radicals generation upon reperfusion.  Myocardial edema from ischemia and reperfusion.
  5. 5. Cessation of Myocardial Blood Flow mitochondria cellular pO2 < 5mmHg within seconds oxidative phosphorilation stops cytosol anaerobic glycolysis glycogen glucose-6-phosphate pyruvate lactate cellular acidosis depletion of ATP
  6. 6. Depletion of ATP < 50% of Normal Level- irreversible lethal cell injury  glycolysis is blocked  increasing cellular acidity  protein denaturation  structural, enzymatic, nuclear changes
  7. 7. Severity and duration of ischemia  The potential for myocardial injury related to duration of warm ischemia To reduce the severity of postischemic injury 1. Rapid arrest 2. Venting LV to decrease O2 requirements 3. Imposing cardiac hypothermia • Safe period 15 to 45 mts. Up to 4hrs with hypothermic intermittant cardioplegia
  8. 8. WHAT DETERMINES MYOCARDIAL OXYGEN DEMAND  Stroke volume  Aortic pressure or wall stress on LV  Heart rate  Basal metabolic rate
  9. 9. How to reduce myocardial oxygen demand ?  CPB and diastolic arrest substantially reduces cardiac load by 50%  Hypothermia  Ventricular decompression with venting  Regional ischemia results in 1. subendocardial infarction 2. contractile dysfunction
  10. 10. REPERFUSION INJURY  Defined as pathology that developes as a consequence of events occuring after restoration of blood flow
  11. 11. Factors contributing reperfusion injury  Calcium influx into cells  Generation of oxygen free radicals(sources mitocondria, vascular endothelium)  Neutrophil activation  Complement activation
  12. 12. Manifestations of Reperfusion injury Produces numerous abnormalities as listed  Reperfusion dysarhythmias  Postischemic systolic and diastolic dysfunction  Myocardial necrosis  Endothelial dysfunction  Apoptosis(cell death)  Myocardial edema  Microvascular injury(no reflow)
  13. 13. How to minimize reperfusion injury ?  Decrease extracellular calcium  Addition of antioxidants like superoxide dismutase,glutathione  Controlled reperfusion  mannitol
  14. 14. Myocardium, Coronary Flow  coronary blood flow: 250 ml/min  entirely during diastole ~ aortic diastolic pressure minus LVDP ~ duration of diastole  pressure < 150 mmHg  oxygenated by superb membrane oxygenator-”the lungs”
  15. 15. Myocardial Protection encompass all the strategies employed during cardiac surgery  preoperative phase  operative phase – global myocardial ischaemic time – reperfusion  postoperative phase
  16. 16. Myocardial oxygen cosumption Reduction Oxygen Demand Normothermic Arrest (37ο C) 1mL/100g/min 90% Hypothermic Arrest (22ο C) 0.30 mL/100g/min Hypothermic Arrest (10ο C) 0.14 mL/100g/min ~ 97%
  17. 17. Myocardial oxygen consumption contd.,  Normal working myocardium consumes 8ml/100gm of oxygen/minute.  Empty beating heart consumes 5.6ml/100gm/minute.  Potassium arrested heart consumes 1.1ml/100gm/mt  Myocardial cooling reduces the consumption to .3ml/100gm/mt of myocardium
  18. 18. HYPOTHERMIA  lowers metabolic rate  decrease myocardial energy requirements  promoting electromechanical quiescence  every 10 0C in temperature, VO2 halved
  19. 19. Normothermic Ischaemia (canine heart)  20 minutes- completely reversible  40 minutes- half the cells are necrotic  1 hour- lethal for all cells
  20. 20. Cardioplegic Strategies  sufficient reduction of oxygen demands  delivery to all cardiac regions
  21. 21. Types of Cardioplegia crystalloid blood
  22. 22. Types of Cardioplegia  crystalloid Pros  Inexpensive  Simplicity  Availability Cons  Hemodilution  No buffering  No oxygen carrying capacity Blood Pros  Oxygen carrying ability  Buffering capacity  Osmolarity,electrolyte  Free radical scavenging ability Cons  Cost  complexity
  23. 23. Cardioplegic Temperature cold (9 0 C) tepid (29 0 C) warm (37 0 C)
  24. 24. Cardioplegic Route antegrade (aorta) retrograde (coronary sinus)
  25. 25. Antegrade Cardioplegia Advantages  Produces prompt arrest.  Simple  Mimics normal coronary flow pitfalls  poor distribution in coronary patients unless delivered through the vein grafts  poor distribution in patients with aortic regurgitation  risk of ostial injury from direct perfusion (during AVR)  interruption of procedure during mitral surgery
  26. 26. Retrograde Cardioplegia  perfusion pressure < 40 mmHg prevent perivascular haemorrhage and oedema!  flow rate = 200mL/min
  27. 27. Retrograde Cardioplegia advantages  distribution of CP to regions supplied by occluded or stenosed vessels  improved subendocardial CP delivery  flushing of air and/or atheromatous debris  Does not impede surgery pitfalls  shunting of CP into ventricular cavities via Thebesian channels  perfusion defects especially right ventricle and posterior septal regions  Catheter placement can be difficult  complex
  28. 28. Blood Cardioplegia 1980’s  improved oxygen carrying capacity and delivery until electromechanical quiescence developed  enhanced myocardial oxygen consumption  preserved high-energy phosphate stores  buffering changes in pH  use of free radical scavengers (superoxide dismutase, catalase, and glutathione)  provide appropriate osmotic environment for myocardial cells and lessen the myocardial oedema
  29. 29. “The heart takes up oxygen over time rather than by dose, so that blood cardioplegic solutions must be delivered over a time interval, rather than by volume”
  30. 30. Cold Blood Cardioplegia advantages  lowers myocardial oxygen demands pitfalls  hypothermic inhibition of mitochondrial enzymes  shifting oxyhaemoglobin dissociation curve to left  activating platelets, leukocytes, complement  impaired membrane stabilization
  31. 31. Microplegia  A cardioplegia technique that mixes blood from CPB circuit with small quantities of concentrated additives.(Pottssium)  Relies on precision pumps to deliver accurate quantities of additives.  Minimizes crystalloid quantity of cardioplegia solution.
  32. 32. Warm Induction “resuscitation of the heart”  severe left ventricular dysfunction  cardiogenic shock preischaemic depletion of energy stores warm induction showed improved aerobic metabolism and LV function in dogs
  33. 33. Warm Reperfusion (hot-shot)  early myocardial metabolic recovery while maintaining electro-mechanical arrest  repletion of energy stores  maintenance of unnecessary contractile activity
  34. 34. Continuous Warm Cardioplegia  avoidance of direct myocellular injury inflicted by any cold solution or environment  increased rate of perioperative stroke and neurological events
  35. 35. Cardioplegia delivery schedule Intermittent Pros  Improved exposure  Lower cardioplegia volume Cons Increased inter-dose myocardial acidosis Continuous Pros  Normal perfusion  Increased postop LV function  Decreased ionotropic requirement Cons  Wet field,Complex
  36. 36. Myocardial monitoring technique Temperature Pros  Ease of use Cons  Location dependent  Temp not equivalent to protection Ph Pros  Potential to alter surgical conduct and improve protection. Cons  Specialized equipment  Efficacy unclear
  37. 37. Cardioplegia Additives Drug Advantage Dis adv Nicorandil Less plegia/Kcl Cost requirement reduced periop coronary spasm preconditioning reduced need of catacolamines post op
  38. 38. Cardioplegia additives contd  L-argine Advantages 1. Decreased myocardial enzyme release 2. Reduced postop cytokine levels 3. Reduced pulmonary artery wedge pressure Disadvantages 1. Cost 2. complexity
  39. 39. Cardioplegia additives contd  Insulin Advantages 1. Increased survival and improved LV function in some studies Disadvantages 1. Complexity 2. Efficacy unclear
  40. 40. Substrate Enhancement of Cardioplegia  Krebs-cycle intermediates – glutamate – aspartate  Insulin-improves LV function  Nitric oxide (NO) / L-arginine decreases myocardial enzyme release,reduces cytokine levels and reduces pulmonary artery wedge pressure
  41. 41. “during all phases ventricular distension must be avoided to prevent the rise of ventricular oxygen demands produced by increased wall tension”
  42. 42. Myocardial protection without cardioplegia  Ventricular fibrillation  Ventricullar fibrillation with intermittent cross clamping.  Off-pump surgery.
  43. 43. Ventricular Fibrillation with Intermittent Aortic Cross-clamping  induces global ischaemia with fibrillation, followed by anoxic arrest and electrical silence on the ECG
  44. 44. Ventricular Fibrillation with Intermittent Aortic Cross-clamping Advantages  cumulative cross-clamp times are less than with cardioplegia  the myocardium is intermittently perfused with oxygenated blood  increasing areas of myocardium are reperfused during the course of the procedure Disadvantages  Repeated aortic clamping  Anastomotic time limited
  45. 45. Therapies Under Investigation Physiological superoxide dismutase catalase nitric oxide Pharmacological mannitol allopurinol antioxidants Physical ischaemic preconditioning hypothermia hypoxic reperfusion
  46. 46. THANK YOU