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Myocardial Protection

Myocardial Protection. Eugene Yevstratov , MD Institute of Cardiology and Cardiovascular Surgery, Favaloro Foundation Buenos Aires, Argentina October/2002. Goals of Myocardial protection. 1. Protect against ischemic injury. 2. Provide a motionless, bloodless field

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Myocardial Protection

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  1. Myocardial Protection Eugene Yevstratov, MD Institute of Cardiology and Cardiovascular Surgery, Favaloro Foundation Buenos Aires, Argentina October/2002

  2. Goals of Myocardial protection 1.Protect against ischemic injury 2.Provide a motionless, bloodless field 3.Allow effective post-ischemic myocardial resuscitation

  3. Spectrum of myocardial ischemic injury • Acute ischemic disfunction • Preconditioning • Stunning • Hibernation • Necrosis vs. Apoptosis

  4. Acute ischemic disfunction • Reversible contractile failure • Perfusion pressure • O2 supply • Inmediate recovery

  5. Preconditioning • Reversible • Slowed energy utilization • Reduction in myocardial necrosis • Increase protective abilities of myocardium • Presented as a normal proper protective reaction of the ischemic myocardium • Recovery Hs,Ds

  6. Stunning • Parcialy Reversible • May be accompained by endothelial disfunction (NO) causing reduced coronary blood flow • Result of ischemia-reperfusion insult • Mediated by increased intracellular Ca accumulation • Recovery in Hs,Wks

  7. Hibernation • Parcialy Reversible • Related to poor myocardial blood flow • Chronic • Recovery Wks,Mo

  8. Necrosis • Irreversible • Hyper contracture - “contracture band necrosis”, “stone heart” • Osmotic/ionic dysregulation, membrane injury • Cell swelling&disruption • Lysis

  9. Apoptosis • Irreversible • Death signal • Cell shrinkage • Cytoplasmic and nuclear condensation • Phagocytosis

  10. Systems involved into membrane injury • MAC( membrane attack complex) • Adenosine dependent receptors • K+ATP dependent chanels • NHE(sodium hydrogen exchanger)

  11. Cellular effects of ischemia • Altered membrane potential • Altered ion distribution(increase intracellularCa++/Na++) • Cellular swelling • Cytoskeletal Disorganisation • Increased hypoxantine • Decreased ATP • Decreased phosphocreatine • Decreased Glutatione • Cellular Acidosis

  12. Straqtegies for Heart protection • Increase the O2 offer • Decreae oxygen demand • Methabolical intervention • Prevention of demand increased • Substrate disponsability

  13. Myocardial O2 consumptions at 37C • Beating (full,perfused) 10ml/100gr/min • Beating (empty,perfused) 5,5ml/100gr/min • Fibrilating(empty,perfused) 6,5ml/100gr/min • K+ Cardioplegia(empty,crossclamp) 1,0ml/100gr/min

  14. Myocardial O2 consumptionml/100gr/min • Temperatura C 37 32 28 22 Beating (empty) 5,5 5,0 4,0 2,9 Fibrilating (empty) 6,5 3,8 3,0 2,0 K+ cardioplegia 1,0 0,8 0,6 0,3

  15. Cardioplegia - Options No cardioplegia Cardioplegia Type ( blood vs crystalloid, cont vs intermittent ) Route ( antegrade vs retrograde ) Temperature ( warm vs cold ) Additives Special consideration ( Acute infarction, Neonate)

  16. Rivero Cardioplegia solutions 1 2

  17. Mechanism of Cardioplegic Protection • Mechanical arrest ( K – induced, 80% reduction in O2 consumption) • Hypotermia (10-15% furter reduction in O2 consumption) • Aerobic metabolism – oxygenated cardioplegia • Maintain hypotermic arrest with readministration every 15-20 min • Retrograde delivery LV RV protection

  18. Protect from rewarming Systemic hypotermia Aortic/ventricular vents Total bypass (caval oclusion) Acute Ischemia Waqrm induction Substrate enhancement Controlled reperfusion Warm,hypocalcemic,alkaline cardioplegia Retrograde or low flow-pressure antegrade perfusion Energy replacement while arrested Uniform warming Other consideration

  19. Cardioplegic Composition • Blood vs Crystalloid • Buffers • Calcium • Potassium • Free radical scavengers • Others

  20. Blood vs Crystalloid O2 carrying capacity ( Hematocrit 15 – 20 %) Buffers –histidine Free radical scavengers in RBCs Improved rheologic / oncotic properties Metabolic substrate

  21. Buffers THAM Histidine NaHCO3 Slightly alkaline reperfusion

  22. Calcium, Potassium Small amounts of calcium ( 0.1 – 0.5 mM/L ) Ca chelated in blood with citrate 10 – mM/L of potassium ( first dose highest ) > 30 mM/L – endothelial dysfunction

  23. Free radical scavengers.Others Allopurinol Propofol Deferoxamine Metabolic substrates ( adenosine, nucleotid transport inhibitors...) K- channel openers ( Nicorandil )

  24. The ways of pharmacological therapy Addition of metabolites or cofactors • Activation of enzymes or complexes involving in generation of reduced equivalents, and their utilisation • Control of synthesis of mitochondrial factors, or genesis of mitochondria, and protection of mitochondria •   Improving Ph balance in the ischemic heart

  25. Institute of Cardiology and Cardiovascular Surgery, Favaloro Foundation Buenos Aires, Argentina The End Eugene Yevstratov E-mail Fax 001775 679 2870

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