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

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Presentation on theme: "Eugene Yevstratov, MD Institute of Cardiology and Cardiovascular Surgery, Favaloro Foundation Buenos Aires, Argentina October/2002."— Presentation transcript:

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

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

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

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6 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

7 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

8 Hibernation Parcialy Reversible Related to poor myocardial blood flow Chronic Recovery Wks,Mo

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

10 Apoptosis Irreversible Death signal Cell shrinkage Cytoplasmic and nuclear condensation Phagocytosis

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

12 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

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

14 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

15 Myocardial O2 consumption ml/100gr/min Temperatura C 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

16 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)

17 Rivero Cardioplegia solutions 12

18 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 min Retrograde delivery LV RV protection

19 Other consideration 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

20 Cardioplegic Composition Blood vs Crystalloid Buffers Calcium Potassium Free radical scavengers Others

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

22 Buffers THAM Histidine NaHCO3 Slightly alkaline reperfusion

23 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

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

25 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

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27 The End Eugene Yevstratov Fax Institute of Cardiology and Cardiovascular Surgery, Favaloro Foundation Buenos Aires, Argentina


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