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Fundamental questions

Fundamental questions. How does the brain damage occur? Can we select at risk patients? What therapies do we have? How do they work? What is the side effect? What is the risk –benefit picture?. CBF & CPP. CBF - 50ml/100g/min -750ml/min – 15-20% CO 20-25 ml/100g/min – cerebral impairment

chelsea-burns
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Fundamental questions

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  1. Fundamental questions • How does the brain damage occur? • Can we select at risk patients? • What therapies do we have? • How do they work? • What is the side effect? • What is the risk –benefit picture?

  2. CBF & CPP • CBF-50ml/100g/min -750ml/min – 15-20% CO 20-25 ml/100g/min – cerebral impairment 15-20 ml/100g/min - isoelectric EEG <10 ml/100g/min - irreversible damage • CPP = MAP – ICP : 80-100 –normal <50 – slowing EEG ,cerebral impairment 25 - 40 – Flat EEG <25 - irreversible damage

  3. CBF- Auto regulation CBF 50 MAP 60 mmHg 160 mmHg

  4. CBF &Variables CBF depends on, • PaCO2 (20-80mmHg)-1-2 ml/100g/min /mmHg • T- 5-7%change/ 1 change • PaO2 <50 mmHg CBF 0

  5. Cerebral protection

  6. Cerebral protection -Strategies • Optimize CPP • Decrease CMR • Block the mediators of cell injury - at ischemic cascade - at reperfusion cascade

  7. Protective techniques • Brain Shrinkage • Hyperventilation Optimize CPP • Appropriate BP • Hypothermia Decrease CMR • Burst suppression • Pharmacological protectors -Block the mediators of cell injury

  8. Brain shrinkage

  9. T regulation o

  10. Mild hypothermia

  11. Moderate hypothermia

  12. Profound hypothermia

  13. ISCHEMIC CASCADE Na-K pump failure Na+ Ca+ Glutamate Phosholipases PL FFA

  14. REPERFUSION CASCADE TAX LT PG OFR Endothelial damage&Platelet,WBC plugs Arachidonic acid PL FFA

  15. Pharmacological intervention • CMR Reduction • Barbiturates: Decreases CMR Decreases Ca+ Decreases OFR Na+ channel blockade Decreases Glucose entry Decreases refractory ICP Inverse steal blood flow

  16. Pharmacological intervention • CMR Reduction • Propofol, Etomidate • Morphine, Fentanil, Sufentanil, Remifentanil • Diazepam, Midazolam • Ketamine, Dexmedetomidine • Halothane, Enflurane, Isoflurane, Sevoflurane, Desflurane

  17. Pharmacological intervention • Neuronal injury protectors A} pre synaptic level- SNX III –Ca+ blocker B} post synaptic level 1.Na+ blocker-All volatile anaesthetic agents -Barbiturates -Lamotrigine - Riluzole -Lubeluzole 2. Ca+ blocker-Nimodipine -Nicardipine 3.NMDA antagonists: Competitive blocker-Selfotel Non Competitive blocker-Dizoclypine -Dexromethorphan -ketamine

  18. Pharmacological intervention 4.Glycine site analogues-felbamate, Licostinel 5.NO synthase inhibitors –lifarizine, 7nitroindazole 6.Mg+-Ca+ blockade, NMDA antagonist 7.steroids-anti inflammatory action, ?neuronal protection -MPS, Tirilazad 8.OFR scavengers- Vit-E, PBN{phenyl derbuyl nitrone}, Tirilazad,Mannitol 9.Cytokinin inhibition-TNF Receptor I, TNF alfa mab 10. Anti adhesion molecule Ab

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