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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

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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 & 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


Cbf auto regulation
CBF- Auto regulation

CBF

50

MAP

60 mmHg

160 mmHg


Cbf variables
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



Cerebral protection strategies
Cerebral protection -Strategies

  • Optimize CPP

  • Decrease CMR

  • Block the mediators of cell injury

    - at ischemic cascade

    - at reperfusion cascade


Protective techniques
Protective techniques

  • Brain Shrinkage

  • Hyperventilation Optimize CPP

  • Appropriate BP

  • Hypothermia Decrease CMR

  • Burst suppression

  • Pharmacological protectors -Block the

    mediators of cell injury







Fundamental questions

ISCHEMIC CASCADE

Na-K pump failure

Na+

Ca+

Glutamate

Phosholipases

PL

FFA


Fundamental questions

REPERFUSION CASCADE

TAX

LT

PG

OFR

Endothelial damage&Platelet,WBC plugs

Arachidonic acid

PL

FFA


Pharmacological intervention
Pharmacological intervention

  • CMR Reduction

  • Barbiturates: Decreases CMR

    Decreases Ca+

    Decreases OFR

    Na+ channel blockade

    Decreases Glucose entry

    Decreases refractory ICP

    Inverse steal blood flow


Pharmacological intervention1
Pharmacological intervention

  • CMR Reduction

  • Propofol, Etomidate

  • Morphine, Fentanil, Sufentanil, Remifentanil

  • Diazepam, Midazolam

  • Ketamine, Dexmedetomidine

  • Halothane, Enflurane, Isoflurane, Sevoflurane, Desflurane


Pharmacological intervention2
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


Pharmacological intervention3
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