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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

slide22

ISCHEMIC CASCADE

Na-K pump failure

Na+

Ca+

Glutamate

Phosholipases

PL

FFA

slide23

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

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