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Physiology of Cerebral Circulation Presenters – Dr. Dalim

Physiology of Cerebral Circulation Presenters – Dr. Dalim Dr. Gurpreet Moderator – Dr.Rani . www.anaesthesia.co.in anaesthesia.co.in@gmail.com. Cerebral Blood Flow. Global – 50-55ml/100g/min Grey matter – 75ml/100g/min White matter – 20ml/100g/min

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Physiology of Cerebral Circulation Presenters – Dr. Dalim

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  1. Physiology of Cerebral Circulation Presenters – Dr. Dalim Dr. Gurpreet Moderator – Dr.Rani www.anaesthesia.co.inanaesthesia.co.in@gmail.com

  2. Cerebral Blood Flow • Global – 50-55ml/100g/min • Grey matter – 75ml/100g/min • White matter – 20ml/100g/min • Children – 95ml/100g/min • Infants – 40ml/100g/min • Cerebral Blood Volume – 5ml/100g.

  3. Adult human brain – 2% of body weight 12-15% of cardiac output 20% of total O2 consumption • CMRO2 – 3.5ml/100g/min • CMRO2 = CBF x AVDO2 = CBF x Hb x1.39 x (SaO2 - SjVO2) • Total energy expenditure = Electrophysiological Cellular function + homeostasis 60% 40%

  4. Regulation of CBF • Regional flow-metabolism coupling • PaCO2 • PaO2 • Auto-regulation • Blood viscosity • Hypothermia

  5. Flow-Metabolism Coupling ↑ metabolism – accumulation of metabolites ( K, H) – local vasodilation (NO, Ca, adenosine, PGs) – ↑ flow

  6. Flow-Metabolism Coupling Effect of anaesthetics : • Suppression of Flow-Metabolism Coupling ( except N2O, ketamine) • Suppress only the component assosciated with electrophysiological function • Progressive suppression of CMRO2 up to the point of complete EEG suppression.

  7. Flow-Metabolism Coupling Effect of temperature : • CMR decreases by 6-7% / ˚C of temperaturereduction • Suppress both the component – electrophysiologic function + cellular integrity • Complete suppression at 18-20˚C • Hyperthermia has opposite effect (up to 42˚C)

  8. PaCO2

  9. CBF changes 1-2ml/100g/min /mmHg change in PaCO2 • CBV change 0.049ml/100g/mmHg change in PaCO2 • Hyperventilation beyond 6-8 hrs may not be effective • Hyperventilation below 20mmHg can cause cerebral ischemia • Hyperventilation should not be abruptly discontinued.

  10. Auto-Regulation of CBF

  11. CBF constant over CPP 50 – 150 mmHg • Below 50mmHg – cerebral ischemia • Above 150mmHg – disruption of BBB • Lag period 30 – 180 sec • Chronic Hypertensives – higher set point. • Impaired by trauma, hypoxia, hypercapnia, ischemia, anesthetics

  12. Mechanism of Autoregulation : • Myogenic Theory : - change in CPP directly change tone of vascular smooth muscle. - Role of NO • Metabolic Theory : - ↓pressure - ↓flow - accumulation of metabolites - ↓ local pH – local vasodilation

  13. PaO2 • Below 50mmHg dramatic rise in cerebral blood flow occurs with further reduction of PaO2

  14. Blood viscosity : • Low hematocrit decreases blood viscosity – increases blood flow • Most obvious in the setting of focal cerebral ischemia • Optimal hematocrit - 30-34% • Not a target of manipulation as it does not reduce the extent of cerebral injury

  15. Effect of Anesthetic drugs • Thiopentone - Dose-dependent decreases CBF & CMRO2 parallel to EEG supression up to iso-electric EEG. - With onset of anesthesia 30% and at iso-electric EEG, 50% decrease in CBF & CMRO2 occurs. - Further increase in dose – no additional effect.

  16. Thiopentone contd. - High dose to cause burst suppression may require vasopressor support. - Tolerance may develop quickly - neuronal metabolism responsible for electrophysiological function is suppressed. - neuronal metabolism responsible for cellular homeostasis is not affected.

  17. Thiopentone contd. - Thiopentone even in high doses dose not abolish cerebral auto-regulation or CO2 reactivity. - Methohexital – may induce seizure in epileptics - ↑ CBF & CMRO2.

  18. Etomidate - Reduces CBF & CMRO2 up to EEG burst suppression - less profound suppression than barbiturates - regional variability in CMR suppression ( predominantly in fore-brain structures) - Myoclonus produced may be misinterpreted as seizure activity - Adrenocortical suppression on prolonged use - CO2 responsiveness preserved

  19. Propofol - Dose related reduction in CBF, CBV & CMRO2 - Substantial reduction in MAP may require vasopressor - Auto-regulation & CO2 responsiveness preserved

  20. Narcotics - Increasing dose progressively decreases CBF & CMRO2 in parallel to progressive slowing of EEG - Burst suppression never achieved - plateau effect - only modest reduction – less than barbiturates and benzodiazepines - sedation, pain control, decrease in arousal may be contributory - presence of control anesthetic

  21. Narcotics contd. - plateau effect is reversible by antagonists - if cerebral vasodilator ( N2O, Halothane) used as control anesthetic - ↓CBF - if vasoconstrictor or no anesthetic is used – usually no effect - Cerebral auto-regulation & CO2 responsiveness maintained

  22. Remifentanil : - low dose (0.05-0.15µg/kg/min) ↑CBF – frontal, parietal, motor cortex ↓CBF – midbrain, cerebellum - higher dose / concominant anesthetics – modest ↓CBF or unaltered CBF.

  23. Ketamine - Increase in CBF & CMRO2 - regional neuro-excitation with concomitant increase in cerebral metabolism - direct cerebral vasodilation - respiratory depression with mild hypercapnia in spontaneously breathing subject - Cerebral auto-regulation & CO2 responsiveness maintained

  24. Benzodiazepines - Small decrease in CBF & CMRO2 even in large doses, ceiling effect may be due to saturation of receptor binding - Effect is less than barbiturates but more than narcotics - Auto-regulation & CO2 responsiveness maintained

  25. Nitrous oxide (N2O) - Administered alone – increases CBF - With barbiturates – effect on CBF attenuated - CMRO2 may be unchanged or increased - Should be considered as a potential cerebro-vasodilator in context of ↑ICP and tight surgical field - CO2 responsiveness preserved

  26. Volatiles : ↓CMRinducedvsdirect vasodilation-induced ↓CBF ↑CBF 0.5MAC - - - 1MAC - - - >1MAC - ↑MAC => ↑CBF Halo >> Enf > Iso ≈ Des > Sevo - ↑MAC => ↓CMR( up to EEG suppression) - ↑ MAC ∞ ↑ CBF/ CMR

  27. Volatiles contd. - CO2 responsiveness is preserved with all - Autoregulation to increasing MAP is impaired - Autoregulation to decreasing MAP is maintaned – clinically more significant

  28. Isoflurane - Increases CBF - Increase in CBF seen in subcortical area - Most potent depressant of CMRO2 - Isoelectric EEG at 2 MAC, reduction in CMRO2 plateaus at this point - Cerebral auto-regulation impaired, CO2 reactivity maintained

  29. Desflurane - Very similar to isoflurane - Dose related decrease in CMRO2 & burst suppression at 2 MAC - Increase in CBF - Cerebral auto-regulation impaired above 1 MAC - CO2 reactivity maintained at 0.5 – 1.5 MAC

  30. Sevoflurane - Very similar to isoflurane - Dose related decrease in CMRO2 & burst suppression at 2 MAC - Increase in CBF - Auto-regulation & CO2 responsiveness maintained at low concentration

  31. Succinylcholine - Increase in CBF & ICP - Secondary to increase in muscle spindle activity with increase in cerebral afferent input – cerebral activation - correlation between observed fasciculation and ↑ICP is poor

  32. Non-Depolarising Muscle-Relaxant - Histamine release by dTC, Atracurium ↓MAP ( due to systemic vasodilation ) ↑ICP ( due to cerebral vasodilation ) ↓CPP - Pancuronium - ↑MAP, ↑ICP ( in case of poor IC compliance and defective auto-regulation)

  33. Thank you www.anaesthesia.co.inanaesthesia.co.in@gmail.com

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