1 / 34

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

zelig
Télécharger la présentation

Physiology of Cerebral Circulation Presenters – Dr. Dalim

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related