Neurophysiology and Cerebral Blood Flow Regulation in Anaesthesia
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The document discusses neurophysiology and factors controlling cerebral blood flow (CBF). Some key points: - The brain has high metabolic needs but no oxygen storage, so it relies on continuous CBF. CBF parallels metabolic activity and averages 50 ml/100g/min. - CBF is controlled by cerebral perfusion pressure (CPP), which depends on mean arterial pressure and intracranial pressure. Autoregulation normally keeps CBF constant over a wide range of pressures. - Important factors influencing CBF include carbon dioxide, which causes vasodilation; oxygen; hematocrit; temperature; and anesthetic agents, many of which are cerebral vasodilators. Barbiturates
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Neurophysiology and Cerebral Blood Flow Regulation in Anaesthesia
- 2. Peculiarities of brain Has a high metabolic rate Has no oxygen stores Unable to maintain its integrity through anaerobic metabolism Neurons don’t require insulin for transport of glucose across cell membrane
- 3. Neurophysiology 2% of body weight 17%-20% of Cardiac output consumption at rest 20% of inspired oxygen 60% - for neuronal activity 40% - to maintain cellular integrity CMR / CMRO2 - 3-3.8ml/100g/min 50ml/min Cerebral glucose consumption - 5mg/100g/min
- 4. cerebral blood flow 80% - Internal carotid arteries 20% - Vertebral arteries Anterior n posterior communicating arteries Circle of Willis Communication between exl & int carotids – opthalmic arteries
- 6. Physiology of CBF Parallels with metabolic activity Can vary from 10 – 300 ml/100g/min Average – 50ml/100g/min Gray matter – 80ml/100g/min White matter- 20ml/100g/min Total CBF- averages 750ml/min < 20-25ml/100g/min- ischemia
- 7. Cerebral blood flow Flow rates below 20-25ml/100g/min slowing of EEG. Flow rates between 15-20ml/100g/min flattening of EEG. Flow rates below 10ml/100g/min irreversible brain damage.
- 9. Cerebral perfusion pressure CPP is the difference between Mean arterial pressure and intracranial pressure (or cerebral venous pressure, which ever is greater) CPP = MAP – ICP
- 10. CPP = MAP - ICP Normal CPP – 80 to 100mmHg More dependent on MAP ICP > 30mmHg compromise CPP CPP < 50mmHg – slowing of EEG 25 – 40 mmHg – flat EEG < 25 mmHg – irreversible brain damage
- 11. Cerebral auto regulation Ability of the cerebral blood vessels to alter their caliber in order to maintain a constant flow in face of variations in blood pressure
- 12. Cerebral auto regulation CBF is kept constant over a wide range of MAP ( 60 – 160 mm Hg ) CPP = MAP – Ven Press = MAP - ICP ↑ MAP Cerebral vasoconstriction ↓ MAP Cerebral vasodilatation Constant CBF is maintained
- 13. Cerebral auto regulation graph Pressures above 160mmHg Disrupts BBB Cerebral edema Haemorrhage
- 14. Auto regulation…… The cerebral vasculature rapidly adapts to change in CPP. (10 - 60 sec) In Hypertensive persons cerebral autoregulation curve shifts to higher pressure levels : 180 – 200mm Hg and towards right.
- 15. Changes in autoregulation Absent ( Vasomotor paralysis ) brain trauma surgical retraction high ICP brain tumor seizures Shift to right Systemic hypertension States of sympathetic activation Shift to left Volatile anesthetic agents
- 16. FACTORS CONTROLLING CBF Intrinsic factors Myogenic Regulation Metabolic Regulation Neuronal Regulation Hormonal regulation Extrinsic factors Respiratory gas Arterial BP Hematocrit Temperature
- 17. Myogenic factors Is the intrinsic response of smooth muscle cells in cerebral arterioles to changes in MAP Protective mechanism against excessive pressure fluctuation at capillary level
- 18. Metabolic regulation Hydrogen ions potassium adenosine prostanoids ↑ CO2 ↑ H+ ↑ K+ ↑ Adenosine EDRF / Nitric Oxide
- 19. Innervation The sympathetic fibers arise mainly from the superior cervical ganglion The parasympathetic from the sphenopalatine and otic ganglia Sensory fibers from the trigeminal ganglion
- 20. Neuronal regulation α-Adrenergic receptors in arterial smooth muscle Postganglionic sympathetic fibers release noradrenaline Causes smooth muscle contraction and arterial constriction Sympathetic innervation is responsible for vascular tone
- 21. Sympathetic Large & Medium sized arteries normally overridden by autoregulation Historically thought to have no role in cerebral circulation Comes into play in states of excessive circulatory activity / pathologic states Role in prevention of cerebral haemorrhage – cerebral vasospasm
- 22. Hormonal regulation Adrenaline Vasopressin Angiotensin II
- 23. Effect of CO2 on CBF CBF œ PaCO2 between 20 – 80 mmHg 1mmHg ↑↓ PaCO2-↑↓ CBF by 1-2ml/100g/min After 24 – 48 hrs CSF HCO3- compensation limits the effects of hypocapnia/ hypercapnia Persistent hyperventilation Leftward shift of oxy-Hb dissociation curve and marked changes in CBF cerebral impairment
- 24. Hypercarbia - CBF The relationship between PaCO2 and CBF is sigmoid with plateaus below 25 mmHg and above 75 mmHg. The slope is approximately linear
- 25. Mechanism of CO2 on CBF The mechanism of CO2 induced changes in vessel caliber An increase in perivascular H+ concentration Associated NOS activation An increase in intracellular cGMP K+ efflux A reduction in intracellular Ca + + resulting in dilation NOS inhibition attenuates the Cyclooxygenase inhibition CBF response to CO2
- 26. Effect of oxygen Hyperoxia – minimal decrease in CBF 10% Severe hypoxia – PaO2 < 50mmHg Increases CBF
- 27. Haematocrit in haematocrit viscosity CBF O2 carrying capacity haematocrit viscosity CBF Optimal haematocrit – 30% to 34%
- 28. Temperature CBF changes 5- 7% per O C Hypothermia CBF & CMR Pyrexia has reverse effect
- 29. Intracranial pressure “ICP means supra tentorial CSF pressure measured in the lateral ventricles or over the cerebral cortex and is normally less than 10mmHg.” Minor variations may occur depending on site measurement but, in lateral recumbent position, lumbar CSFpressure normally approximates supratentorial pressure.
- 30. Intracranial pressure MONRO-KELLIE DOCTRINEMONRO-KELLIE DOCTRINE The cranial vault is a rigid structure with fixed volume Brain 80% Blood 12% CSF 8% Any increase in one component must be offset by an equivalent decrease in another to prevent rise in ICP
- 31. Intracranial pressure ICP normally 10mmHg and less. Intracranial elastance determined by measuring the change in ICP in response to change in intracranial volume Initially increases in volume are initially well compensated until it reaches a point which further increase can cause rise in ICP
- 33. Intracranial pressure Major compensatory mechanisms include a)Displacement of CSF from cranial to spinal compartment b)An increase in CSF resorption c)Decrease in CSF production d)Decrease in total cerebral blood volume
- 34. Applied aspects Effects of anesthetic drugs on CBF Volatile anesthetics Induction agents Anesthetic adjuncts Vasopressors Vasodilators Neuromuscular blocking agents
- 35. Volatile agents Volatile agents – dose dependent dilatation of cerebral vessels Impair auto regulation Response to CO2 retained May increase cerebral blood volume May result in elevated ICP
- 36. Halothane Has greatest effect on CBF Con.> 1% - abolishes auto regulation Generalized increase in CBF At equivalent MAC CBF up to 200% Prior hyperventilation to be initiated Isoflurane CBF Auto regulation maintained up to 1 MAC is > in sub cortical than neocortical areas At equivalent MAC CBF up to 20% Simultaneous hyperventilation can prevent in ICP
- 37. Sevoflurane: CBF effects similar to isoflurane Produce slightly less vasodilation Auto regulation maintained up to 1.5 MAC Desflurane: CBF similar to isoflurane Autoregulation progressively abolished as dose increases
- 38. Nitrous Oxide: When administered on its own- increases both CBF and metabolism. when added to a background of another anesthetic, it increases CBF without changing metabolism It is a direct acting and potent cerebral vasodilator
- 39. IV induction agents Intravenous anesthetics reduce CBF in a dose dependent fashion coupled to the reduction in metabolism Once maximal suppression of metabolism occurs, no further reduction in CBF occurs
- 40. Barbiturates Barbiturates maximal 50% reduction in CBF and metabolism CO2 reactivity is maintained but is quantitatively reduced compared to the awake response Cerebral auto regulation maintained intact
- 41. Propofol Propofol produces a coupled dose dependent reduction in CMRO2 and CBF High doses vasodilator effect overcomes the coupling & CBF increases Both CO2 responses and auto regulation are maintained intact in the normal brain In head injured patients static auto regulation may be impaired by high propofol infusion rates
- 42. Ketamine Dilates the cerebral vasculature and increases CBF ( 50 – 60%) Increases in CBF, CBV, CSF volume can increase ICP markedly in patients with decreased IC compliance
- 43. Opioids Opioids at low doses produce very little effect on CBF (provided CO2 is not allowed to rise) Auto regulation remains intact Some opioids in ICP BP vasodilatation to maintain CBF cerebral blood volume increase intracranial pressure.
- 44. Vasopressors With intact auto regulation & BBB in CBF occurs when MAP<50 -60mmHg MAP>150 – 160mmHg In the absence of auto regulation, vasopressors CBF by direct effect on CPP.
- 45. Vasodilators In the absence of hypotension Cerebral vasodilatation CBF With Hypotension CBF is maintained or increased CBV & ICP in patients with IC compliance
- 46. NMBD No direct effect on CBF Histamine releasing agents can cause hypotension , CPP
- 47. What is Luxury perfusion ? Intra cerebral steal ? Reverse steal phenomenon ?
- 48. Luxury perfusion The combination of a decrease in CMRO2 and increase in CBF has been termed luxury perfusion met. Demand met. Supply
- 49. Luxury perfusion… Seen in Acute cerebral infarction Vessels – max. dilated Induced hypotension with isoflurane
- 50. Intracerebral Steal In a setting of focal ischemia , vasodilatation in a normal area would shunt blood away from the diseased area. ischemic normal
- 51. Steal Seen in in PaCO2 in cerebral ischemia Volatile anesthetic agents Results in vasodilatation in normal areas not in ischemic areas
- 53. Reverse Steal phenomenon Diversion or redistribution of blood flow from normal to ischemic areas in the brain is termed Reverse Steal / Robin Hood phenomenon ischemicnormal
- 54. Thank you