Neurophysiology and anesthesia point of view

Neurophysiologie on anesthesia

1. Neurophysiology and anaesthesia Dr. Ibrahim Elkathiri

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 / CMRO 2 - 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

5. Circle of willis

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 .

8. FACTORS CONTROLLING CBF

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 CO 2 on CBF CBF œ PaCO2 between 20 – 80 mmHg 1mmHg ↑↓ PaCO2-↑↓ CBF by 1-2ml/100g/min After 24 – 48 hrs CSF HCO 3 - 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 CO 2 on CBF The mechanism of CO 2 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 CO 2

26. Effect of oxygen Hyperoxia – minimal decrease in CBF 10% Severe hypoxia – PaO 2 < 50mmHg Increases CBF

27. Haematocrit in haematocrit viscosity CBF O 2 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 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

32. Intracranial elastance

33. Intracranial pressure Major compensatory mechanisms include Displacement of CSF from cranial to spinal compartment An increase in CSF resorption Decrease in CSF production 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 CO 2 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 CMRO 2 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 CMRO 2 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 PaCO 2 in cerebral ischemia Volatile anesthetic agents Results in vasodilatation in normal areas not in ischemic areas

52. Reverse Steal phenomenon Diversion or redistribution of blood flow from normal to ischemic areas in the brain is termed Reverse Steal / Robin Hood phenomenon ischemic normal

53. Surgery for Brain Tumors

54. Glasgow coma scale 1. Severe, GCS < 8–9 (In trauma, a GCS of 8 or less indicates a need for endotracheal intubation) 2. Moderate, GCS 9–12 3. Minor, GCS ≥ 13

55. Cerebral Aneurysm Surgery

56. Trans- sphenoidal Surgery

57. Cont ,

58. Awake Craniotomy (Temporal lobe surgery)

59. Cont ,

60. Cont ,

61. Anesthesia for Traumatic Brain Injury 1 . is defined as trauma to the head other than superficial injuries 2. Maintenance of airway and breathing is of paramount significance in critical care setting and more importantly for patients with head injury as brain is very sensitive to the effects of hypoxemia and hypercapnia 3. Maintenance of cerebral blood flow has to be adequate to avoid cerebral ischemia, thereby minimizing secondary injury to brain. Hypotension, hypoxia, raised ICP and anemia should be avoided.

62. Cont , TBI 4. There is 10% incidence of unstable cervical spine injury with TBI. Risk factors include GCS score less than 8 and motor vehicle accident. Thus manual in line stabilization should be maintained to avoid neurological damage 5. Patients with TBI should be orally intubated because of potential presence of basilar skull fracture, risk of which may be exacerbated with nasal intubation

63. Cont , 6 . All intravenous induction agents except ketamine cause a fall in CBF, CMRO2 and ICP. Etomidate causes a little change in blood pressure despite reducing CMRO2 and may be advantageous but may lead to adrenal insufficiency leading to delayed hypotension

64. Cont , TBI 7. Risk of aspiration during airway procedure should be minimized. Administration of Muscle relaxant prevents coughing thereby preventing sudden increase in ICP. Argument against succinyl choline is the potential to increase ICP, however the suspected rise of ICP is only transient and may be blunted with adequate dose of induction agent such as thiopentone

65. Cont , TBI 8 . Hypotension is extremely detrimental to brain. Goal is to maintain SBP above 90 mmHg, CPP in range of 50-70 mmHg. In absence of ICP monitoring an ICP of 20 mmHg should be assumed and MAP should be kept above 60 mmHg.

66. Cont , 9. The optimal Hemoglobin level in TBI patients is still unclear but there is no benefit of a liberal transfusion strategy (transfusion when Hb <10 g/dl) in moderate to severe TBI patients and it is not recommended.

67. Cont , TBI 10 . Reduction of ICP in patients with head injuries can be accomplished effectively using osmotic diuretics. a. Mannitol is the most commonly used agent (0.25 to 1 g/kg) and is available for IV administration in either a 20% or 25% solution. With repeated doses one must be cautious that serum osmolarity should not be allowed to exceed 320 mOsm . Intravascular volume depletion should be avoided. b. In patients with severe TBI and elevated ICP refractory to mannitol treatment, 7.5% hypertonic saline administered as second tier therapy can increase cerebral oxygenation and improve cerebral and systemic hemodynamics.

68. Cont , TBI c. Hyperventilation is an effective way to reduce ICP. It is useful in the setting of an acutely increased ICP that needs to be controlled until more definitive therapy can be initiated. d. Barbiturates may be used as an adjunct to other therapy for controlling ICP. Barbiturate therapy is appropriate only in patients who are hemodynamically stable and have been adequately resuscitated. Propofol is a reasonable alternative to barbiturates for ICP management. e. Current recommendations are that patients with TBI should be maintained at normocapnia except when hypocapnia is necessary to control acute increases in ICP.

69. Cont , TBI 11 . Coagulation disorders are a common problem after TBI . Hemostatic drugs such as antifibrinolytics , such as trenaxamic acid and procoagulants such as recombinant factor VII are sometimes used in treatment of coagulopathy after TBI.

70. Cont , TBI 12. Hyperglycemia after TBI is associated with increased morbidity and mortality. Tight glucose control with intensive insulin therapy remains controversial due to recurring dangerous episodes of hypoglycemia. Evidence shows a target glucose range of 80–180 mg/dl seems reasonable in postoperative period .

71. Cont , TBI 13. Patients may present with head injuries in isolation or in conjunction with other injuries. Up to 50% of patients with severe traumatic brain injury have major extra cranial injuries. As a result the presence of coexisting injuries should be actively sought and excluded. A systematic approach to evaluation and initial management, such as that proposed by Advanced Trauma Life Support, should be adopted for these patients .

72. Cont , 14. Prophylactic hypothermia is of no use unless it is maintained for more than 48 hrs (decreases mortality). 15. High dose methyl prednisolone is of no use in moderate to severe TBI, rather it increases mortality.

73. Referance Morgan and Mikhails clinical anesthesiology 7 th edition Anesthesia for neurosurgery (Part II) by Lalit Gupta1, Bhavna Gupta, Indian Journal of Clinical Anaesthesia , July-September, 2018;5(3):299-305

74. Thank you