Neuro 1

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  1. What is CMRO2
    cerebral metabolic rate of O2 consumption
  2. Brain wt
    • 1500 g
    • 2% of body weight
  3. How much of the CO and O2 uptake does the brain use?
    • 15% of CO
    • Consumes 20% of O2 uptake
  4. Total cerebral blood flow
    • 750 ml or
    • 50 ml / 100 g/ min
  5. Brain O2 consumption
    60 ml or 0.04 ml / 100 g
  6. Is CMRO2 evenly distributed throughout the brain?
    No, the white matter has low metabolism and the gray matter has increased metabolic activity
  7. How can CMRO2 be measured
    • Theoretically with Fick principle
    • Clinically via MRI
  8. How much ATP is produced in aerobic vs. anaerobic metabolism?
    • Aerobic 38 molecules ATP / 1 molecule glucose
    • Anaerobic 2 ATP / 1 glucose
  9. Does anaerobic metabolism produce enough ATP to meet the brain's metabolic demands?
  10. What are some possible reasons that increased metabolic demand results in increased blood flow?
    • 1) Increased K+ or H+ in brain ECF result in dilation and hence increased flow
    • 2) Ca++/ adenosine/ NO/ prostaglandins help with coupling of increased metabolism leading to increased flow
  11. Intercerebral steal syndrome
    With increased CO2 the arterioles in the brain are maximally dilated and can not dilate any more to direct flow to areas of increased demand (ischemic area).
  12. Robin hood phenomenon
    If pt is hyperventilated or metabolism is decreased due to thiopental there is overall reduction in cerebral blood flow, but vessels in the ischemic area will be dilated due to metabolites and decreased pH in the area causing increased flow.  AKA inverse steal.
  13. What effect does hyperventilation have on cerebral blood flow and CSF pH?  What about on systemic pH?
    • Cerebral blood flow is decreased.
    • CSF pH is increased.
    • Both will normalize within 6-8 hours tho.
    • Systemic alkalosis will continue as long as hyperventilation continues.
  14. In what MAP range does CBF auto regulate?
    • 50-150 mmHg
    • Within this range, cerebral vascular rx adjusts to maintain cerebral blood flow.
  15. What happens to CBF at MAP < 50?  < 40 mmHg?
    • < 50 CBF is reduced
    • < 40 cerebral ischemia occurs
  16. How does auto regulation differ in a HTN pt?
    • The curve is shifted to the right, so a higher pressure is required to maintain CBF.  
    • Caused by hypertrophy of the vessel wall.  
    • Shift may go back towards normal with anti-HTN treatment
  17. Can hypoxia or trauma abolish auto regulation?
  18. How does PaCO2 affect CBF?
    • As PaCO2 increases, so does CBF (linear relationship)
    • Absolute change of 1-2 ml/ 100g/ min for each mmHg change in PaCO2
  19. How does PaO2 affect CBF?
    • PaO2 of >50 mmHg has little effect on CBF
    • PaO2 of < 50 mmHg causes a marked increase in CBF
    • Hypoxemia is a potent VD
  20. Autoregulation of CBF occurs between MAPs of 50-150 mmHg, beyond those limits how does CBF vary?
    • <50 mmHg CBF decreases
    • > 150 mmHg CBF increases
  21. What type of cells form the BBB?
    Brain capillary endothelial cells
  22. What type of junctions make up the BBB?
    Tight junctions that prevent the passage of substances.  Impedes the flow of large molecules (glucose) and ions.
  23. What types of molecules can cross the BBB?
    Gases (volatiles) and lipid soluble compounds
  24. How is glucose transported to the brain
    Via a carrier mediated process- it can only be transported if the concentration in the blood exceeds that of the brain.
  25. Why are intraop hypoglycemia and hypoxia so dangerous?
    • Lack of glucose or O2 causes impairment of neural activity
    • Difficult to recognize s/sx of hypoglycemia under GA
    • Glucose deficiency may result in permanent brain damage
  26. How does the tight junction of the BBB help us therapeutically pull excess water from the brain?
    • Brain edema can be alleviated by giving a large molecule (like mannitol) which does not cross the BBB
    • Or by giving an ion (like 3% NaCl) which also can not cross
    • This produces an osmotic effect drawing fluid from the brain
    • BBB needs to be intact for either to work
  27. What can cause disruption of the BBB?
    • acute hypertension
    • osmotic shock
    • disease
    • tumor
    • radiation
    • trauma
    • ischemia
  28. Where is CSF formed?
    In the choroid plexus of the cerebral ventricles
  29. What type of cells form the blood CSF barrier?
    epithelial cells of the choroid plexus which have tight junctions
  30. CSF volume in the brain
    120 ml
  31. Rate of CSF formation and reabsorption
    0.3-0.4 ml / min
  32. How often does complete replacement of the CSF occur?
    3-4x / day
  33. T or F, the blood-CSF barrier is similar to the BBB in that it allows free movement of water, gases, and lipid-soluble compounds, but it requires carrier mediated transport for glucose and ions
  34. 3 components of the cranial vault
    • 1 brain tissue
    • 2 blood perfusing the brain
    • 3 CSF and ECF
  35. CPP
    CPP = MAP - ICP
  36. What deleterious effects (2) does increased ICP and intracranial volume have?
    • 1 Decreased CPP leading to ischemia
    • 2 Increased ICP can directly cause brain herniation leading to neuro damage and death
  37. Normal ICP
    5-15 mmHg
  38. What is considered intracranial HTN
    ICP > 20 mmHg
  39. How do small increases in ICV affect ICP?
  40. How is intracerebral compliance achieved?
    • CSF is moved from the brain to the spinal space
    • Venous blood is moved from the cranium to the extracranial veins
  41. What factors can increase ICP?
    • 1) Increased brain tissue volume (tumor or edema)
    • 2) Increased CSF / ECF volume (blockage of CSF absorption or circulation)
    • 3) Increased blood volume (VD from volatiles, hypercarbia, hypoxia, hematoma)
  42. How can increased ICP due to increased arterial CBF be managed?
    Decrease CBF (avoid VD due to volatiles, hypercapnea, or hypoxia)
  43. How can increased ICP due to increased venous CBF be managed?
    • Improve cerebral venous drainage (elevating head)
    • Avoid activities which decrease cerebral venous drainage and increase venous engorgement (like coughing or straining against an ETT)
  44. What is the patho behind ischemia to cerebral tissue?
    • Main factor causing damage to neurons under ischemic conditions is reduced energy production
    • Lack of O2 decreases ATP production by 95% / molecule of glucose
    • Lack of ATP leads to loss of energy dependent homeostatic mechanisms (intracellular Na and Ca increase while intracellular K decreases)
    • Ion changes cause the cell to be polarized and excitatory AA (like glutamate) to be released
    • Glutamate causes more depolarization so...
    • More Ca enters the cell which triggers ischemic damage
  45. How does the high intracellular Ca concentration trigger ischemic damage?
    • Increased activity of proteases and phospholipases
    • Increased level of free FA and free radicals
    • Build up of lactate and H+ ions
  46. Why do trauma pts often have high BP?
    Due to SNS stimulation and catecholamine release
  47. Cushing's Triad
    • s/sx of increased ICP
    • HTN
    • bradycardia
    • irregular respirations
  48. What VS abnormalities contribute to poor outcome in head injury pts?
    • Increased ICP
    • SBP < 90 mmHg
  49. 3 categories evaluated with GCS
    • Eye opening
    • Best verbal response
    • Best motor response
  50. GCS minor injury
  51. GCS moderate injury
  52. GCS major injury
    < 9
  53. Epidural hematoma
    • Classic presentation- pt initially appears lucid but then rapidly deteriorates into a coma
    • Usually a skull fracture involved
    • Hematoma between dura mater and the skull
  54. Why do pts with epidural hematomas often experience a lucid period before rapidly deteriorating?
    • Pt bleeds, but then a spasm or clot occurs in the vessel, so bleeding stops temporarily (and the pt becomes lucid)
    • But over the next several hours the bleeding resumes and pt deteriorates
  55. Treatment of epidural hematoma
    Emergency hematoma evacuation
  56. Where do epidural hematomas often occur?
    In the temporal parietal region where the skull fracture interrupts the middle meningeal artery and causes unconsciousness
  57. Subdural hematoma
    • Occur between the dura and arachnoid mater
    • Usually caused by lacerations of the venous sinuses (sudden head deceleration)
    • Usually occur slowly
    • Always causes a degree of brain damage
    • Difficult to distinguish between SAH and SDH
  58. Intracerebral hematoma
    • Collection of blood deep in the brain
    • Usually in the temporal or frontal lobe
    • Usually can't be surgically evacuated and must be medically managed
  59. What type of hemorrhage has the best prognosis
    Epidural hematoma
  60. How are intracranial hematomas best diagnosed?
    CT scan
  61. When is a CT scan indicated in a head injury pt?
    GCS < 15 or LOC
  62. How is a c spine cleared?
    • Not by xray alone (26% fail to show a fracture)!
    • Need normal xray, normal mental status, and asymptomatic pt
  63. T or F, an unconscious pt s/p acute head injury has a stable c-spine?
  64. What drug would be contraindicated for induction for an acute head injury pt?
    Ketamine as it increases CMRO2, CBF, and ICP
  65. What drug would be indicated for induction for an acute head injury pt?
    Propofol- it will decrease CMRO2 and vasoconstrict to lower ICP; but don't want to lower BP, so ok if pt has normal or high BP
  66. Is succ ok to use with an acute head injury pt?
    • Not ideal, but airway control and CO2 control are priorities
    • If have to use, defasciculate first!
    • Succ increases ICP by increasing primary muscle activation with depolarization
    • Can minimize ICP with a defasciculating dose of a non depolarizing NMB!
  67. T or F, hyperventilation should always be used with acute head injury?
    F, it should be used on a selective basis
  68. What are examples of when we might hyperventilation a pt with an acute head injury?
  69. Acute neuro deterioration
    • High ICP refractory to other methods of control
    • Neurosurgery to facilitate surgical exposure per surgeon request
  70. What should CPP be maintained at?  What MAP is needed to maintain this CPP?
    • CPP- > or = to 70 mmHg
    • MAP- > or = to 90 mmHg
  71. Primary treatment of acute severe head injury
    • airway control
    • ventilation to a PCO2 of low normal
    • volume restoration
    • maintain MAP >= 90 mmHg
    • neuro exam
  72. Interventions to treat elevated ICP
    • hyperventilate
    • mannitol
    • foley
    • head CT
  73. Evidence of elevated ICP on CT
    • loss of cisterns
    • mass effect and shift
    • hematoma
  74. TIA
    • sudden vascular related focal neuro deficit
    • resolves within 24 hours
    • evidence of impending stroke (30-40% chance of developing thrombotic stroke within 5 years)
  75. S/sx of TIA suggestive of carotid disease
    • unilateral vision impairment
    • numbness
    • weakness of a single extremity
    • aphasia
  76. S/sx of TIA suggestive of vertebral basilar disease
    • bilateral vision impairment
    • bilateral weakness
    • dizziness
    • ataxia (uncoordinated muscle movement)
    • amnesia
  77. Major arterial blood supply to the brain
    2 pairs of vessels: internal carotid arteries and vertebral arteries
  78. Basilar artery
    • Formed from the vertebral arteries
    • Branches off to form the intracranial vessels
  79. Intracranial vessels
    • Branch off of the basilar artery
    • Anterior cerebral artery
    • Middle cerebral artery
    • Posterior cerebral artery
    • Circle of Willis
  80. What neuro deficits does occlusion of middle cerebral artery produce?
    • -most common in epidural hematoma
    • -contralateral hemiparesis
    • -hemisensory deficit
  81. What neuro deficits does occlusion of vertebral or basilar arteries produce?
    Global symptoms such as aphasia, ataxia, bilateral vision impairment
  82. Can pts with TIAs undergo elective surgery?
    Yes, but need doppler flow studies first
  83. How long post CVA should elective surgery be delayed for?
    • No definite waiting period
    • Usually postponed for at least 6 weeks post stroke
  84. Post stroke changes in cerebral blood flow, CO2 responsiveness, and BBB
    • Regional blood flow and metabolic rate abnormal for 2 weeks post CVA
    • CO2 responsiveness and BBB are not normal for 4 weeks or greater post CVA
  85. In a pt with hemiparesis, on what side should the nerve stimulator be placed on
    Non paretic side
  86. Why should succ be avoided in pts with CVA, SCI, denervation injuries, or extensive muscle wasting? 
    Risk of hyperkalemia due to up-regulation of Ach receptors
  87. How does upregulation of Ach receptors occur?
    Due to decreased release of Ach or blockade of Ach receptors causes a greater number of Ach receptors to be produced.  
  88. In CVA how does up-regulation of Ach receptors occur?  What effect does this have on succ and NDMR?  
    Ach receptors are spread over a large portion of the affected muscle.  Many more ion channels open after administration of such, so this causes increased K+ levels.  Sensitivity to succ.  

    Also, there is resistance to NDMR- related to spread of receptor sites in the extra junctional area. Extrajunctional receptors bind NDMR poorly.  
  89. After SCI, how long does it take for up regulation of Ach receptors to occur?
    4-7 days
  90. What conditions are associated with upregulation of Ach receptors?
    • SCI
    • stroke
    • burns
    • prolonged immobility
    • prolonged exposure to NMB
    • MS
    • Guillian-Barre syndrome
  91. What conditions are associated with DOWNregulation of Ach receptors?
    • Myasthenia gravis
    • Ach poisoning
    • Organophosphate poisoning
  92. After burn injury how long does it take for up regulation to occur?
    Takes 24 hours, so ok to use such immediately after the burn.  
  93. Hydrocephalus
    • Accumulation of excess CSF
    • Obstructive or nonobstructive, usually obstructive
  94. Non obstructive hydrocephalus
    Overproduction of CSF or inadequate absorption of CSF
  95. Where is CSF usually absorbed into?
    Into the venous system by the villi in the arachnoid membrane of the brain.

    When CSF pressure exceeds the pressure in the venous sinuses, the arachnoid villi will allow 1 way flow of CSF from subarachnoid space into the venous system.  
  96. Obstructive hydrocephalus
    Blockage of the arachnoid villi or the foramen connecting the ventricles.  Pressure builds and hydrocephalus develops.  
  97. Hydrocephalus causes
    • congenital
    • neoplastic disease
    • trauma
    • meningitis
    • SAH
  98. V-P shunt
    ventricular-peritoneal shunt to move CSF from the brain ventricles to the peritoneum

    used for treatment of hydrocephalus
  99. Pathway of CSF flow
    • Formed in choroid plexus of the lateral ventricles
    • Passes into 3rd ventricle thru Foramen of Monro
    • Goes along Aqueduct of Sylvius into 4th ventricle
    • Goes out of 4th ventricle thru 3 small openings (2 lateral Foramen of Luschka and midline Foramen of Magendie) into Cisterna Magna (continuous with subarachnoid space)
    • Fluid is reabsorbed from arachnoid villi into venous sinuses and enters the venous blood
  100. S/sx increased ICP
    • H/A
    • N/V
    • MS changes
    • Altered LOC
    • Often occur in early morning (during sleep CO2 increases and VD occurs)
    • Fatigue
    • Drowsiness
    • Vision disturbances
    • Seizures
  101. Generalized seizures
    • Involve bilateral neurons
    • Usually originate from a subcortical or deeper brain focus
    • Consciousness always impaired or lost
  102. Partial seizures
    • AKA focal seizures
    • Involve neurons unilaterally
  103. How do seizures affect O2 and ATP demand?
    • ATP requirement increased 250%
    • Cerebral O2 demand increased 60%
  104. What types of pts are likely to have seizures?
    • Brain tumor
    • Diabetic
    • Seizure disorder
    • Post-op metabolic derangements (hypoglycemia, hyperglycemia, acidosis, hypoxia)
  105. Peri-op management of a pt with a seizure disorder
    • Check labs on emergence and intra-op more frequently
    • Early awakening to check neuro status
    • Continue anti-seizure meds to maintain therapeutic levels
    • Avoid eliptogenic drugs
  106. If a pt is on Dilantin, how will this affect metabolism of anesthetic drugs?
    Dilantin causes enzyme induction so metabolism will be sped up
  107. Drugs that do not lower the seizure threshold or predispose seizure activity
    • barbs
    • opioids
    • benzos
    • volatiles except enflurane
  108. Drugs that DO lower the seizure threshold or predispose seizure activity
    ketamine, brevital, and enflurane

    atracurium and cisatrocurium have a metabolite called laudanosine which has CNS stimulating effects
  109. How does hyperventilation affect the seizure threshold?
    It lowers it
  110. Seizure complications
    • aspiration
    • hypoxemia
    • cerebral injury from prolonged hypoxemia 
    • hypotension
    • resp depression from anti-convulsant therapy
Card Set:
Neuro 1
2013-10-07 14:57:17
BC NU 590

BC Nurse Anesthesia
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