NEUROMONITRING IN ANESTHESIOLOGY USING DIFFERENT BRAIN FUNCTIONING MONITORING DEVICES. CEREBRAL PROTECTIVE AGENTS PERIOPERATIVELY

1. NEUROPROTECTION AND
NEUROMONITORING
MODERATOR: DR KISHORE KEERTHY
CHAIRPERSON: DR VIJAYANAND S
PRESENTER: DR NEELAMBIKA RAGATE

2. • The brain normally consumes 20% of total body oxygen.
• Relatively high oxygen consumption and the absence of significant oxygen
reserves, interruption of cerebral perfusion usually results in unconsciousness
within 10 sec, as oxygen tension rapidly drops below 30 mm Hg. If blood flow is
not reestablished within 3–8 min under most conditions, ATP stores are depleted,
and irreversible cellular injury begins to occur.
60% cerebral oxygen : NEURONAL ELECTRICAL
ACTIVITY
40%: Maintains CELLULAR INTEGRITY

3. • Cerebral metabolic rate of O2 consumption (CMRO2) ~ 3–3.8 mL/100 g/min (50
mL/min)
• Total CBF averages 50 mL/100 g/min,
• Flow in gray matter is about 80 mL/100 g/min,
• white matter is estimated to be 20 mL/ 100 g/min.
• Total CBF in adults averages 750 mL/min (15% to 20% of cardiac output).
• CBF below 20–25 mL/100 g/min : Cerebral impairment,
evidenced by slowing on the electroencephalogram (EEG).
• CBF rates between 15 and 20 mL/100 g/min typically produce a flat (isoelectric)
EEG, whereas
• Rates below 10 mL/ 100 g/min are usually associated with irreversible brain
damage.

6. CEREBRAL PROTECTION
Includes measures instituted before or after an insult to prevent or ameliorate the
harmful effects on the brain for a known cerebral insult.
High requirement of glucose(5.5mg/100g/min) and oxygen(3.5ml/100g/min) by
the neuronal tissue makes it prone for ischemic and hypoxic injury.
GOALS:
• INCREASE OXYGEN SUPPLY
• DECREASE OXYGEN DEMAND

9. CEREBRAL PROTECTION MODALITIES:
1.MEASURES TO DECREASE CEREBRAL METABOLISM:
• Physiological(hypothermia) and Pharmacological
2. MEASURES TO INCREASE MICROCIRCULATORY FLOW:
• Induced hypertension
• Hemodilution
• Anticoagulants
3.REDUCTION OF SECONDARY INJURY:
• Calcium channel blockers
• Excitatory amino acid antagonists
• Free radical scavengers
• Prostaglandin inhibitors
• Steroids

10. 1. Maintain physiologic parameters:
i. AVOID hyperthermia:
Increase temperature  Increase CMRO2  exacerbate
ischemia.
ii. AVOID Hyperglycemia and Hypoglycemia:
Hyperglycemia aggravates ischemia by worsening lactic
acidosis.
Hypoglycemia= Ischemic brain injury by reduced ATP
formation.
Persistence Seizure activity and neuronal injury.

11. iii. AVOID hypotension, hypoxia and hypercapnia
iv.NORMALISATION OF RAISED ICP:
• Moderate hyperventilation to PaCO2 of 25-30mm hg.
Hyperventilation is a temporary measure to reduce CBF.
• Head end elevation to 30 degree.
• Mannitol/ furosemide diuresis
• CSF drainage via ventriculostomy.
• Limited fluid restriction.

12. v. PROMPT correction of acidosis and electrolyte imbalance.
vi. AVOID high hematocrit/ hypercoagulable state:
• HEMODILUTION: Hct of 32-34% increases CBF by decreasing viscosity.
Hence O2 delivery improves.
NOTE: Excessive dilution reduces oxygen carrying capacity of blood.
• ANTICOAGULATION
iv. rTPA(recombinant tissue plasminogen activator):
• IV rTPA 0.9mg/kg,max dose 90mg for selected patients, treated within 3hrs of
onset of ischemic stroke
• Recent updates: administered within 3 - 4.5 hrs after onset of stroke.

13. 2. HYPOTHERMIA:
• Decreases both functional and metabolic activities of the brain
• CMRO2 changes every 10 degree change in temperature.
• For most biological rxns
CMRO2 reduces by 50% for every 10 degree reduction in temperature
• Neuroprotection from mild to mod hyperthermia: mechanism is multifactorial:
• CMR reduces
• Metabolism downregulation
• Reduced calcium influx
• Reduced EAA release
• Prevention of lipid peroxidation
• Decrease in edema fluid
• Modulation of inflammatory response
• Apoptotic cell death

14. • Hypothermia needs to be instituted early, defined endpoint maintained for
prolonged time.
• COMPLICATIONS OF HYPOTHERMIA:
a) CVS: myocardial depression, dysrhythmia, hypotension, Inadequate tissue
perfusion.
b) COAGULATION: thrombocytopenia, fibrinolysis, platelet dysfunstion.
c) Metabolism of drugs is delayed.
d) Shivering: O2 desaturation, increase in O2 demand and increased CO2
production.

15. 3. ANAESTHETIC DRUGS AND ADJUVANTS:
• BARBITUARATES:
• Produce isoelectric eeg.
• To treat cerebral edema resistant to other approaches
i. THIOPENTAL:
• Reduces CMRO2( upto 55%), CBF, CBV and ICP.
• CO2 reactivity: Preserved.
• Effective anticonvulsant

16. • Mechanism:
a) Gaba antagonism
b) Free radical scavenging
c) Reduced membrane lipid peroxidation and damage.
d) NMDA antagonism
e) Calcium channel blockade
f) Maintenance of protein synthesis.
• Dose for focal ischemia: 3-5mg/kg titrated every 5-10 mins to EEG burst
suppression upto 15-20mg/kg.

17. ii. PENTOBARBITAL:
• Longer acting, duration of action:3-4hrs
• Elimination t1/2: 15-50hrs
• Current clinical indication:
• Barbituarate coma in pts with increased ICP resistant to standard therapy.
• Loading dose: 3-10mg/kg over 0.5-3hrs
• Maintenance infusion:0.5-3mg/kg/hr titrated to EEG burst suppression.
• Therapeutic plasma conc. : 2.5-4mg/dL

18. • ETOMIDATE:
• Cerebral vasoconstriction
• EEG burst suppression with higher doses
• Reduces CMRO2 (50%), CBF and ICP.
• CO2 reactivity: preserved
• Myoclonic activity and seizures may occur.
• PROPOFOL:
• Reduces CMRO2,ICP and CBF
• Reduction of CBF is larger than the reduction of CMRO2.
• Reduction in CPP greater than with barbituarates
• Maintain MAP and CPP when propofol is given.

19. • Propofol interferes minimally with electrophysiologic monitoring including MEP.
• Burst suppression of EEG with large doses of propofol.
• BENZODIAZEPINES:
• Enhance inhibitory Gaba neurotransmission and reduced CMRO2 and CBF while
preserving CO2 reactivity.
• DEXMEDETOMEDINE: reduces CBF without significantly aletring CMRO2.
• KETAMINE:
• Markedly increases ICP and CBF(60%) via cerebrovasodilatation.
• CMRO2 unchanged/slightly reduced.
• Autoregulation is abolished.
• Seizures can occur.
• Non competitive NMDA antagonist, not recommeneded for patients with
intracranial pathology.

20. • LIDOCAINE:
• Sodium channel blocking drugs.
• Seizures at toxic doses.
• Reduces CMRO2 with non seizure inducing doses.
• With pentobarbital lidocaine may reduce CMRO2 by additional 15-20%.

21. INHALATIONALANESTHETICS
• Cerebrovasodilators, hence increase CBF and ICP
• Effect can be attenuated by prior hyperventilation.
• Reduce CMRO2
• CO2 reactivity preserved.
• Delay neuronal death.
• Reduce ischemic cerebral injury.

22. • ISOFLURANE:
• Large reduction in CMRO2(40-50%)
• Small increase in CBF
• Isoelectric EEG at 2 MAC-2.4MAC
• No effect on production of CSF, increase CSF resorption.
• SEVOFLURANE:
• Slight increase in CBF and ICP.
• Reduction in CMRO2
• Nephrotoxic inorganic fluoride may accumulate
• Rapid induction and emergence.

23. • DESFLURANE:
• ICP may increase
• May be protective after brain ischemia
• NITROUS OXIDE:
• Increase in CBF, CMRO2, ICP
• Increase in CBF attenuated by hypocapnia and IV drugs(barbituarates, opioids,
benzodiazepines, propofol)
• N2O diffuses into air containing body cavities, can enlarge air embolus.
• Avoided in pneumocephalus, in any surgery within 2wks of craniotomy.

24. • ANTICONVULSANT DRUGS:
• Seizure activity exacerbated effects of ischemia
• CBF, CMRO2, intracellular calcium increase during seizures.
• Once seizures occurs, patients airway must be secured immediately.
• Adequate ventilation
• Midazolam:1-5mg
• Thiopental:25-100mg
• Pentobarbital:100mg(upto 500mg)
• Fosphenytoin: 15-20mg/kg or Phenytoin 15mg/kg
• 75mg fosphenytoin~ 50mg phenytoin
• Phenytoin administration limited to 50mg/min as it may induce hypotension
• Loading dose of fosphenytoin in 5-7mins compared to 15-20 mins of equivalent
phenytoin dose.

25. • CALCIUM CHANNEL BLOCKERS:
• Cause vasodilatation
• Diminution of consequences of calcium influx
• Recommended for prophylaxis against cerebral vasospasm after aneurysmal SAH.
• NIMODIPPINE: decreases incidence and severity of vasospasm
• Oral form:60mg Q4h for 21days.
• Do not give IV nimodipine
• Blocking influx into vascular smooth muscle and hypercontraction.
• MAGNESIUM: reduces calcium influx into cells.
• Blocks transmitter release and NMDA channels.

26. • GLUTAMATE RECEPTOR ANTAGONIST:
• Prevents neuronal damage from excessive accumulation of excitatory
neurotransmitter glutamate.
• Magnesium and Xenon.
• SODIUM CHANNEL BLOCKING DRUGS:
• Riluzole: may reduce glutamate release during ischemia.
• Lamotrigine: Na+ channel blocking activity  may reduce ischemic damage.
• Lidocaine: clinical studies have been ambiguous, ?improve neurologic recovery.
• TIRILAZAD: lipid soluble 21 aminosteroid, crosses blood brain barrier.
• Lipid antioxidant, inhibits free radical formation and lipid peroxidation.
• No clinical trials have shown improved outcome after stroke.

27. • FREE RADICAL SCAVENGERS: SOD, Desferoxamine, vitamin E, mannitol
and glucocorticoids.
• Limitation of SOD: short elimination(t1/2:8mins( and poor blood brain barrier
penetration.
• Glucocorticoids: membrane stabilising properties, reduce cerebral edema from
brain tumours, no improved clinical outcome in stroke.
• MODIFICATION OF ARACHIDONIC ACID SYNTHESIS:
• Thromboxane synthesis inhibitors and PGI2 synthetase stimulation to prevent
excessive cerebral vasoconstriction.

28. • NO SYNTHASE: catalyzes formation of NO, decreases neuronal damage, 3 forms
i. Neuronal NOS: enhances glutamate release, NMDA mediated neurotoxicity.
Selective nNOS inhibitors: neuroprotective.
ii. Immunologic NOS(iNOS): causes delayed neuronal cell death, can exacerbate
glutamate excitotoxicity.
Inhibition of iNOS by aminoguanidine reduces ischemic damage in experimental
models.
iii. Endothelial NOS:stimulation by an ischemia induced increase in intracellular
Calcium improves CBF by dilatation of cerebral blood vessels.
• ERYTHROPOIETIN:
• Reduce inflammation, inhibit neuronal apoptosis, stimulate neurogenesis,angiogenesis and
production of the protein of repair.

29. NEUROMONITORING
• There are four key principles of intraoperative neurologic monitoring.
• The pathway at risk during the surgical procedure must be amenable to
monitoring.
• The monitor must provide reliable and reproducible data.
• If evidence of injury to the pathway is detected, there must be some intervention
possible.
• If changes in the neurologic monitor are detected, and no intervention is
possible, although the monitor may be of prognostic value, it does not have the
potential to provide direct benefit to the patient from early detection of impending
neurologic injury.

30. BRAIN FUNCTION MONITORING
ELECTROPHYSIOLOGY
EEG
PROCESSED EEG:
•BIS
ENTROPY
PATIENT SAFETY
INDEX
NARCOTREND
EVOKED
POTENTIALS
SENSORY
MOTOR
CRANIAL NERVE
INTRACRANIAL
HEMODYNAMICS
CEREBRAL BLOOD FLOW :
INTRACRANIAL
PRESSURE
MONITORING
METABOLISM
CEREBRAL OXYGENATION
INVASIVE:
JUGULAR VENOUS OXIMETRY
BRAIN TISSUE OXYGENATION
NON INVASIVE:
NIRS
INTRACRANIAL
BIOCHEMISTRY
NEURONAL BIOMARKERS

31. • The brain can be monitored in terms of:
Function
Cerebral blood flow (CBF) & intracranial pressure (ICP)
Brain oxygenation and metabolism

32. MONITORING OF FUNCTION
Electroencephalograms (EEG):
 Raw EEG
 Computerized Processed EEG: Compressed spectral array, Density spectral array, Aperiodic
analysis, Bispectral analysis (BIS)
Evoked Potential :
Sensory EP:
 Somatosensory EP
 Visual EP
 Brain stem auditory EP
Motor EP:
 Transcranial magnetic MEP
 Transcranial electric MEP –
 Direct spinal cord stimulation
 EMG - Cranial nerve function (V, VII, IX, X, XI, XII)

33. ELECTROENCEPHALOGRAM
• Surface recordings of the summation of
excitatory and inhibitory postsynaptic
potentials generated by pyramidal cells in
cerebral cortex.
• EEG:
 Measures electrical function of brain
 Indirectly measures blood flow
 Measures anesthetic effects

34.  Electrodes placed so that mapping system relates surface head anatomy to underlying
brain cortical
• regions.
3 parameters of the signal:
• Amplitude – size or voltage of signal
• Frequency – number of times signal oscillates
• Time – duration of the sampling of the signal

35. • EEG Waves :
• Beta: high frequency , low amp (awake
state)
• Alpha: med frequency, high amp (eyes
closed while awake)
• Theta: Low frequency (not
predominant)
• Delta: very low frequency high amp
(depressed functions/deep
coma)

36. Regional problems - asymmetry in frequency, amplitude or unpredicted patterns
of such
• Epilepsy – high voltage spike with slow waves.
• Ischemia – slowing frequency with preservation of amplitude or loss of amplitude
(severe)
Global problems – affects entire brain, symmetric abnormalities. Anesthetic
agents induce global changes similar to global ischemia or hypoxemia (control of
anesthetic technique is important.)

37. Subanesthetic doses of inhaled anesthetics (0.3 MAC):Increases frontal beta
activity (low voltage, high frequency)
Light anesthesia (0.5 MAC): Larger voltage, slower frequency
General anesthesia (1 MAC): Irregular slow activity
Deeper anesthesia (1.25 MAC):Alternating activity
Very deep anesthesia (1.6 MAC): Burst suppression eventually isoelectric

39. BISPECTRAL INDEX
• 1994 by Aspect Medical systems
• To monitor anesthetic state in patients receiving GA and sedation.
• Development of BIS:
i. Collection of more than 2000 high fidelity EEG recordings from patients
receiving a wide range of anesthetic techniques.
ii. Segments of EEG in these records were used to compute bispectral and power
variables.
iii. These variables were correlated with a clinical score that represented level of
hypnosis and sedation.

40. • BIS algorithm is proprietary hence actual computation is not public knowledge.
• BIS combines information from 3 EEG analyses;
a) SPECTROGRAM: decomposition of EEG into power content by frequency as a
function of time.
b) BISPECTRUM: degree of non linear coupling between pairs of frequencies.
c) TIME DOMAIN ASSESSMENT OF BURST SUPPRESSION.
• Index value of BIS: 0-100
• For most anesthetics EEG shows low frequency, high amplitude oscillations as
patients achieve deeper states of unconsciousness; exceptions are:
i. Ketamine: prominent high frequency oscillations, but unconsciousness
ii. Dexmedtomedine: low oscillations,reduction in beta oscillations.BIS values in
unconscious ranges but patient is arousable.
iii. Nitrous oxide: increases amplitude of low frequency EEG and decreases
amplitude of low frequency EEG.

41. • BIS in older adults
• BIS works poorly in older adults as in this age patients tend to have lower
amplitude oscillations
• BIS can interpret as awake state/unconsciousness.
• Children have much more power across a broader range of frequency bands.
• Hence children may be well anesthetised, but BIS algorithm provides numbers
suggesting sedation rather than unconsciousness.

45. ENTROPY
• Degree of randomisation of EEG.
• As level of consciousness decreases EEG becomes less random and more regular
Entropy reduces.
• Entropy monitor has 2 component:
• State entropy(SE)
• Response entropy(RE)
• State entropy:corresponds to cortical activity
• Tracks EEG changes in 0.8-32Hz.
• Response entropy: describes electromyographic activity
• Tracks eeg power changes in 0.8-47Hz
• RE declines faster than SE when patient is profoundly unconscious
• RE:0-100
• SE-0-91

48. NON ANESTHETIC FACTORS AFFECTING EEG
SURGICAL PATHOPHYSIOLOGIC
1. Cardiopulmonary bypass 1. Hypoxemia
2. Occlusion of major cerebral 2. Hypotension
vessel (carotid cross-clamping, 3.Hypothermia
aneurysm clipping) 4. Hypercarbia and
3. Retraction on cerebral cortex hypocarbia
4. Surgically induced emboli to
brain

49. USES OF EEG
• 1. Carotid endarterectomy
• 2. Cerebral aneurysm surgery when temporary clipping is
• used.
• 3. Cardiopulmonary bypass procedure
• 4. Extracranial-intracranial bypass procedure
• 5. Deliberate metabolic suppression for cerebral protection.
• 6.Surgeries that place the brain at risk (difficulties: restricted
• access)
• 7. Seizure monitoring in ICU

50. PROCESSED EEG
• The gold standard for intra-op EEG monitoring:
• continuous visual inspection of a 16- to 32-channel analog EEG by
experienced electroencephalographer
• “Processed EEG”: methods of converting raw EEG to a plot showing
voltage, frequency, and time.
• Monitors fewer channels, less experience required.
• Reasonable results obtained.

51. • Electrical activity generated in response to
sensory or motor stimulus
Stimulus is given, then neural response is
recorded at different points along pathway
• Sensory evoked potential
• Latency – time from stimulus to onset of
SER
• Amplitude – voltage of recorded response

52. SENSORY EVOKED POTENTIAL
Sensory evoked potentials
 Somatosensory (SSEP)
 Auditory (BAEP)
 Visual (VEP)
SSEP – produced by electrically stimulating a cranial or peripheral nerve
• If peripheral n. stimulated – can record proximally along entire tract (peripheral
n., spinal cord, brainstem, thalamus, cerebral cortex)
As opposed to EEG, records subcortically.

53. SSEP
Time-locked, event related, pathway
specific EEG in response of peripheral
stimulus
Monitor integrity of the pathway from
periphery to the cortex
Electrical stimulator placed at median,
ulnar, or posterior tibial nerves

54. INDICATIONS OF SSEP
 Scoliosis correction
Spinal cord decompression and stabilization after acute injury
Brachial plexus exploration
Resection of spinal cord tumour
Resection of intracranial lesions involving sensory cortex
 Clipping of intracranial aneurysms
Carotid endarterectomy
Thoracic aortic aneurysm repair

55. CAROTID ENDARTERECTOMY
 Similar sensitivity has been found between SSEP and EEG
 SSEP has advantage of monitoring subcortical ischemia
 SSEP disadvantage do not monitor anterior portions -frontal or temporal lobes
CEREBRAL ANEURYSM
• SSEP can gauge adequacy of blood flow to anterior cerebral circulation
• Evaluate effects of temporary clipping and identify unintended occlusion of
perforating vessels supplying internal capsule in the aneurysm clip

56. DRAWBACKS
Motor tracts not directly monitored
• Posterior spinal arteries supply dorsal columns
• Anterior spinal arteries supply anterior (motor) tracts
• Possible to have significant motor deficit postoperatively despite normal SSEPs
SSEP’s generally correlate well with spinal column surgery.

57. • Visual Evoked Potential (VEP):
• Using LED goggles to create stimulus
• Difficult to perform
• Brainstem Auditory Evoked Potential (BAEP)
• Repetitive clicks delivered to the ear
• Reflects the VIII nerve & brainstem “well-being”

59. AEP
• Auditory (BAEP) – rapid clicks elicit responses
 CN VIII, cochlear nucleus, rostral brainstem, inferior colliculus,
auditory cortex
 Procedures near auditory pathway and posterior fossa:
 Decompression of CN VII, resection of acoustic neuroma, sectioning
CNVIII for intractable tinnitus
Resistant to anesthetic drugs.

62. DRAWBACKS
Responds to injury by increased latency, decreased amplitude, ultimately
disappearance.
Problem is response non-specific
• Surgical injury
• Hypoperfusion/ischemia
• Changes in anesthetic drugs
• Temperature changes
 Signals easily disrupted by background electrical activity (ECG, EMG activity of
muscle movement, etc)
Baseline is essential to subsequent interpretation.

63. ANESTHETIC AGENTS AND SEPS
 Most anesthetic drugs increase latency and decrease amplitude
 Exceptions:
• Nitrous oxide: latency stable, decrease amplitude
• Etomidate: increases latency, increase in amplitude
• Ketamine: increases amplitude
• Opiods: no clinically significant changes
• Muscle relaxants: no changes

64. PHYSIOLOGICAL FACTORS AFFECTING SEPS
 Hypotension
 Hyperthermia and hypothermia
 Mild hypothermia (35-36 degrees) minimal effect
 Hypoxemia
 Hypercapnia
 Significant anemia (HCT <15%)
Technical factor: poor electrode-to skin-contact and high electrical impedance (eg
electrocautery)

66. MOTOR EVOKED POTENTIALS
Motor EP:
1. Transcranial magnetic MEP
2. Transcranial electric MEP
3. Direct spinal cord stimulation

67. • Transcranial electrical MEP
monitoring.
• Stimulating electrodes placed on scalp
overlying motor cortex.
• Application of electrical current
produces MEP.
• Stimulus propagated through
descending motor pathways.

68. MOTOR EVOKED POTENTIALS
• MEPs very sensitive to anesthetic agents
• Possibly due to anesthetic depression of anterior horn cells in spinal cord
• Intravenous agents produce significantly less depression
• TIVA often used
• No muscle relaxant

69. EMG
Early detection of surgically induced
nerve damage and assessment of level
of nerve function intra-operatively.
Active or passive.
Uses:
• 1. Facial nerve monitoring
• 2. Trigeminal nerve monitoring
• 3. Spinal Accessory nerve

71. FACIAL NERVE MONITORING
• The most common cranial nerve monitored during surgery.
• This nerve may be intertwined within brainstem tumors (e.g., acoustic neuroma).
• Monitoring of the facial nerve allows identification of the nerve in the
operative site and warning of the unrecognized proximity of the nerve
to surgical activity.
• Because of the improvement in outcome in posterior fossa surgery seen with facial
nerve monitoring, NIH concluded, “The benefits of routine intraoperative
monitoring of the facial nerve have been clearly established [in vestibular
schwannoma]. This technique should be included in surgical therapy.”
• The muscles used for monitoring are the orbicularis oculi and orbicularis oris
muscles ipsilateral to the surgical site.

72. TRANSCRANIAL DOPPLER
Measures the blood flow velocity in major cerebral blood vessels.
Examination carried out through the temporal window, orbital foramen or foramen
magnum.
 Using 2MHz probe.
 MCA commonly used.
 Change in velocity is proportional to change in flow considering the vessel
diameter is constant.
Normal velocity in the middle cerebral artery is approximately 55 cm/ sec.
Velocities greater than 120 cm/sec can indicate cerebral artery vasospasm
following subarachnoid hemorrhage or hyperemic blood flow.

75. CLINICALAPPLICATIONS OF TCD
• 1. Noninvasive monitor of CBF.
• 2. Diagnose cerebral vasospasm and monitor response to therapy in patients with
subarachnoid hemorrhage and head injury.
• 3. Study autoregulation of CBF and cerebral vascular response to carbon dioxide.
• 4. Assess intracranial circulatory status in raised ICP.
• 5. Identify intraoperative cerebral embolization during surgery on carotid artery
and cardiopulmonary bypass procedures.
• 6. Optimise CPP and hyperventilation in patients with head injury.

76. INTRAVASCULAR TRACER COMPOUNDS
Method originally described by Kety and Schmidt.
Administration of radioactive isotope of xenon-133
Measurement of radioactivity washout with gamma detectors.
Disadvantages:
• 1.Exposure to radioactivity
• 2.Cumbersome detector equipment
• 3.Focal areas of hypoperfusion missed
• 4.Snapshot of CBF, not a continuous monitor

77. THERMAL DIFFUSION CEREBRAL BLOOD FLOW
MONITORING
The rate at which heat dissipates in a tissue depends on the tissue’s thermal
conductive properties and the blood flow in that area.
Measurement is automatically suspended if the passive thermistor measures a
brain temperature of 39.1°C.
The inability to monitor during a febrile episode may constitute a true limitation of
the technique

78. MONITORING OF CEREBRAL OXYGENATION AND
METABOLISM
Brain tissue oxygenation
 Jugular bulb venous oximetry monitoring
 Microdialysis catheter
 Near Infrared Spectroscopy (NIRS)

79. JUGULAR VENOUS OXIMETRY
(A-V)DO2x CBF = CMRO2
When CMRO2 is constant, any change in CBF is associated with a reciprocal
change in the cerebral arteriovenous oxygen difference.
 Based on the principle of reflectance oximetry.

80. Continuous monitoring of jugular
venous oxygen saturation (SjVO2 ) is
carried out by a catheter placed
retrograde through the internal jugular
vein into the jugular bulb.
For accurate measurement, the tip of the
catheter must be within 1 cm of the
jugular bulb.

81. INDICES
• 1.Jugular venous oxygen saturation (SjVO2)
• 2. Cerebral arteriovenous oxygen difference (A-VDO2) (the difference between
arterial and jugular venous oxygen content) and
• 3. Cerebral oxygen extraction(CEO2) (the difference between SaO2 and SjVO2).

82. • Interpretation of jugular venous oxygen saturation (SjvO2)
 Increased values: >90% indicates absolute/relative hyperemia
• Reduced metabolic need comatose/brain death
• Excessive flow severe hypercapnia
• AVM
Normal Values: 60-70% focal ischemia?
Decreased Values: <50% increased O2 extraction, indicates a potential risk of
ischemia injury
• Increased demand: seizure / fever
• Decreased supply: decreased flow, decreased hematocrit
• As ischemia progress to infarction: O2 consumption decreases

83. NEAR INFRA RED SPECTROSCOPY(NIRS)
The principle of absorption of near-infrared light by chromophores in the body
like oxyhaemoglobin, deoxyhaemoglobin and cytochrome aa3.
Light in the near-infrared region (70-1000 nm) is very minimally absorbed by
body tissues. It can penetrate tissues upto 8 cm.
 Measure regional cerebral blood flow, cerebral blood volume, cerebral oxygen
saturation and cerebral metabolism.

86. LIMITATIONS
Inability to assess the contribution of extracranial tissue to the signal changes.
 Presence of intracranial blood in the form of haematomas and contusions can
interfere with the measurements.
• Measures small portion of frontal cortex, contributions from non-brain sources
• Temperature changes affect NIR absorption water spectrum
• Degree of contamination of the signal by chromophores in the skin can be
appreciable and are variable
• Not validated – threshold for regional oxygen saturation not known (20%
reduction from baseline?

87. TISSUE PARTIAL PRESSURE OXYGEN MONITORING
Based on an oxygen-sensitive electrode originally described by Clark.
The diffusion of oxygen molecules through an oxygen permeable membrane into
an electrolyte solution causes an electric current that is proportional to Po2.
 The catheter is placed into the brain tissue through a twist drill hole into the
subcortical white matter.
 Normal values for brain tissue oxygen tension are 20-40 mmHg.
 In patients with cerebral ischemia the values are 10 ± 5 mmHg as against 37 ± 12
mmHg in normal individuals.

88. CEREBRAL MICRODIALYSIS
• Small catheter inserted with ICP/tissue PO2 monitor.
• Artificial cerebrospinal fluid, equilibrates with extracellular fluid, chemical
composition analysis.
• Markers:
• Lactate/pyruvate ratio : onset of ischemia
• High level glycerol: inadequate energy to maintain cellular integrity- membrane
breakdown
• Glutamate: neuronal injury and a factor in its exacerbation.

89. • Catheter placement is usually in
‘high risk’ tissue.
• Uses:
• 1.Ischemia/trauma
• 2.epilepsy
• 3.Tumor chemistry

91. REFERENCES
• MILLERS ANESTHESIA, 9TH EDITION
• COTTRELL AND YOUNG’S NEUROANESTHESIA, 5TH EDITION
• MORGAN AND MIKHAIL,
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