Intraoperative neurophysiological monitoring is a crucial component of neurosurgery.

2. Indications Cervical or thoracic level spinal surgeries
 Posterior fossa surgeries
 Hemispheric or deep brain surgeries
 Surgeries that place peripheral nerves at risk

3. Contraindications of NIOM:
 Presence of cardiac pacemaker
 Cranial and other implants(MEP)
 History of epilepsy….??

4. Types
Basic techniques of neurophysiologic intraoperative
monitoring (NIOM):
 Electromyography (EMG).
 Motor nerve conduction studies.
 Somatosensory evoked potentials (SEPs).
 Motor evoked potentials (MEPs).
 Brainstem auditory evoked potentials (BAEPs).
 Electroencephalography (EEG) are all discussed.

5. Anaesthetic considerations
Four phases of general anaesthesia:
• Premedication
• Induction
• Maintenance
• Recovery

6. Premedication
 Prior to entering the operating suite, “premedications”
 may be administered to prepare the patient for the
perioperative period. Usually this takes the form of
mild sedation for anxiolysis, analgesics for
preprocedural pain, antihypertensives, antiemetics for
patients with a
 high likelihood of postoperative nausea and vomiting,
antisialagogues to facilitate intubation,etc.

7. Induction
• Intravenous rout
• Inhalational( volatile gases)

9. 18th Century Surgery
General & Local Anesthetics, (AAM) 9
Original in the Royal College of Surgeons of England, London.

10. The Ideal Anesthetic
 The ideal anesthetic drug will cause:
 loss of sensation esp. pain.
 loss of noxious reflexes.
 induce muscular relaxation.
 induce smooth onset and recovery.
 induce amnesia.
 causes no systemic amnesia.
 causes no systemic toxicity.
 presents no hazard to others
10

11. Inhalation Anesthetics
• Original agents were vapours from volatile liquids
or gases:
• Nitrous oxide, ether (diethylether), chloroform
• Induction of anesthesia
Rarely seen today as induction is usually by injected anesthetic.
Inhalation drugs used to maintain depth of anesthesia.
• Only nitrous oxide still in routine use.
11

12. Anesthesia Criteria
• Applying a gas rather than a solid or a liquid required a special
set of terms.
• Concentration – although blood concentration in µg/litre or
µM is possible to measure, the volatility of the drug makes it
difficult. Gases in the lung alveolus are in equilibrium with
gases in solution in the blood, so alveolar concentration is
expressed as a partial pressure or percent of total gas.
• MAC – minimum alveolar concentration (as a percentage) that
eliminates pain when 1 cm incision in 50% of patients.
12

13. MAC Value
• N2O = 105%
• Halothane = 0.75%
• Isoflurane = 1.16%
• Euflurane = 1.68%
• Sevoflurane = 2%
• Deslurane = 6%
• N2O alone is unable to produce adequate
anesthesia ( require high conc. )
December 17 13

14. 14

15. INTRAVENOUS ANESTHETICS
• Mainly selected members of sedative drug classes.
• Act by
• a) potentiating the action of an inhibitory ionophore (the GABAA receptor).
• b) blocking the action of excitatory ionophores (Nicotinic Ach & NMDA
receptors).
• ADVANTAGES - Rapid onset, controlled dosage, ease of administration.
• DISADVANTAGES - Overdose not readily corrected, no antagonists or antidotes,
prolonged after effects (hangover).
15

16. Barbiturates
• Pharmacokinetics important - ULTRA SHORT ACTING
• Methohexital, Thiopental, Pentobarbital
• Very lipid soluble, induces anesthesia (hypnosis) in 1 circulation
time.
• Redistribution occurs at a rate proportional to blood supply. i.e.
brain → lean tissues → fat.
• Metabolism is slower but slow leaching from stores keeps blood
levels low; effect restricted to a hangover.
16

17. Alkylphenols
• Propofol (“Milk of Amnesia”)- newer drug.
 Comparable kinetics to thiopental (t½α = 2-4 min), but t½ß = 1-
3hr) - Patients recover more rapidly and feel less “hangover”.
 Contraindicated for sedation in children due to acidosis and
possible neurological sequelae.
 Slightly greater incidence of pain and excitation on induction.
 Emulsificant can cause reactions (Cremophor vs Intralipid)
 Significant but transient fall in blood pressure and a rise in
heart rate -
17

18. Benzodiazepines
 Common drugs are diazepam or lorazepam BUT not water
soluble and too slow an onset.
 Midazolam - water soluble but slower in onset than
barbiturates.
 Mainly used preoperatively.
 Prolonged recovery with amnesia.
 MAINLY USED PREOPERATIVELY
 Flumazenil - receptor antagonist; used to speed recovery,
or act as antidote in overdose.
18

19. Cyclohexylamines
 Ketamine - Channel blocking agent related to Phencyclidine (Angel dust)
 Blocks both nicotinic ACh and NMDA (glutamic acid) receptor channels
 Dissociative anesthesia - catatonia, amnesia, analgesia BUT NOT true surgical
anesthesia.
 Cardiovascular stimulation
 muscle tone maintained
 emergence reactions - dreams and hallucinations (Less in children) (Control with
diazepam or dropridol)
 Indicated mainly in outpatient procedures, children and burn dressings.
19

20. 20

21. Muscle Relaxants
21
Drugs used in
muscle Relaxation
Neuromuscular
blockers
Nondepolarizing
Short action
(mivacurium)
Long action
(tubocurarine)
Depolarizing
(succinylcholine)
Spasmolytics
Acute use
(cyclobenzaprine)
Chronic use
CNS action
(baclofen,
diazepam,
tizanidine)
Muscle action
(dantrolene)

22. Nondepolarizing NMJ Blockers
• Pharmacokinetics
• All agents are given parenterally, metabolized (eg,
mivacurium by plasma cholinesterase), eliminated by
kidney (eg, pancuronium, tubocurarine). Atracurium
clearance involves rapid spontaneous breakdown
(Hofmann elimination) to form laudanosine and other
products and is largely in dependent of hepatic or renal
function.
• Mechanism of action
• Prevention Ach attachment at N receptors
22

23. Oxygen is
bubbled in
volatile Anesth.
agnet
Mixture vapor
Anesthetic
machine
Lungs
Diffuse across
alveolar capillary
membrane
blood Brain
December 17 23

24. * Hyperthermia
* Chronic drug abuse (ethanol)
* Acute use of amphetamines
* hyperthyroidism
* Increasing Age
* hypothermia
* Other anesthetic (opioids)
* Acute drug intoxication (ethanol)
* Pregnancy
* Hypothyroidism
* Other drugs ( clonidine ,reserpine)
December 17 24

25. Propofol
• Intravenous
anaesthetic/hypn
otic.
• Akylphenol.
• Propofol is a
sweet drug in the
OR, but definitely
not for home use.
December 17 Dr. Med. Khaled Radaideh 25

26. Propofol
Physical and chemical properties
Emulsion consists of:
1% propofol 10mg/ml
10% soyabean oil.
2.25 %glycerol
1.2% purified egg
phosphatide.
December 17 Dr. Med. Khaled Radaideh 26

27. Propofol
Physical and chemical properties so Propofol is a highly lipid soluble oil that’s combined with glycerol,
egg, and soya bean oil for IV administration.
 It’s appearance is similar to that of a 2% milk.
 It has a pH of 7 and is supplied in 20 ml ampoules with a concentration
of 10 mg/ml.
 Neither precipitates histamine release nor triggers malignant
hyperthermia.
 Has no effects on muscle relaxants.
 Associated with low incidence of nausea & vomiting.
December 17 27

28. Dose•For healthy unpremedicated 2.5-3 mg/kg.
•For premedicated 1.5-2 mg/kg.
•Elderly patients <= 1 mg/kg.
•Maintenance of anesthesia (50-150 mcg/kg/min) combined with N2O
and Opioids (Continuous Infusion: Total intravenous Anesthesia
TIVA)
•For IV conscious sedation for operative procedures with local
anaesthesia 25-75 mcg/kg/min.
December 17 28

29. Effects on organs
Cerebral:
decreases cerebral blood flow and
intracranial pressure. Propofol has
antiemetic, antipruritic, and anticonvulsant
properties.
Cardiovascular:
decrease in arterial blood pressure secondary
to a drop in systemic vascular resistance,
contractility, and preload. Hypotension is
more pronounced than with thiopental.
Propofol markedly impairs the normal
arterial baroreflex response to hypotension.
December 17 29

30. Respiratory:
propofol causes profound respiratory
depression. Propofol induced depression of
upper airway reflexes exceeds that of
thiopental.
Venous irritation:
• Pain on injection is more common than with
thiopental esp. if given in a small vein in the
hand.
• To solve this problem:
1. small doze of lidocaine with propofol.
2. administering propofol through a fast flowing more proximal IV catheter.
December 17 30

31. Propofol
indications
indication Approved Patient Population
Initiation and maintenance of
Monitored Anesthesia Care
sedation
Adults only
Combined sedation and regional
anesthesia
Adults only
(See PRECAUTIONS)
Induction of General Anesthesia Patients ≥ 3 years of age
Mainenance of General Anesthesia Patients ≥ 2 months of age
Intensive Care Unit (ICU) sedation
of intubated, mechanically
ventilated patients
Adults only
December 17 31

32. Propofol
Contraindications
1. Egg allergy.
2. Lack of resuscitation equipment or knowledge of the
drug.
3. Inability to maintain a patent airway.
4. Conditions in which reduction in blood pressure can’t
be tolerated. E.g. patients with fixed cardiac output
(severe aortic or mitral stenosis, IHSS, pericardial
tamponade) and those in shock status.
December 17 32

33. Ketamine
 It’s a dissociative anesthetic agent.
 by dissociative we mean that the
patient is unconscious but appears
awake and doesn’t feel pain.
 It has anesthetic and analgesic effect
December 17 33

34. Ketamine
Physical & chemical
Properties chemically related to the psychotropic drug ( e.g.
phencyclidine).
 Water soluble, and 10x more lipid soluble than
thiopental.
 pH=3.5 - 5.5
December 17 34

35. Ketamine
Pharmacokinetics
Route of administration
• I.V. : 2mg/kg
• IM. 5-10 mg/Kg
• Oral.
• Rectal. Needs higher doze due to extensive first pass
metabolism and decreased absorption.
December 17 35

36. Ketamine
Pharmacokinetics
Dosage
• IM  5 – 10 mg/kg. peak plasma level reach
approx 15 minutes
• IV  1 – 2 mg/kg. dissociated stage is noted in
15 seconds. intense analgesia, amnesia &
unconciousness occur within 45-60 minutes
subsequent IV doses of 1/3 – ½ of the initial
dose maybe required
December 17 36

37. KETMINE
METABOLISM
 It has a rapid absorption and distribution to the
vessel rich groups like THIOPENTAL
 Hepatic metabolism is required for elimination
 <5% excreted unchanged in urine
December 17 37

38. KETMINE
Pharmacodynamics
CNS :
1. ketamine increases cerebral oxygen consumption, cerebral
blood flow, and intracranial pressure
2- generalized increase in the muscle tone and purposful
movements.
3- Unpleasant dreams, hallucinations or frank delirium (esp.
females & large doze of ketamine).
incidence of dilirium in 15-35 year old pts is approx. 20%
December 17 38

39. KETMINE
Pharmacodynamics
• Respiratory system:
It preserves laryngeal &pharyngeal airway reflexes.
• Ketamine is a potent bronchodilator.
• The CO2 response curve is shifted to the left with its slope
unchanged (similar to opiates).
• FRC  unchaged.
• Minute ventilation  unchanged.
• Tidal volume  unchanged.
• Hypoxic pulmonary vasoconstriction  unchanged.
• Ketamine causes increased secretions but this can be
limited by anti-cholinergic drugs.
December 17 39

40. KETMINE
Indications
1- sole anesthetic for diagnosis and surgical procedures
2- induction of anesthesia
3- to supplement regional or local anesthetic techniques
4- for anesthetic induction in severe asthmatic pts. Or patients with
cardiovascular collapse requiring emergency surgery
December 17 40

41. KETMINE
Contraindications
1- lack of knowledge of the drug
2- lack of resuscitative equipment
3- inability to maintain a patent airways
4- allergy to ketamine
5- history of psychosis
6- cerebro-vascular disease
December 17 41

42. Benzodiazepines
• Features which result in their popularity as adjuvant
IV anaesthetic agents:
1 – amnesia
2 – minimal cardiarespiretory depressant effect.
3 – anticonvulsant activity.
4 – low incidence of tolerance and dependence.
42

43. Benzodiazepines
Mode of action They inhibit the actions of glycine (by increasing the conc. Of a
glycine inhibitory neurotransmitter) which will lead to antianxiety and
skeletal muscle relaxant effects.
 They facilitate the actions of the inhibitory neurotransmitter GABA
which results in the sedative and anticonvulsant effects.
 Benzodiazepines are highly lipid soluble.
 They are highly protein bound (albumin).
 They are metabolized by the liver through conjugation with glucoronic
acid and excreted by the kidneys.
 Midazolam and Diazepam are the most commonly used benzodiazepines
during operative procedures.
December 17 43

44. Benzodiazepines
Midazolam and diazepam
• They are commonly used to provide:
1- IV sedation.
2- amnesia.
3- reducing anxiety.
December 17 44

45. Narcotic Agonists
• Opium derived from
dried juice of poppy plant
which contains over 20
plant alkaloids. including
morphine & codiene.
December 17 45

46. Narcotic Agonists
Site of Action
• Opioid receptors are predominantly located in the:
1. Brain stem (amygdala, corpus striatum, periaqueductal gray
matter and medulla).
2. Spinal cord(substantia gelatinosa).
3. GIT.
 They act on 3 types of receptors:
1. Mu receptors (μ): analgesia, respiratory depression, euphoria, &
physical dependence.
2. Kappa receptors (K): analgesia, sedation, respiratory depression,
miosis.
3. Segma receptors(a): dysphoria, hallucination, tachypnea,
tachycardia.
December 17 46

47. Narcotic Agonists
Pharmacodynamics
Respiratory
• They result in dose related depression of respiratory
rate and minute ventilation and increase the tidal
volume which will lead to a slow deep respiration.
Reversed by naloxone administration.
December 17 47

48. Narcotic Agonists
Pharmacodynamics
CVS
 Opioids have little myocardial depressant effect
even when administered in high doses.
 Supplementation with either N2O or
benzodiazepines may depress cardiac output.
 They decrease systemic vascular resistance
either by decreasing sympathetic outflow or by
releasing histamine (as morphine) which
produces vasodilation & decrease SVR.
 Synthetic opioids are less likely to release
histamine.
 They produce bradycardia by stimulation vagal
nucleus in the brain stem.
December 17 48

49. Narcotic Agonists
Pharmacodynamics
GIT
• Narcotics slow GI mobility and may result in
constipation or post operative ileus.
• All narcotics increase biliary tract tone which may lead
to biliary colic with patients with bile stones.
Others
• Increases the bladder sphincter’s tone  urine
retention.
• Anaphylactic reactions, bronchospasm, chest wall
rigidity and pruritis.
December 17 49

50. Narcotic Agonists
Fentanyl and Morphine
• Fentanyl is the most narcotic agent used during
induction of anaesthesia due to its rapid onset (highly
lipid soluble) and predictable duration of action (30
minutes).
• Morphine is used in the perioperative period to provide
long lasting analgesia. And it should be administered
slowly at a rate < 5 mg/min to avoid excessive
histamine release.
December 17 50

51. Effects of various agents on
NIOM

52. Effects of anaesthetic agents on
Electroencephalogram
December 17 52

53. Effects of Intravenous agents on
Evoked Potentials
December 17 53

54. December 17 54

55. 55

56. New drugs
• Dexmeditomidine

57. Pharmacology
• Establish and maintain adequate drug concentration
at effector site to produce desired effect
• sedation
• hypnosis
• analgesia
• paralysis
• Predict the time course of drug onset + offset

58. Pharmacodynamics
• Relationship between drug conc + effect
• Interaction of drug with receptor
• Receptor
• cell component
• interacts with drug
• biochemical change
• Examples of receptors:
• AchR, GABA, opioid,  +  adrenergic

59. Receptors
• Coupled to ion channels
• neural signaling, 2nd messenger effects
• Drug effects at receptor
• agonist, antagonist or mixed effects
• stereospecificity, racemic mixture of
isomers
• Receptor alterations
• upregulated or downregulated (e.g., CHF)
•  or  number (e.g., burns, myasthenia
gravis)

60. Pharmacodynamics
• Sedation/hypnosis
• Anxiolysis
• Analgesia
• Sympatholysis (BP/HR, NE)
• Reduces shivering
• Neuroprotective effects
• No effect on ICP
• No respiratory depression

61. Pharmacokinetics
• Rapid redistribution: 6 min
• Elimination half-life: 2 h
• Vd steady state: 118 L
• Clearance: 39 L/h
• Protein binding: 94%
• Metabolism: biotransformation in liver to inactive
metabolites + excreted in urine
• No accumulation after infusions 12-24 h
• Pharmacokinetics similar in young adults + elderly

62. 2 Agonists
Clonidine
• Selectivity: 2:1 200:1
• t1/2  8 hrs1
• PO, patch, epidural
• Antihypertensive
• Analgesic adjunct
• IV formulation not
available in US
Dexmedetomidine
• Selectivity: 2:1 1620:1
• t1/2  2 hrs
• Intravenous
• Sedative-analgesic
• Primary sedative
• Only IV 2 available for use
in the US

63. Perioperative Dex Infusion
Protocol
Example: 70 kg patient. Assess BP, HR, volume status
2 mL Dex in 48 mL 0.9% saline= 200 ug/50 mL, or 4 ug/ml
Hypovolemic
Start at 40 mL/hr
Stop load if  HR
Usual load: 25 to 35 ug or 6 to 9 mL over 10-15 min
Monitor BP/HR
throughout
If bradycardia,
 infusion
Maintenance: 0.2 to 0.7 ug/kg/hr [4 to 12 mL/hr]
Volume preload
500 to 1000 cc LR
Normovolemic
Dex=dexmedetomidine.

64. Considerations With Anesthesia
Use of Dexmedetomidine
• Dilute in 0.9% saline: 4 mcg/mL
• Requires infusion pump: mcg/kg/h
• Transient HTN: with rapid bolus
• Hypotension may occur, especially if hypovolemia
•  HR (attenuation of tachycardia): usually desirable
•  conc of inhaled agents: BIS monitoring
• Continue infusion after extubation for 30 min [PACU]
• L + D: not studied
• Pediatrics: abstracts + case reports [Lerman, Toronto]
• Geriatrics: more hypotension + bradycardia:  dose

65. Properties of remifentanil
1. Egan TD. Clin Pharmacokinet 1995; 29: 80–94.
2. GlaxoSmithKline. Remifentanil HCl (Ultiva) Summary of Product Characteristics, June 2005.
• Unique, very short-acting opioid, rapidly cleared by blood
and tissue esterases1
• Rapid onset of action: t1/2ke0 = 1.3 minutes1
• Rapid offset of action: context-sensitive half-time = 3.65
minutes1
• Predictable offset of
action, independent of
duration of infusion1
• Pharmacokinetics are
unaltered by obesity
and renal or hepatic
function1,2
• Precise intra-operative
control and fast, clear-
headed recovery1

66. Intra-operative control
• Remifentanil is suitable for use in many different
types of surgery1–5
• Remifentanil’s fast onset and short duration of action
enables rapid titration to effect6
• Remifentanil offers a unique approach to the
management of surgical patients by providing:
• More effective control of intra-operative responses than
alfentanil or fentanyl7,8
• More effective at maintaining haemodynamic stability than
alfentanil or fentanyl5,9
• Control in difficult-to-treat patients with renal or hepatic
impairment, with no initial dose adjustment needed10-12
1. Sneyd J et al. Br J Anaesth 2005; 94: 778–83.
2. Demirbilek et al. J Clin Anesth 2004; 16: 358–63.
3. Howie MB et al. Anesth Analg 2001; 92: 1084–93.
4. Fish W. Anaesthesiology 1999; 54: 1002–6.
5. Mackey J. et al. J Clin Anesth 2000; 12: 427–32.
6. Egan T. Pharmacokinet 1995; 29: 80–94.
7. Schuttler J et al. Anaesthesia 1997; 52: 307–317.
8. Sneyd J et al. Eur J Anaesthesiol 2001; 18: 605–14.
9. Kallar SK et al Anesthesiol 1994; 81: A32.
10. Dershwitz M et al. Anesthesiology 1996; 84: 812–20.
11. Dershwitz M et al. J Clin Anesthesia 1996; 8: 88S–90S
12. GlaxoSmithKline. Remifentanil HCl (Ultiva) SPC, June 2005.

67. Recovery
• Remifentanil provides fast, clear-headed
recovery1–3
• Recovery with remifentanil is more rapid than
with fentanyl or alfentanil2,3
• Remifentanil facilitates rapid extubation and
reduces the need for ICU admission1–5
• Remifentanil enables early post-operative
neurological assessment1–3
• Post-operative pain can be effectively
managed6
1. Wilhelm W et al. Br J Anaesth 2001; 86: 44–9.
2. Kovac A et al. J Clin Anesth 1997; 9: 532–41.
3. Bekker A et al. Anesth Analg 2000; 91: 117–22.
4. Park G et al. Eur J Anaes 2000; 17: 111–19.
5. Eberhart L et al. Eur J Anaesthesiol 2004; 21: 107–14.
6. Minkowitz H. Can J Anesth 2000; 47: 522–28.

68. Reconstitution
• Available as lyophilised powder for reconstitution in 1mg, 2mg and 5mg
vials
• To reconstitute add recommended diluent to powder in vial and shake
well
• After reconstitution, further dilute to recommended dilution
• 50µg/ml is the recommended dilution for adults
Target
concentration
Remifentanil
vial size
Total volume of
recommended
diluent required
Volume of diluent
required for
reconstitution
Volume of diluent
required for
dilution
50µg/ml
1mg 20ml 3ml 17ml
2mg 40ml 5ml 35ml
5mg 100ml 10ml 90ml
See factsheet: Reconstitution Guidelines
GlaxoSmithKline. Remifentanil HCl (Ultiva) Summary of Product Characteristics, June 2005.
• 20–25µg/ml is recommended for paediatric patients aged 1 year and
over

69. Dosing protocol for general anaesthesia
– induction
• Remifentanil is indicated as an analgesic agent for use during
induction and/or maintenance of general anaesthesia under
close supervision1
• Induction of anaesthesia in adults:*
• Remifentanil: continuous infusion 0.5–1µg/kg/min1
• Mackey et al used an infusion rate of 0.5µg/kg/min for 2 minutes
prior to intubation2
• Warner et al used an infusion rate of 0.5–1µg/kg/min for 1 minute
prior to intubation3
• Isoflurane: starting dose 0.5 MAC1
• Propofol: starting dose 100μg/kg/min1
Details of infusion rates required for target dosages according to patient weight
are supplied in the corresponding factsheet
*When given by bolus injection at induction remifentanil should be administered over not less
than 30 seconds1
See factsheet: Dosing Protocol for General Anaesthesia
1. GlaxoSmithKline. Remifentanil HCl (Ultiva) Summary of Product Characteristics, June 2005.
2. Mackey J. et al. J Clin Anesth 2000; 12: 427–32.
3. Warner DS. Anesth Analg 1999; 89: S33–39.

70. Dosing protocol for general anaesthesia
– maintenance
Maintenance of anaesthesia in adult ventilated patients:
• The administration of remifentanil should be
individualised based on the patient’s response
• During anaesthesia, the rate of administration can be
titrated:
• upward in 25–100% increments every 2–5 minutes
• downward in 25–50% decrements every 2–5 minutes
• When used with isoflurane: starting rate 0.25µg/kg/min
(range 0.05–2µg/kg/min)*
• When used with propofol: starting rate 0.25µg/kg/min (range
0.05–2µg/kg/min)*
See factsheet: Dosing Protocol for General Anaesthesia
GlaxoSmithKline. Remifentanil HCl (Ultiva) Summary of Product Characteristics, June 2005.
*For cardiac patients refer to the Summary of Product Characteristics

71. Dosing protocol for general
anaesthesia – summary
INTUBATION
STOP
remifentanil
and propofol
EXTUBATION
See factsheet: Dosing Protocol for General Anaesthesia
1. GlaxoSmithKline. Remifentanil HCl (Ultiva) Summary of Product Characteristics, June 2005.
2. Muñoz HR et al. Br J Anaesth 2002; 88: 814–18.
3. Minkowitz H. Can J Anesth 2000; 47: 522–28.
Morphine
Propofol
Remifentanil
Morphine 150–200μg/kg
bolus more than 40
minutes before end
of surgery2,3
Remifentanil: titrate as required1
Increments: 25–100% every 2–5 minutes
Decrements: 25–50% every 2–5 minutes
Range: 0.05–2.00μg/kg/min
Start propofol
100μg/kg/min1
Start remifentanil
0.5μg/kg/min1
SCHEMATIC
REPRESENTATION
ONLY
Remifentanil at
0.25μg/kg/min1

72. Hypnotic sparing effects in general
anaesthesia
Combining remifentanil with
Isoflurane1 Sevoflurane2 Propofol3
0.05 µg/kg/min
remifentanil is
associated with a 50%
reduction in isoflurane
MAC
Use of remifentantanil
(0.34μg/kg/min) with low
concentrations of
sevoflurane (0.5 MAC)
facilitates early recovery
Increasing remifentanil
concentrations produces
a dose-dependent
reduction in propofol
requirements
• It is appropriate to maintain a low concentration of hypnotic
agent and titrate remifentanil to produce adequate
anaesthesia1-3
See factsheet: Hypnotic Sparing Effects in General Anaesthesia
1. Lang E et al. Anesthesiology 1996; 85: 721–28.
2. Breslin DS et al. Anaesthesia 2001; 56: 114–19.
3. Milne S et al. Br J Anaesth 2003; 90: 623–29.

73. Recent regimen for anaesthetic
planHigh dose Remifentanil infusion
Low dose propofol-Ketamine based
anaesthetic
+/- ½ MAC Sevoflorane

74. Other factors that may affect
NIOM

75. Temperature Significant effect in nerve function specially the
axon.
 Relative hypothermia causes slowed latency
 The opposite is true with hyperthermia specially
with Evoked potentials.
 Patient ‘s temperature must be kept greater than 36
C .

76. Blood flow Somatosensory Evoked Potentials can be lost when
blood flow falls below 15 mL/min/100 gm.
 Crudely this can be achieved by the mean arterial blood
pressure monitoring and cerebral perfusion monitoring.
 Mean ABP can be maintained between 70-50 mmHg .

77. Ventilation Hypo or hypercapnea can alter cellular metabolism
by changing the acid base status of the individual.
 Unless pH of the patient drops below 7.2, neural
mechanisms are maintaiined .
 Extremes in hypocarbia (20 mmHg) can alter SEP.
 Profound hypoxia is poorly tolerated specially in
surgical blood loss and potential hypotension.

78. Hematology Generally accepted hemoglobin levels should be kept
above 8 g/dl, ideally 10 g/dl minimal.
 This is crucial for optimizing the oxygen carrying
capacity , specially when deliberate hypotension is
required .

79. Intracranial pressure
 Increase ICP is well documented cause of shifts in
cortical responses of EPs and prolonged motor
evoked potentials( MEPs) .
 There is a pressure-related increase in latency and
decrease in amplitude of cortical SEPs.
 If intracranial pressure becomes pathologic , uncal
herniation occurs with subsequent loss of subcortical
SEP responses and Brain stem auditory evoked
potential ( BAEPs) .

80. Other factors
 Potassium, Calcium and Sodium , are essential for
the integrity of neural function .
 Profound hyper- or hypoglycemia should be avoided
as both can cause cellular dysfunction .

81. Train-Of- Four monitoring

82. Testing
When pressing the train-of-four button, the stimulus is
sent as a group of 0.2-millisecond pulses (to avoid direct
muscle stimulation or repetitive nerve stimulation going
over the refractory period) in a square-wave pattern
spaced 500 milliseconds apart. This is repeated every
10 seconds

83. • The response is measured as follows:
• When 4 twitches are seen, 0-75% of the receptors
are blocked.
• When 3 twitches are seen, at least 75% of the
receptors are blocked.
• When 2 twitches are seen, 80% of the receptors are
blocked.
• When 1 twitch is seen, 90% of the receptors are
blocked.
• When no twitches are seen, 100% of receptors are
blocked.

84. Tailoring of the Regimen
 Remember that you are dealing with a patient who will be
operated upon so he/she must be “Deep” enough, and
meanwhile he/she must be “ light “ enough for the NIOM to be
successful…….. !!!!.
 Complete cooperation between all operative staff must be
fulfilled , specially between the anaesthetist, neurophysiologist
and surgeon.
 Due to the previously described effects of anaesthetic agents
, we nowadays shifted to “ Balanced anaesthesia” .