INDUCTION AGENTS IN ANAESTHESIA

1. Dr. ASHISH NAIR
MBBS, MD ANAESTHESIA
FELLOW IN REGIONAL ANESTHESIA
IDCCM
JDept of Anesthesiology
BVUMC & Hospital – Pune

2. By the end of presentation;we should know
 What are IV induction agents.
 Properties
 Metabolism
 Pharmacokinetics
 MOA
 Systemic Action
 CNS
 CVS
 RS
 Doses
 Uses
 Side effects.
6/23/2017 2

3. Case Scenarios
6/23/2017 3

4. Case scenario-1
A patient with intestinal
obstruction having wheezing
requires an emergency laparotomy.
Which induction drug would you
use?
6/23/2017 4

5. Case scenario-2
A patient a history of golttic cancer;
has signs of respiratory distress
and marked stridor; requires a
tracheostomy.
Which IV induction drug would
you use?
6/23/2017 5

6. Case scenario-3
A patient requires a burns
dressing change.
Which induction drug would you
use?
6/23/2017 6

7. Case scenario-4
A patient with a history of heart
failure and MI requires a general
anaesthetic for cholecytectomy .
Which induction drug would you
choose?
6/23/2017 7

8. Case Scenario-5
Which IV induction drug would
be most appropriate to use in a
hypovolaemic patient.
(Blunt Trauma abdomen)
6/23/2017 8

9. Case Scenario-6
A patient with porphyria comes for
an inguinal hernia repair and is
requesting a general anaesthetic.
Which induction drug would you
use?
6/23/2017 9

10. Case Scenario-7
An adult patient requires sedation
on the intensive care unit.
Which of the induction drugs
would be appropriate to run as an
infusion?
6/23/2017 10

11. Case Scenario-8
Patient coming for Fibroadenoma
excision under GA (Day care
surgery).
Drug of choice for induction ??
6/23/2017 11

12. HISTORY
1872
• PIERRE-CYPRIEN ORE’ (French Surgeon) used chloral hydrate
1864
• ADOLF VON BAYER – On Saint Barbara’s Day discovered barbituric
acid. Coined the term Barbitute as acombination of Barbara and urea.
(no sedative properties)
• 1n 1903 – Emil fischer discovered hexobarbital. Helmut Weese studied
it
1934
• JOHN LUNDY of clinic of mayo studied sod .thiopental – balanced
anesthesia
• In 1941 – pearl harbour – many deaths with use of STP due to
cardiovascular depressant effects.

13. HISTORY
1956 - Replacements like
• HYDROXYDIONE (thrombophlebitis)
• ALTHESIN (mixture of alphaxolone and alphadolone; has rapid onset
and recovery; rejected because of hypersensitivty reactions)
• PROPANIDID (rejected because of hypersensitivity reactions)
In 1973 – Etomidate – minimal hemodynamic
depression .
1962 – 1978
• Ketamine –
• Benzodiazepines were studied for anxiolysis without same degree of
sedation as thiopentone ;1963 – diazepam 1978 - midazolam
1977
• Propofol was discovered

14. What are IV induction
drugs
 These are drugs that, when given intravenously in an
appropriate dose, cause a rapid loss of
consciousness.
 They are used:
To induce anaesthesia prior to other drugs being given
to maintain anaesthesia.
As the sole drug for short procedures.
To maintain anaesthesia for longer procedures by
intravenous infusion.
To provide sedation

15. IDEAL IV INDUCTION DRUG
Physical properties
• Water soluble & stable in solution
• Stable on exposure to light
• Long shelf life
• No pain on intravenous injection
• Non-irritant when injected subcutaneously
• Low incidence of thrombophlebitis
• Cheap

16. Pharmacokinetic properties
 Rapid onset in one arm-brain circulation time
 Rapid redistribution to vessel rich tissue
Rapid clearance and metabolism
No active metabolites
Pharmacodynamics properties
 High therapeutic ratio
Minimal cardiovascular and respiratory effects
No histamine release/hypersensitivity reactions
 No emetic effects
 No involuntary movements
No emergence nightmares
No hang over effect
No adrenocortical suppression
 Safe to use in porphyria

17. Drugs
BARBITURATES
PROPOFOL
KETAMINE
ETOMIDATE
BENZODIAZEPINE
OPIOIDS

18. e.g.
 Thiopental
 Thiamylal
 Pentobarbital
 Secobarbital
 Methohexital
Mechanisms of Action
 Depress the reticular activating
 Suppress transmission of excitatory
neurotransmitters (acetylcholine)
 Enhance transmission of inhibitory
neurotransmitters (GABA)
BARBITURATES

19. Structure
 Barbiturates are barbituric acid derivatives
 Pale yellow colored powder
 Kept in environment of nitrogen
 The sodium salts of the barbiturates are water
soluble
 pH of 2.5% thiopental: 10.5 (highly alkaline)
 Shelf life : 2 wk 2.5% thiopental solution
BARBITURATES

20. Pharmacokinetics
 Highly protein bound (80%)
 The duration of action of is determined by redistribution,
not metabolism or elimination
 Maximal brain uptake within 30 s
 Subsequent redistribution to the peripheral lowers plasma and brain
concentration to 10% of peak levels within 20–30 min
 This pharmacokinetic profile correlates with clinical
experience—patients typically lose consciousness
within 30 s and awaken within 20 min.
BARBITURATES

21. BARBITURATES
 BIOTRANSFORMATION
 Hepatic oxidation to inactive water-soluble metabolites.
 EXCRETION
 Renal excretion
 Important for less protein-bound and less lipid-soluble agents such as
phenobarbital,
 Water-soluble end products of hepatic biotransformation.

22. Route and dose
BARBITURATES

23. Effects on Organ Systems
CARDIOVASCULAR
 First effect dose dependent peripheral vasodilatation
 Negative inotropic effect - ↓ Ca to myocardial fiber
 ↓BP
 ↓ CO (↓venous return , vasodilatation, -veinotropic effect , ↓CNS symp outflow
)
 Tachycardia ( 10-36 %) Via baroreceptor mediated symp reflex in response to ↓
CO & BP
 CAD patient on induction ↑HR - ↑myocardial demand of O2
 ECG changes :-prolonged QT , flattened T wave ,vent arrhythmia
BARBITURATES

24. RESPIRATORY
 Ventilatory response to hypercapnia and hypoxia ---
Decreases
 Tidal volume --- decreased
 Respiratory rate --- decreased
 Bronchospasm in asthmatic patients or laryngospasm
in lightly anesthetized patients
 Barbiturates do not completely depress noxious
airway reflexes Airway reflexes preserved;not
suitable for LMA insertion ,may cause coughing and
laryngospasm
 Release of histamine
6/23/2017 24

25. RESPIRATORY SYSTEM
 Dose related resp depression,peak resp depression
after (1-1.5 min) after adm of bolus dose .
 More susceptible patient ch lung disease,Airway obst
 Apnea :- transient apnea for 25 sec only in 20 % cases.
 Double apnea :- 1 st during adm of drug > transient
>after 4-5 breath 2 nd apnea last for longer period .
 during this period ventilation must be assessed –
controlled ventilation .

26. CNS EFFECT
 Sedation and loss of consciousness
 Retrograde amnesia and depression of vasomotor centre.
 Induction and maintenance of anesthesia
 Rate of adm α onset
 Termination of effect take 5-10 min to awake ( after bolus )
 Awakening depend on :-
 Volume of distribution
 Plasma concentration
 Redistribution and Clearance
 Alteration in metabolism
 CNS sensitivity ↑ with age

27. CNS
 Pupil and eye :- initially pupil contract but then dilate .
 Pupillary response is lost with surgical anaesthesia .
 loss of eyelash reflex is commonly used as endpoint for
adequate induction dose .
 Following traumatic brain injury, infusion of thiopental to
produce a “barbiturate coma” lowers intracranial pressure
and may improve neurological outcome.
 Anticonvulsant property
 Burst suppression of EEG can be induced with high doses
when used in treatment of status epilepticus or intractable
rise in ICP following head injury .

28. BARBITURATES
 Cerebral blood flow --- Decrease
 Intracranial pressure---Decrease
 Cerebral perfusion pressure--- Increased
 (CPP equals cerebral artery pressure minus cerebral venous pressure or
intracranial pressure.)
 Cerebral oxygen consumption --- Decrease
(This effect of barbiturates may protect the brain from transient
episodes of focal ischemia (eg, cerebral embolism) but probably not
from global ischemia (eg, cardiac arrest).
 have an antianalgesic effect by lowering the pain threshold

29. BARBITURATES
 RENAL
 Reduce renal blood flow and glomerular filtration rate in
proportion to the fall in blood pressure.
 HEPATIC
 Hepatic blood flow is decreased.
 Induction of hepatic enzymes increases the rate of metabolism of
some drugs
 The induction of aminolevulinic acid synthetase stimulates the formation of
porphyrin (an intermediary in heme synthesis), which may precipitate
acute intermittent porphyria or variegate porphyria in susceptible
individuals.
 IMMUNOLOGICAL
 Sulfur-containing thiobarbiturates evoke mast cell histamine
release in vitro, whereas oxybarbiturates do not.

30. SODIUM THIOPENTONE
Indications
 Induction of anaesthesia
 Control convulsions
 Decreases ICP
 Neuroprotection
Contraindications
 COPD
 Severe asthama
 Porphyria
 Previous hypersensitivity
 Allergy to sulphur
PRECAUTIONS :
 Stenoticvalvular disease
 Severe hepatic disease
 Renal impairment

31. BARBITURATES
Intra-arterial Injection
 Immediate, intense vasoconstriction and excruciating
pain that radiates along the distribution of the artery.
 Severe Vasoconstriction may obscure distal arterial
pulses.
 Gangrene and permanent nerve damage may occur.
SPECIFIC COMPLICATION :

32. Mechanism of Damage
 Due to be the precipitation of thiopental crystals
inflammatory response and arteritis
microembolization that follows, eventually results in
occlusion of the distal circulation.
Treatment
 Immediate attempts to dilute the drug --- injection of saline
 Prevention of arterial spasm & sustain adequate blood flow—
 lidocaine, papaverine, or phenoxybenzamine
 stellate ganglion block or brachial plexus block
BARBITURATES

33. 6/23/2017 33

34.  Structure
Alkylphenol
 Propofol (2,6-diisopropylphenol)
 Propofol is not water soluble
 1% solution (10 mg/mL) --- an oil-in-water emulsion
Containing
 soybean oil
 glycerol
 egg lecithin
 Mechanisms of Action
 Facilitation of inhibitory neurotransmission mediated by
GABA.
Propofol

35. Pharmacokinetics
 DISTRIBUTION
 High lipid solubility
 onset of action that is almost as rapid as that of thiopental
(one-arm-to-brain circulation time).
 Awakening from a single bolus dose is also rapid due to a
very short initial distribution half-life (2–8 min).
 Recovery --- rapid
 Hangover --- less
 This makes it a good agent for outpatient anesthesia.
 BIOTRANSFORMATION
 Hepatic and extra hepatic metabolism
 EXCRETION
 Primarily excreted in the urine
 chronic renal failure does not affect clearance of the parent drug.
Propofol

36. Effects on organ
CARDIOVASCULAR
 Blood pressure
Propofol causes the most marked fall in blood
pressure of all the induction drugs & is d/t fall in
systemic vascular resistance accompanied with slight
increase in heart rate
The fall in blood pressure is dose dependent and is
most marked in the elderly and in shocked patients.
This can be minimized by slow injection – avoiding
inadvertent overdose.
 HEART RATE
No change /Bradycardia
Propofol

37. RESPIRATORY
 Profound respiratory depressant following an induction
dose---apnea
 Inhibits hypoxic ventilatory drive and depresses the
normal response to hypercarbia.
 Depression of upper airway reflexes
 Helpful during intubation or laryngeal mask placement in the
absence of paralysis.
 Lower incidence of wheezing
 Safe in asthmatic patients
6/23/2017 37

38. Propofol
CEREBRAL
 Cerebral blood flow---- decreases
 Intracranial pressure---- decreases.
 Antiemetic effects
 preferred drug for outpatient anesthesia.
 Anticonvulsant properties (ie burst suppression)
 used to terminate status epilepticus.
 Safely administered to epileptic patients.
 Intraocular pressure----Decreases

39. Use :
 Induction of Anesthesia 1.5 to 2.5 mg/kg
 Intravenous Sedation 25 to 100 µg/kg per minute IV
 Maintenance of Anesthesia 100 to 300 µg/kg per minute
IV
 Nonhypnotic Therapeutic Applications
 Antiemetic Effects
 Mech –unknown
 10 to 15 mg IV
 Anticonvulsant Activity
 Attenuation of Bronchoconstriction
Propofol

40. Propofol
Specific complication
 Lactic Acidosis or propofol infusion syndrome
 Prolonged high-dose infusions of propofol (>75 µg/kg per minute)
for longer than 24 hours.
 Mechanism –
 Unclear
 Cytopathic hypoxia of the electron transport chain and impaired
oxidation of long-chain fatty acids
 C/F
 Unexpected tachycardia
 Diagnosis
 Arterial blood gases and serum lactate concentrations
 Treatment
 Metabolic acidosis in its early stages is reversible with
discontinuation of propofol administration.

41.  Pain on Injection
 Most common
 Reduced by
 1% lidocaine
 Potent short-acting opioid eg Fentanyl
 Bacterial Growth
 Supports the growth of Escherichia coli and Pseudomonas aeruginosa.
 Recommendation:
 An aseptic technique be used in handling propofol.
 The contents of the ampule containing propofol should be withdrawn into a
sterile syringe immediately after opening and administered promptly.
 The contents of an opened ampule must be discarded if they are not used within
6 hours.
Propofol

42. PROPOFOL
Advantages
 Rapid induction
 Anti emetic effect
 TIVA
 Agent of choice for day care
surgery
Disadvantages
 Induction apnoea
 Hypotension
 Dose dependant bradycardia
 Dose dependant resp
depression
 Pain during injection
 It is also euphorigenic but
does not have residual
psychotic effects like
Ketamine

43. 6/23/2017 43

44. Ketamine Mechanisms of Action
 NMDA(N-methyl-D-
aspartate) receptor
antagonist.
 Produce dissociative
Anaesthesia
Structure :
 structural analogue of
phencyclidine
6/23/2017 44

45. PHARMACOKINETICS
 ABSORPTION
 Intravenously or intramuscularly
 Peak plasma levels are usually achieved within 10–15 min
after intramuscular injection.
 DISTRIBUTION
 Ketamine is more lipid soluble and less protein bound than
thiopental
 Half-life is 10–15 min
 Awakening is due to redistribution to peripheral
compartments.
 BIOTRANSFORMATION
 Liver to several metabolites (eg, norketamine)
 EXCRETION
 End products of biotransformation are excreted renally
KETAMINE

46. Ketamine
uses
Induction of general anesthesia 0.5-2 mg/kg IV;
4-6 mg/kg IM
Maintenance of general anesthesia 0.5-1 mg/kg IV with N2O 50% in
O2
15-45 µg/kg/min IV with N2O 50-
70% in O2
30-90 µg/kg/min IV without N2O
Sedation and analgesia 0.2-0.8 mg/kg IV over 2-3 min 2-
4 mg/kg IM
Preemptive/preventive analgesia 0.15-0.25 mg/kg IV
Intra thecal ketamine 0.5-0.75 mg/kg

47. Effects on organ system
Central Nervous System
 cerebral blood flow --- Increase
 CMRO2---Increase
 Intracranial Pressure--- Increase
Cardiovascular System
 Sympathetic nervous system stimulation
 Systemic and pulmonary arterial blood pressure---- increased
 Heart rate ---- increased
 Cardiac output---- increased
 Myocardial oxygen requirements ---- increased
KETAMINE

48.  But in Critically ill patients
 Unexpected decreases in systemic blood pressure and cardiac output,
which may reflect a depletion of endogenous catecholamine stores and
exhaustion of sympathetic nervous system compensatory mechanisms.
 Unmasking of ketamine's direct myocardial depressant effects.
Ventilation and Airway
 Depression of ventilation: not significant
 Upper airway skeletal muscle tone:maintained,
 Upper airway reflexes : intact
 Salivary and tracheobronchial mucous gland: Increased secretions are
increased
 Use antisialagogue before ketamine
 Bronchodilatory effects
 Drug of choice for induction patients with asthma
KETAMINE

49. Specific Complications
Emergence Delirium (Psychedelic Effects)
• In postoperative period visual, auditory, proprioceptive,
and confusional illusions, which may progress to delirium.
• Dreams and hallucinations can occur up to 24 hours after
the administration of ketamine.
• Mechanisms
• Emergence delirium probably occurs secondary to
ketamine-induced depression of the inferior colliculus
and medial geniculate nucleus, thus leading to the
misinterpretation of auditory and visual stimuli.
KETAMINE

50.  The loss of skin and musculoskeletal sensations results in a decreased ability to
perceive gravity producing a sensation of bodily detachment or floating in space
 FACTORS ASSOCIATED WITH AN INCREASED
INCIDENCE
 Age greater than 15 years
 Female gender
 Dose greater than 2 mg/kg IV
 History of frequent dreaming
 PREVENTION OF KETAMINE-INDUCED EMERGENCE
DELIRIUM
 Midazolam (administer IV about 5 minutes before induction
of anesthesia with ketamine)
 Prospective discussion with patient about side effects of
ketamine
KETAMINE

51. KETAMINE
 ADVANTAGE
 increase HR,BP,CO
 In asthmatic
 For short procedure
 Combination with BZD
can use in cardiac
catheterization and
angiography .
 In OPD surgical procedure
 Good analgesic property
 DISADVANTAGE
 limb movement and
Nystagmus
 Emergence phenomenon
in 50 %
 Hypertensive
 Increased ICP , IOT
 Uterine stimulation
 Schizophrenia , psychosis
 Poor muscle relaxation

52. KETAMINE
 INDICATION
 CVS except IHD
 Resp. disorder
 Hemodynamica compromised
states ( pericarditis , cardiac
tamponade , CM , shock )
 Traumatic and septic shock
 As component in TIVA with
midaz and propofol provide
better hemodynamic stability
 In cancer patient , neuropathy
 Phantom or ischaemic limb pain
 Fibromyalgia , visceral pain
 Migraine
 CONTRAINDICATION
 ↑ ICP , SOL brain
 Large size Infarct
 Ophthalmic injury
 IHD
 Vascular aneurysm
 Schizophrenia

53. 6/23/2017 53

54.  Structure
 Carboxylated imidazole-containing compound
 Commercial Preparation
 Etomidate is prepared as a fat emulsion, and pain on
injection and venous irritation is unlikely.
 Mechanism of Action
 GABA receptors
ETOMIDATE

55. Uses
 Etomidate (0.2 to 0.4 mg/kg IV)
 As an alternative to propofol or barbiturates for the
induction of anesthesia, especially in the presence of
an unstable cardiovascular system.
ETOMIDATE

56. Effects on organ system
Central Nervous System
 Potent direct cerebral vasoconstrictor that decreases cerebral blood
flow and CMRO2
 Activate seizure foci
 Caution in patients with focal epilepsy
 Facilitate the localization of seizure foci in patients undergoing
the cortical resection of epileptogenic tissue.
ETOMIDATE

57. Cardiovascular System
 Cardiovascular stability (minimal changes in heart rate, stroke
volume, cardiac output)
 Preferred for Induction of anesthesia in patients with little or no
cardiac reserve.
6/23/2017 57
ETOMIDATE

58.  Ventilation
 Depressant effects on ventilation
 Pain on Injection
 Pain on injection and venous irritation has been virtually
eliminated with use of etomidate preparations utilizing a lipid
emulsion vehicle rather than propylene glycol
 Myoclonus (spontaneous movements)
 Caution in the use of this drug for the induction of anesthesia in patients
with a history of seizure activity.
 Adrenocortical Suppression
 lasts 4 to 8 hours after an intravenous induction dose of
etomidate.
 Be considered desirable from the standpoint of “stress-free”
anesthesia.
ETOMIDATE

59. ETOMIDATE
Clinical use Dose
Induction of general anaesthesia 0.2-0.6mg/kg I.V
Maintainance of general
anaesthesia
10mcg/kg/min I.V. with N2o & an
opiate
Sedation & Analgesia Limited to periods of brief sedation
because of inhibition of steriod
synthesis

60. 6/23/2017 60

61.  E.g.
 Midazolam
 Diazepam
MECHANISM OF ACTION
 Facilitating the actions of γ-aminobutyric acid (GABA),
the principal inhibitory neurotransmitter in the CNS
 Benzodiazepines do not activate GABAA receptors but
rather enhance the affinity of the receptors for GABA.
BENZODIAZEPINE

62. BENZODIAZEPINE
Uses and Doses of Commonly Used Benzodiazepines

63. EFFECTS ON ORGAN SYSTEMS
CARDIOVASCULAR
Minimal cardiovascular depressant effects even at induction
doses.
Arterial blood pressure
Cardiac output decline slightly
Peripheral vascular resistance
Heart rate ---- slight rise
Midazolam tends to reduce blood pressure and peripheral
vascular resistance more than diazepam.
BENZODIAZEPINE

64. RESPIRATORY
Depress the ventilatory response to CO2
Apnea may be less common after benzodiazepine
induction than after barbiturate induction.
Ventilation must be monitored in all patients receiving
intravenous benzodiazepines, and resuscitation
equipment must be immediately available.
BENZODIAZEPINE

65. CEREBRAL
 Cerebral oxygen consumption, cerebral blood flow, and
intracranial pressure----Reduce
 Anti seizures properties
 Antegrade amnesia------premedication
 Mild muscle-relaxant property --- mediated at the
spinal cord level, not at the neuromuscular junction.
 Slower loss of consciousness and a longer recovery
BENZODIAZEPINE

66. 6/23/2017 66

67.  E.g.
 Morphine
 Fentanyl
 Sufentanyl
 Meperidine
Mechanisms of Action
 Opioids bind to specific receptors located throughout the central
nervous system and other tissues.
 Four major types of opioid receptor
 µ
 Κ
 σ
 δ
 Opiate–receptor activation inhibits the presynaptic release and postsynaptic response to
excitatory neurotransmitters (eg, acetylcholine, substance P) from nociceptive neurons.
OPIOIDS

68. Uses and Doses of Common
Opioids
OPIOIDS

69. EFFECTS ON ORGAN SYSTEMS
CARDIOVASCULAR
Do not seriously impair cardiovascular function.
Cardiac contractility--- do not depress (except meperidine)
Heart rate
 Increase ----Meperidine
 Decrease ---High doses of morphine, fentanyl, sufentanil.
Blood pressure --- Decreased
 As a result of bradycardia, venodilation, and decreased sympathetic reflexes
 Meperidine and morphine --- can lead to profound drops in systemic
vascular resistance and arterial blood pressure due to histamine release
 The effects of histamine release can be minimized in susceptible patients by
slow opioid infusion, adequate intravascular volume, or pretreatment with
H1 and H2 histamine antagonists.
OPIOIDS

70. RESPIRATORY
 Respiratory rate– decrease
 Apneic threshold( the highest PaCO2 at which a patient remains
apneic) --- elevated
 Hypoxic drive -- decreased.
 Histamine-induced bronchospasm --- Morphine and meperidine
 Chest wall rigidity ( fentanyl, sufentanil, and alfentanil)
 Enough to prevent adequate ventilation.
 Centrally mediated muscle contraction
 After large drug boluses
 Effectively treated with neuromuscular blocking agents.
 Blunt airway reflex
OPIOIDS

71. CEREBRAL
 Effects on cerebral perfusion and intracranial pressure -
--variable
 Cerebral oxygen consumption, cerebral blood flow, and
intracranial pressure--- slight reduction.
 Stimulation of the medullary chemoreceptor trigger
zone is ----high incidence of nausea and vomiting.
 Physical dependence
 Use of opioids in epidural and subdural spaces has
revolutionized pain management.
 Management of perioperative shivering ---Intravenous
meperidine
OPIOIDS

72.  GASTROINTESTINAL
 slow gastric emptying time by reducing peristalsis.
 Biliary colic may result from opioid-induced
contraction of the sphincter of Oddi.
 ENDOCRINE
 Stress response to surgical stimulation ---decresed
 Ischemic heart disease patients may benefit from
attenuation of the stress response .
OPIOIDS

73. Case Scenario 1
A patient with intestinal obstruction having
wheezing requires an emergency laparotomy. Which
induction drug would you use?

74. Ketamine
Porpofol
6/23/2017 74

75. Case Scenario 2
A patient a history of golttis cancer has signs of
respiratory distress and marked stridor requires a
tracheostomy. Which IV induction drug would you
use?

76.  Any difficult airway
 Avoid ----IV induction drugs and muscle relaxants
(respiratory depressant properties)
 It may not be possible to perform facemask ventilation
should this patient become apnoeic.
 Inhalational induction with halothane or sevoflurane
should be employed.
6/23/2017 76

77. Case Scenario 3
A patient requires a burns dressing change. Which
induction drug would you use?

78.  Ketamine is an ideal drug to be used for minor
procedures. For burns dressing changes, a sub-
anaesthetic dose can be used.
 It will provide sedation and analgesia, preserving the
protective airway reflexes.
 Propofol + ketamine
 Propofol + fentanyl
6/23/2017 78

79. A patient with a history of heart failure and MI requires
a general anaesthetic for cholecytectomy . Which
induction drug would you choose?
Case Scenario 4

80.  Etomidate due to its limited effect on the
cardiovascular system.
 High dose Fentanyl
 Be cautious while using Propofol and thiopental
 Avoid Ketamine
The lowest possible dose is given, it is given slowly
and it is titrated to effect with Intra-arterial blood
pressure monitoring.
6/23/2017 80

81. Case Scenario 5
Which IV induction drug would be most appropriate to use
in a hypovolaemic patient. (Blunt Trauma abdomen)

82.  Ketamine
 Etomidate
6/23/2017 82

83. Case Scenario 6
A patient with porphyria comes for an inguinal hernia repair
and is requesting a general anaesthetic. Which induction
drug would you use?

84.  Avoid ---Thiopental
 Most preferred ---Propofol
6/23/2017 84

85. Case Scenario 7
 An adult patient requires sedation on the
intensive care unit. Which of the induction
drugs would be appropriate to run as an
infusion?

86.  Preferred -- Midazolam , Propofol
 Avoid
 Thiopental
 due to accumulation
 etomidate
 effect on adrenal steroid hormone synthesis
6/23/2017 86

87. Case Scenario 8
 Patient coming for Fibroadenoma excision under GA
( Day care surgery). Drug of choice for induction ??

88. Propofol
6/23/2017 88