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KM (Spring 2024) Anesthesia Pharm ** > *Induction Drugs (Etomidate & Ketamine) (Exam II) > Flashcards

*Induction Drugs (Etomidate & Ketamine) (Exam II) Flashcards

1
Q

In general, thiobarbiturates are much more _____ soluble and have a greater _______ than oxybarbiturates.

What atom do thiobarbiturates have in lieu of an oxygen in the second position (like oxybarbiturates)?

A
  • Lipid; potency
  • Sulfur
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2
Q

What is unique about Etomidate’s organic chemical structure?

A

It is the only carboxylated imidazole containing compound.

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3
Q

When is etomidate water-soluble vs lipid-soluble?

A
  • H₂O-soluble at acidic pH.
  • Lipid-soluble at physiologic pH.
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4
Q

What percentage of etomidate is propylene glycol?
What is the result of this?

A
  • 35% propylene glycol
  • resulting in pain on injection and venous irritation.
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5
Q

Which induction agent can be given without an IV?
How is this?

A

Etomidate - can be given sub-lingual.

Only drug with direct systemic absorption in oral mucosa that bypasses hepatic metabolism

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6
Q

Why does etomidate have a low incidence of myoclonus?

A
  • Trick Question. Etomidate has a high incidence of myoclonus, just like all other induction agents.
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7
Q

What is the onset of Etomidate?

A

1 minute

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8
Q

How much of Etomidate is protein bound?
What protein does it bind to?

A

76% albumin bound

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9
Q

What is etomidate’s Vd?
How does clearance compare to thiopental?
What is the result of this clearance?

A
  • Large Vd
  • 5x faster clearance than thiopental resulting in a prompt awakening.
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10
Q

What metabolizes Etomidate?

A

Hydrolysis by hepatic microsomal enzymes and plasma esterases.

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11
Q

What is the Elimination Half-time and profile of Etomidate?

A

Elimination 1/2 time: 2-5 hours

Elimination:
* 85% in urine
* 10% - 13% in bile

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12
Q

What is the induction dosage range for Etomidate?

A

0.3 mg/kg IV

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13
Q

What is Etomidate an alternative for IV induction?

A

Propofol or Barbituates

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14
Q

Drug effects that Etomidate does not have?

A

No hangover or cumulative drug effect

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15
Q

What is the best use for Etomidate?

A
  • Induction for unstable cardiac patients.

Especially with little or no cardiac reserve

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16
Q

What needs to be used concurrently with etomidate when performing a laryngoscopy/tracheal intubation?
Why?

A
  • use with Opioids
  • etomidate has no analgesic effects.
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17
Q

What is Etomidate’s most common side effect?
How often does this occur?

A
  • Involuntary Myoclonic Movements
  • that occurs with 50 - 80 % of administrations.
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18
Q

What should be administered with Etomidate to prevent involuntary myoclonic movements?

A

Fentanyl 1-2 μg/kg IV

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19
Q

Etomidate has a dose dependent inhibition of the conversion of cholesterol to _________________.

What does this mean clinically?

A
  • Cortisol
  • Etomidate decreases SNS capability to respond to stress (longer vent times, hypotension, etc.)
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20
Q

How long does adrenocortical suppression with etomidate last?

A
  • 4-8 hours.
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21
Q

What two pathologies would cause you to hesitate before giving Etomidate?

A

Caution with sepsis and hemorrhage

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22
Q

Compared to Thiopental, Etomidate will lower plasma concentrations of what substance?

A

Cortisol

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23
Q

What are etomidate’s effects on CBF & CMRO₂ ?
Why is this and what does it do?

A

↓CBF & ↓CMRO₂ 35%-45% due to being
a potent direct cerebral vasoconstrictor.

  • Will also ↓ICP.
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24
Q

CMRO₂ is couple with both CBF and _______.

A

CMRG (cerebral metabolic requirement of glucose)

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25
Q

What is the EEG profile of etomidate?

A
  • More excitatory than thiopental
  • May activate seizure foci
  • Augments SSEP amplitude.
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26
Q

positive side effects of Etomidate

A
  • CV stable
  • minimal changes in HR, SV, CO, and contractility
  • No intra-arterial damage
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27
Q

Etomidate results in significant hypotension if _________not treated prior to induction?

A
  • Hypovolemia

esp. high 0.45 mg/kg IV

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28
Q

Histamine release via etomidate is mediated through what?

A
  • Trick question. Etomidate does not release histamine.
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29
Q

What is the pulmonary profile of etomidate?

A
  • No change in minute ventilation.
    d/t increase in respiratory rate compensate decrease in tidal volume
  • Less respiratory depression than barbiturates
  • Rapid IV produces apnea
    -Stimulates CO₂ medullary centers
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30
Q

What type of drug is ketamine?

A
  • Phenycyclidine derivative;
    NMDA receptor antagonist (PCP; “angel dust”)
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31
Q

What type of anesthesia does Ketamine produce?

A

Dissociative anesthesia

32
Q

What two properties does Ketamine possess?

A

Amnestic & intense analgesia

33
Q

What signs and symptoms does dissociative anesthesia (ketamine) produce?

A

“Zonked” state

  • Non-communicative but awake
  • Hyptonus & purposeful movements
  • Cataleptic state: eyes open with a slow nystagmic gaze (“no one’s home”)
34
Q

What are Ketamine’s two greatest advantages over Propofol or Etomidate?

A
  • No pain at injection (no propylene glycol)
  • Profound analgesia at sub-anesthetic doses.
35
Q

What are the two greatest disadvantages of ketamine?

A
  • Emergence delirium
  • Abuse potential
36
Q

What is Benzethonium Chloride?

A

Ketamine preservative that inhibits ACh receptors

37
Q

Differentiate S(+)Ketamine vs R(-)Ketamine.

A

S-Ketamine (left-handed isomer) is essentially better.

  • More intense analgesia
  • ↑ metabolism & recovery
  • Less salivation
  • Lower emergence delirium
38
Q

What benefits does a racemic ketamine mixture offer?

A
  • Less fatigue & cognitive impairment
  • Inhibits catecholamine reuptake at nerve endings (like cocaine).
39
Q

What is Ketamine’s main mechanism of action?

A
  • Non-competitive inhibition of NMDA (N-methyl-D-aspartate) receptors by inhibiting pre-synaptic release of glutamate.

Glutamate is most abundant excitatory NT in CNS

40
Q

What are Ketamine’s secondary receptor sites?

A
  • Weak GABA-A effects.
  • Opioid (μ, δ, and κ)
41
Q

What is Ketamine’s time of onset? (IV & IM)
When would this drug be utilized IM?

A
  • IV: 1 min
  • IM: 5 min (mostly for pediatric patients)
42
Q

What is Ketamine’s duration of action?

A

10-20 min

43
Q

What is Ketamine’s lipid solubility?
What is the result of this?

A
  • Highly lipid soluble (5-10x greater than thiopental).
  • Results: Brain →** non plasma bound** → peripheral tissue.
44
Q

What is the Vd of ketamine?

A

3L/kg (large)

S20

45
Q

What is the Elimination 1/2 time of Ketamine?

A

2-3 hours

46
Q

Name the pharmacokinetic profile of ketamine:
- Clearance:
- Metabolism:
- Excretion:

A
  • Clearance: high hepatic clearance (1L/min)
  • Metabolism: CYP450’s
  • Excretion: kidneys

S21

47
Q

What is the primary metabolite of ketamine and what its its significance?

A

Norketamine is metabolite (⅓ potency and prolongs analgesia).

S21

48
Q

In what patient population is ketamine tolerance most often seen?

A

Burn patients

S21

49
Q

What is the induction dose of ketamine IV?
What if it is given intramuscularly?

A
  • 0.5 - 1.5 mg/kg IV
  • 4 - 8 mg/kg IM

S22

50
Q

What is the maintenance dosing of ketamine?

A
  • 0.2 - 0.5 mg/kg IV
  • 4 - 8 mg/kg IM

S22

51
Q

What is the subanesthetic/analgesic dose of ketamine?

A

0.2 - 0.5 mg/kg IV

S22

52
Q

What is the post-operative sedation and analgesia dosing for ketamine in pediatric cardiac surgery cases?

A

1-2 mg/kg/hour

S22

53
Q

What is the neuraxial epidural analgesia dosing of ketamine?
What about intrathecal route?

A
  • 30mg epidural
  • 5 - 50 mg via intrathecal/spinal/subarachnoid

S22

54
Q

Ketamine is a potent sialagogue.
What does this mean for your clinical practice?

A
  • Manage excessive salivary secretions during intubation & watch for coughing/laryngospasm.
55
Q

What drug and dosing to treat excessive salivary secretions from ketamine administration?

A

Glycopyrrolate: 0.2mg

S23

56
Q

You gave ketamine and the patient fell asleep within 30 seconds. If you gave no more doses when would you expect the patient to:
- Wake up?
- Be fully conscious?
- Start remembering things?

A

*- Wake up *in 10-20 minutes

- Full consciousness in 60 - 90 min

  • Amnestic effects should also wear off in 60 - 90 min.

S23

57
Q

What patient populations is ketamine best used for?

A
  • Acutely hypovolemic patients
  • Asthmatics
  • Mental health patients

S25

58
Q

When would you do an IM induction of a patient?

A

Uncooperative and difficult-to-manage mentally challenged patients.

S25

59
Q

Though ketamine has many indications, when should it be avoided?

A
  • Patients with pulmonary HTN and ↑ICP.

S26

60
Q

What are Ketamine’s Clinical Uses?

A
  • Burn dressing changes
  • debridement
  • skin grafting procedures
  • Reversal of opioid tolerance
  • Improvement of psych disorders
  • Restless leg syndrome

S26

61
Q

What are Ketamine’s effects on ICP? Why?

A
  • ↑ICP via ↑CBF by 60%
  • Potent cerebral vasodilator.

S27

62
Q

At what dosing will the ICP increasing effects of ketamine plateau?

A

2mg/kg IV

S27

63
Q

Due to ketamine’s increased excitatory EEG activity, how much does seizure potential increase with administration?

A

Trick question. No increase in seizure potential with ketamine.

Increased amplitude with SSEP is reduced by N20

S27

64
Q

What does the cardiovascular profile of ketamine look like?
How can this side effect profile be blunted?

A
  • SNS stimulation ( ↑ in sBP, PAP, HR, CO, etc.)
  • Blunted via pre-med with benzo’s, volatiles, or nitrous.

S28

65
Q

Say you just gave ketamine and you have an unexpected drop in systolic BP and CO.
What happened?
How do you treat it?

A
  • Depleted catecholamine stores
  • Treat with direct-acting SNS agents (ex. phenylephrine) vs indirect (ex. ephedrine).

S28

66
Q

What is the Pulmonary profile of ketamine?

A
  • No depression of ventilation
  • CO₂ response maintained.
  • ↑ salivary excretion
  • Intact upper airway tone & reflexes.
  • Bronchodilator with no histamine release.

S30

67
Q

What does emergence delirium present like with ketamine?

aka Psychedelic Effects

A
  • Visual, auditory, proprioceptive illusions. Morbid & vivid dreams up to 24 hours.

S31

68
Q

What is the proposed physiologic mechanism of action for emergence delirium occurrence with ketamine?

A

Depression of inferior colliculus & medial geniculate nucleus.

S31

69
Q

What percentage of patients will develop ketamine induced emergence delirium?
How can it be prevented?

A
  • Psychedelic effects in 5 - 30% of patients.
  • Pre-med with midazolam & glycopyrrolate.

S31

70
Q

What “other systems” effects does ketamine have?

A
  • Non-depolarizing NMBs enhancement.
  • Succinylcholine prolongation via plasma cholinesterase inhibition.
  • PLT aggregation inhibition

S32

71
Q

What are ketamine’s most common drug interactions?

A
  • Volatiles→ hypotension
  • Non-depolarizing NMBs → enhancement
  • Succinylcholine → prolongation

S33

72
Q

Why does ketamine prolong succinylcholine’s effects?

A

Ketamine is a plasma cholinesterase inhibitor.

S32

73
Q

Which induction agent has the highest analgesic properties?

A
  • Ketamine

S35

74
Q

Why would ketamine be a decent induction drug for an OSA patient?

Why not?

A
  • Preservation of upper airway reflexes & ventilatory function
    .
  • Risks: Sialagogue, Psych effects, SNS activation

S34

75
Q

What is Ketafol?

A

Ketamine and Propofol mix

S37

76
Q

What is combining, admixing, diluting, pooling, reconstituting, repackaging, or otherwise altering a drug or bulk drug substance to create a sterile preparation?

A

Sterile compounding

S37

77
Q

What are the rules for Pharmaceuctical Compounding?

A
  • Immediate use: 1 hr to 4 hr rule
  • Single dose
  • Aseptic process maintained

S37

KM (Spring 2024) Anesthesia Pharm ** (101 decks)

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