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Anesthesia Pharm (Spring '24) - A > 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.
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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.

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

A
  • Onset: 1 minute
  • 76% albumin bound
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8
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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9
Q

What metabolizes etomidate?
What is the elimination profile?

A
  • CYP450’s & plasma esterases
  • Elimination ½ time = 2-5 hours with 85% via urine and 10 - 13% via bile.
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10
Q

What is the induction dosage range for etomidate?

A
  • 0.2 - 0.4 mg/kg
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11
Q

What is the best use for etomidate?

A
  • Induction for unstable cardiac patients.
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12
Q

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

A
  • Opioids, etomidate has no analgesic effects.
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13
Q

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

A
  • Involuntary Myoclonic Movements ( 50 - 80 %) of administrations.
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14
Q

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

A

Fentanyl 1-2 μg/kg IV

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15
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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16
Q

How long does adrenocortical suppression with etomidate last?
What two pathologies would cause you to hesitate before giving etomidate?

A
  • 4-8 hours.
  • Sepsis & hemorrhage (anything where you need an intact cortisol response).
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17
Q

Compared to thiopental, etomidate will lower plasma concentrations of what substance?

A

Cortisol

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18
Q

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

A
  • Etomidate = ↓CBF & ↓CMRO₂ due to being a direct cerebral vasoconstrictor.
  • Will also ↓ICP.
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19
Q

CMRO₂ is couple with both CBF and _______.

A

CMRG (cerebral metabolic requirement of glucose)

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20
Q

What is the EEG profile of etomidate?

A
  • More excitatory than thiopental
  • May activate seizure foci
  • Augments SSEP amplitude.
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21
Q

Though etomidate is great for cardiac patients, what condition can result in significant hypotension if not treated prior to induction?

A
  • Hypovolemia
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22
Q

Histamine release via etomidate is mediated through what?

A
  • Trick question. Etomidate does not release histamine.
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23
Q

What is the pulmonary profile of etomidate?

A
  • No change in minute ventilation.
  • Less respiratory depression than barbiturates
  • Rapid IV produces apnea
  • Stimulates CO₂ medullary centers
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24
Q

What type of drug is ketamine?
What type of anesthesia does it produce?
What two properties does it possess?

A
  • Phenycyclidine derivative; NMDA receptor antagonist (PCP; “angel dust”)
  • Dissociative anesthesia
  • Amnestic & intense analgesia
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25
Q

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

A

“Zonked” state

  • Non-communicative but awake
  • Hyptonus & purposeful movements
  • Eyes open but “no one’s home”.
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26
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.
27
Q

What are the two greatest disadvantages of ketamine?

A
  • Emergence delirium
  • Abuse potential
28
Q

What is Benzethonium Chloride? What is it’s relevance?

A
  • Ketamine preservative that inhibits ACh receptors
29
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
30
Q

What benefits does a racemic ketamine mixture offer?

A
  • Less fatigue & cognitive impairment
  • Inhibits catecholamine reuptake at nerve endings (like cocaine).
31
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.
32
Q

What are Ketamine’s secondary receptor sites?

A
  • Weak GABAA effects.
  • Opioid (μ, δ, and κ)
33
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)
34
Q

What is Ketamine’s duration of action?
What about its lipid solubility?
What is the result of this?

A
  • 10-20 min
  • Highly lipid soluble (5-10x greater than thiopental).
  • Results: Brain → non plasma bound → peripheral tissue.
35
Q

What is the Vd and E½ time of ketamine?

A
  • Vd = 3L/kg
  • E ½ = 2-3 hours
36
Q

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

A
  • Clearance: high hepatic clearance (1L/min)
  • Metabolism: CYP450’s.
  • Excretion: kidneys
37
Q

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

A

Norketamine is metabolite (⅓ potency and prolongs analgesia).

38
Q

In what patient population is ketamine tolerance most often seen?

A

Burn patients

39
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
40
Q

What is the maintenance dosing of ketamine?

A
  • 0.2 - 0.5 mg/kg IV
  • 4 - 8 mg/kg IM
41
Q

What is the subanesthetic/analgesic dose of ketamine?

A
  • 0.2 - 0.5 mg/kg IV
42
Q

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

A

1-2 mg/kg/hour

43
Q

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

A
  • 30mg epidural
  • 5 - 50 mg via intrathecal/spinal/subarachnoid
44
Q

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

A
  • Manage excessive secretions during intubation & watch for coughing/laryngospasm.
45
Q

What drug and dosing of said drug should be used to treat excessive salivary secretions from ketamine administration?

A

Glycopyrrolate: 0.2mg

46
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.
47
Q

What patient populations is ketamine best used for?

A
  • Acutely hypovolemic patients
  • Asthmatics
  • Mental health patients
48
Q

When would you do an IM induction of a patient?

A
  • Uncooperative and difficult-to-manage mentally challenged patients.
49
Q

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

A
  • Patients with pulmonary HTN and ↑ICP.
50
Q

What are Ketamine’s effects on ICP? Why?

A
  • ↑ICP via ↑CBF by 60%
  • Potent cerebral vasodilator.
51
Q

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

A
  • 2mg/kg IV
52
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.

53
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.
54
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).
55
Q

What is the Pulmonary profile of ketamine?

A
  • No depression of ventilation with CO₂ response maintained.
  • ↑ salivary excretion
  • Intact upper airway tone & reflexes.
  • Bronchodilator with no histamine release.
56
Q

What does emergence delirium present like with ketamine?

A
  • Visual, auditory, proprioceptive illusions. Morbid & vivid dreams up to 24 hours.
57
Q

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

A

Depression of inferior colliculus & medial geniculate nucleus.

58
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.
59
Q

What “other systems” effects does ketamine have?

A
  • Non-depolarizing NMBs enhancement.
  • Succinylcholine prolongation via plasma cholinesterase inhibition.
  • PLT aggregation inhibition
60
Q

What are ketamine’s most common drug interactions?

A
  • Volatiles → hypotension
  • Non-depolarizing NMBs → enhancement
  • Succinylcholine → prolongation
61
Q

Why does ketamine prolong succinylcholine’s effects?

A

Ketamine is a plasma cholinesterase inhibitor.

62
Q

Which induction agent has the highest analgesic properties?

A
  • Ketamine
63
Q

Why would ketamine be a decent induction drug for an OSA patient? Why not?

A
  • Preservation of upper airway reflexes & ventilatory function.
  • Sialagogue.

Anesthesia Pharm (Spring '24) - A (20 decks)

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