Induction Meds: Ketamine Flashcards

(45 cards)

1
Q

What type of drug is ketamine?

A
  • Phenycyclidine derivative;
    NMDA receptor antagonist (PCP; “angel dust”)
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2
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”)
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3
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.
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3
Q

What are the two greatest disadvantages of ketamine?

A
  • Emergence delirium
  • Abuse potential
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4
Q

What is Benzethonium Chloride?

A

Ketamine preservative that inhibits ACh receptors

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5
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
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6
Q

What benefits does a racemic ketamine mixture offer?

A
  • Less fatigue & cognitive impairment
  • Inhibits catecholamine reuptake at nerve endings (like cocaine).
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7
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

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8
Q

What are Ketamine’s secondary receptor sites?

A
  • Weak GABA-A effects.
  • Opioid (μ, δ, and κ)
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9
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)
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10
Q

What is Ketamine’s duration of action?

A

10-20 min

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11
Q

What is the Vd of ketamine?

A

3L/kg (large)

S20

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12
Q

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

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

S21

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13
Q

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

A

Norketamine is metabolite (⅓ potency and prolongs analgesia).

S21

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14
Q

In what patient population is ketamine tolerance most often seen?

A

Burn patients

S21

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15
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

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16
Q

What is the maintenance dosing of ketamine?

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

S22

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17
Q

What is the subanesthetic/analgesic dose of ketamine?

A

0.2 - 0.5 mg/kg IV

S22

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18
Q

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

A

1-2 mg/kg/hour

S22

19
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

20
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.
21
Q

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

A

Glycopyrrolate: 0.2mg

S23

22
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

23
Q

What patient populations is ketamine best used for?

A
  • Acutely hypovolemic patients
  • Asthmatics
  • Mental health patients

S25

24
When would you do an IM induction of a patient?
Uncooperative and difficult-to-manage mentally challenged patients. ## Footnote S25
25
Though ketamine has many indications, when should it be avoided?
- Patients with **pulmonary HTN and ↑ICP**. ## Footnote S26
26
What are Ketamine's effects on ICP? Why?
- ↑ICP via ↑CBF by 60% - **Potent cerebral vasodilator**. ## Footnote S27
27
At what dosing will the ICP increasing effects of ketamine plateau?
2mg/kg IV ## Footnote S27
28
Due to ketamine's increased excitatory EEG activity, how much does seizure potential increase with administration?
Trick question. **No increase in seizure potential with ketamine**. | Increased amplitude with SSEP is reduced by N20 ## Footnote S27
29
What does the cardiovascular profile of ketamine look like? How can this side effect profile be blunted?
- SNS stimulation ( ↑ in sBP, PAP, HR, CO, etc.) - Blunted via pre-med with benzo's, volatiles, or nitrous. ## Footnote S28
30
Say you just gave ketamine and you have an unexpected drop in systolic BP and CO. What happened? How do you treat it?
- *Depleted catecholamine stores* - **Treat with direct-acting SNS agents (ex. phenylephrine)** vs indirect (ex. ephedrine). ## Footnote S28
31
What is the Pulmonary profile of ketamine?
- No depression of ventilation - CO₂ response maintained. - ↑ salivary excretion - Intact upper airway tone & reflexes. - Bronchodilator with no histamine release. ## Footnote S30
32
What does emergence delirium present like with ketamine? | aka Psychedelic Effects
- Visual, auditory, proprioceptive illusions. Morbid & vivid dreams up to 24 hours. ## Footnote S31
33
What is the proposed physiologic mechanism of action for emergence delirium occurrence with ketamine?
Depression of inferior colliculus & medial geniculate nucleus. ## Footnote S31
34
What percentage of patients will develop ketamine induced emergence delirium? How can it be prevented?
- Psychedelic effects in **5 - 30%** of patients. - **Pre-med with midazolam & glycopyrrolate**. ## Footnote S31
35
What "other systems" effects does ketamine have?
- Non-depolarizing *NMBs enhancement*. - Succinylcholine prolongation via p*lasma cholinesterase inhibition.* - *PLT aggregation inhibition* ## Footnote S32
36
What are ketamine's most common drug interactions?
- **Volatiles**→ hypotension - **Non-depolarizing NMBs** → enhancement - **Succinylcholine** → prolongation ## Footnote S33
37
Why does ketamine prolong succinylcholine's effects?
Ketamine is a plasma cholinesterase inhibitor. ## Footnote S32
38
Which induction agent has the highest analgesic properties?
- Ketamine ## Footnote S35
39
Why would ketamine be a decent induction drug for an OSA patient? Why not?
- Preservation of upper airway reflexes & ventilatory function . - Risks: Sialagogue, Psych effects, SNS activation ## Footnote S34
40
What type of anesthesia does Ketamine produce?
Dissociative anesthesia
41
What two properties does Ketamine possess?
Amnestic & intense analgesia
42
What is Ketamine's lipid solubility? What is the result of this?
- **Highly lipid soluble** (5-10x greater than thiopental). - Results: **Brain** →** non plasma bound** → **peripheral tissue**.
43
What is the Elimination 1/2 time of Ketamine?
2-3 hours
44
What are Ketamine's Clinical Uses?
* Burn dressing changes * debridement * skin grafting procedures * Reversal of opioid tolerance * Improvement of psych disorders * Restless leg syndrome ## Footnote S26