Induction Drugs (Etomidate & Ketamine) (Exam II) Flashcards by Katie Johnson

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)?

Lipid; potency
Sulfur

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What is unique about Etomidate’s organic chemical structure?

It is the only carboxylated imidazole containing compound.

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When is etomidate water-soluble vs lipid-soluble?

H₂O-soluble at acidic pH.
Lipid-soluble at physiologic pH.

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

35% propylene glycol resulting in pain on injection.

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

Etomidate - can be given sub-lingual.

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Why does etomidate have a low incidence of myoclonus?

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

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

Onset: 1 minute
76% albumin bound

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

Large Vd
5x faster clearance than thiopental resulting in a prompt awakening.

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What metabolizes etomidate?
What is the elimination profile?

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

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What is the induction dosage range for etomidate?

0.2 - 0.4 mg/kg

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What is the best use for etomidate?

Induction for unstable cardiac patients.

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

Opioids, etomidate has no analgesic effects.

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

Involuntary Myoclonic Movements ( 50 - 80 %) of administrations.

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

Fentanyl 1-2 μg/kg IV

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Etomidate has a dose dependent inhibition of the conversion of cholesterol to _________.
What does this mean clinically?

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

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

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

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

Cortisol

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

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

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CMRO₂ is couple with both CBF and _______.

CMRG (cerebral metabolic requirement of glucose)

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What is the EEG profile of etomidate?

More excitatory than thiopental
May activate seizure foci
Augments SSEP amplitude.

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

Hypovolemia

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Histamine release via etomidate is mediated through what?

Trick question. Etomidate does not release histamine.

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What is the pulmonary profile of etomidate?

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

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

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

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

**"Zonked" state** - Non-communicative but awake - Hyptonus & purposeful movements - Eyes open but "no one's home".

What are ketamine's two greatest advantages over propofol or etomidate?

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

What are the two greatest disadvantages of ketamine?

- Emergence delirium - Abuse potential

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

- Ketamine preservative that inhibits ACh receptors

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

S-Ketamine (left-handed isomer) is essentially better. - More intense analgesia - ↑metabolism & recovery - Less salivation - Lower emergence delirium

What benefits does a racemic ketamine mixture offer?

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

What is Ketamine's main mechanism of action?

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

What are Ketamine's secondary receptor sites?

- Weak GABA_A effects. - Opioid (μ, δ, and κ)

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

- IV: 1 min - IM: 5 min (mostly for pediatric patients)

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

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

What is the Vd and E½ time of ketamine?

- Vd = 3L/kg - E ½ = 2-3 hours

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

- Clearance: high hepatic clearance (1L/min) - Metabolism: CYP450's. - Excretion: kidneys

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

Norketamine is metabolite (⅓ potency and prolongs analgesia).

In what patient population is ketamine tolerance most often seen?

Burn patients

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

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

What is the maintenance dosing of ketamine?

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

What is the subanesthetic/analgesic dose of ketamine?

- 0.2 - 0.5 mg/kg IV

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

1-2 mg/kg/**hour**

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

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

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

- Manage excessive secretions during intubation & watch for coughing/laryngospasm.

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

**Glycopyrrolate: 0.2mg**

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?

- Wake up in 10-20 minutes - Full consciousness in 60 - 90 min - Amnestic effects should also wear off in 60 - 90 min.

What patient populations is ketamine best used for?

- Acutely hypovolemic patients - Asthmatics - Mental health patients

When would you do an IM induction of a patient?

- Uncooperative and difficult-to-manage mentally challenged patients.

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

- Patients with **pulmonary HTN and ↑ICP**.

What are Ketamine's effects on ICP? Why?

- ↑ICP via ↑CBF by 60% - **Potent cerebral vasodilator**.

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

- 2mg/kg IV

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**.

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.

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).

What is the Pulmonary profile of ketamine?

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

What does emergence delirium present like with ketamine?

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

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

Depression of inferior colliculus & medial geniculate nucleus.

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**.

What "other systems" effects does ketamine have?

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

What are ketamine's most common drug interactions?

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

Why does ketamine prolong succinylcholine's effects?

Ketamine is a plasma cholinesterase inhibitor.

Which induction agent has the highest analgesic properties?

- Ketamine

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

- Preservation of upper airway reflexes & ventilatory function. - Sialagogue.