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Clinical Meds > Induction: Prop/Etom/Ket > Flashcards

Induction: Prop/Etom/Ket Flashcards

1
Q

For Propofol, what are the doses for:
1. Induction
2. Maintenance
3. Conscious sedation

A
  1. Induction = 1.5 - 2.5 mg/kg IV
  2. Maintenance = 100 - 300 μg/kg/min
  3. Conscious sedation = 25 - 100 μg/kg/min
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2
Q

What are the inactive ingredients in propofol? Why is one particularly important?

A
  • 1.2% Lecithin (from egg yolks) can cause anaphylaxis with egg allergies.
  • 2.25% glycerol
  • 10% soybean oil
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3
Q

What are the disadvantages of propofol’s inactive ingredient composition?

A
  • ↑ bacterial growth
  • ↑ plasma triglycerides with prolonged infusions
  • Pain on injection
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4
Q

What is the mechanism of action of propofol?

A
  • GABA receptor modulator that increases Cl⁻ conductance.
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5
Q

How does propofol cause immobility through spinal cord-depression?

A
  • Trick question. Immobility from propofol is not from drug-induced spinal cord depression.
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6
Q

What are the clearance characteristics of propofol?

A

The clearance of propofol is primarily through hepatic metabolism, with minor contributions from renal clearance and pulmonary elimination.

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7
Q

What metabolizes propofol?

A
  • CYP450 and UGT1A9
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8
Q

What is the E ½ time of propofol?

A
  • 30 - 90 minutes
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9
Q

What is the context-sensitive half-time of propofol? Is this a relatively low or high context half-time?

A
  • 40 minutes (for an 8 hours infusion)
  • Low CS ½ time.
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10
Q

What are the following characteristics of propofol:
1. Elimination ½ time.
2. Volume of distribution
3. Clearance (mL/kg/min)

A
  1. E ½ time = 30 - 90 minutes
  2. Vd = 3.5 - 4.5
  3. Clearance = 30 - 60 mL/kg/min
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11
Q

Differentiate blood pressure and heart rate changes that occur with propofol vs thiopental.

A
  • Propofol: ↓BP & ↓HR
  • Thiopental: ↓BP & ↑HR
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12
Q

Does propofol cross the placenta? What are the consequences of this?

A
  • Yes but is rapidly cleared from neonatal circulation.
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13
Q

Do cirrhosis and renal dysfunction have significant effects on propofol metabolism?

A

No

(Induction drugs 1, slide 43)

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14
Q

What is the induction dose of propofol in adults? Children?

A
  • Adults: 1.5-2.5 mg/kg IV
  • Pediatrics: higher doses due to larger central volume and clearance rate.
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15
Q

What is the induction dose of propofol in the elderly?

A
  • 1 mg/kg IV (25 - 50% lower than regular adult)
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16
Q

What plasma propofol levels would correlate with unconsciousness?
What about awakening?

A
  • Unconscious: 2 - 6 μg/mL
  • Awake: 1 - 1.5 μg/mL
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17
Q

What are the characteristics of propofol in the context of conscious sedation?

A
  • Minimal analgesia but has anti-convulsive and amnestic properties.
  • Prompt recovery w/ low residual sedation
  • ↓ risk of PONV
  • Midazolam or opioids as adjuncts.
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18
Q

What are the anti-emetic properties of propofol?
Why is this thought to occur?

A
  • Very anti-emetic (more effective than ondansetron)
  • Direct depressant of vomiting center
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19
Q

What is the sub-hypnotic dosing for propofol?

A
  • 10 - 15 mg IV, followed by 10 mcg/kg/min
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20
Q

What is the anti-pruritic dosing of propofol?

A
  • 10 mg IV
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21
Q

What is the anti-convulsant dosing of propofol?

A

1mg/kg IV

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22
Q

What are “other” category benefits of propofol?

A
  • Bronchodilation
  • Anti-emetic
  • Anti-pruritic
  • Anti-convulsant
  • Low dose analgesia
  • Antioxidant
  • Does not trigger MH
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23
Q

What are propofol’s effects on CMRO₂, CBF, and ICP?

A
  • ↓ CMRO₂, CBF, and ICP
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24
Q

Large doses of propofol may ______ cerebral perfusion pressure.

A

decrease

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25
Q

Though propofol will not produce seizures, it will produce _______.

A

myoclonus

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26
Q

What is the mechanism for propofol-induced hypotension?
What conditions will exaggerate this effect?

A
  • SNS inhibition causing ↓SVR and ↓ ICF Ca⁺⁺.
  • Hypovolemia, elderly, and LV compromise
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27
Q

How is propofol-induced hypotension from induction usually counteracted?

A
  • Intubation (from laryngeal stimulation).
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28
Q

Why is bradycardia seen with propofol?
What would occur with propofol overdose?

A
  • ↓SNS response & baroreceptor reflex
    depression.
  • Profound bradycardia & eventual asystole.
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29
Q

What are the pulmonary effects of propofol?
How does this change with opioids?

A
  • Dose-dependent depression of respiratory drive.
  • Synergistic resp depression with opioids
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30
Q

What severe condition(s) can occur with prolonged propofol infusions?

A
  • Hepatocellular injury or Propofol Infusion Syndrome.
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31
Q

What is Propofol Infusion Syndrome?

A
  • Metabolic acidosis thought to occur from poisoning of electron transport chain and impaired oxidation of fatty acids.
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32
Q

What relatively benign condition(s) can occur from prolonged propofol infusions?
Why does this happen?

A

Green and cloudy urine from phenols and uric acid crystals.

Neither alters renal function.

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33
Q

What sort of infusion dosing can result in propofol infusion syndrome?

A
  • > 75 μg/kg/min for longer than 24 hours
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34
Q

What is the worst side effect in children who have propofol infusion syndrome?

A
  • Severe, refractory, fatal bradycardia
35
Q

What are the symptoms of propofol infusion syndrome?
How is propofol infusion syndrome diagnosed?

A
  • Urine changes, lactic acidosis, brady-dysrhythmias, and rhabdomyolysis.
  • ABG & serum lactate concentrations.
36
Q

What are the “other” organ system side effects of propofol?

A
  • Injection pain (lido before)
  • ↓ IOP
  • Plt aggregation inhibition
  • Allergic reactions (lecithin)
  • Prolonged myoclonus
  • Abuse/misuse
37
Q

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

A

Etomidate - can be given sub-lingual.

38
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
39
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.
40
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.
41
Q

What is the best use for etomidate?

A
  • Induction for unstable cardiac patients.
42
Q

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

A
  • Opioids, etomidate has no analgesic effects.
43
Q

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

A
  • Involuntary Myoclonic Movements ( 50 - 80 %) of administrations.
44
Q

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

A

Fentanyl 1-2 μg/kg IV

45
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.)
46
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).
47
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.
48
Q

What is the EEG profile of etomidate?

A
  • More excitatory than thiopental
  • May activate seizure foci
  • Augments SSEP amplitude.
49
Q

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

A
  • Hypovolemia
50
Q

Histamine release via etomidate is mediated through what?

A
  • Trick question. Etomidate does not release histamine.
51
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
52
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
53
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”.
54
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.
55
Q

What are the two greatest disadvantages of ketamine?

A
  • Emergence delirium
  • Abuse potential
56
Q

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

A
  • Ketamine preservative that inhibits ACh receptors
57
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
58
Q

What benefits does a racemic ketamine mixture offer?

A
  • Less fatigue & cognitive impairment
  • Inhibits catecholamine reuptake at nerve endings (like cocaine).
59
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.
60
Q

What are Ketamine’s secondary receptor sites?

A
  • Weak GABAA effects.
  • Opioid (μ, δ, and κ)
61
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.
62
Q

What is the Vd and E½ time of ketamine?

A
  • Vd = 3L/kg
  • E ½ = 2-3 hours
63
Q

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

A
  • Clearance: high hepatic clearance (1L/min)
  • Metabolism: CYP450’s.
  • Excretion: kidneys
64
Q

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

A

Norketamine is metabolite (⅓ potency and prolongs analgesia).

65
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
66
Q

What is the maintenance dosing of ketamine?

A
  • 0.2 - 0.5 mg/kg IV
  • 4 - 8 mg/kg IM
67
Q

What is the subanesthetic/analgesic dose of ketamine?

A
  • 0.2 - 0.5 mg/kg IV
68
Q

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

A

1-2 mg/kg/hour

69
Q

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

A
  • 30mg epidural
  • 5 - 50 mg via intrathecal/spinal/subarachnoid
70
Q

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

A

Glycopyrrolate: 0.2mg

71
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.
72
Q

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

A
  • Patients with pulmonary HTN and ↑ICP.
73
Q

What are Ketamine’s effects on ICP? Why?

A
  • ↑ICP via ↑CBF by 60%
  • Potent cerebral vasodilator.
74
Q

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

A
  • 2mg/kg IV
75
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.
76
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).
77
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.
78
Q

What does emergence delirium present like with ketamine?

A
  • Visual, auditory, proprioceptive illusions. Morbid & vivid dreams up to 24 hours.
79
Q

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

A

Depression of inferior colliculus & medial geniculate nucleus.

80
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.
81
Q

What “other systems” effects does ketamine have?

A
  • Non-depolarizing NMBs enhancement.
  • Succinylcholine prolongation via plasma cholinesterase inhibition.
  • PLT aggregation inhibition
82
Q

What are ketamine’s most common drug interactions?

A
  • Volatiles → hypotension
  • Non-depolarizing NMBs → enhancement
  • Succinylcholine → prolongation
83
Q

Why does ketamine prolong succinylcholine’s effects?

A

Ketamine is a plasma cholinesterase inhibitor.

84
Q

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

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

Clinical Meds (5 decks)

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