Hypnotics Flashcards

1
Q

Propofol Class

A

Hypnotic

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2
Q

Propofol Clinical Use

A
  • Induction, maintenance of general anesthesia, and monitored anesthesia care
  • Anticonvulsant and antiemetic
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3
Q

Propofol MOA

A

Mimics GABA at the receptor, directly activating chloride channels, which hyperpolarizes the postsynaptic membrane.

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4
Q

Propofol Doses

A
  • Induction of GA: 1-2.5 mg/kg
  • Maintenance of GA: 25-300 mcg/kg/min IV
  • Sedation: 25-100 mcg/kg/min
  • Antiemetic 10-20 mg can repeat every 5-10 minutes, or start infusion of 10 mcg/kg/min
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5
Q

Propofol Pharmacokinetics

A
  • Onset after induction dose: 30 seconds
  • DOA induction dose: 5 – 15 minutes
  • Metabolized via hepatic and extra hepatic metabolism (mostly lungs), no active metabolite
  • Excreted by the kidney
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6
Q

Propofol Contraindications

A
  1. Allergy to propofol or its contents
  2. Caution with cardiac dysfunction and hypovolemia.
  3. Can cause severe hypotension
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7
Q

Propofol Considerations

A
  • There is no evidence that propofol should be avoided in egg or soy allergic patients
  • Contains sulfites
  • Painful on injection
  • Thrombophlebitis and extravasation risk
  • Bacterial infection risk
  • Can trigger propofol infusion syndrome
    If given >48 hours, especially with pedi
  • Raises seizure threshold
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8
Q

Etomidate Class

A

Hypnotic

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9
Q

Etomidate Clinical Use

A

Induction of anesthesia

Considered for CV stability and trauma

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10
Q

Etomidate MOA

A

Binds to the GABA-a receptor, increasing chloride conduction

Lower doses: potentiates GABA at its receptors

Higher doses: directly stimulates the GABA receptor

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11
Q

Etomidate Dose

A

Induction Dose: 0.3 mg/kg

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12
Q

Etomidate Pharmacokinetics

A

Onset: 1 minute

Duration: 5 -15 minutes

Metabolism: Hepatic P450 enzymes and plasma esterases

No active metabolite

Excretion: kidneys and in bile

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13
Q

Etomidate Contratindications

A

Seizures – can induce further seizures

Avoid if adrenally suppressed

Porphyria

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14
Q

Etomidate Considerations

A

Reduces ICP/CBR, CMO2

Minimal cardiac effects

Does not blunt SNS response to laryngoscope

Hyperventilation –> apnea and mild resp depression

INHIBITS CORTISOL; ADRENAL SUPPRESSION VIA 11 BETA-HYDROXYLASE

N/V in 30-40% of patients

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15
Q

Ketamine Class

A

phencyclidine derivative

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16
Q

Ketamine Clinical Use

A

May be used for GA induction and maintenance, and monitored anesthesia care.

Used as an anesthetic, analgesic and antidepressant.

17
Q

Ketamine MOA

A

non competative NMDA receptor antagonist.

Blocks postsynaptic reflexes in the spinal cord and inhibits excitatory neurotransmitters in selected areas of the brain. Dissociates thalamus from the limbic system involved in awareness.

It also binds with opioid, MAO, serotonin, NE, muscarinic and sodium channels.

18
Q

Ketamine Dose

A

IV Induction 1-2 mg/kg

IM Induction 4-6 mg/kg
Onset: 20 minutes

Sedation 1-3 mcg/kg/min or 0.5-1 mg/kg boluses as needed

Multimodal infusion – 3-5 mcg/kg/minute

19
Q

Ketamine Pharmacokinetics

A

IV Onset: 2-5 minute
IV DOA: 10-20 minutes (may require an hour for full orientation)

Metabolism = ­P450 enzymes in the liver
­Chronic ketamine use induces enzymes that metabolize it
­Active metabolite: norketamine is 1/3 as potent as ketamine and is renally excreted

 - Excretion = kidneys
20
Q

Ketamine Contraindications

A
  • Hypertension
  • Angina
  • CHF
  • Increased intracranial pressure
  • Increased ocular pressure
  • Auditory/Visual hallucinations
  • Airway problems d/t increase secretions
  • Emergence reactions
    vivid dreams, hallucinations (lasts 1-3 hours) and can be reduced with propofol and/or benzodiazepines
21
Q

Ketamine Considerations

A

Increases CMRO2, CBF, ICP

Dissociative, analgesic, depression, emergence delirium, nightmares and hallucinations

SNS stimulant. Increased SVR, HR, myocardial O2 consumption, PVR, mild cardiac depression
Bronchodilator, maintains RR, preserves reflexes low dose, increases secretions (pair with antisialagogue)

Causes nystagmus

22
Q

Dexmedetomidine Class

A

Selective alpha 2 adrenergic agonist

23
Q

Dexmedetomidine Use

A

May be used for induction, monitored anesthesia care, analgesia and prevention of emergence delirium

24
Q

Dexmedetomidine MOA

A

Centrally and peripherally alpha 2 adrenergic receptor agonist thereby producing sedation by decreasing sympathetic nervous system activity and the level of arousal.

Regulates the cardiovascular system by inhibiting norepinephrine release

Reduces blood pressure and heart rate by decreasing the tonic levels of sympathetic outflow from the CNS and augmenting cardiac vagal activity.

25
Q

Dexmedetomidine Dose

A

For procedural sedation: start at 1 mcg/kg over 10 minutes

followed by a maintenance infusion from 0.2 to 1 mcg/kg/hr.

26
Q

Dexmedetomidine Pharmacokinetics

A
Onset: 5 min
DOA: 1 - 2 hrs
Metabolized by the P450 system in the liver		
Excreted by the liver
Inactive metabolites
27
Q

Dexmedetomidine Contraindications

A

Bradycardia

28
Q

Dexmedetomidine Considerations

A

Hypotension and bradycardia
Minimal respiratory depression
Analgesia, enhances neuraxial blockage
Reduces emergence delirium with pediatrics, reduces inhalational agent requirements

29
Q

Midazolam Class

A

Hypnotic + (Benzodiazepine?)

30
Q

Midazolam Use

A

sedative, anxiolytic, amnestic, anticonvulsant, muscle relaxant

31
Q

Midazolam MOA

A

enhances the response to GABA A receptor

32
Q

Midazolam Dose

A

Premed = titrated 0.5-2 mg IV (adult)
or 0.2-0.6 mg/kg PO
Induction dose: 0.1 - 0.3 mg/kg

33
Q

Midazolam Pharmacokinetics

A

Onset = 1 min
Peak = 2-5 min
DOA induction dose = 6-15 min

Metabolized by CYP450 in liver
Active metabolite = 1-hydroxymidazolam

Excreted by kidney

34
Q

Midazolam Contraindications

A

Post op delirium with elderly

35
Q

Midazolam Considerations

A

Highly protein bound
Induction dose causes BP and SVR to decrease
Reduces muscular tone in upper airway
Decrease O2 and hypoxia response
COPD causes more sensitive depressive effects
Anterograde amnesia, anticonvulsant, anxiolysis, antispasmodic, no analgesia