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Pharm > IV Sedatives > Flashcards

IV Sedatives Flashcards

1
Q

Define sedative

A

a drug that induces a state of calm or sleep

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2
Q

Define hypnotic

A

a drug that induces hypnosis or sleep

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3
Q

Define anxiolytic

A

any agent that reduces anxiety

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4
Q

Define sedative-hypnotics

A

drugs that reversible depress the activity of the central nervous system

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5
Q

Describe the mechanism of action of barbiturates

A

GABA-A agonist (GABA is the primary inhibitory NT in the brain)
- increase the DURATION of opening of chloride channels

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6
Q

What substance are barbiturates derived from?

A

barbituric acid

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7
Q

What effect does substituting a sulfur molecule to the 2nd position of a barbiturate have on PK/PD? What are 2 examples?

A

increases lipid solubility and potency
- thiobarbiturates -
Ex: thiopental, thiamylal

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8
Q

What effect does substituting an oxygen molecule on the second position of a barbiturate have on PK/PD? What are 2 examples?

A

effect unknown..
- oxybarbiturates -
Ex: methohexital, pentobarbital

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9
Q

Adding a methyl group to a nitrogen of a barbiturate has what effect?

A

lowers the seizure threshold and increases potency
(ex: methohexital)

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10
Q

What effect does adding a phenyl group the 5th carbon of a barbiturate have?

A

increases anticonvulsant effect
(ex: phenobarbital)

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11
Q

Describe the effects of low/normal dose versus high-dose thiopental

A

low/normal: increase affinity of GABA for its binding site
high: directly stimulates GABA-A receptor

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12
Q

What is the typical dose of thiopental for adults? Peds?

A

adult: 2.5-5mg/kg
peds: 5-6mg/kg

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13
Q

Give the onset and duration of thiopental

A

onset = 30-60 seconds
duration = 5-10 minutes

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14
Q

How is thiopental metabolized?

A

liver via P450 enzymes
*awakening is determined by redistribution (not metab)

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15
Q

What effect does repeated doses of thiopental have on wake-up?

A

repeated doses leads to tissue accumulation which results in prolonged wake-up time and hangover effect

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16
Q

Thiopental cardiovascular effects:

A
  • hypotension d/t venodilation, decreased preload, and histamine release
  • baroreceptor reflex is preserved
  • less hypotension than propofol
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17
Q

Thiopental respiratory effects:

A
  • respiratory depression (shifts CO2 response curve to the right)
  • bronchoconstriction d/t histamine release
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18
Q

Thiopental CNS effects:

A
  • decreased CMRO2
  • decreased cerebral BF
  • decreased ICP
  • decreased EEG activity
  • NO analgesia
  • neuroprotective in focal ischemia (not global)
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19
Q

Does thiopental have an active metabolite?

A

after high dose = pentobarbital

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20
Q

Describe acute intermittent porphyria

A
  • caused by a defect in heme synthesis resulting in the accumulation of heme precursors
  • most common and dangerous type of inducible porphyria
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21
Q

What factors worsen acute intermittent porphyria?

A
  • stimulation of ALA synthase
  • emotional stress
  • prolonged NPO status
  • CYP450 induction
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22
Q

List the signs and symptoms of acute intermittent porphyria

A

GI: severe abdominal pain, NV
CNS: anxiety, confusion, sz, psychosis, coma
PNS: skeletal muscle weakness, bulbar weakness

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23
Q

Which drugs should be avoided in patients with acute intermittent porphyria?

A

-barbiturates
-etomidate
-ketamine
-ketorolac
-amiodarone
-many CCBs
-birth control pills

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24
Q

How does anesthesia manage acute intermittent porphyria?

A
  • HYDRATION
  • glucose supplementation to dec. ALA synthase activity
  • heme arginate (same)
  • prevent hypothermia
  • regional anesthesia
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25
Q

List the medications that are safe for patients with acute intermittent porphyria

A
  • volatile anesthetics
  • N2O
  • NMBs
  • NMB reversal agents
  • narcotics
  • midazolam
  • ondansetron
  • vasopressors
  • beta-blockers
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26
Q

What happens if thiopental is injected interarterially? How is it treated?

A

vasoconstriction, crystal formation, inflammation, tissue necrosis

treatment= inject vasodilator (phentolamine or phenoxybenzamine), or sympathectomy via stellate ganglion block or brachial plexus block

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27
Q

Which medication is the gold-standard for ECT?

A

Methohexital (induction dose 1-1.5mg/kg)

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28
Q

What is unique about phenobarbital when compared to other barbiturates?

A

phenobarb is excreted unchanged in the urine
(the rest are metabolized by the CYP450 system)

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29
Q

What is the mechanism of action of propofol?

A
  • direct GABA-A agonist
  • activity at the glycine receptors, too
  • increases transmembrane Cl- conductance
  • hyperpolarizes postsynaptic membrane
  • inhibition of postsynaptic neuron
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30
Q

What is the chemical name for propofol?

A

2,6-diisopropylphenol

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31
Q

What is the typical induction dose of propofol? infusion dose?

A

induction: 1.5-2.5mg/kg
infusion: 25-200 mcg/kg/min

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32
Q

What is the onset and duration of propofol?

A

onset: 30-60 seconds
duration: 5-10 minutes

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33
Q

How is propofol metabolized?

A

via the liver (P450) + extrahepatic clearance in the lungs

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34
Q

What effect does renal impairment have on propofol metabolism/elimination? liver impairment?

A

renal: none
liver: none

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35
Q

What subset of patients have a decreased rate of plasma clearance of propofol?

A

patients >60

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36
Q

What is propofol’s effect on the cardiovascular system?

A
  • decreased BP d/t decreased SNS tone, vasodilation
  • decreased SVR
  • decreased venous tone –> decreased preload
  • decreased myocardial activity
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37
Q

What effect does propofol have on the respiratory system?

A
  • shifts CO2 response curve down and to the R
  • respiratory depression
  • inhibits hypoxic ventilatory drive
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38
Q

What effect does propofol have on the CNS?

A
  • decreased CMRO2
  • decreased cerebral BF
  • decreased ICP
  • decreased IOP
    NO analgesia
  • some anticonvulsant properties
  • myoclonus possible
  • seizures?
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39
Q

What effect can propofol have on the urine?

A

green –> phenol excretion
cloudy –> increased uric acid excretion

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40
Q

List three beneficial effects of propofol?

A

antioxidant properties
antipruritic effect
antiemetic effect

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41
Q

What are the risk factors for propofol infusion syndrome?

A
  • dose > 4mcg/kg/hr
  • duration >48 hours
  • sepsis
  • continuous catecholamine infusions
  • high-dose steroids
  • significant cerebral injury
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42
Q

Describe the clinical presentation of PIS

A

*acute refractory bradycardia –> asystole
one of the following:
- metabolic acidosis
- rhabdo
- enlarged fatty liver
- renal failure
- hyperlipidemia
- lipemia

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43
Q

How do you treat PIS?

A
  • d/c propofol
  • maximize gas exchange
  • cardiac pacing
  • phosphodiesterase inhibitors
  • glucagon
  • ECMO
  • CRRT
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44
Q

Propofol syringe is good for _ hours
Propofol tubing is good for _ hours

A

syringe = 6
tubing = 12

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45
Q

Which propofol preservative can cause issues?

A

generic formulation: metabisulfite can cause bronchospasm, benzyl alcohol is avoided in infants

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46
Q

What is the MOA of fospropofol?

A

it is a prodrug; metabolized to propofol by alkaline phosphatase in the blood

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47
Q

What is the chemical name of fospropofol?

A

phosphono-O-methyl-2,6-diisopropylphenol

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48
Q

What is the onset and duration of fospropofol?

A

onset: 5-13 minutes
duration: 15-45 minutes

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49
Q

What is the active metabolite of fospropofol?

A

propofol
formaldehyde is metabolized to formate (excreted in the urine)

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50
Q

What is a major side effect of fospropofol?

A

genital and anal burning

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51
Q

What is the most commonly used IV anesthetic for induction and sedation?

A

propofol

52
Q

What is the MOA of etomidate?

A
  • direct GABA-A agonist
  • increased transmembrane Cl- conductance
  • hyperpolarization of postsynaptic cell membrane
  • inhibition of postsynaptic neuron
53
Q

What is the chemical name of etomidate?

A

R-1-methyl-1-(a-methylbenzyl) imidazole-5-carboxylate

54
Q

What drug class is etomidate part of?

A

imidazoles

55
Q

Describe how etomidate acts at normal pH and acidic pH

A

normal pH: imidazole ring closes, increased lipid solubility
acidic pH; imidazole ring opens, increased water solubility

56
Q

What are the 2 formulations of etomidate and what is the important difference?

A

1) 35% propylene glycol (painful to inject)
2) lipid emulsion (less pain on injection)

57
Q

What is the onset and duration of etomidate?

A

onset: 30-60 seconds
duration: 5-15 minutes

58
Q

How is etomidate metabolized?

A

liver (P450) and plasma esterases

59
Q

Rapid awakening after etomidate can be attributed to what?

A

redistribution (not metabolism)

60
Q

Etomidate cardiovascular effects:

A
  • minimal change in HR, SV, or CO
  • decreased SVR causes a small reduction in BP
  • does NOT block SNS response to laryngoscopy
61
Q

Etomidate respiratory effects:

A

mild respiratory depression (less than propofol or barbiturates)

62
Q

Etomidate CNS effects:

A
  • decreased CMRO2
  • decreased cerebral blood flow
  • decreased ICP
  • stable CPP
    NO analgesia
63
Q

Which IV sedative can increase the risk of seizures?

A

etomidate – if the patient has a history of seizures

64
Q

How does etomidate affect the adrenal system?

A

inhibits 11-beta-hydroxylase and 17-alpha-hydroxylase (needed for cortisol and aldosterone synthesis) for 5-8 hours

65
Q

What is the MOA of benzodiazepines?

A
  • GABA-A agonist
  • increases frequency of channel opening
  • neuronal hyperpolarization
66
Q

What are the most common side effects of benzos?

A

fatigue and drowsiness

67
Q

What side effects can occur when benzos are used in combination with CNS depressants or opioids?

A
  • decreased motor coordination
  • impaired cognitive functions
  • increased ventilatory depression
  • anterograde amnesia
68
Q

What effect do benzos have on the hypothalamic-pituitary-adrenal axis?

A

suppression of cortisol levels

69
Q

How long does dependence on benzos take to develop?

A
  • therapeutic doses may cause physical dependence
  • > 6 months of use
70
Q

What are the risks of giving benzos to an aging adult?

A
  • increased sensitivity
  • gait instability, falls, fractures
  • accelerated cognitive decline with long-term use
  • confusion with withdrawal
71
Q

What chemical structure describes midazolam?

A

imidazole ring

72
Q

Give the dose ranges for midazolam:

A

IV sedation: 0.01-0.1 mg/kg
IV induction: 0.1-0.5mg/kg
PO sedation (peds): 0.5-1.0 mg/kg (50% bioavail d/t first pass metab)

73
Q

What is the onset and duration of midazolam?

A

onset: 30-60 seconds
duration: 20-60 minutes

74
Q

How is midazolam metabolized?

A

liver (P450)
intestines (P450)

75
Q

What is the active metabolite of midazolam?

A

1-hydroxymidazolam
- 1/2 the potency of midaz
- rapidly conjugated to an inactive compound
- renal failure prolongs the effects

76
Q

Respiratory effects of midazolam:

A
  • sedation dose: minimal
  • induction dose: respiratory depression
  • effects are potentiated by opioids
  • pts with COPD are more sensitive
77
Q

Cardiovascular effects of midazolam:

A
  • sedation dose: minimal
  • induction dose: decreased BP and SVR
78
Q

CNS effects of midazolam:

A
  • decreased CMRO2
  • decreased CBF
  • anterograde amnesia
  • anticonvulsant
  • anxiolysis
  • skeletal muscle relaxation at spinal neurons
    NO analgesia
79
Q

Why is diazepam not frequently used in surgery?

A

undergoes hepatic recirculation making its elimination half-time 43 hours

80
Q

What are 3 beneficial features of diazepam?

A
  • anticonvulsant properties
  • prevents emergence delirium following ketamine
  • antispasmodic agent
81
Q

Lorazepam is (more/less) potent than midaz and diazepam?

A

more (side effects remain consistent)

82
Q

What is the onset of lorazepam?

A

1-2 minutes (peak effect at 20-30 minutes) which limits its usefulness as an anticonvulsant

83
Q

Key features of oxazepam:

A
  • active metabolite of diazepam
  • shorter DOA than diazepam
  • elim half-time 5-15 hours
84
Q

Key features of alprazolam:

A

more prominent inhibition of adrenocorticotrophic hormone and cortisol secretion than other benzos

85
Q

Key feature of clonazepam:

A

effective in controlling and preventing seizures

86
Q

Key features of flurazepam:

A
  • used exclusively to treat insomnia
  • has an active metabolite that can cause daytime sedation
87
Q

Key feature of temazepam:

A
  • used exclusively to treat insomnia
  • daytime drowsiness is unlikely
88
Q

Key features of triazolam:

A
  • effective in treating insomnia (difficulty in falling asleep)
  • shortest acting (1.7 hours)
  • daytime drowsiness unlikely
  • decreased dose by 50% in elderly
89
Q

What is the MOA of flumazenil?

A

competitive antagonist of GABA-A receptor (high affinity)

90
Q

What is the duration of flumazenil?

A

30-60 minutes (may need to re-dose)

91
Q

What is the dose of flumazenil?

A

initial: 0.2mg
titrated in 0.1 mg Q1min

92
Q

Describe the effects of flumazenil:

A
  • does not increase SNS tone, anxiety, or stress
  • may cause withdrawal symptoms including sz in dependent patients
  • reverses sedative effects better than amnestic effects
93
Q

What is the MOA of ketamine?

A

NMDA receptor antagonist (antagonizes glutamate)
- dissociates the thalamus from the limbic system

*also targets opioid, MAO, serotonin, NE, muscarinic, and Na+ channels/receptors

94
Q

Ketamine belongs to which class of drugs?

A

arylcyclohexylamine

95
Q

What are the doses for ketamine?

A

induction: 1-2mg/kg
maintenance: 1-3mg/min
analgesia: 0.1-0.5mg/kg
IM: 4-8mg/kg
PO: 10mg/kg

96
Q

What is the onset of ketamine?

A

IV: 30-60 seconds
IM: 2-4 minutes
PO: varies

97
Q

What is the duration of ketamine?

A

10-20 minutes; 60-90 to return to “normal”

98
Q

How is ketamine metabolized?

A

liver (P450)

99
Q

What is the active metabolite of ketamine?

A

norketamine

1/3-1/5 the potency of ketamine

100
Q

Cardiovascular effects of ketamine

A
  • increase SNS tone
  • increase CO, HR, SVR, PVR
  • myocardial depressant
101
Q

Respiratory effects of ketamine:

A
  • bronchodilation
  • maintain respiratory drive
  • no significant effect on CO2
  • increase oral and pulmonary secretions
102
Q

CNS effects of ketamine:

A
  • increased CMRO2, CBP, ICP, IOP, EEG activity
  • nystagmus
  • emergence delirium (esp in Peds)
103
Q

Ketamine is better at relieving (somatic/visceral) pain

A

somatic

104
Q

Which IV sedative is a good adjunct for patients with chronic pain?

A

ketamine

105
Q

List 3 other facts about ketamine:

A
  • treatment for depression
  • chronic use can cause ulcerative colitis
  • avoid in patients with acute intermittent porphyria
106
Q

Which IV sedative undergoes the least plasma binding?

A

ketamine = 12%
etomidate = 75%
lorazepam = 90%
dexmedetomidine & midaz = 94%
propofol & diazepam = 98%

107
Q

What is the MOA of dexmedetomidine?

A
  • alpha-2 agonist
  • decreases cAMP
  • inhibits locus coeruleus in the pons causing sedation
108
Q

What is the loading dose of dex? maintenance dose?

A

loading: 1mcg/kg over 10 minutes
maintenance: 0.4-0.7 mcg/kg/hr

109
Q

What is the onset and duration of dex?

A

onset with loading dose: 10-20 minutes
duration after infusion is stopped: 10-30 minutes

110
Q

How is dex metabolized?

A

liver (P450)

111
Q

What is the active metabolite of dex?

A

none

112
Q

Cardiovascular effects of dex:

A
  • bradycardia
  • hypotension
  • transient hyPERtension if given rapidly
113
Q

Respiratory effects of dex:

A
  • no respiratory depression
  • no change in oxygenation
  • no change in blood pH
  • no change in CO2 response curve
114
Q

CNS effects of dex:

A
  • decrease CBF
  • no change in CMRO2
  • no change in ICP
  • sedation caused by decreased SNS tone
  • unreliable amnesia
  • patients easily aroused
115
Q

Dex provides analgesia through what mechanism?

A

alpha-2 stimulation in the dorsal horn of the spinal cord (decreases substance P and glutamate release)

116
Q

List some other effects of dex:

A
  • impairs thermoregulatory response (anti-shivering)
  • reduces emergence delirium in peds
  • NO impairment of evoked potentials
  • used for “wake-up” test in scoliosis surgery
  • nasal and buccal routes have high bioavailability
117
Q

What is the MOA of scopalamine?

A
  • anticholinergic
  • binds to muscarinic cholinergic receptors
  • decreases the activity of the RAS
  • lipid-soluble tertiary amine
  • crosses BBB
118
Q

How is scopolamine eliminated?

A

hepatic and renal pathways

119
Q

What is the elimination half-life of scopolamine?

A

4.5 hours

120
Q

Scopolamine belongs to which class of drugs?

A

anticholinergic

121
Q

What are some beneficial side effects of scopolamine?

A
  • amnesia
  • antisialagogue
  • antiemetic
122
Q

What is the dose of scopolamine for sedation?

A

0.3-0.5mg IM or IV
also available via transdermal patch

123
Q

What is the reversal agent for scopolamine?

A

physostigmine 2mg IV

124
Q

What are two negative side effects of scopolamine?

A
  • mydriasis and cycloplegia (caution in patients with glaucoma)
  • central anticholinergic syndrome
125
Q

What are the symptoms of central anticholinergic syndrome? What is the treatment?

A

symptoms: restless, hallucinations, somnolence, unconsciousness
treatment: physostigmine 15-60mcg/kg IV every 1-2 hours until symptoms improve

Pharm (19 decks)

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