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APEX > Unit 4 - IV Anesthetics > Flashcards

Unit 4 - IV Anesthetics Flashcards

1
Q

chemical name of propofol

A

2,6-diisopropylphenol

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2
Q

propofol protein binding

A

98%

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3
Q

preservatives in propofol

A
  • Preservative in Diprivan = disodium edetate
  • Preservative in generic = sodium metabisulfite
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4
Q

MOA of propofol

A

direct GABA-A agoinst

  • Prolongs time channel stays open
  • Increases Cl- conductance = neuronal hyperpolarization = decreased RMP
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5
Q

onset & duration of propofol

A

Onset: 30-60 seconds

Duration: 5-10 minutes

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6
Q

pKa of propofol

A

11

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7
Q

clearance of propofol

A

Liver (P450) + extrahepatic metabolism (mostly lungs)

Clearance > liver blood flow

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8
Q

when does brain concentration of propofol peak

A

~1 minute

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9
Q

kinetics of propofol: what results in awakening

A

redistribution from brain

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10
Q

CV effects of propofol

A
  • ↓BP (↓ SNS tone, vasodilation, myocardial depression)
  • ↓SVR
  • ↓venous tone (↓ preload)
  • ↓ contractility
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11
Q

respiratory effects of propofol

A

Shifts CO2 response curve down and right (less sensitive to CO2) = resp depression, apnea

Inhibits hypoxic ventilatory drive

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12
Q

CNS effects of propofol

A
  • ↓ CMRO2, ↓ CBF, ↓ ICP
  • No analgesia; anticonvulsant properties; myoclonus can occur
  • Few reports of propofol-induced seizures
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13
Q

IV anesthetic with antioxidant properties

A

propofol

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14
Q

how can propofol change urine appearance

A
  • Green urine = phenol excretion
  • Cloudy urine = increased uric acid excretion (doesn’t indicate renal impairment or infection)
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15
Q

is propofol safe with allergies to eggs, soy, and peanuts?

A

yes - Most egg allergies are allergic to albumin in egg whites

lecithin derived from yolk

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16
Q

what causes propofol infusion syndrome

A
  • Contains long-chain triglycerides (LCT)
  • increased LCT load impairs oxidative phosphorylation and fatty acid metabolism
  • Cells starved of O2 (particularly cardiac and skeletal muscle)
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17
Q

risk factors for propofol infusion syndrome

A
  • dose > 4 mg/kg/hr (67 mcg/kg/min)
  • gtt > 48 hours
  • sepsis
  • continuous catecholamine infusions
  • high-dose steroids
  • significant cerebral injury
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18
Q

clinical presentation of Propofol Infusion Syndrome

A

acute refractory bradycardia - asystole + at least one:

  • Metabolic acidosis (base deficit > 10 mmol/L)
  • Rhabdomyolysis
  • Enlarged or fatty liver
  • Renal failure
  • Hyperlipidemia
  • Lipemia (cloudy plasma or blood) may be early sign
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19
Q

propofol infusion syndrome treatment

A
  • d/c propofol
  • maximize gas exchange
  • cardiac pacing
  • PDE inhibitors
  • glucagon
  • ECMO
  • renal replacement therapy
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20
Q

preservatives in propofol

A
  • Diprivan contains EDTA as a preservative = no bronchial irritation
  • Generic contains different preservatives = metabisulfite (can precipitate bronchospasm in asthmatics), benzyl alcohol (avoid in infants)
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21
Q

when should opened propofol be discarded

A

syringe within 6 hours

infusion within 12 hours (tubing included)

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22
Q

methods to mimimize or eliminate pain on propofol injection

A
  • Injecting into larger and more proximal vein
  • Give opioid before propofol injection
  • Give lidocaine before injection - mixing together in syringe is controversial (theoretical risk of microemboli)
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23
Q

dose of propofol to decrease itching from spinal opioids and cholestasis

A

10 mg

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24
Q

chemical name of fospropofol

A

phosphono-O-methyl-2,6-diisopropylphenol

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25
Q

what class is propofol

A

isopropylphenol, alkylphenol

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26
Q

class of fospropofol

A

isopropylphenol

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27
Q

formulation of fospropofol

A

aqueous solution

prevents burning, doesn’t support microbial growth like lipid emulsion (no preservative)

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28
Q

MOA of fospropofol

A

prodrug

metabolized to propofol by alkaline phosphatase (present in vascular endothelium & liver)

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29
Q

dosing fospropofol

A

initial bolus 6.5 mg/kg

repeat 1.6 mg/kg not more than q4min

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30
Q

onset & duration of fospropofol

A

Onset: 5-13 min

Duration: 15-45 min

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31
Q

side effects of fospropofol

A

genital and anal burning

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32
Q

chemical name of ketamine

A

2-(o-Cholophenyl)-2 (methylamino) cyclohexanone hydrochloride

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33
Q

class of ketamine

A

arylcyclohexylamine (phencyclidine derivative)

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34
Q

IV anesthetic with the least amount of protein binding

A

ketamine (12%)

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35
Q

ketamine formulation

A

aqueous solution available as 1%, 5%, and 10% solutions

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36
Q

pKa of ketamine

A

7.5

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37
Q

MOA of ketamine

A
  • NMDA receptor antagonist - antagonizes glutamate
  • Secondary receptor targets: opioid, MAO, serotonin, NE, muscarinic, Na+ channels
  • Dissociates thalamus (sensory) from limbic system (awareness)
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38
Q

NMDA receptor is permeable to which electrolytes

A

sodium

calcium

potassium

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39
Q

ketamine dosing

A
  • Induction: 1-2 mg/kg
  • Maintenance: 1-3 mg/min
  • Low dose infusion: 1-3 mcg/kg/min (opioid sparing effect)
  • Analgesia: 0.1-0.5 mg/kg
  • IM: 4-8 mg/kg
  • PO: 10 mg/kg
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40
Q

ketamine onset

A
  • IM: 30-60 sec
  • IM: 2-4 min
  • PO: variable
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41
Q

duration of ketamine

A

10-20 min (may require 60-90 min to return to full orientation)

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42
Q

clearance of ketamine

A

Liver (P450) - chronic use induces enzymes that metabolize it (rapid ↑ tolerance)

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43
Q

active metabolite of ketamine & its potency

A

norketamine (1/3 – 1/5 potency of ketamine)

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44
Q

what is the “wind up” phenomenon with NMDA receptor agonism

A
  • wide dynamic range neurons ↑ firing rate for given stimulus
  • can contribute to hyperalgesia
  • ketamine counteracts this process
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45
Q

CV effects of ketamine

A

↑ SNS tone, ↑ CO, ↑ HR, ↑ SVR, ↑ PVR

Direct myocardial depression - unmasked in pt with depleted catecholamine stores (sepsis) or sympathectomy

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46
Q

resp effects of ketamine

A
  • Bronchodilation; upper airway muscle tone/airway reflexes intact
  • Maintains resp. drive (may have brief period of apnea)
  • No significant effect on CO2 response curve
  • ↑ salivation (glycopyrrolate helps)
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47
Q

CNS effects of ketamine

A

↑ CMRO2, ↑ CBF, ↑ ICP, ↑ IOP, ↑ EEG activity, nystagmus

dissociative anesthesia

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48
Q

increased risk of emergence delirium with ketamine

A
  • age > 15
  • female
  • dose > 2 mg/kg
  • personality disorder
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49
Q

prevention of emergence delirium in ketamine

A

benzos (versed)

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50
Q

only induction agent that provides good analgesia and opioid sparing effects

A

ketamine

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51
Q

analgesic effects of ketamine

A
  • Relieves somatic pain > visceral pain
  • Blocks central sensitization and wind-up in dorsal horn
  • Prevents opioid-induced hyperalgesia after remifentanil gtt
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52
Q

IOP with ketamine

A

increased only with high doses

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53
Q

when is ketamine contraindicated

A

acute intermittent porphyria

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54
Q

uses of esketamine

A

resistant depression

major depressive disorder with acute SI

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55
Q

chemical name of etomidate

A

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

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56
Q

what causes rapid awakening with etomidate

A

redistribution (NOT metabolism)

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57
Q

class of etomidate

A

imidazole

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58
Q

how does etomidate function in different pH

A
  • Acidic pH = imidazole ring opens - increased water solubility
  • Physiologic pH = imidazole ring closes - increased lipid solubility
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59
Q

formulations of etomidate

A
  1. 35% propylene glycol (pain with injection)
  2. lipid emulsion (less pain)
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60
Q

MOA of etomidate

A

GABA-A agonist

61
Q

onset and duration of etomidate

A

onset 30-60 seconds

duration 5-15 minutes

62
Q

clearance of etomidate

A

P450 + plasma esterases

63
Q

CV effects of etomidate

A
  • minimal change in HR, CO, SV
  • ↓ SVR (accounts for small reduction in BP)
64
Q

does etomidate block SNS response to DL

65
Q

resp effects of etomidate

A

Mild respiratory depression ( < propofol, barbiturates)

66
Q

neuro effects of etomidate

A

↓ CMRO2, CBF, ICP

  • Cerebral vasoconstriction
  • Cerebral perfusion remains stable
  • increased risk seizures if hx seizures
67
Q

does etomidate have analgesic effects

68
Q

why can etomidate cause myoclonus

A

likely d/t imbalance between inhibitory and excitatory pathways in thalamocortical tract

69
Q

why does etomidate cause adrenocortical suppression

A

Cortisol & aldosterone synthesis dependent on 11-b-hydroxylase (in adrenal medulla) - inhibited by etomidate

70
Q

when should etomidate be avoided

A

sepsis, adrenal failure

71
Q

PONV is the most common with which induction agent

72
Q

how long does etomidate cause adrenal suppression

A

Single dose suppresses adrenocortical function for 5-8 hrs

73
Q

acute intermittent porphyria triggering agents

A
  • ketamine
  • etomidate
  • barbiturates
  • ketorolac
  • amiodarone
  • CCBs
  • birth control
  • lidocaine
74
Q

examples of thiobarbiturates

A

thiopental, thiamylal

75
Q

which type of barbiturate has a sulfur molecule in 2nd position

what is the effect of this

A

thiobarbiturates

increases lipid solubility and potency

76
Q

barbiturate with oxygen molecule in 2nd

A

oxybarbiturates

77
Q

examples of oxybarbiturates

A

methohexital, pentobarbital

78
Q

barbiturate with methyl group on nitrogen

effects of methyl group

A

methohexital

decreased seizure threshold, increased potency

79
Q

barbiturate with phenyl group added to carbon in 5th position

effect?

A

phenobarbital

increased anticonvulsant effect

80
Q

chemical name of thiopental

A

5-ethyl-5-(1-methylbutyl)-2-thiobarbituric acid

81
Q

pH of thiopental

A

9 (highly alkaline)

precipitates in acidic solution

82
Q

MOA of thiopental

A

GABA-A agonist

  • Depresses RAS in brainstem
  • Low/normal dose: increases affinity of GABA for its binding site
  • High dose: directly stimulates GABA-A receptor
83
Q

thiopental dosing

A

Adults 2.5-5 mg/kg

Children 5-6 mg/kg

84
Q

duration of thiopental

A

5-10 minutes

85
Q

thiopental clearance

86
Q

what determines awakening with thiopental

A

redistribution - not metabolism

87
Q

which causes more hypotension - propofol or thiopental

88
Q

IV anesthetic associated with hangover effect

A

thiopental

89
Q

CV effects of thiopental

A
  • ↓ BP r/t venodilation & ↓ preload
  • -myocardial depression
  • Non-immunologic histamine release can ↓ BP (short lived)
  • Baroreceptor reflex preserved = reflex tachy maintains CO
90
Q

resp effects of thiopental

A

Respiratory depression = shifts CO2 response curve to right

Histamine release can cause bronchoconstriction

91
Q

neuro effects of thiopental

A
  • ↓ CMRO2, CBF (cerebral vasoconstriction), ↓ ICP, ↓ EEG
  • ↓ EEG activity can cause burst suppression or isoelectric EEG
  • No analgesia (low dose may ↑ pain perception)
  • Neuroprotection against focal ischemia, not global
92
Q

treatment of intra-arterial thiopental injection

A
  • injection of vasodilator (phentolamine or phenoxybenzamine)
  • Or treat with sympathectomy: stellate ganglion block or brachial plexus block
93
Q

gold standard for ECT

why

A

methohexital

↓ seizure threshold and produces a better quality seizure

94
Q

induction dose of methohexital

A

1-1.5 mg/kg

95
Q

how is phenobarbital excreted

A

unchanged in urine

96
Q

how are barbiturates metabolized

A

CYP450

except phenobarb- excreted unchanged in urine

97
Q

what causes acute intermittent porphyria

A

defect in heme synthesis promotes accumulation of heme precursors

98
Q

what 3 things is heme a key component of

A

Hgb

myoglobin

CYP450

99
Q

4 situations that make acute intermittent porphyria worse

A
  1. emotional stress
  2. prolonged NPO
  3. CYP450 induction
  4. stimulation of ALA synthase
100
Q

GI symptoms of acute intermittent porphyria

A

severe abdominal pain (most common, typically 1st)

N/V

101
Q

CNS effects of acute intermittent porphyria

A

anxiety, confusion, seizures, psychosis, coma

102
Q

PNS effects of acute intermittent porphyria

A

skeletal muscle weakness (risk resp failure)
bulbar weakness (risk aspiration)

103
Q

anesthesia implications for acute intermittent porphyria

A
  • liberal hydration
  • glucose supplementation (dec. ALA synthase activity)
  • heme arginate (dec. ALA synthase activity)
  • prevent hypothermia
104
Q

why might regional anesthesia be avoided in pts with acute intermittent porphyria

A

difficult to establish block-related complications from acute porphyria attack

105
Q

chemical name of precedex

A

(S) – 4 – [1-(2,3-Dimethylphenyl)ethyl] – 1H – imidazole monohydrochloride

106
Q

class of dexmedetomidine

107
Q

precedex formulation

A

preservative free, water soluble, pKa = 7.1

108
Q

MOA of precedex

A

presynaptic alpha-2 agonism in CNS = ↓ cAMP = inhibits locus coeruleus in pons

  • Produces negative feedback loop that reduces NE release from presynaptic nerve terminal
  • ↓ SNS tone, produces sedation
109
Q

dose of precedex

A
  • Loading: 1 mcg/kg over 10 min
  • Maintenance: 0.4-0.7 mcg/kg/hr
110
Q

onset and duration of precedex

A
  • onset: 10-20 min for loading dose
  • duration: 10-30 min after infusion stopped
111
Q

clearance of precedex

A

CYP450 enzymes

112
Q

PO bioavailability of midazolam

A

50% d/t significant first-pass metabolism

113
Q

how can rapid admin of precedex cause HTN

A

a2 stim. in vasculature = vasoconstriction

short lived

114
Q

most common side effects of precedex

A

bradycardia

hypotension

115
Q

neuro effects of precedex

A

↓ CBF; no change in CMRO2 or ICP (CMRO2-CBF uncoupling)

116
Q

which IV anesthetic most resembles natural sleep

117
Q

how does precedex have an antishivering effect

A

impairs thermoregulatory response

118
Q

does precedex have analgesic effects?

A

yes via a2 stimulation in dorsal horn (↓substance P & glutamate release)

119
Q

precedex dose for preop sedation in peds

A

3-4 mcg/kg 1 hour preop for preop sedation in peds

120
Q

relative potency of benzos

A

lorazepam > midazolam > diazepam

121
Q

additive in diazepam and lorazepam that causes venous irritation

A

propylene glycol

122
Q

chemical name of midazolam

A

8-chloro-6-(2-fluorophentl)-1-methyl-4 H-imidazol[1,5-a][1,4]benzodiazepine

123
Q

formulation of midazolam

A

imidazole ring = hydrophilic & lipophilic properties

124
Q

how does midazolam function in different pH

A
  • Acidic pH = imidazole ring opens = increased water solubility
  • Physiologic pH = imidazole ring closes = increased lipid solubility = crosses BBB freely
125
Q

preservatives in midazolam

A

0.01% disodium edetate, 1% benzyl alcohol

126
Q

MOA of midazolam

A

GABA-A agonist = increased frequency of channel opening = neuronal hyperpolarization

127
Q

dosing of midazolam

A
  • IV sedation: 0.01-0.1 mg/kg
  • Induction: 0.1-0.4 mg/kg
  • PO in children: 0.5-1 mg/kg
128
Q

metabolite of midazolam

A

1-hydrozymidazolam (active)

  • 0.5x potency of midazolam
  • Rapidly conjugated to inactive compound
  • Renal failure prolongs effects
129
Q

midazolam clearance

A

CYP450 (liver and intestine)

130
Q

onset and duration of midazolam

A

onset 30-60 sec IV

duration 20-60 min IV

131
Q

CV effects of midazolam

A

Minimal with sedation dose

Induction dose: ↓ BP and SVR

132
Q

patients more sensitive to resp depressant effects of midazolam

133
Q

neuro effects of midazolam

A

sedation dose: minimal

induction dose: decreased CMRO2, CBF

134
Q

can midazolam produce isoelectric EEG

135
Q

IV anesthetics with skeletal muscle antispasmodic effects

136
Q

why does diazepam remain in the body for such a long time?

whats its elimination half time?

A

Undergoes enterohepatic recirculation

43 hours

137
Q

how long do amnestic effects of lorazepam last

A

up to 6 hours

138
Q

indications of remimazolam

A

induction & maintenance for adults undergoing procedural sedation lasting 30 min or less

139
Q

dosing of remimazolam

A
  • procedural sedation induction = 5 mg IV per 1 min (2.5 mg for sicker pts)
  • Maintenance of procedural sedation = 2.5 mg IV over 15 seconds, min q2min
140
Q

when does peak sedation occur with remimazolam

A

3-3.5 minutes after admin

141
Q

T½ of remimazolam

A

0.5-2 minutes

142
Q

when does remimazolam have to be discarded

A

discard single-use vial after 8 hours

143
Q

key benefits of remimazolam over midazolam

A

faster onset, deeper sedation, faster recovery

144
Q

when is remimazolam contraindicated

A

pts with hx severe hypersensitivity reaction to Dextran 40

145
Q

metabolism of remimazolam

A

Rapidly metabolized by non-specific plasma esterases

146
Q

remimazolam dosing in liver dysfunction

A

pts with severe liver dysfunction should still receive decreased dose

147
Q

MOA of flumazani

A

Competitive GABA-A receptor antagonist

148
Q

dosing of flumazanil

A

Initial dose 0.2 mg IV, titrated in 0.1 mg increments q1min

149
Q

IV anesthetic that is a carboxylated imidazole structure

APEX (54 decks)

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