Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pharmacodynamics anesthesia > IV Anesthetics > Flashcards

IV Anesthetics Flashcards

1
Q

Propofol MOA

A

GABA-A
Directly stimulates GABA A and potentiates the actions of endogenous GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Propofol onset

A

30-60 seconds (one circulation time)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Propofol duration

A

5-15 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Propofol induction dose

A

1-2.5 mg/kg IV bolus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Propofol maintenance of gen anesthesia dose

A

100-300 mcg/kg/min (when only TIVA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ketamine induction dose

A

1-4.5 mg/kg IV lasts 5-10 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Etomidate induction dose

A

0.2-0.4 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Dex loading dose

A

1mcg/kg over 10 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ketamine IM dose

A

4-8 mg/kg lasts 12-25 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ketamine sedation dose

A

0.1-0.5 mg/kg IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ketamine dose for chronic pain

A

0.1-0.3 mg/kg/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ketamine depression dose

A

0.5 mg/kg over 30-40 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Flumazenil dose for benzo reversal

A

0.2 mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Remimazolam dose for adult induction

A

5mg over 1 minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Remimazolam dose for adult maintenance

A

After 2 minutes of loading, 2.5 mg over 15 seconds prn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Midazolam induction dose

A

0.1-0.2 mg/kg over 30 to 60 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Midazolam adult sedation dose

A

0.25 -2.5 mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Propofol sedation dose

A

25-75 mcg/kg/min (or 10-20 mg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Propofol sedation bolus dose

A

1-2 ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Propofol antiemetic dose

A

10-15 mcg/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Mechanism of action of Barbiturates

A

Potentiating GABA A channel activity.
(also work on glutamate, adenosine, and neuronal nicotinic ACh receptors)
Increase affinity of GABA for it’s binding site, thereby increasing the duration of GABA A activated opening of chloride channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

MOA of Barbiturates at higher doses

A

Mimic action of GABA by directly activating GABA A receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Type of metabolism of barbiturates

A

Hepatic, mostly oxidation, EXCEPT phenobarbitol.
Increases production of porphyrins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Elimination of phenobarbitol

A

Unchanged via renal excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Important considerations for induction dose of thiopental

A

Age, weight, and MOST importantly, cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Barbiturate used for anticonvulsant therapy

A

Methohexital - has decreased anticonvulsant effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

CNS effects of barbiturates

A

Dose-dependent CNS depression
Decreased CMRO2 and CBF
Decreased ICP
Decreased EEG activity
NO analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Respiratory effects of barbiturates

A

HIstamine release - SEVERE
Resp Depression
Dose-Dependent depression of medullary and pontine ventilatory centers
Laryngeal and cough reflexes not depressed until large doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

CV effects of thiopental

A

5mg/kg IV produces 10-20mm decrease in BD.
Due to vasodilation but also depression of medullary vasomotor center and decreased SNS outflow.
Offset by compensatory 15-20 bpm increase in HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Induction dose Methohexital

A

1-1.5 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is propofol used for

A

sedation, induction, maintenance of anesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

2, 6-diisopropyl phenol

A

Propofol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

pH and pKa of diprivan

A

7-8.5
11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

pH of generic Propofol

A

4.5-6.4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

hours prop syringe is good for

hours prop tubing is good for

A

6

12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Propofol antipruritic dose

A

10 mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What type of transmitter is GABA

A

inhibitory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What happens when GABA A receptors are activated

A

Transmembrane chloride conductance increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Reason why you can use propofol when monitoring evoked potentials

A

Spinal motor neuron excitability is not altered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Propofol - time to awakening is dependent on what

A

dose and patients (5-15 min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Prop distribution half life

A

2-4 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Prop elimination half life

A

1-5 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Propfol % protein binding

A

98%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Two IV agents that are not highly protein bound

A

Etomidate - 75%
Ketamine - 12%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is context sensitive half time and what does it depend on?

A

The time needed for the pasma levels of a drug to drop by 50% after stopping the infusion.
Depends of duration for which an infusion has been run

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Does Propofol have analgesic properties?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

CNS effects of propofol

A

Decreased CMRO2
Decreased cerebral blood flow
Decreased cerebral blood volume
Decreased ICP
Decreased Intraocular pressure
Large doses cause burst suppression on EEG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

CV effects of propofol

A

Decreased BP - transient and within 10 minutes of induction.
Decreased CO, CI, stroke volume index, SVR, sympathetic tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What does of prop reduces SBP by 25-40%

A

induction dose of 2-2.5 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What factors make CV effects of Prop more pronounced

A

Elderly
ASA > 3
Baseline MAP <70
Given with high doses of fentanyl (synergistic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Respiratory effects of Prop

A

Dose-dependent resp depression
Decreased Tidal Volume
Apnea
Decreased sensitivity to CO2
Minimal bronchodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Other properties of Propofol

A

Anti-emetic
Antipruritic
Pain on injection
Easily passes placental barrier
Green urine - phenols
Cloudy urine - uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What propofol does NOT do

A

Does not:
Enhance neuro-muscular blockade
Trigger MH
Affect corticosteroid synthesis
Normally affect hepatic or renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the allergic components of propofol

A

Phenyl nucleus
Disopropyl side chain (rare)
In lipid emulsion formulations - Lecithin (egg yolk)
Generic - Metabisulfite or benzyl alcohol preservative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Clinical characteristics of PRIS

A

-Impaired systemic microcirculation with tissue hypoperfusion and hypoxia
EKG changes (arrhythmias, wide QRS)*
Severe Metabolic Acidosis *
Refractory bradycardia -requires pacing
Hypotension
Hyperlipidemia
Renal failure
Rhabdo
Fever
Hyperkalemia
Hypoxia
Hepatic disturbances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Risk factors for PRIS

A

Long-term high dose infusions of propofol
Dose > 5mg/kg per hour
Duration >48 hours
ICU setting
High-fat low-carb intake (keto)
Inborn errors of mitochondrial fatty acid oxidation
Concomitant catecholamine infusion/steroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Management of PRIS

A

D/C propofol
Sedate with versed or precedex
Supportive measures
Cardiac pacing
NO established guidelines
Success of tx r/t earlier diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

IV anesthetic with hypnotic but not analgesic properties and with minimal hemodynamic effects

A

Etomidate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Etomidate is _______ soluble at an acidic pH and _______ soluble at physiologic pH

A

water soluble at acidic
lipid soluble at physiologic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

MOA of Etomidate

A

Single isomer (stereoisomer)
Anesthetic effect resides in the R+ isomer
Relatively selective as a modulator of GABA A receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Onset of etomidate

A

100 seconds

62
Q

DOA of etomidate

A

Usually 5-15 minutes
Depends on redistribution to inactive tissue sites

63
Q

Metabolism of etomidate

A

Hepatic by ester hydrolosis to inactive metabolites, then excreted in urine and biles.

64
Q

Initial distribution half life of etomidate

A

2.7 minutes

65
Q

Redistribution half life of etomidate

A

29 minutes

66
Q

elimination half life of etomidate

A

2.9 - 5.3 hours

67
Q

CNS effects of etomidate

A

Dose-dependent CNS depression within one arm-brain circulation-hypnotic via GABA.
NO analgesia
CBF and CMRO2 decreased
ICP decreased (but no change in MAP so CPP stays the same)
Myoclonia
IOP Decreased

68
Q

CV effects of etomidate

A

PRIMARY advantage is hemodynamic stability in modestly debiliated patients.
No change in HR, PAP, CI, SVR, and SBP (unless pt has aortic or mitral valve disease)
NO effect on SNS/baroreceptor

69
Q

How does etomidate mediate increased BP

A

Acts as agonist at a2B-adrenoceptors

70
Q

Respiratory effects of etomidate

A

Dose-dependent decrease in tidal volume, but RESP RATE INCREASES.
Decreased ventilatory response to CO2.
Brief periods of apnea.
Little effect on bronchial tone
NO histamine release

71
Q

Etomidate’s mechanism of adrenocortical suppression

A

Dose dependent inhibition of the conversion of cholesterol to cortisol.
Inhibits 11 b-hydroxylase.
Lasts 8-12 hours after SINGLE induction dose.

72
Q

Primary advantage of etomidate

A

Hemodynamic stability in modestly debilitated patients

73
Q

When is etomidate contraindicated

A

Known sensitivity
Adrenal suppression
Acute porphyrias

74
Q

enzyme inhibited by etomidate

A

11beta hydroxylase

75
Q

Etomidate effect on nausea/vomiting

A

increases

76
Q

Fade is observed with which type of NMBDs

A

Nondepolarizing

77
Q

What causes fade during TOF stimulation

A

Antagonism of the presynaptic nicotinic receptors by nondepolarizing NMBDs

78
Q

At rest, is the inside of the cell generally positive or negative

A

Negative

79
Q

What drugs are metabolized by pseudocholinesterase

A

Succ, mivacurium, and ester local anesthetics

80
Q

Primary location of acetycholinesterase

A

Neuromuscular junction

81
Q

Primary location of pseudocholinesterase

A

Plasma

82
Q

Treatment for hyperkalemia that stabilizes the myocardium

A

IV calcium

83
Q

Treatment for hyperkalemia that shifts potassium into the cell

A

Glucose + insulin
Sodium bicarb
Hyperventilation
Albuterol

84
Q

Treatment for kyperkalemia that promotes K elimination

A

Lasix
Volume resuscitation
Hemodialysis
Hemofiltration

85
Q

Benzylisoquinolinium nondepolarizing drugs

A

Atracurium
Cisatracurium
Mivacurium

86
Q

Aminosteroid nondepolarizing drugs

A

Rocuronium
Vecuronium
Pancuronium

87
Q

What is Hofmann elimination dependent on

A

Normal blood pH and temperature

88
Q

NMBDs that don’t produce an active metabolite

A

Rocuronium
Mivacurium

89
Q

NMBDs that produce active metabolite Laudanosine

A

Atracurium
Cisatracurium

90
Q

Metabolism of Atracurium

A

Plasma: Hofmann and ester hydrolysis

91
Q

Metabolism of Cisatracurium

A

Plasma: hofmann elimination

92
Q

Metabolism of Mivacurium

A

Plasma: Pseudocholinesterase

93
Q

Metabolism of Rocuronium

A

None: Undergoes biliary excretion

94
Q

Metabolism of Vecuronium

A

Liver

95
Q

Metabolism of Pancuronium

A

Liver
85% eliminated from kidneys

96
Q

Which NMBDs release histamine

A

Succ
Atracurium
Mivacurium

97
Q

Hofmann elimination is faster with

A

Alkalosis and hyperthermia

98
Q

Hofmann elimination is slower with

A

Acidosis and hypothermia

99
Q

Reversal agent of diazepam, midazolam, and lorazepam

A

Flumazenil - selective antagonist

100
Q

Desired effects of benzos

A

Anxiolysis and anterograde amnesia, sedation, hypnosis, and anticonvulsant

101
Q

MOA of Benzos

A

Agonist action at benzodiazepine receptor binding sites on the GABA A receptor throughout the CNS

102
Q

How does the GABA A receptor exert its action

A

Modulating chloride channels

103
Q

Is midaz lipid soluble or water soluble in vivo/blood

A

Lipid at pH >4

104
Q

Which effect of midazolam greater, amnestic or sedative

A

Amnestic

105
Q

Does midazolam cross the placenta

A

Yes

106
Q

How are benzos metabolized

A

Selectively metabolized by hepatic cytochrome P450 to single dominant ACTIVE metabolite

107
Q

CNS effects of benzos

A

Dose-dependent CNS depression
Anticonvulsant effects, amnesia, muscle-relaxing properties
Not all antiemetic (midaz is antiemetic)
Reduce CMRO2 and CBF at higher doses
Dose-related anterograde amnesia
NO ANALGESIA

108
Q

CV effect of benzos

A

Sedation dose= minimal effects
*unless elderly, cv disease, or given with opioids
Induction dose= decrease in SBP and SVR

109
Q

Resp effects of benzos

A

Dose-dependent depression
Midazolam is MOST respiratory depressing

110
Q

Most common adverse effects of benzos

A

Unexpected respiratory depression and over-sedation
Avoid in patients with porphyria

111
Q

Sedation dose of Midazolam
Onset
Peak
Duration

A

IV: 0.25-2.5 mg
Onset: 30-60 seconds
Peak: 5 minutes
Duration: 15-80 minutes

112
Q

Induction dose of Midazolam

A

0.1-0.2 mg/kg IV over 30-60 seconds

113
Q

Remimazolam metabolism

A

Rapid via nonspecific tissue esterases to an inactive carboxylic acid

114
Q

Remimazolam Dose for adults

A

5mg IV over 1 minutes

115
Q

Remimazolam dose for ASA 3-4 adults

A

2.5 - 5mg IV over 1 minutes

116
Q

Remimazolam maintenance dose

A

After AT LEAST 2 minutes, 2.5 mg over 15 seconds

117
Q

Remimazolam preparation

A

Powder needs reconstituted
20 mg vial
8ml NSS = 2.5 mg/ml
10ml NSS = 2 mg /ml
For infusion, reconstitute to 1 mg/ml

118
Q

Remimazolam Onset

A

1-1.5 minutes
Peak sedation 3-3.5 minutes

119
Q

Remimazolam Duration

A

11-14 minutes

120
Q

Initial dose of flumazenil

A

0.2 mg IV

121
Q

Onset of flumazenil

A

2 minutes

122
Q

DOA of flumazenil

A

30-60 minutes

123
Q

Subsequent dosing of flumazenil

A

0.1 mg IV at 60 second intervals

124
Q

When should flumazenil not be given

A

For patients being treated with antiepileptic drugs for control of seizure activity

125
Q

MOA of flumazenil

A

Competative Benzo receptor antagonist

126
Q

Effects of ketamine

A

Dissociative Anesthesia
Amnesia
Intense analgesia
Retains protective reflexes
Eyes remain open with slow nystagmus

127
Q

MOA of ketamine

A

Antagonism at NMDA receptors in brain
Dissociates thalamus (sensory) from limbic system (awareness)
Direct inhibition of cytokines in blood
Inhibit TNF-a and interluken 6

128
Q

Ketamine’s primary site of analgesic action

A

Thalamo-neocortical system

129
Q

When is the NMDA receptor activated

A

When glutamine and glycine bind to it

130
Q

How does ketamine work on the NMDA receptor

A

Deactivates. Decreases presynaptic release of glutamate

131
Q

Metabolism of Ketamine

A

Extensively by hepatic microsomal enzymes. Demethylation by P450 to form active metabolite Norketamine.
<4% unchanged in urine.
<5% fecal excretion

132
Q

What is elimination of ketamine dependent upon

A

Hepatic blood flow. High hepatic extraction.

133
Q

Onset of ketamine

A

3-5 minutes

134
Q

Ketamine elimination half life

A

2-3 hours

135
Q

CNS effects of Ketamine

A

Cerebral dilator
Increases CBF and CMRO2
Emergence delirium
Can increase CBF up to 60%
Nystagmus, Increased IOP
Increased EEG activity

136
Q

CV effects of Ketamine

A

Stimulant
Increases BP, HR, Contractility, CO, CVP via centrally mediated sympathetic stimulation
Increased myocardial O2 consumption

137
Q

Ketamine not used for patients with:

A

Increased ICP
Recent MI or severe heart disease

138
Q

Respiratory effects of Ketamine

A

Minor and short duration
Reflexes and tone remain intact
Central response to CO2 maintained
Increases pulm compliance and decreases resistance
NO histamine release
ONLY active bronchodilating IV induction agent
Increases secretions

139
Q

IV induction drug of choice for active asthma/wheezing for urgent surgery

A

Ketamine

140
Q

Dexmedetomidine class

A

highly selective alpha 2 agonist.
Targets high density of alpha 2 receptors in the pontine locus ceruleus

141
Q

Primary effects of Dex

A

sedation, analgesia, anxiolysis, reduced postop shivering and agitation, CV sympatholytic actions

142
Q

What class of alpha 2 agonist is Dex

A

Imidazolines

143
Q

MOA of Dex

A

Stimulates a2 receptors resulting in decreased catecholamine release.
Activates sleep pathways
Analgesic effects at the dorsal horn of spinal cord

144
Q

Metabolism of Dex

A

Rapid hepatic involving conjugation, n-methylation, and hydroxylation.
Metabolites excreted in urine and bile.
No active metabolites

145
Q

Onset of Dex

A

10-20 minutes after loading dose

146
Q

DOA of Dex

A

10-30 minutes after infusion stopped

147
Q

Loading dose for Dex

A

1 mcg/kg over 10 minutes

148
Q

Maintenance dose of Dex

A

0.2-0.7 mcg/kg iv infusion

149
Q

CNS effects of Dex

A

Does not interfere with electrophysiologic monitoring.
No change in CMRO2.
CBF decreased due to vasoconstriction.
Reduces postop agitation and delirium.

150
Q

CV effects of Dex

A

Hypotension and bradycardia
Transient hypertension with rapid loading dose.
NO direct effect on contractility
Reduces myocardial O2 demand
Transient profound HTN with glyco

151
Q

Resp effects of Dex

A

Respirations maintained
Responsiveness to CO2 is normal
Airway patency and reflexes present or slightly diminished
Decrease airway reactivity in pts with COPD or Asthma

152
Q
A

pharmacodynamics anesthesia (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions