Brainscape's Knowledge GenomeTM

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


See full index

614 General Principles Of Anesthesia > Week 5- Induction Agents > Flashcards

Week 5- Induction Agents Flashcards

1
Q

Primary MOA of propofol

A

GABA- A receptor agonist (enhance GABA inhibition)

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

Chemical name for propofol

A

2-6-diisopropylphenol

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

Protein binding of propofol

A

98%

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

Make up of propofol

A

1% propofol
10% soybean oil
2.25% glycerol
1.2% egg phospholipid emulsifier

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

What is added to propofol to decrease microbial growth

A

EDTA

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

T or F: propofol has an unpredictable CSS

A

False- predictable

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

T or F: propofol causes PONV

A

F- antiemetic properties

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

What component of propofol causes veno irritation

A

The glycerol

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

CNS effects of propofol

A

CNS depressant
- neuroprotective
- anticonvulsant
- decrease CMRO2, CBF, and ICP

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

CV effects of Propofol

A

Significant decrease in SVR, SV, and CO

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

Pulmonary reactions to propofol

A

Respiratory depressant and potent bronchodilator

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

Major side effects of propofol

A

Pain with injection

Propofol infusion syndrome

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

sign of propfol infusion syndrome

A

Green urine

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

Clinical uses of propofol

A
  • general, induction, maintenance
  • TIVA
  • Conscious/deep sedation including ambulatory centers
  • ICU
  • PONV prevention
  • safe for MH patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Propofol is metabolized in

A

Liver
inactive/water soluble metabolites excreted by kidneys

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

Most common extra hepatic site of metabolism of Propofol. How much metabolism occurs here

A

Kidney and lungs

30%

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

Which model explains elimination of propfol

A

3-compartment model

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

What causes unconscious states of propofol

A

Enhancement of GABA inhibitory pathways and central cholinergic transmission, NMDA, or a- adrenergic sites

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

What does low dose propofol produce

A
  • sedation
    -possible paradoxical excitation at higher doses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

T or f: propfol can be used to treat status epilepticus

A

T

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

Why would you use propofol for ECT

A

Shorten seizure duration

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

When are you more likely to have a CV response to Propofol?

A

Induction dosing compared to continuous
*drop in BP without increased HR (decreased CO, SV, SVR)

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

What can maintenance doses of propfol do to tidal volume and RR

A

Decrease Tv and increased RR

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

Why is propofol a good bronchodilator

A

Direct effect on intracellular calcium

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

IV and infusion dose of Propofol to prevent PONV

Why does this seem to prevent PONV

A

IV = 10-15 mg
Infusion = 10 mcg/kg/min

direct effect on chemoreceptor trigger zone

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

What can you use to effectively treat opioid-induced pruritus, what dose, and what mechanism is this related to

A

Propofol
10 mg IV
Spinal cord suppression

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

Induction of anesthesia with propofol:
- dose
- produces unconsciousness in ____

A
  • 2 mg/kg
  • 30 seconds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Intravenous sedation of propofol (MAC)

Maintenance dose of propofol (GA)

A

25-75 mcg/kg/min

100-200 mcg/kg/min

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

Usual concentration of propofol

A

200 mg/20 mL –> 10 mg/mL

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

What cause cause propofol allergies?

A
  • phenyl nucleus and di-isopropyl side chain (anaphylaxis reported)
  • generic brand have sodium metabisulfite —> contrainidicated with sulfite sensitivity
  • eggs or soy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Cautious using propofol in (5 examples)

A
  • elderly —> increased sensitivity d/t decreased CO and clearance
  • children —> large Vd and faster clearance
  • chronic alcoholics —> require more
  • CV disease
  • trauma/ hypotension/ bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How long is propofol good for?

A

12 hours in opened vial, 6 hours in syringe

read the vial IT CAN SUPPORT BACTERIA

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

What doses can cause propofol infusion syndrome

A

4 mg/kg/hr > 48 hours

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

Most important side effects of propofol infusion syndrome

A

Bradycardia/ asystole

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

Etomidate is __________ stable.
It also can cause post-operative __________.

A

Hemodynamically ;

PONV

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

MOA of etomidate

A

GABA-A receptor agonist

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

T or F: etomidate should be avoided in elderly

A

F- good for cardiac, trauma, elderly

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

Critically ill patients administered etomidate should be monitored for

A

Adrenocortical supression

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

Chemical makeup of etomidate

A

Carboxylated imidazole derivative

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

Why is the continuous infusion of etomidate limited?

A

Due to possible adrenal suppression.

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

T or F: etomidate follows 1 compartment model

A

F- 3 compartment model

**Fast resolution of effect secondary to redistribution

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

Etomidate (_________)

A

Amidate

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

Metabolization and excretion of etomidate

A

Liver and plasma esterases

Excreted by kidney (80%) and bile (20%)

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

Protein binding of etomidate

A

75% (Highly protein bound)

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

Etomidate

Initial distribution half-life:

Redistribution of half-life:

Elimination half-life:

Volume of distribution:

A

2.7 minutes

29 minutes

3-6 hours.

2.5-4.5L/kg

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

Induction dose of etomidate

the usual concentration of etomidate

A

0.2-0.3 mg/kg

2 mg/cc

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

CNS effects of etomidate

A
  • potent vasoconstrictor that reduces CBF, ICP, CMRO2
  • seizure like, myoclonic movements on induction –versed/opioid
  • proconvulsant and lowers seizure threshold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

CV effects of etomidate

A
  • hemodynamically stable on induction
  • minimal to no side effects on CV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Why does etomidate cause adrenocortisol suppression

A

Inhibit activity of 11B-hydroxylase and prevents conversion of cholesterol to cortisol

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

Ketamine (_________)

A

Ketalar

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

Ketamine’s active metabolite

A

Norketamine

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

Ketamine is a _________ anesthetic. Emergence was associated with __________.

A

Dissociative;

Delirium and hallucinations.

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

Ketamine is a __________ derivative.

A

Phenylcyclohexyl piperidine(PCP)

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

T or F- ketamine is a racemic mixture with a chiral compound

A

T

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

Bioavailability of routes of administration of ketamine

A

IM (93%)
Transnasal (25-50%)
Rectal or oral (16%)

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

Protein binding of Ketamine

A

20%

** it has a high lipid solubility/ rapid redistribution

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

How is ketamine metabolized

A

by Cytochrome p450 enzymes

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

where is Ketamine metabolized and what is the metabolite of Ketamine

A

Liver

Demethylation to norketamine (1/3-1/5 as active)

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

Ketamine

Onset:

Duration:

Induction dose:

K-dart dose:

Usual concentration

A

O: 30-60 sec

D: 10-20 min (dose depedent)

ID: 0.5-2 mg/kg IV
4-5 mg/kg IM (K dart)

Usual conc: 10 mg/cc

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

Ketamine’s CNS effect are primarily related to its _______ activity at the NMDA receptor

A

antagonistic

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

MOA of Ketamine

A
  • function dissociation between thalamocortical and limbic systems
  • CNS effects primarily related to antagonistic activity of NMDA receptor
62
Q

Where else does Ketamine bind

A
  • non NMDA glutamate receptor
  • Nicotinic receptors
  • cholinergic receptors
  • monoaminergic receptors
  • mu, delta, and kappa-opioid receptors
  • inhibit neuronal NA+ channel and Ca2+
63
Q

Ketamine uses:

A
  • Sedation
  • Analgesia and acute post- op pain (part of non-opioid protocol)
  • ERAS protocol (enhanced recovery after surgery.
  • Opioid abuse patients
  • Acute and CHRONIC pain.
  • Depression
64
Q

Why Ketamine clinically

A
  • dissociative amnestic state
  • unconscious with eyes open, maintain RR and do not react to painful stimulus
  • good choice for hemo stable (induction dose associated with increased HR and BP)
  • OB
  • acute/chronic pain
  • depression
65
Q

In what pt should you be cautious of using Ketamine

A

Cardiac, cardiac cripple, and severe right heart dysfunction (increases PVR)

66
Q

CNS effects of Ketamine

A
  • POTENT CEREBRAL VASODILATOR
  • increased CBF 60-80% during normocapnia (attenuated with hyperventilation)
  • relatively contraindicated in elevated ICP
67
Q

Why is there increase of secreations in Ketamine use

A

Effect of muscarinic receptors

**can give glycopyrollate

68
Q

T or F: Ketamine is a good bronchodilator

A

T

**maintains protective airways/ does not produce significant depression of ventilation.

69
Q

Ketamine resembles _________ on the CV system

A

SNS stimulation

70
Q

CV effects of Ketamine

A

Everything up
- MAP, CO, myocardial O2 requirements, SVR

71
Q

Why should Ketamine be avoided in critically ill or shock like pt

A

Due to chatecholomine depletion leading to unopposed direct myocardial depression

72
Q

How to medically prevent Ketamine emergence delerium

A

Midazolam preoperative and awake in calm and quiet environment

** becareful in pt’s with PTSD

73
Q

Incidence of emergence delerium in Ketamine and what is the dose at which it occurs

A

5-30%

> 2 mg/kg

74
Q

MOA of dexmedetomidine

A

Highly selective, specific, potent a2-adrenergic agonist

75
Q

Dexmotidine produces dose-dependent sedation and analgesia with _________ respiratory depression.

A

MILD

76
Q

dexmedetomidine is ______ times more selective for a2 receptors than clonidine

A

7-8

77
Q

Protein binding of dexmedetomidine

A

94%

**highly protein bound

78
Q

Metabolism of dexmedetomidine

A

Rapid hepatic metabolism involving conjugation, N-methylation, and hydroxylation

79
Q

Excretion of dexmedetomidine

A

Urine and feces

80
Q

rapid redistribution: with distribution half life of dexmedetomidine

A

6 minutes

81
Q

Short elimination half life of dexmedetomidine

A

2 hours

82
Q

dexmedetomidine could cause increased plasma concentration of ________

and why?

A

Opioids

precedex has weak inhibitory properties in the CYP-450 system

83
Q

CNS effects of dexmedetomidine

A
  • sedative, anxiolytic, analgesic (spinal cord and brain)
  • sedated but easily arousable
  • Analgesic effects reduce opioid requirement
84
Q

Respiratory effects of dexmedetomidine

A
  • less ventilator depression compared to others.
  • bolus dose reduces minute ventilation
85
Q

CV effects of dexmedetomidine

A
  • increase potential hypotension and bradycardia (esp in kids)
  • blunt effects of hemo dynamic effects of direct laryngoscopy and improves hemo dynamic stability when given as anesthetic adjunct
86
Q

Sedation and infusion dose of dexmedetomidine

typical syringe concentration

A

Sedation: 0.5- 1 mcg/kg over 10 minutes

Infusion: 0.2-0.7 mcg/kg/hr

Conc: 4 mcg/mL

87
Q

Side effects of dexmedetomidine

A
  • hypotension
  • bradyacardia
  • dry mouth and nausea
  • rebound hypertension
88
Q

Benefits of using benzodiazepines

A
  • amnesia
  • minimal CV and respiratory depression
  • anticonvulsant
  • anxiolysis and sedation
  • skeletal muscle relaxant
89
Q

MOA of benzodiazepines

A

Effect central inhibitory GABA-A

Bind to alpha subunits increasing chloride conductance –> hyperpolarization of cell

90
Q

Benzodiazepine have rapid absorption from the gut, with _________% first- pass hepatic extraction.

A

> 50%

** watch for patients with kidney and liver dysfunction, age, cormobidities,

91
Q

T or F: benzodiazepines burn on injection

A

False- does not burn d/t being water soluble in bottle

92
Q

Protein binding of benzodiazepines

A

94-98%

**high lipid solubility

93
Q

benzodiazepines effects (5)

A
  • descrease CMRO2, CBF, little effect on ICP
  • decreased upper airway reflexes
  • decreased central Resp drive
  • decrease SVR and BP
  • anterograde amnesia (OB)
94
Q

Reversal dose of benzodiazepine with flumazenil (_________):

A

Romazicon

0.2 mg IV over 15 seconds

If after 45 seconds, no response, give 0.2 mg

Can repeat at 1 min intervals (not exceed 4 doses)

95
Q

Oral dose of benzodiazepines in kids and adults

A

Kids: 0.5 mg/kg 30 min before OR

Adults: 1-2 mg in preoperative (IV)

96
Q

3 most common benzodiazepines

A
  • midazolam, lorazepam, diazepam
97
Q

Which of the benzodiazepines is water soluble

a. midazolam
b. lorazepam
c. diazepam

A

Midazolam

***undergoes conformational change in the bloodstream becoming more lipophilic

98
Q

Barbiturates 2 classes

A
  • oxybabrbiturates
  • thiobarbiturates
99
Q

Why is methohexital a oxybarbiturate

A

Retains an O2 atom on the #2 carbon atom

100
Q

Why is thiopental a thiobarbiturates

A

Replacement of the O2 atom with sulfur on the #2 carbon atom

101
Q

Primary metabolism Barbiturates

A

Hepatic, inactive metabolites excreted in urine and bile

102
Q

What accounts for rapid termination after a single dose of Barbiturates

A

Rapid distribution of highly perfused compartments

103
Q

MOA of Barbiturates

A

Cortical and brain stem GABA inhibitory pathways

104
Q

Concerning side effects of Barbiturates

A
  • LOC, respiratory and CV depression
105
Q

What causes hypnotic effects of Barbiturates

A

Inhibiton of central excitatory pathway

** mediated by glutamate via the NMDA receptors and acetylcholine

106
Q

Thiopental may be used for induction of anesthesia in patients with ________, as well as the treatment of _______ that is resistant to hyperventilation.

A

increase ICP

Increase ICP

107
Q

Thiopental is generally considered an ___________ and used to treat ___________.

A

anticonvulsant;

status epilepticus

108
Q

Elimination 1/2 life of thiopental

A

12 Hours

109
Q

thiopental precipitates with (3)

A
  • SCh
  • rocuronium
  • lidocaine
110
Q

Thiopental stimulates the release of histamine from:

A

mast cells

111
Q

T or F: thiopental is neuroprotective

A

T

*** by drug induced cerebrovascular vasoconstriction.
- This leads to decreased cerebral blood flow.
- subsequent decrease in intracranial pressure
- decreased cerebral metabolic O2 consumption.

112
Q

Barbiturates should be avoided in patients with what disorder:

A

AIP ( acute intermittent porphyria )

113
Q

Other name for methohexital

A

Brevital

114
Q

Elimination half life of Brevital

A

4 hours

** more efficient hepatic extraction

115
Q

Drug of choice for Electroconvulsive therapy

A

Methohexital (brevital)

**proconvulsant activity

116
Q

Methohexital (brevital)

IV dose
Rectal dose

A

IV: 1-2 mg/kg
Rectal: 20-30 mg/kg

***may cause pain on injection

117
Q

Induction dose of thiopental

A

2.5-5 mg/kg

***reduce dose by 30-35% in elderly

118
Q

low dose of IV anesthetics produce ______ and high doses produce ______

A

sedation

unconsciousness

119
Q

T or F: all IV anesthetics are sedative-hypnotics and produce dose-dependent CNS depression

A

T

120
Q

uses for IV induction medications

A
  • induction of anesthesia
  • TIVA
  • MAC
  • sedation during local and regional anesthesia
121
Q

the time it takes for the plasma concentration of a drug to decreas to 50% of its original concentration (after 1 bolus dose)

A

elimination half-time (t 1/2)

122
Q

T or F: elimination half-time can describe a three-compartment model for a drug only in the blood phase or a drug administered only once (bolus)

A

F- one-compartment model

123
Q

the time to achieve a 50% reduction in concentration after stopping a continuous infusion

A

context-sensitive half time

124
Q

describes the transfer of drug out of the plasma into the peripheral compartments followed by the reverse process once the infusion is stopped back into the central compartment

A

context-sensitive half time

125
Q

the best example of Css

A

remifentanil

126
Q

which induction agent can cause an increase in “sexual tendencies”

A

propofol

127
Q

T or F: Ketamine is a bronchodilator

A

T

128
Q

other name for etomidate

A

amidate

129
Q

T or F: etomidate can cause PONV

A

T

130
Q

what contributes to the veno-irritation and phlebitis of etomidate

A

solvents in the formation (propylene glycol)

131
Q

etomidate has a _______ onset of action

A

quick
**(vein to brain)

132
Q

the initial distribution half-life of etomidate

A

2.7 minutes

133
Q

redistribution half-life of etomidate

A

29 minutes

134
Q

elimination half life of etomidate

A

3-6 hours

135
Q

volume of distribtuion of etomidate

A

2.5-4.5 L/kg

136
Q

T or F: Ketamine is a phencyclidine derivative

A

T

137
Q

T or F: Ketamine is also known as Vitamin K

A

T

138
Q

T or F: ketmine can cause emergence delerium and hallucinationsn

A

t

139
Q

t or f: ketamine only has anesthetic effects, not analgesic effects

A

F, has both

140
Q

Ketamine has ____________ effects

a. associative
b. dissociative

A

dissociative

141
Q

why would ketamine be used in a pt with acute or chronic pain

A

NMDA receptor is associated with central sensitization and winds up at the spinal cord associated with chronic pain. studies suggest ketamine analgesia occurs by prevention of hyperalgesia and decreases in CNS sensitization that occurs with acute pain

142
Q

T or F: Ketamine produces significant depresison of ventilation

A

F - does NOT produce … maintain protective airway reflexes

143
Q

t or F: Precedex produces dose-dependent sedation and analgesia with mild respiratory depression

A

T

144
Q

Why is precedex a good IV adjunct during induction or maintenance of general anesthesia `

A

will blunt acute SNS response to laryngoscopy

145
Q

uses of dexmedetomidine

A
  • procedural sedation (awake fiberoptic)
  • rigid bronchs
  • used as adjuvant during local and regional anesthesia
146
Q

how can you decrease the incidence of bradycardia with precedex use and how can you treat it?

A
  • ommit loading dose
  • treat with atropine, ephedrine, or volume
147
Q

rapid absorption in the gut with ________ first-pass hepatic extraction of benzos

A

> 50%

148
Q

rapid absorption in the gut with ________ first-pass hepatic extraction of benzos

A

> 50%

149
Q

which barbiturate is associated with accumulation in poorly perfused compartments and slow elimination (prolonged Css and delayed recovery)

A

Thiopental

150
Q

may be used for induction of anesthesia in patients with increased ICP as well as the treatment of increased ICP that is resistant to hyperventilation alone

A

Thiopental

151
Q

CNS effects of thiopental

A
  • cerebrovascular vasoconstriction
  • decrease cerebral blood flow
  • decreased intracranial pressure
  • decreased cerebral metabolic O2 consumption

**anticonvulsant

152
Q

T or F: thiopental stimulates the release of histamine from mast cells

A

T

614 General Principles Of Anesthesia (14 decks)

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