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S5 - Regional/OB - Test 1 > Local Anesthetics - Test 1 > Flashcards

Local Anesthetics - Test 1 Flashcards

1
Q

if the same dose of an LA is given to the same person via both tracheal and epidural routes, at which site will the block wear off fastest?

why?

A

tracheal block will be shorter d/t higher rate of blood flow and higher rate of uptake

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2
Q

goals for regional anesthesia (3)

already know I’m gonna read this twice, put 5/5 and move on 4ever

A
  1. understanding peripheral nerve anatomy
  2. understanding LAs, US equipment, and nerve block techniques
  3. practice
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3
Q

vertebrae that correlates with the xiphoid

A

T9

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4
Q

which is more likely to cause an allergic reaction - ester or amide?

why?

A

esters

metabolite: PABA

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5
Q

nerve fibers that carry reflexes

A

Aγ fibers

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6
Q

what is the best (but most complicated) method to sustain a patient with cardiac toxicity from LA?

A

cardiac bypass

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7
Q

onset and duration of ropivacaine

A

slow onset

duration 180-600 min (long)

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8
Q

amides bind the lipid side of the chain with ____

A

NHC

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9
Q

max dose of bupivacaine

why is it especially important to pay attention to max dose with this drug?

A

2.5 mg/kg

bupivacaine is particularly cardiotoxic and is very lipophilic - so it’s long-lasting and its effect doesn’t “wear off” quickly

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10
Q

effect of epinephrine on LA & why

A

potentiates effects

  • causes vasoconstriction = decreased blood flow = decreased circulatory uptake = decreased metabolism
  • increased duration of action, potency, and reduction of absorption into tissue
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11
Q

why is 5% lidocaine not used much anymore for subarachnoid blocks?

A

neurotoxicity

(specifically cauda equina syndrome when catheters were used to continuously infuse; TNS has been reported from single injections)

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12
Q

function of Aα nerve fibers

A

motor signals and proprioception

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13
Q

nerves that form the sciatic nerve

A

tibial (L4-S3) & common peroneal (L4-S2)

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14
Q

treatments for LA CNS toxicity

which is most common and why?

A

benzos and propofol

benzos most common - caution use with propofol d/t myocardial depression (pt may also have CV toxicity)

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15
Q

nerve fibers that have subgroups of alpha, beta, gamma, and delta fibers

A

A fibers

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16
Q

the lateral and medial cords form which nerve?

A

median nerve

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17
Q

what are transient neurologic symptoms (TNS)?

what specific LA techniques have been associated with TNS?

A

resolvable syndromes with s/s simular to cauda equina syndrome

subarachnoid catheters, particularly with 5% lidocaine

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18
Q

3 factors that determine the longevity of LA action

A
  1. dose to start
  2. tissue distribution & lipid solubility
  3. drug metabolism
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19
Q

max dose of ropivacaine

A

3 mg/kg

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20
Q

LA with metabolite that is a precursor for methemoglobin

what is the metabolite?

there’s two

A

prilocaine

o-toluidine

and benzocaine

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21
Q

max dose of prilocaine

A

8 mg/kg

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22
Q

2 main concerns of bupivacaine use

A
  • particular propensity to cause cardiac effects
  • prolonged duration may be concerning because it doesn’t “wear off”
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23
Q

onset and duration of lidocaine

A

fast onset

duration 90-120 min (medium)

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24
Q

How many pairs of spinal nerves are there?

What are the groups of spinal nerves?

A

31 pairs:

  • 8 cervical
  • 12 thoracic
  • 5 lumbar
  • 5 sacral
  • 1 coccygeal
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25
Q

functional unit of the peripheral nerve

A

axon

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26
Q

MOA of local anesthetics

A
  • interrupt Na+ current in the nerve
  • prevents depolarization
  • (Stoelting - bind to voltage-gated Na+ channels, inhibiting passage of Na+ ions and preventing transmission of nerve impulses)
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27
Q

which form of the LA binds to the Na+ receptor - ionized or nonionized?

is this its water or lipid-soluble form?

A

ionized

water soluble

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28
Q

how does tissue distribution (blood flow to tissues) affect LAs?

A

the higher the blood flow to the tissue LA is injected into, the faster the LA will enter the bloodstream to be metabolized

(increased blood flow = increased entry into bloodstream = increased metabolism = decreased effect on nerve)­­­

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29
Q

effect of clonidine on LAs & why

A

increases potency and duration of blocks by delaying repolarization

(has alpha 2 agonist properties)

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30
Q

effect of opioids on LA block

A

increased potency (sometimes recognized as increased speed of onset)

density of block/total duration of action won’t change

He said that it probably doesnt really speed onset, but instead juast makes for a less spotty block because other receptors are covered with opioids

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31
Q

function of B nerve fibers

difference vs. A fibers

A

carry autonomic signals

less myelination

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32
Q

how are nerve fiber sizes classified?

A

A, B, and C

A is the largest

C is the smallest

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33
Q

vertebrae that is the most prominent cervical level (“vertebral prominens”)

A

C7

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34
Q

why can CNS effects be seen with LA toxicity?

A

crossing blood-brain barrier & depression of inhibitory neurons

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35
Q

uses of liposomal bupivacaine (Exparel)

A

long-acting pain relief for ortho surgeries

peripheral nerve blocks

given as a single injection

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36
Q

rates of LA uptake from fastest to slowest

A

tracheal > intercostal > caudal > epidural > brachial plexus > femoral/sciatic

(aka- highest to lowest bloodflow)

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37
Q

what characteristics of a nerve fiber make it harder to block with LAs?

A

the larger and more myelinated, the harder to block

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38
Q

components of PNS order of physical size

A

afferent and efferent fibers > fascicles (bundles of axons) > individual nerve fibers (axons)

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39
Q

typical timing of systemic toxicity

why does this occur?

A

occurrence is usually rapid

most often in < 1 min, majority < 5 min from time of injection

d/t direct injection of LA intravascularly rather than into tissue

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40
Q

max dose of procaine

A

12 mg/kg

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41
Q

How is ropivacaine similar to bupivacaine?

How is it different?

A

similar: onset, time, duration
different: less cardiotoxic effects, generally less pronounced motor block potency

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42
Q

esters bind the lipid side of the chain with ____

A

CO

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43
Q

nerve roots that form the radial nerve

A

C5-T1

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44
Q

onset and duration of chloroprocaine

A

fast onset

short duration (30-60 min)

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45
Q

how does clonidine improve LA blockade duration and potency?

A

inhibits peripheral nerve signal conduction in A and C fibers

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46
Q

key to classifying types of local anesthetics

A

the link between the lipophilic ring and the hydrocarbon

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47
Q

hallmark s/s of both cauda equina syndrome and TNS

A

deficits of:

  • bowel
  • bladder
  • lower extremity motor
  • lower extremity sensory
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48
Q

what is dibucaine?

what do the following mean:

dibucaine no. 80

dibucaine no. 20

A

dibucaine is an LA that inhibits plasma cholinesterase

dibucaine no 80 - plasmacholinesterase is 80% inhibited when exposed to dibucaine (normal)

dibucaine no 20 - plasmacholinesterase only 20% inhibited when exposed to dibucaine (expect longer recovery from ester LAs, ~3 hrs)

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49
Q

LA used to evaluate for the presence of normal enzyme function

In normal patients, how much pseudocholinesterase is inhibited by this LA?

A

dibucaine - exposing a patient’s pseudocholinesterase to dibucaine should inhibit the action of the enzyme

normal pts - 80% (Dibucaine no. 80)

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50
Q

direction of spinous processes at cervical vs. lumbar levels

A

cervical - caudad

lumbar - straight

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51
Q

what organ removes a large portion of the LA, especially lidocaine?

A

lungs

brand new info- thought lidocaine was metabolized by ur lil liver

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52
Q

metabolism of esters vs. amides

which is generally faster?

A
  • esters: pseudocholinesterases
  • amides: liver
  • generally faster: esterases
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53
Q

vertebrae that is the plane of Ludwig

what does this correlate?

A

T4

carina and angle of Louis

54
Q

onset and duration of tetracaine

A

slow onset

long duration

55
Q

3 states of sodium channel

in which state/states can a LA block?

A
  1. activated open
  2. inactivated closed
  3. rested closed

LAs can block in channels 1&2 only

56
Q

primary mediator for influx of Na+ into peripheral nerves

A

voltage-gated sodium channels

57
Q

LAs associated with methemoglobinemia

How is methemoglobinemia treated?

A

prilocaine & benzocaine

1-2 mg/kg methylene blue IV

58
Q

CNS communication to the body occurs via the __________.

is this motor or sensory?

A

ventral root from ventrolateral aspect of the cord

motor (efferent)

59
Q

acute and significant uptake of LA may result in what adverse effect?

A

hypoventilation, respiratory arrest

60
Q

MOA of 20% lipid solution for LAST

A

lipids absorb the LA, which accelerates its removal from cardiac receptors

61
Q

how does the dose of LA impact systemic absorption?

A

larger doses increase concentration gradient of the LA

62
Q

vertebrae that correlates with the umbilicus

A

T10- dermatome

L4- vertbrae

63
Q

function of Aδ nerve fibers

A

fast pain, temperature, and touch

64
Q

part of LA chemical structure that is lipophilic

A

aromatic benzene ring

65
Q

where does the spinal cord terminate in most adults?

what does it transition into?

A

L2

transitions into collection of nerves called cauda equina

66
Q

component of amides that can cause an allergic reaction

which amide is most likely to cause an allergic reaction?

A

preservatives such as methylparaben

prilocaine

67
Q

nerve roots that form the brachial plexus

where does the brachial plexus emerge?

A

C5-T1

between the anterior and middle scalene muscles

68
Q

conditions that increase risk of toxicity with use of esters vs. amides

A
  • esters: plasma cholinesterase deficiency
  • amides: liver dysfunction
69
Q

MOA of cardiotoxicity seen with LAs

A

blockade of excitatory neurons resulting in cardiac dysrhythmias and arrest

70
Q

CNS communication from the body is via the _____________.

is this motor or sensory?

A

dorsolateral aspect of the cord

sensory

71
Q

what is pKa?

what is the effect of pH lower than the pKa of the drug?

A

pH at which half of the drug is nonionized and the other half is ionized

if pH of patient is lower than pKa of the drug, the LA becomes more ionized and less able to enter the nerve

72
Q

onset and duration of procaine

A

slow onset

duration 60-90 min (short, I think?)

73
Q

non-nerve blockade uses of LAs (4)

A
  1. inhibition of ventricular dysrhytmias
  2. reduced CBF (for high ICP during intubation)
  3. pain management
  4. use of lidocaine to blunt respiratory stimulation (via smooth muscle relaxation)
74
Q

what is the max dose of mepivacaine

does the max dose change if epinephrine is added?

A

4.5 mg/kg

yup, with epi max is 7 mg/kg

75
Q

onset and duration of mepivacaine

A

onset: fast
duration: 120-240 min (medium)

76
Q

vertebrae that correlates with superior angle of the scapula and sternal notch

A

T2

77
Q

vertebrae that correlates with the superior iliac crest, L4-5 disc space, and the umbilicus

A

L4

78
Q

nerve fiber recovery from LA

A

heavy myelinated fibers

A delta fibers

C fibers

B fibers

79
Q

function of Aβ fibers

A

touch and pressure recognition

80
Q

max dose of chloroprocaine

A

12 mg/kg

81
Q

how does lipophilicity of LA impact its potency and duration of action?

A

increased lipophilicity = increased potency & longer duration of action

82
Q

where are the cervical spinal nerves in relation to the vertebral bodies?

A

lying above the like-named vertebral body

83
Q

T/F - liposomal bupivacaine (Exparel) must be given via indwelling catheter

A

false - single injection can be used for same effect d/t long duration of

feel free to reword

84
Q

general order of nerve fiber blockade

A

B fibers

C fibers

A delta fibers

heavily myelinated fibers

85
Q

LA components that increase cardiotoxicity

which LA is particularly associated with CV tox?

A

likely r/t high protein binding, more assoc. with longer-acting drugs

bupivicaine

86
Q

keys to prevent LAST (5)

A
  • aspiration
  • incremental dosing
  • use of US
  • test dosing
  • knowledge of toxic levels
87
Q

which LA class names have 2 i’s

A

amides

ex - lidocaine, mepavicaine, bupivicaine, prilocaine, ropivicaine

88
Q

active LA in “hurricaine spray”

A

benzocaine

89
Q

sustained-release LA

what explains its prolonged duration of action?

how long does the block last?

A

liposomal bupivacaine (Exparel)

prolonged duration presumably from delayed uptake

allegedly lasts 24-48 hours

90
Q

myelinated vs. unmyelinated fibers

(size, speed, function)

A

myelinated:

  • larger
  • faster conduction
  • assoc. with motor and sensory function

unmyelinated:

  • slower conduction
  • transmit pain, temperature, and autonomic impulses
91
Q

LA with particular propensity to cause cardiac effects more than others

A

bupivicaine

92
Q

where are nerve Na+ channels located?

A

Nodes of Ranvier

93
Q

what is EMLA cream?

when should it be applied?

A

equal parts lidocaine & prilocaine for topical use

apply 1 hour in advance (lol we always went with 20-30 min in the ER)

94
Q

3 factors that affect systemic LA absorption

A
  1. site of injection
  2. dose
  3. properties of specific drug
95
Q

what is toxicity?

what is the MOA of LA toxicity?

A

a dose that enters circulation and brain faster than it can be cleared (not necessarily just a large dose)

LA toxicity results from blocking inhibitory neurons, leaving excitatory neurons “unchecked”, or unopposed

96
Q

nerve roots that form the ulnar nerve

A

C8 & T1

97
Q

if CV toxicity is seen with LA use, ACLS guidelines are used with what exception?

A

use smaller doses of epi

ex. 100 mcg vs. 1000 mcg

98
Q

LA most commonly used in aerosolized form for topical use in airway anesthesia

A

benzocaine

99
Q

1% lidocaine = _____ mg/mL

A

10

100
Q

onset and duration of bupivacaine

A

slow onset

180-600 min duration (long)

101
Q

hallmark symptoms of LA CNS toxicity

what other s/s normally follow?

A

seizures, hyperexcitation

followed by ringing ears, circumoral numbness, tongue numbness

102
Q

effect of adding bicarbonate to LA

A

addition of an alkalinizing agent increases the nonionized portion of the drug to allow access to the nerve

this improves pain of injection & onset of block

103
Q

part of LA chemical structure that is hydrophilic

A

tertiary amine

104
Q

preferred method of long-acting pain relief for orthopedic surgery

A

liposomal bupivacaine (Exparel)

105
Q

CV effects seen with LA toxicity with typical vs. high concentrations

what is the MOA?

A

typical - decreased contractility and conductivity

high - smooth muscle relaxation (hypotension)

MOA - same inhibitory mechanism of action on Na+ channels

106
Q

effect of opioids on LAs

A

potentiate LA

increase intensity & speed of onset for blocks

107
Q

what does eutectic mean?

which LA has this property?

A

has a lower melting point

ex) EMLA cream

108
Q

why is benzocaine primarily used topically?

A

it is permanently nonionized (stays lipid-soluble) - crosses into cell and attaches to Na+ channel directly

109
Q

how does blood flow to tissues affect an LA’s risk of toxicity?

A

a site with higher blood flow will have increased circulatory uptake and increased risk of toxicity

110
Q

how do patients with infections respond differently to LAs?

A

less effect of the drug when injected

onset is slower & less dense

(d/t decreased patient pH)

111
Q

in which form does the LA enter the nerve - ionized or nonionized?

is this in its water-soluble or lipid-soluble form?

A

nonionized

lipid soluble

112
Q

vertebrae that correlates with the inferior angle of the scapulae

A

T7

113
Q

how does the addition of epinephrine to LA solution improve the margin of safety?

A

epinephrine reduces circulatory uptake/metabolism of LA, leading to reduced toxicity

114
Q

RMP of peripheral nerves

A

-60 to -90 mV

115
Q

effect of adding decadron to LA

which route is best - IV or perineural?

A

increases duration of action

trick question - studies say effects are similar either way

116
Q

max dose of procaine

A

12 mg/kg

117
Q

Does adding sodium bicarbonate improve the potency or duration of LA?

A

nope - only improves speed of onset and reduces pain of injection

118
Q

what is cauda equina syndrome?

what can cause this?

A

toxicity in the intrathecal space

can be caused by LA in prolonged exposure, infection, compression/hematoma, or structural changes

119
Q

max dose of lidocaine

max dose of lidocaine w/ epi

A

4.5 mg/kg

w/ epi - 7 mg/kg

120
Q

esters are metabolized by pseudocholinesterases. what is the exception to this?

A

cocaine - metabolized by liver

121
Q

what is the cauda equina?

A

the terminal end of the spinal cord - fibrous strands in the subarachnoid space

122
Q

which nerve fibers are not myelinated?

A

C fibers

123
Q

location of thoracic, lumbar, sacral, and coccygeal spinal nerves in relation to respective vertebral bodies

A

below vertebral body

124
Q

factors that increase risk of LAST (LA systemic toxicity)

A
  • unintended uptake into circulation (fastest - ex. vascular injection)
  • fast uptake from highly perfused areas
  • higher potency = more toxicity
125
Q

interspaced among the axon at spaces that are not myelinated

A

nodes of Ranvier

126
Q

max dose of tetracaine

A

3 mg/kg

127
Q

which nerve fibers are the smallest and are unmyelinated?

what is the function of these fibers?

A

C fibers

carry pain and temperature signals (C - dorsal root)

128
Q

vertebrae that correlates with cricoid cartilage

A

C6

129
Q

nerve fibers from largest to smallest (7)

A
  1. Aα
  2. Aβ
  3. Aγ
  4. Aδ
  5. B
  6. C - dorsal root
  7. C - sympathetic
130
Q

rank the nerve fibers’ conduction velocity from fastest to slowest (7)

A
  1. Aα
  2. Aβ
  3. Aγ
  4. Aδ
  5. B
  6. C - dorsal root
  7. C - sympathetic

PTL that this is the same order as size biggest to smallest

S5 - Regional/OB - Test 1 (13 decks)

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