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APEX > Unit 5 - Local Anesthetics > Flashcards

Unit 5 - Local Anesthetics Flashcards

1
Q

which LA does not undergo protein binding

A

chloroprocaine

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2
Q

what is conduction velocity

A

measure of how fast an axon transmits AP

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3
Q

what increases conduction velocity

A

myelination and a larger fiber diameter

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4
Q

insulates axons

A

myelin

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5
Q

what is saltatory conduction

A

the way an electrical impulse skips from node to node down the full length of an axon

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6
Q

what are nodes of ranvier

A

a gap in the myelin sheath of a nerve, between adjacent Schwann cells

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7
Q

myelination of A fibers

A

alpha & beta - heavy
gamma & delta - medium

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8
Q

function of A alpha nerve fibers

A

skeletal muscle motor
proprioception

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9
Q

function of A beta nerve fibers

A

touch, pressure

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10
Q

function of A gamma nerve fibers

A

skeletal muscle tone

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11
Q

function of A delta nerve fibers

A

fast pain, temperature, touch

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12
Q

function of B nerve fibers

A

preganglionic ANS fibers

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13
Q

function of C sympathetic nerve fibers

A

postganglionic ANS fibers

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14
Q

function of C dorsal root nerve fibers

A

slow pain, temperature, touch

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15
Q

peripheral nerve fiber block onset

A
  1. B fibers
  2. C fibers
  3. A gamma & delta
  4. A alpha & beta

block regression is in opposite order

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16
Q

what is Cm

A

minimum effective concentration

unit of measure that quantifies the concentration of LA required to bloc

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17
Q

what is Cm analogous to

A

ED50, MAC

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18
Q

are fibers easier or harder to block if Cm is increased

A

harder

(more resistant to blockade)

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19
Q

what reduces Cm

A

higher tissue Ph
high frequency of nerve stimulation

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20
Q

Cm is typically higher in nerves with diameter that is wider or more narrow?

A

wider

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21
Q

what is a differential blockade

A
  • Provides analgesia at lower concentrations & spares motor function
  • As concentration increases, it anesthetizes resistant nerve types (motor function, proprioception)

ex - epidural bupivacaine

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22
Q

MOA of LAs

A
  • conjugate acid reversibly binds to alpha subunit of voltage-gated sodium channel
  • Reduces Na+ conductance, blocks nerve conduction

LAs do NOT affect RMP or TP

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23
Q

what forms ion-conducting pore of Na+ channel in a nerve fiber

A

alpha subunit

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24
Q

3 possible states of Na+ channel

A
  1. resting
  2. active
  3. inactive
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25
Q

what determines the state of the Na+ channel

A

Voltage near the sodium channel determines the state of the channel

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26
Q

voltage of Na+ channel in resting state

A

-70 mV

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27
Q

when does the nerve fiber’s voltage-gated Na+ channel open

A

Channel opens when threshold potential is reached

Open channel allows Na+ to follow concentration gradient (outside to ins

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28
Q

what state of Na+ channel is repolarization

A

inactive state

Inactivation gate plugs channel until RMP is re-established

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29
Q

voltage of Na+ channel in inactive state

A

+35 to -70 mV

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30
Q

what converts Na+ channel from inactive to resting state

A

restoration of RMP

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31
Q

what is the guarded receptor hypothesis

A

LAs can only bind to Na+ channels in active (open) and inactive (closed refractory) states

The more frequently the nerve is depolarized and the voltage-gated Na+ c

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32
Q

3 things that influence RMP

A

1) Chemical force (concentration gradient)
2) Electrostatic counterforce
3) Na+/K+ ATPase (3 Na+ out for every 2 K+ in)

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33
Q

primary determinant of RMP

A

serum K

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34
Q

primary determinant of threshold potential

A

serum calcium

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35
Q

how does serum Ca2+ affect threshold potential

A
  • ↓ Ca2+ = TP more negative (easier to depolarize)
  • ↑ Ca2+ = TP more positive (harder to depolarize)
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36
Q

how does serum K affect RMP

A
  • ↓ serum K+ = RMP more negative
  • ↑ serum K+ = RMP more positive
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37
Q

what makes a cell depolarize

A

when Na+ or Ca2+ enters cell

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38
Q

what causes a cell to repolarize

A

K+ leaves or Cl- enters

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39
Q

what is hyperpolarization

A

movement of a cell’s membrane potential to more negative value beyond baseline RMP

More difficult to depolarize (RMP further from TP)

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40
Q

primary determinant of LA onset

A

LA’s pKa

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41
Q

primary determinant of LA potency

A

lipophilicity

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42
Q

primary determinant of LA duration of action

A

protein binding

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43
Q

how do LAs produce effects

A

via voltage-gated Na+ channels and excitable tissue

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44
Q

what is the Henderson-Hasselbach equation

A

pH = pKa + log ([base]/[conjugate acid])

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45
Q

3 possible things LA can do once in ECF

A

1) diffuse into nerve
2) diffuse into surrounding tissue and bind to other proteins
3) diffuse into systemic circulation

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46
Q

are LAs weak acids or weak bases

A

weak bases

pKa > 7.4

can predict that > 50% of the LA will exist as the ionized conjugate acid

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47
Q

what happens to LA after it’s injected near a nerve

A

rapidly dissociates into an uncharged base (LA) and an ionized conjugate acid (LA+)

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48
Q

how does uptake of LAs occur

A

Diffusion into bloodstream (removal of LA from tissue into blood)

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49
Q

how does blood flow affect LA duration

A

Highly vascular areas remove LA faster than sites with less blood flow

decreased LA duration and increased plasma concentration

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50
Q

what characteristic of LAs guards against precipitation

A

Solution has low pH

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51
Q

how do vasoconstrictors like epi affect LA admin

A

prolong LA duration (↓ rate of vascular uptake)

Most useful with LAs that exhibit significant intrinsic dilating activit

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52
Q

how does LA enter axoplasm

A

by diffusing through lipid-rich axolemma

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53
Q

what makes a greater fraction of inoized conjugate acid once inside the cell

A

ICF is slightly more acidic than ECF

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54
Q

what part of LA binds to alpha subunit inside voltage-gated Na+ channel

A

nonionized conjugate acid

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55
Q

what happens to ester LAs after entering bloodstream

A

metabolized by pseudocholinesterase in plasma

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56
Q

what happens to amide LAs after entering bloodstream

A

delivered to liver for metabolism by CYPP450 system

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57
Q

3 key components of LA molecule

A

benzene ring, intermediate side chain, tertiary amine

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58
Q

what molecular component of LA determines lipophilicity

A

benzene ring

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59
Q

what molecular component of LA determines metabolism & allergic potential

A

intermediate chain

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60
Q

what molecular component of LA determines hydrophilicity

A

tertiary amine

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61
Q

what molecular component of LA accepts proton

A

tertiary amine

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62
Q

what molecular component of LA makes molecule a weak base

A

tertiary amine

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63
Q

which LA class has the structure -COO-

A

esters

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64
Q

which LA class has the structure -NHCO-

A

amides

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65
Q

how to distinguish amides from esters by LA name

A

amides have 2 i’s in the name

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66
Q

metabolism of cocaine

A

pseudocholinesterase + liver

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67
Q

which LA class has a higher allergic potential

A

esters

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68
Q

do amides have cross sensitivity in the same class?

A

no

esters do

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69
Q

do amides have cross sensitivity in the same class?

A

no

esters do

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70
Q

component of esters assocated with allergic reactions

A

PABA

some multi-dose vials contain methylparaben

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71
Q

primary & secondary variables that determine onset of action

A

primary: pKa
secondary: dose, concentration

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72
Q

primary & secondary variables that determine potency

A

primary: lipid solubility
secondary: intrinsic vasodilating effect

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73
Q

primary & secondary variables that determine duration of action

A

primary: protein binding
secondary: lipid solubility, intrinsic vasodilating effect, addition of vasoconstrictors

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74
Q

how does pKa affect LA onset

A

if pKa of LA is closer to blood pH, a larger fraction of molecules are lipid soluble (uncharged base) - more molecules diffuse across axolemma = faster onset

pKa further away from blood pH = fewer molecules to penetrate cell membr

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75
Q

why does chloroprocaine have a rapid onset even with a high pKa

A
  • Not very potent, large dose required
  • giving more molecules creates a mass effect
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76
Q

which has a faster onset - 0.75% or 0.25% bupivacaine

A

0.75% (more molecules given)

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77
Q

LA structural component that increases lipid solubility

A

alkyl group substitution on amide group and benzene ring

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78
Q

how is LA removed from site of action

A

absorption into systemic circulation

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79
Q

what kind of response do nearly all LAs have on vascular smooth muscle

A

biphasic response

lower concentration = vasoconstriction (inhibit NO)
higher concentration

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80
Q

how does a greater degree of intrinsic vasodilation affect vascular uptake

A

results in faster rate of vascular uptake, prevents some of the dose from accessing the nerve

ex. lidocaine

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80
Q

how does a greater degree of intrinsic vasodilation affect vascular uptake

A

results in faster rate of vascular uptake, prevents some of the dose from accessing the nerve

ex. lidocaine

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81
Q

how does protein binding affect LA duration

A
  • Molecules that bind to plasma proteins serve as a tissue reservoir
  • extends duration
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82
Q

how does protein binding affect LA duration

A
  • Molecules that bind to plasma proteins serve as a tissue reservoir
  • extends duration
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83
Q

how does a strong acid or base behave in water

A

will completely dissociate

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84
Q

how does a weak acid or base behave in water

A
  • a fraction will ionize, remaining fraction non-ionized
  • Ionization depends on pH of solution & pKa of drug

LAs are weak bases that are ionized at physiologic pH

85
Q

relationship between pKa and degree of ionization

A

As pKa gets further from physiologic pH, degree of ionization ↑

86
Q

relationship between LA pKa and onset

A

The closer the pKa is to pH of blood, the faster the onset (exception: chloroprocaine)

87
Q

which has higher pKa - esters or amides

A

All esters have higher pKa than amides

88
Q

only available LA with pKa well below physiologic pH

A

Benzocaine

pKa = 3.5

89
Q

uses of benzocaine

A

topical anesthesia of mucus membranes during endoscopy, TEE, bronchoscopy

90
Q

significant risk with benzocaine

A

methemoglobinemia

91
Q

Factors that influence vascular uptake & Cp

A
  • site of injection
  • tissue blood flow
  • physiochemical properties of LA
  • metabolism
  • addition of vasoconstrictor
92
Q

fastest to slowest sites for LA uptake

A

IV > tracheal > interpleural > intercostal > caudal > epidural > brachial plexus > femoral > sciatic > sub-q

93
Q

what determines final LA plasma concentration

A

Total dose of LA (not concentration or speed of injection)

94
Q

what protein do most LAs bind to

A

alpha-1 acid glycoprotein

95
Q

how does adding a vasoconstrictor like epi affect LA duration

A

↓ systemic absorption by up to 1/3 and prolong duration

Effect greatest with LAs that have significant intrinsic dilating activi

96
Q

liposomal bupivacaine

97
Q

key benefits of Exparel

A

duration of action up to several days, ↓ opioid consumption

98
Q

how does Exparel work

A

As lipid membranes in suspension erode and reorganize over time, bupivacaine is released

99
Q

max dose of Exparel

100
Q

how should Exparel be administered if a larger volume is needed to extend coverage

A

20 mL (266 mg) expanded with up to 300 mL NS or LR

101
Q

Exparel contraindication

A

paracervical block in OB population

Not recommended for epidural or intrathecal anesthesia, intraarticular a

102
Q

when should Exparel be used cautiously

A

hepatic and/or renal dysfunction

103
Q

can other LAs be admin with Exparel?

A

co-administration of other LAs can disrupt liposomal suspension & cause immediate release

If used, lidocaine must be infiltrated at surgical site min. 20 min prior to Exparel injection

104
Q

when can bupivacaine be given after exparel admin

A

must be 96+ hours after exparel

105
Q

what determines systemic levels of LA

A
  • drug
  • dose
  • site of injection
  • technique
106
Q

max dose of levobupivacaine

A

2 mg/kg
max total = 150 mg

107
Q

max dose of bupivacaine

A

2.5 mg/kg
max total = 175 mg

108
Q

max dose of bupicavaine + epi

A

3 mg/kg
max total = 200 mg

109
Q

max dose of ropivacaine

A

3 mg/kg
max total = 200 mg

110
Q

max dose of lidocaine

A

3.5 mg/kg
max total = 300 mg

111
Q

max dose of lidocaine + epi

A

7 mg/kg
max total = 400 mg

112
Q

max dose of mepivacaine

A

7 mg/kg
max total = 500 mg

113
Q

max dose of prilocaine

A

9 mg/kg
max total < 70 kg = 500 mg
max total > 70 kg = 600 mg

114
Q

max dose of procaine

A

7 mg/kg
max total = 350-400 mg

115
Q

max dose of chloroprocaine

A

11 mg/kg
max total = 800 mg

116
Q

max dose of chloroprocaine + epi

A

14 mg/kg
max total = 1,000 mg

117
Q

what determines plasma concentration of LA

A

net balance of vascular uptake relative to redistribution & metabolism

118
Q

how to reduce risk of LAST

A

use test dose and incremental dosing with period aspiration

119
Q

Most common cause of toxic LA plasma concentration

A

inadvertent intravascular injection

120
Q

most frequent 1st symptom of LAST

A

seizure

exception: cardiac arrest may be first with bupivacaine

121
Q

when are LAs more assoc. with LAST

A

peripheral nerve blocks (not epidural)

122
Q

CV effects of lidocaine at plasma concentration > 25 mcg/mL

A

CV collapse

123
Q

effects of lidocaine at plasma concentration 15-25 mcg/mL

A

coma
respiratory arrest

124
Q

effects of lidocaine at plasma concentration 10-15 mcg/mL

A
  • seizures
  • LOC
125
Q

CNS effects of lidocaine at plasma concentration 5-10 mcg/mL

A
  • tinnitus
  • skeletal muscle twitching
  • lip/tongue numbness
  • restlessness
  • vertigo
  • blurred vision
126
Q

CV effects of lidocaine at plasma concentration 5-10 mcg/mL

A
  • hypotension
  • myocardial depression
127
Q

plasma concentration of lidocaine assoc. with analgesia

A

1-5 mcg/mL

128
Q

3 things that increase risk of CNS toxicity with LA use

A
  • hypercarbia
  • hyperkalemia
  • metabolic acidosis
129
Q

why does hypercarbia contribute to increased risk of LAST

A
  • ↑ CBF
  • ↑ drug delivery to brain
  • ↓ protein binding
  • ↑ free fraction
130
Q

why does hyperkalemia contribute to increased risk of LAST

A

↑ RMP = neurons are more likely to depolarize

131
Q

why does metabolic acidosis contribute to increased risk of LAST

A

↓ convulsion threshold, favors ion trapping inside brain

132
Q

3 things that decrease risk of CNS toxicity with LAs

A
  • hypocarbia
  • hypokalemia
  • CNS depressants
133
Q

how does hypocarbia protect against CNS toxicity with LAs

A

↓ CBF, ↓ drug delivery to brain

134
Q

how does hypokalemia protect against CNS toxicity with LAs

A

↓ RMP = requires larger stimulus to depolarize nerve

135
Q

how do LAs disrupt hemodynamics

A

altering cardiac AP, myocardial performance, and vascular resistance

136
Q

how do LAs cause myocardial depression

A

by impairing intracellular Ca2+ regulation

137
Q

what 2 features determine extent of cardiotoxicity with LAs

A

1) affinity for voltage-gated Na+ channel in active and inactive states
2) rate of dissociation from receptor during diastole

138
Q

why is cardiac morbidity with bupivacaine is higher & cardiac resuscitation is so difficult

A
  • Bupivacaine has a greater affinity for Na+ channel & slower rate of dissociation vs. lidocaine
  • bupivacaine remains at the receptor for longer
139
Q

LAs with greatest to least difficulty of CV resuscitation

A

bupivacaine > levobupivacaine > ropivacaine > lidocaine

140
Q

4 factors that increase risk of bupivacaine toxicity

A
  • pregnancy
  • beta blockers
  • CCBs
  • digoxin
141
Q

Primary risk of cocaine toxicity

A

excessive SNS stimulation

142
Q

meds to avoid with cocaine toxicity

A
  • MAOIs
  • TCAs
  • sympathomimetics
  • beta blockers
143
Q

Cocaine dose range

A

1.5 – 3 mg/kg (max 150-200 mg depending on text)

144
Q

best med to use to decrease BP in cocaine toxicity

A

Vasodilator like nitroglycerin

Labetalol or another mixed alpha agonist is a reasonable choice

145
Q

treatment of LAST

A
  • 100% FiO2
  • treat sz with benzos
  • lipid emulsion therapy
146
Q

why might you give NMB for LAST

A

to stop muscle contraction (seizures)

minimize O2 consumption, hypoxemia, acidosis

147
Q

why should propofol be avoided in treatment of LAST

A

augments myocardial depression

148
Q

ACLS modifications for LAST

A
  • If epi is used, give < 1 mcg/kg doses
  • For ventricular arrythmias: avoid lidocaine and procainamide, use amiodarone
149
Q

dosing of lipid emulsion therapy for LAST

A

> 70 kg:
* 100 ml bolus over 2-3 min
* 250 ml over 15-20 min

< 70 kg:
* Bolus 20% 1.5 mL/kg (LBW) over 1 minute
* infusion = 0.25 mL/kg/min
* Can repeat bolus up to 2 more times and increase infusion to max 0.5 mL/kg/min
* Continue infusion 10 min after HD stability

150
Q

max recommended dose of lipid emulsion therapy for LAST

A

10 mL/kg in first 30 min

151
Q

theoretical complication of lipid emulsion therapy for LAST

A

pancreatitis

152
Q

meds to avoid in treatment of LAST

A
  • code-dose epi
  • lidocaine
  • procainamide
  • beta blockers
  • CCBs
153
Q

treatment of LAST if unresponsive to modified ACLS and lipid emulsion

154
Q

proposed MOA of lipid emulsion therapy for LAST

A
  • lipid sink: sequesters LA
  • metabolic effect: enhanced myocardial fatty acid metabolism
  • inotropic effect: increased Ca influx
  • membrane effect: impairs LA binding to Na+ channels
155
Q

most common cause of death from liposuction

A

pulmonary embolism

156
Q

what is Tumescent anesthesia

A
  • Dilute solution of sodium chloride, lidocaine, epi, & bicarb injected into adipose tissue
  • firms adipose tissue & increases ease of removal
157
Q

function of epi & lidocaine in tumescent anesthesia

A
  • Lidocaine prevents discomfort
  • epi minimizes vascular uptake of LA & tumescent solution
158
Q

current American Academy of Dermatology recommendation for max lidocaine in tumescent anesthesia

159
Q

metabolism of lidocaine in Tumescent anesthesia

A
  • metabolized by CP3A4 & 1A2
  • completely eliminated from body at 36 hours
160
Q

peak Cp of lidocaine in tumescent anesthesia

161
Q

when is GA recommended over MAC if tumescent anesthesia used

A

if > 2-3 L injected (due to risk of fluid shifts)

162
Q

complications of tumescent anesthesia

A

Fluid overload & pulmonary edema may occur as a result of intravascular volume expansion

163
Q

subunits of Hgb molecule

A
  • 2 alpha
  • 2 beta
164
Q

how is methemoglobin produce

A

when the iron moiety in heme is oxidized from ferrous state (Fe+2) to ferric state (Fe+3)

165
Q

2 ways methemoglobin decreases CaO2

A

1) methemoglobin can’t bind oxygen molecules
2) shifts oxyhemoglobin

166
Q

why does methemoglobin result in physiologic anemia

A

Oxyhgb shift ↑ HgbA’s affinity for O2, which makes it harder to release O2 to tissues

167
Q

why does methemoglobinemia cause pulse ox errors

A
  • Methemoglobin absorbs 660 nm and 940 nm infrared wavelengths equally
  • tends to push SpO2 towards 85%
168
Q

why is a co-oximeter required to diagnose methemoglobinemia

A

Uncouples normal relationship between SpO2 & SaO2

169
Q

LAs assoc. with methemoglobinemia

A
  • benzocaine
  • cetacaine
  • prilocaine
  • EMLA
170
Q

presentation of methemoglobinemia with 0-20% HgbMet

A

usually well tolerated

171
Q

presentation of methemoglobinemia with 20-50% HgbMet

A
  • tachypnea
  • tachycardia
  • AMS
  • slate-gray pseudocyanosis
172
Q

presentation of methemoglobinemia with 50-70% HgbMet

A

dysrhythmias, coma

173
Q

% HgbMet not compatible with life

174
Q

s/s that is highly suggestive of methemoglobinemia

A

Cyanosis in the presence of a normal PaO2

175
Q

1st line treatment of methemoglobinemia

A

methylene blue

Helps accelerate reduction of methemoglobin

176
Q

methylene blue dosing

A
  • 1-2 mg/kg over 5 min
  • Max dose 7-8 mg/kg
  • May require redosing (rebound can occur up to 12 hours after methylene blue admin)
177
Q

how does methylene blue treat methemoglobinemia

A

Metabolized by methemoglobin reductase to form leucomethylene blue – electron donor, reduces methemoglobin back to hemoglobin

178
Q

treatment of methemoglobinemia in a patient with G6PD deficiency

A
  • exchange transfusion
  • don’t possess methemoglobin reductase – methylene blue can precipitate hemolytic crisis
179
Q

population at higher risk for developing methemoglobinemia & why

A

neonates

Fetal hemoglobin is relatively methemoglobin reductase deficient (suscep

180
Q

what is EMLA cream made of

A

50/50 combination of 2.5% lidocaine and 2.5% prilocaine

181
Q

what characteristic of EMLA cream facilitates its absorption

A

Melting point is lower than either of its constituents

182
Q

effects of EMLA cream

A

Produces analgesia within 1 hour, max effect in 2-3 hours

183
Q

increases risk of toxicity with EMLA cream

A

eczema, psoriasis, skin wounds d/t altered pharmacokinetics

184
Q

can be applied simultaneously with EMLA cream to hasten absorption

A

nitroglycerin

185
Q

metabolite of prilocaine

A

o-toludine

186
Q

max dose of EMLA cream:
- 0-3 months or < 5 kg
- 3-12 months and > 5 kg
- 1-6 years and > 10 kg
- 7-12 years and > 20 kg

A
  • 0-3 months or < 5 kg: 1 g
  • 3-12 months and > 5 kg: 2 g
  • 1-6 years and > 10 kg: 10 g
  • 7-12 years and > 20 kg: 20 g
187
Q

max application area of EMLA cream:
- 0-3 months or < 5 kg
- 3-12 months and > 5 kg
- 1-6 years and > 10 kg
- 7-12 years and > 20 kg

A
  • 0-3 months or < 5 kg: 10 cm2
  • 3-12 months and > 5 kg: 20 cm2
  • 1-6 years and > 10 kg: 100 cm2
  • 7-12 years and > 20 kg: 200 cm2
188
Q

additives that prolong LA duration

A
  • epi
  • decadron
  • dextran
189
Q

additives that supplement LA analgesia

A
  • clonidine
  • epi
  • opioids (neuraxial only)
190
Q

additive that shortens LA onset

A

sodium bicarbonate

191
Q

additive that improves LA diffusion through tissues

A

hyaluronidase

192
Q

LA that decreases effectiveness of epidural opioids

A

chloroprocaine

193
Q

how does epi prolong block duration & enhance block quality

A
  • decreases systemic LA uptake
  • better matching of uptake and metabolism
  • decreased LA in plasma
194
Q

epi is best at prolonging which LAs

A

intermediate duration

ex. extends duration of lidocaine > bupivacaine

195
Q

how does dexamethasone extend LA duration

A

glucocorticoid activity - acts on steroid receptor, affects systemic uptake

Can increase duration of brachial plexus block by up to 50%

196
Q

how does dextran affect LA

A

prolongs block duration by ↓ systemic uptake

197
Q

how does clonidine affect LA

A

alpha agonism = analgesia

198
Q

how does sodium bicarb affect LA

A
  • Alkalinization ↑ number of lipid soluble molecules = speeds onset of action
  • Can also increase quality of block and ↓ pain on injection

Mix 1 mL of 8.4% of bicarb with 10 mL LA solution

199
Q

how does sodium bicarb affect LA

A
  • Alkalinization ↑ number of lipid soluble molecules = speeds onset of action
  • Can also increase quality of block and ↓ pain on injection

Mix 1 mL of 8.4% of bicarb with 10 mL LA solution

200
Q

how does hyaluronidase affect LA

A

Hydrolyzes hyaluronic acid
facilitates diffusion of substances in tissues

201
Q

what is an AP an how does it depolarize a nerve

A
  • AP = temporary change in transmembrane potential followed by return to transmembrane potential
  • Na+ or Ca2+ must enter cell for neuron to depolarize
  • once threshold potential occurs, cell depolarizes and propagates AP
202
Q

what is an AP an how does it depolarize a nerve

A
  • AP = temporary change in transmembrane potential followed by return to transmembrane potential
  • Na+ or Ca2+ must enter cell for neuron to depolarize
  • once threshold potential occurs, cell depolarizes and propagates AP
203
Q

what happens when a nerve repolarizes

A

removal of positive charges from inside the cell

accomplished by removing potassium

204
Q

RMP and threshold potential of peripheral nerves

A

RMP = - 70 mV
TP = - 55 mV

205
Q

after peripheral nerve repolarization, how is RMP maintained until the nerve is depolarized again

A

Na/K-ATPase

206
Q

why is epi avoided in the treatment of LAST

A

decreases efficacy of lipid emulsion therapy

207
Q

possible adverse effect of giving a beta blocker in cocaine overdose

A

heart failure

allows unopposed alpha 1 stimulation
high SVR and reduced inotropy set t

208
Q

possible adverse effect of giving a beta blocker in cocaine overdose

A

heart failure

allows unopposed alpha 1 stimulation
high SVR and reduced inotropy set t

209
Q

which nerve fibers do not experience saltatory conduction

A

C fibers

no myelination

209
Q

which nerve fibers do not experience saltatory conduction

A

C fibers

no myelination

210
Q

which LA is assoc. with neurotoxicity and therefore not used in spinal anesthesia

A

chloroprocaine

APEX (54 decks)

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