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Advanced Clinical Nursing Theory > Analgesia: Local Anaesthetics > Flashcards

Analgesia: Local Anaesthetics Flashcards

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1
Q

how does conduction of an electrical impulse through a nerve occur?

A

all or nothing event called the action potential

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2
Q

what is an action potential?

A

all or nothing event that facilitates conduction of electrical impulse through nerves

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3
Q

what is an action potential caused by?

A

voltage dependent opening of sodium and potassium channels in the cell membrane

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4
Q

what ion channels are involved in the creation of an action potential?

A

Na+ and K+

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5
Q

describe the Na+ concentration outside a nerve cell

A

high

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6
Q

describe the K+ concentration outside a nerve cell

A

low

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7
Q

describe the Na+ concentration inside a nerve cell

A

low

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8
Q

describe the K+ concentration inside a nerve cell

A

high

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9
Q

how is the concentration of sodium and potassium within a nerve cell maintained?

A

Na+/K+ pump uses ATP to move 2 potassium ions and 3 sodium ions against their concentration gradients

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10
Q

how many sodium and potassium ions are exchanged by the Na+/K+ pump?

A

2K+ ions into the cell and 3Na+ ions out

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11
Q

what is the method of cell transport used in the Na+/K+ pump?

A

active transport

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12
Q

why is active transport required in the Na+/K+ pump?

A

as sodium and potassium are being moved against their concentration gradient

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13
Q

what causes the nerve cell membrane to become depolarised?

A

rate of Na+ entry to the cell exceeds K+ exit

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14
Q

what is occurring when a nerve cell becomes depolarised?

A

membrane looses negative electrical gradient

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15
Q

what is set off by the depolarisation of nerve cell membranes?

A

Na+ positive feedback which causes more voltage gated Na+ channels to open to cause the membrane to become even more depolarised

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16
Q

what is caused by increasing number of voltage gated Na+ channels opening in response to membrane depolarisation?

A

more voltage gated Na+ channels open to cause the membrane to become even more depolarised

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17
Q

what is the threshold for generation of an action potential?

A

15mV higher than RMP

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18
Q

what happens when the membrane potential reached 15mV higher than RMP?

A

an action potential is generated

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19
Q

when does the cell membrane repolarise following generation of an action potential?

A

when Na+ channels become inactivated and K+ channels open to allow K+ to exit the axon

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20
Q

how is the membrane potential returned to -70mV following generation of a action potential?

A

Na+ channels become inactivated and a set of K+ channels open to allow K+ to leave the axon
Na+ cells regain resting excitable state and Na+/K+ pump returns membrane potential to normal

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21
Q

describe how an action potential is generated

A

rate of Na+ entry to the cell exceeds K+ exit
membrane looses negative electrical gradient
Na+ positive feedback causes more voltage gated Na+ channels to open to cause the membrane to become even more depolarised
when a threshold of 15mV higher than RMP is reached an action potential is generated

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22
Q

how do local anaesthetic drugs affect action potential generation?

A

block Na+ channels and prevent generation of action potential

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23
Q

where are voltage operated Na+ channels found in the body?

A

all excitable tissue (not just nerve tissue)

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24
Q

what are voltage operated Na+ channels sensitive to?

A

membrane potential

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25
Q

what is the role of voltage operated Na+ channels?

A

selective passing of Na+ ions

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26
Q

what effect on the membrane are local anaesthetics said to have?

A

membrane stabilising

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27
Q

why are local anesthetics said to be membrane stabilising?

A

less likely that Na+ will move into the cell and begin membrane depolarisation

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28
Q

what are the 3 broad nerve types?

A

motor
sensory
autonomic

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29
Q

what are the types of motor nerves?

A

alpha
beta
gamma

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30
Q

what are the types of sensory nerves?

A

proprioceptors
mechanoreceptors
nociceptors

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31
Q

what types of nerve fibre are proprioceptors?

A

Aalpha
Abeta

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32
Q

what types of nerve fibre are mechanoreceptors?

A

Abeta
Adelta

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33
Q

what types of nerve fibre are nociceptors?

A

Adelta
C

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34
Q

what are the types of autonomic nerves?

A

preganglionic B
postganglionic C

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35
Q

what axons are more resistant to LA block?

A

larger diameter

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36
Q

why are larger diameter axons more resistant to LA block?

A

more heavily myelinated

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37
Q

why does level of myelination affect LA block efficacy?

A

myelin slows/resists movement of LA into nerve cells

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38
Q

what nervefibre types are more susceptible to LA block?

A

C fibres and Adelta

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39
Q

why are C fibres and Adelta fibres more susceptible to LA block?

A

C fibres are unmyelinated
Adelta fibres are only thinly myelinated

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40
Q

what fibres are preferentially blocked?

A

C fibres
Adelta fibres

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41
Q

why does preferential blocking occur?

A

due to sensitivity of some nerve fibres to LA block because of their level of myelination

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42
Q

what nerve fibres are blocked first due to preferential blocking?

A

nociceptive

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43
Q

what order will nerve blocking occur in due to preferential blocking?

A

nociceptive
proprioceptive
mechanoreceptive
motor

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44
Q

where is LA site of action

A

within nerve cells at the Na+ channel

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45
Q

where on the cell does LA have its action>

A

within the cell rather then on the outside

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46
Q

what are LA drugs made up of?

A

aromatic group (lipophillic)
basic side chain / tertiary aimide (hydrophillic)
linkage by either ester or amide

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47
Q

what are the aromatic group and basic side chain / tertiary aimide of a LA drug linked by?

A

ester or amide linkage

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48
Q

what type of molecules are LA drugs?

A

weak bases

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49
Q

what is the pKa of most LA drugs?

A

8-9

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50
Q

what form of LA can enter cells?

A

only the uncharged form can cross the lipid membrane

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51
Q

in order to have maxiumum LA effect what form does the drug need to be in?

A

uncharged

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52
Q

what is the proportion of uncharged LA governed by?

A

pH of the solution the LA is in
pKa of the LA
Henderson-Hasselbach equation

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53
Q

what affects how much of the LA is uncharged?

A

pKa of LA itself
pH of the solution it is in

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54
Q

what will lead to more uncharged fraction of LA?

A

if solution is closer to the pKa of the LA

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55
Q

what can lead to more ionised / charged LA?

A

more acidic solution so pH is further from pKa

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56
Q

what does pKa affect?

A

onset of LA action

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57
Q

what is the pKa of lidocaine?

A

7.8

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58
Q

what is the pKa of bupivacaine?

A

8.1

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59
Q

what is the pH of plasma?

A

7.4

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60
Q

of lidocaine and bupivacaine which has the slower onset of action?

A

bupivacaine

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61
Q

why does bupivacaine have a slower onset of action than lidocaine?

A

at plasma pH a greater proportion of bupivacaine is ionized and so less is able to cross into the cell

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62
Q

why is a greater fraction of bupivacaine than lidocaine ionised in plasma?

A

plasma pH is further from bupivacaine pKa

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63
Q

in what type of tissue is LA less effective?

A

inflamed tissue

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64
Q

why is LA less effective in inflamed tissue?

A

pH is decreased so a greater proportion of LA is ionised and so less can penetrate the cell membrane to bind to the Na channel

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65
Q

what is the effect of inflammation on tissue pH?

A

decreases - more acidic

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66
Q

what is drug potency a measure of?

A

drug activity expressed in terms of the amount required to produce an effect of given intensity

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67
Q

what is the potency of lidocaine?

A

2

68
Q

what is the potency of bupivacaine?

A

8

69
Q

what happens to LA toxicity as potency increases?

A

increases

70
Q

what are the factors which affect LA duration of action?

A

lipid solubility
strength of binding to the channel
speed of drug removal
metabolism of LA

71
Q

why does lipid solubility affect duration of action?

A

ease of penetration of membrane
amount of drug reaching Na+ channel

72
Q

what is the speed of removal of LA dependent on?

A

tissue perfusion

73
Q

what does metabolism of the LA depend on?

A

ester or amide linkages

74
Q

what can be added to LA drugs to reduce speed of removal?

A

vasoconstrictors

75
Q

what vasoconstrictor is often added to LA drugs?

A

adrenaline

76
Q

what is the benefit of adding adrenaline to LA drugs?

A

vasoconstriction reduces blood flow to and from the area which reduces the removal of LA

77
Q

how can you identify LA drugs that have an ester linkage?

A

no i before caine

78
Q

how can you identify LA drugs that have an amide linkage?

A

i before caine

79
Q

how stable are ester linkages?

A

unstable

80
Q

how stable are amide linkages?

A

more stable than ester

81
Q

what are ester linkages broken down by?

A

plasma pseudocholinesterase

82
Q

how long is the plasma half life of ester linkage LAs?

A

short - rapidly broken down by plasma pseudocholinesterase

83
Q

how long is the plasma half life of amide linkage LAs?

A

longer than ester

84
Q

how are amide linkage LAs broken down?

A

subject to biotransformation with conjugation in the liver

85
Q

how do plasma esterases breakdown ester linked LA?

A

hydrolysis of ester link

86
Q

what is formed as a result of the hydrolysis of the ester link in LA drugs?

A

PABA

87
Q

why is there a risk of allergic reactions with ester linked LA drugs?

A

PABA is produced by the hydrolysis of ester link which can cause allergic reactions

88
Q

where in the body are esterases not found?

A

CSF

89
Q

what enzyme breaks down amide linkages?

A

cytochrome P450

90
Q

what disease may contraindicate the use of amide linkage LA drugs?

A

hepatic

91
Q

why may hepatic disease contraindicate the use of amide LA drugs?

A

can prolong or limit LA metabolism

92
Q

what effect can barbiturates have on amide LA breakdown?

A

increase drug breakdown

93
Q

what drugs may cause an increase in amide LA breakdown?

A

barbiturates

94
Q

how can barbiturates increase amide LA breakdown?

A

induce enzymes in the liver that breakdown the LA

95
Q

what drugs can inhibit amide LA breakdown?

A

midazolam

96
Q

why may midazolam inhibit amide LA breakdown?

A

inhibit P450 enzymes that breakdown amide linkage

97
Q

what are the main formulations of lidocaine available?

A

sterile solution for parenteral use
aerosol or spray
topical patches

98
Q

why are LAs often supplied in a salt solution?

A

as they are poorly water soluble

99
Q

what is the effect to the patient of placing local anaesthetics in a salt solution?

A

lowers pH so can cause stinging on injection

100
Q

what is baricity?

A

weight of one substance compared to the weight of an equal volume of another

101
Q

what is the comparator substance for baricity for spinal anaesthesia?

A

CSF

102
Q

why must baricity be considered in local anaesthesia?

A

dont want LA to spread high into the epidural space and affect muscles of respiration

103
Q

how can upward spread of LA in spinal anaesthesia be avoided?

A

ensuring LA is heavier / has higher baricity than the CSF

104
Q

how is baricity of LA increased for spinal anaesthesia to prevent spread?

A

glucose is added to make then heavier

105
Q

why is adrenaline commonly added to LA?

A

vasoconstrictor to prolong duration
reduction of risk of toxicity
reduction of bleeding

106
Q

when should LA with vasoconstrictors in be used with caution?

A

end arterial sites (e.g. tail/toes) as risk of ischemia

107
Q

what is the issue with LA being absorbed systemically?

A

available for systemic effects including toxicity

108
Q

what is required for a drug to be systemically active?

A

unbound and unionised

109
Q

what does plasma protein binding of LA depend on?

A

concentration
pH

110
Q

when does percentage binding of plasma proteins to LA decrease?

A

as concentration rises
as pH falls

111
Q

what is the effect of low plasma protein on LA toxicity?

A

less protein = more free, unbound LA
leads to more systemic effects

112
Q

in what species is lidocaine licensed?

A

cats
dogs
horses

113
Q

what is the onset of action of lidocaine?

A

2-5 minutes

114
Q

what is the duration of action of lidocaine?

A

20-40 minutes

115
Q

how cardiotoxic is lidocaine when compared to bupivacaine?

A

less as less potent

116
Q

what species is bupivacaine licensed for use in?

A

no veterinary species so should be used under cascade

117
Q

what is the duration of action of bupivacaine?

A

up to 6 hours

118
Q

what is the onset of action of bupivacaine compared to lidocaine?

A

linger

119
Q

is EMLA licenced?

A

no

120
Q

what is EMLA made up of?

A

lidocaine and prilocaine

121
Q

what leads to maximum absorption of EMLA into the skin?

A

covering with an occlusive dressing

122
Q

when is full effect of EMLA seen?

A

30-45 mins after application

123
Q

what are the main areas of LA toxicity?

A

neurotoxicity
cardiotoxicity

124
Q

what is the safe maximum dose for lidocaine?

A

8-10mg/kg

125
Q

what is the safe maximum dose for bupivacaine?

A

1-2mg/kg

126
Q

what is the main risk factor for LA toxicity?

A

overdosing

127
Q

how can LA toxicity be avoided?

A

never exceed safe dose limits
consider injection site
care with small patients
use correctly sized syringes

128
Q

are CVS or CNS toxicity signs seen at lower concentrations of LA?

A

CNS

129
Q

what is seen with CNS LA toxicity?

A

generalised CNS depression proportional to unbound drug in bloodstream
minor behavioural changes
muscle twicthing and tremors
tonic-clonic convulsions
CNS depression/respiratory depression and death

130
Q

how is LA CNS toxicity treated?

A

symptomatic
benzodiazepines to control seizures
O2 supplementation
intubation and ventilation if needed

131
Q

what can LA CVS toxicity lead to?

A

hypotension
dysrhythmias

132
Q

how does LA CVS toxicity lead to hypotension?

A

depression of myocardial contractility
direct relaxation of vascular smooth muscle
loss of vasomotor sympathetic tone

133
Q

how does LA CVS toxicity lead to dysrhythmias?

A

lipophilicity means rapid entry of LA to open sodium channels during systole
drug remains bound to the sodium channel during diastole

134
Q

how does LA CVS toxicity present as arrhythmias?

A

re-enterant arrhythmias

134
Q

what LA most commonly causes arrhythmias if cardiotoxicity occurs?

A

bupivacaine

135
Q

how is LA CVS toxicity treated?

A

symptomatic
manage bradycardia
fluid therapy with inotropic support if needed
intralipid IV

136
Q

how should brady cardia be managed?

A

anticholinergic

137
Q

how can LA toxicity be prevented?

A

don’t exceed safe maximum dose
dilute LA with 0.9% NaCl if larger volume needed
use appropriately sized syringes
use appropriately sized needles to minimise tissue trauma
aspirate before injection

137
Q

what is the role of intralipid IV in CVS LA toxicity?

A

mop up unbound LA

138
Q

according to the RCVS guidance on the VS act (1966) what LA blocks can RVNs carry out?

A

any block that doesn’t enter a body cavity
cannot perform epidural/pleural block

139
Q

what are the main loco-regional techniques?

A

epidural
regional/local
topical
infiltration

140
Q

where is epidural anesthesia placed?

A

into epidural space after L7 / around sacrum

141
Q

what structure are spinal and epidural anaesthesia both performed within?

A

the vertebral canal

142
Q

what is the epidural space?

A

space within vertebral canal which surrounds the sac containing spinal cord, nerves and CSF

143
Q

what is spinal anaesthesia?

A

injection into sac containing CSF, spinal cord and nerves

144
Q

what is epidural anesthesia?

A

injection into the epidural space

145
Q

can epidural anaesthesia be performed by an RVN?

A

no involves entry into a body cavity

146
Q

in what patients is epidural anaesthesia more complex?

A

pregnant
obese
those were anatomical landmarks have been affected

147
Q

how should the skin be prepped for epidural?

A

sterile prep

148
Q

when should epidural not be performed?

A

if sin infection at puncture site
sepsis
coagulation impairment

149
Q

what LA must be used for epidurals?

A

sterile
preservative free

150
Q

what may be added to LA in an epidural?

A

opioids (may use alone)
ketamine
medetomidine

151
Q

what are the side effects of epidural?

A

hypotension
hypothermia
urinary retention
infections
slowed hair regrowth

152
Q

define local anaesthesia

A

infiltration - small discrete action

153
Q

define regional anaesthesia

A

blocking a larger area (e.g. brachial plexus)

154
Q

what is the role of local / regional anesthesia?

A

surround a specific peripheral nerve or set of nerves to provide anaesthesia

155
Q

what are 4 examples of local/regional blocks?

A

ophthalmic
dental
limb nerve blocks
wound soaker catheters

156
Q

what forms may topical LA come in?

A

spray / cream /liquid

157
Q

what are 3 examples of topical LA?

A

eyedrops
intubeeze
EMLA

158
Q

what topical LA products are licensed for veterinary use?

A

none except for intubeeze

159
Q

where can infiltration LA occur?

A

anywhere on the body provided there is enough tissue to infiltrate

160
Q

what are 4 examples of infiltration LA?

A

ring block of distal limb/tail
around skin tumour to be excised
incisional line block
intraperitoneal

161
Q

how is infiltration LA performed?

A

injection into either V-shape or inverse pyramid

162
Q

how is intraperitoneal LA infiltration performed?

A

instilled into peritoneal space of open abdomen before closure (more difficult if abdomen closed

163
Q

can RVNs perform infiltration LA blocks?

A

some - not any that require entry into a body cavity but could at as VS hands (e.g. under instruction do intraperitoneal while scrubbed in)

164
Q
A

Advanced Clinical Nursing Theory (36 decks)

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