Neuromuscular Blocking Flashcards
1
Q
what may be an effect of ketamine being given alone as an anaesthetic drug?
A
muscle ridgidity
2
Q
what methods can be used to provide muscle relaxation under anaesthesia?
A
local anaesthetics
benzodiazipines
alpha-2 adrenoreceptor agonists
guaiphenesin (GGE)
neuromuscular blocking drugs
3
Q
what is often sufficient to provide muscle relaxation for most procedures?
A
GA
4
Q
what type of drug is guaiphenesin (GGE)?
A
centrally acting muscle relaxant
5
Q
what areas of the body does guaiphenesin (GGE) work at?
A
internuncial neurones of the spinal cord, brainstem and subcortical areas of the brain
6
Q
does guaiphenesin (GGE) have analgesic or anaesthetic properties?
A
no
7
Q
when is guaiphenesin (GGE) most commonly used?
A
infusion during induction
part of a triple for GA maintenance
8
Q
what species is guaiphenesin (GGE) used in?
A
horses
9
Q
why is guaiphenesin (GGE) useful in equine anaesthesia?
A
counteracts ketamine muscle rigidity
10
Q
what are the main considerations for guaiphenesin (GGE)?
A
can cause haemolysis at higher concentrations
can cause tissue damage if given perivascularly
11
Q
when can guaiphenesin (GGE) cause haemolysis?
A
at concentrations greater than 10%
12
Q
what can happen at guaiphenesin (GGE) concentrations greater than 10%?
A
haemolysis
13
Q
how can tissue necrosis from perivascular guaiphenesin (GGE) administration be prevented?
A
clean stick IVC
patency confirmed
14
Q
what are the clinical indications for the use of NMBAs?
A
relax skeletal muscles for surgical access
facilitate control of ventilation
facilitate tracheal intubation in cats and pigs
ophthalmic surgery
assist reduction of dislocated joints and fractures
reduction of anaesthetic needed to relax muscles
15
Q
how can relaxation of skeletal muscles by NMBAs increase surgical access?
A
aids retraction
16
Q
how can relaxation of skeletal muscles by NMBAs facilitate control of ventilation?
A
prevents patients bucking the vent which can cause physiological disturbance
17
Q
how can administration of NMBAs aid ophthalmic surgery?
A
creation of a central and stable eye to aid surgery
18
Q
how does administration of NMBAs aid reduction of dislocated joints and fractures?
A
can aid closed reduction as muscles will relax and so traction easier to perform
19
Q
when may administration of NMBAs not be of use for fracture or dislocation reduction?
A
if the injury is older and scar tissue has formed
20
Q
why may NMBAs not be useful in the reduction of old fractures or dislocations?
A
fibrosis will be present which will not be responsive to NMBAs
21
Q
how can NMBAs reduce the amount of anaesthetic drug needed?
A
MAC sparing as less volatile needed to produce muscle relaxation
fewer analgesic drugs needed to produce muscle relaxation so fewer side effects
22
Q
what must you ensure about your patient when they are anaesthetised and have a NMBA on board?
A
anaesthetic depth is adequate
23
Q
what is the anaesthetic triad?
A
narcosis
analgesia
muscle relaxation
24
Q
why were NMBAs initially unsuccessfully used in dogs?
A
patients weren’t ventilated
25
describe the process of an impulse passing through the neuromuscular junction
acytylcholine (ACh) released from presynaptic neurone due to change in charge of cell
acytylcholine (ACh) passes across synapse and binds to post-synaptic nicotinic receptor
once two acytylcholine (ACh) subunits are bound there is a resulting muscle contraction
acytylcholine (ACh) is then rapidly hydrolysed within the synaptic cleft by acytylcholineesterase
26
what is the neuromuscular junction formed of?
motor neurone
muscle cell
seperated by synaptic cleft
27
what is the role of acytylcholine (ACh)?
passes across synapse and binds to muscle cell to instigate muscle contraction
28
what receptor on the post synaptic cell does acytylcholine (ACh) bind to?
nicotinic receptor
29
how may subunits of the post synaptic nicotinic receptor must be bound to acytylcholine (ACh) in order to stimulate muscle contraction?
two
30
how is muscle contraction kept brief?
acytylcholine (ACh) is broken down rapidly in synaptic cleft by acytylcholinesterase
31
what enzyme breaks down acytylcholine (ACh)?
acytylcholinesterase
32
what is the role of acytylcholinesterase?
break down of acytylcholine (ACh) remaining in the synaptic cleft to keep muscle contraction short
33
what must be available before neuromuscular blocking drugs are given?
facilities for ET intubation
IPPV
robust analgesic and anaesthetic protocol
appropriate anaesthetic depth
34
why is a robust analgesic and anaesthetic plan vital when NMBAs are used?
they have no anaesthetic or analgesic effects
35
what muscles are most sensitive to the action of NMBAs?
peripheral
36
what muscles are least sensitive to NMBAs?
central - diaphragm and intercostals
37
are all muscle groups equally sensitive to NMBAs?
no - peripheral much more sensitive and central (e.g. diaphragm and intercostals) much less so
38
what are the 2 main groups of NMBAs?
depolarizing
non-depolarizing
39
what is an example of a depolarising NMBA?
Suxamethonium
40
what is Suxamethonium formed from?
2 ACh molecules
41
how does Suxamethonium exert its action at the NMJ?
administered IV, moves into synaptic cleft down concentration gradient
binds to post synaptic receptors
42
how is Suxamethonium broken down by the body?
cannot be broken down by acytylcholineesterase in the synapse so moves out of synapse and is broken down in the plasma
43
what is Suxamethonium broken down by?
pseudocholinesterase / plasma cholinesterase
44
can Suxamethonium be broken down within the synapse?
no - must diffuse out into the plasma and be broken down by pseudocholinesterase / plasma cholinesterase
45
what is the speed of onset of Suxamethonium?
2-3 minutes
46
how many doses of Suxamethonium can be given?
only one
47
what is seen in the patient on initial administration of Suxamethonium?
muscle fasiculation
48
why is muscle fasiculation seen in the patient on initial administration of Suxamethonium?
due to the binding of the molecule to the post synaptic cell
49
what can occur if multiple doses of Suxamethonium are given?
accumulation leading to phase II block
50
how long is the duration of action of Suxamethonium in cats?
5 minutes
51
how long is the duration of action of Suxamethonium in dogs?
20 minutes
52
how may Suxamethonium be used in cats and pigs?
aid intubation
53
what are some of the risks with using Suxamethonium?
may trigger malignant hyperthermia
can increase serum potassium levels and so should not be used with burns patients
54
with what conditions must the use of Suxamethonium be carefully considered?
urinary issues
burns
due to raised K+
55
how do non-depolarising NMBAs work?
compete with acytylcholine (ACh) for binding sites on the post synaptic cell which prevents binding of endogenous acytylcholine (ACh)
56
how does competative inhibition of acytylcholine (ACh) prevent muscle contraction?
prevents binding of endogenous acytylcholine (ACh) and so prevents mscle contraction
57
are initial muscle fasiculations seen with non-depolarizing NMBAs?
no as there is no initial binding
58
why are no initial muscle fasiculations seen with non-depolarizing NMBAs?
there is no initial binding of the drug to the receptor sites
59
what is the speed of onset of non-depolarizing NMBAs?
relatively slow
60
can non-depolarizing NMBAs be topped up?
yes with 1/3 of initial dose
or given as an infusion
61
how much can non-depolarizing NMBAs be topped up by?
1/3 original dose
62
what is the main safety aspect of non-depolarizing NMBAs?
can be antagonised
63
can non-depolarizing NMBAs be antagonised?
yes
64
can depolarizing NMBAs be antagonised?
no
65
what is the most common non-depolarizing NMBA?
atracurium
66
what type of compound is atracurium?
bis-isoquinolinium
67
what is atracurium made up of?
mixture of 10 isomers
68
how may of the isomers which form atracurium are active?
only one
69
what is Hoffman elimination?
temperature dependent reaction seen in plasma which is involved in drug metabolism
70
how is atracurium broken down by the body?
cannot be broken down in the synapse so diffuses out of cell
some hepatic metabolism
mostly Hoffman elimination
71
is atracurium broken down by acytylcholinesterase?
no - cannot be broken down in the synapse so diffuses out of cell
some hepatic metabolism
mostly Hoffman elimination
72
what pre-existing conditions is atracurium suitable for use with?
hepatic
renal
73
why is atracurium agent of choice for animals with hepatic or renal compromise?
not 100% metabolised by the liver
74
what is a risk when giving atracurium IV?
histamine release
75
how can histamine release following atracurium IV administration be avoided?
slow IV
76
what compound can be produced by metabolism of atracurium?
laudanoustine
77
what is the risk associated with laudanoustine?
has neuro effects but not at clinical doses
78
what is cisatracurium?
the active isomer in atracurium
79
why is cisatracurium not often used?
expensive
80
where should atracurium be stored?
the fridge
81
does atracurium need to be reconstituted/
no
82
what is vecuronium?
non-depolarizing NMBA
83
what type of compound is vecuronium?
steroid
84
does vecuronium have corticosteroid effects as it is a steroid compound?
no
85
is there a risk of histamine release with vecuronium?
no
86
how much vecuronium is metabolised though the liver?
40-50% undergoes hepatic metabolism
87
what form is vecuronium supplied in?
powder - must be reconstituted
88
how long can reconstituted vecuronium be stored for?
24 hours
89
where can vecuronium be stored?
shelf
90
what are the 3 other NMBAs?
rocuronium
mivacurium
pancuronium
91
what must be monitored about the equipment when the patient is undergoing NMB?
ensure ventilator is working and IPPV is resulting in effective ventilation
check tube is not kinked or dislodged
ensure breathing system remains connected
92
what patient parameters are key when monitoring a patient with NMBAs on board?
movement of thoracic wall
EtCO2
SpO2
93
why can't you use traditional methods to check anaesthetic depth when a patient is undergoing a NMB?
muscle movement is lost so reflexes cannot be checked and jaw will be lax
94
what are the signs of inadequate anaesthetic depth for the NMBA patient?
increase in pulse rate
increase in blood pressure
salivation or lacrimation
vasovagal response
increased EtCO2 unrelated to ventilation change
slight muscle twitching
pupillary dilation
95
what is the vasovagal response?
bradycardia
hypotension
96
what parameter is critical when monitoring patients with NMBAs?
blood pressure
97
why must a neuromuscular blockade be monitored?
to check if the degree of muscle relaxation is adequate
98
how is a neuromuscular blockade monitored?
peripheral nerve stimulator used to generate twitches
99
does peripheral nerve stimulation assess anaesthetic depth?
no only degree of neuromuscular blockade
100
what nerves can be used for monitoring a neuromuscular blockade?
ulnar
peroneal
facial
101
what is the main monitoring method for NMB?
train of 4
102
how does train of 4 NMB monitoring work?
4 electrical impulses supplied to the nerve over 2 seconds
103
how may electrical impulses are used in train of 4 NMB monitoring?
4
104
how long does testing of the NMB last in train of 4 NMB monitoring
2 seconds
105
what is the most common NMB monitoring pattern?
tain of 4
106
what pattern would be see if a train of four was used in a non-NMB patient?
4 twitches of equal strength
large twicthes
107
how does the train of 4 show the effect of an NMBA?
as NMBA is administered twitch strength will decline
eventually all should be absent
108
how frequently should the NMB be checked using the train of four?
every 5 minutes
109
what factors influence the duration of NMB?
volatile agent used
hypothermia
hepatic or renal insufficiency
electrolyte or acid base abnormalities
muscle diseases (e.g. myaesthenia gravis)
aminoglycoside antibiotics
dose of NMBA administered
110
what is the effect of hypothermia on the duration of NMBAs?
prolongs action
111
what is the effect of hepatic or renal insufficiency on the duration of NMBAs?
prolongs action
112
what is the effect of myesthenia gravis on the duration of NMBAs?
prolongs action
113
how does the dose of NMBA adminstered affect NMBA action?
higher dose leads to longer action
114
how do aminoglycoside antibiotics affect NMBA action?
prolong action
115
what type of NMBAs can be antagonised?
non-depolarising
116
when should non-depolarising NMBAs be antagonised?
once 1 or 2 twitches return on train of four
117
what type of drug is used to antagonise non-depolarising NMBAs?
anticholinesterases
118
why are anticholinesterases used to antagonise non-depolarising NMBAs?
interfere with the action of acytycholinesterase and so increase the concentration of acytylcholine (ACh) available in the synapse
this competes with NMBA and eventually there is high enough concentration that muscle contrction will return
119
what do anticholinesterases interfere with?
acytylcholinesterases
120
what are the side effects of anticholinesterases?
bradycardia
salivation
bronchospasm
diarrhoea
121
why are the side effects of anticholinesterases seen?
due to an increase in ACh at other receptors as acytylcholinesterases is inhibited
122
what are the main anticholinesterases used to antagonise NMBAs?
neostigmine
edrophonium
123
what type of drugs are given alongside anticholinesterases?
anticholinergic
124
when are anticholinergic drugs given?
alongside anticholinesterases
125
why are anticholinergic drugs given alongside anticholinesterases?
to counteract side effects of anticholinesterases
126
what are the main anticholinergic drugs given alongside anticholinesterases?
atropine
glycopyrrolate
127
when can ventilation be stopped in patients where NMBA has been antagonised?
must be supported until spontaneous ventilation seen
128
what must be monitored for following extubation of patient who has had a NMBA?
URT weakness
return of paralysiswh
129
at may indicate return of paralysis following NMBA antagonism?
cyanosis
URT noise
paradoxical ventilation
130
who must be informed if a patient has received a NMBA?
recovery and wards nurses
131
what other NMBA and antgonist is available but expensive?
rocuronium
cyclodextrins to antagonise
132
