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APEX > Unit 5 - Neuromuscular Blockers > Flashcards

Unit 5 - Neuromuscular Blockers Flashcards

1
Q

what are the 2 types of nicotinic AChRs at NMJ

A
  • prejunctional Nn receptor: regulates ACh release
  • postsynaptic Nm receptor: responds to ACh (depolarizes muscle)
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2
Q

enzyme in synaptic cleft

A

AChE

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3
Q

5 subunits of postsynaptic nicotinic receptor

A
  • 2 alpha
  • 1 beta
  • 1 delta
  • 1 epsilon
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4
Q

what causes postsynaptic nicotinic receptor to open

A

when 2 ACh molecules simultaneously occupy both alpha subinits

Na+ and Ca2+ enter cell, K+ exits

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4
Q

what causes postsynaptic nicotinic receptor to open

A

when 2 ACh molecules simultaneously occupy both alpha subinits

Na+ and Ca2+ enter cell, K+ exits

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5
Q

electrolyte movement when ACh activates Nm

A

Na+ flows down concentration gradient and enters cell

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6
Q

how is muscle contraction initiated after ACh binds to Nm receptor

A
  • Na+ enters cell
  • muscle cell depolarization instructs SR to release Ca2+ into cytoplasm
  • engages in myofilaments, initiates muscle contraction
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7
Q

why don’t anions pass through Nm

A

repelled by negative charge

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8
Q

what is acetylcholinesterase metabolized to

A

choline + acetate

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9
Q

what terminates action of ACh

A

metabolism and diffusion away from receptor

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10
Q

what allows extrajunctional receptors to return later in life

A

denervation
prolonged immobility

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11
Q

where are EJRs distributed

A

NMJ & sarcolemma

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12
Q

conditions that increase EJRs
(avoid succs)

A
  • Upper or lower motor neuron injury
  • Spinal cord injury
  • Burns
  • Skeletal muscle trauma
  • Cerebrovascular accident
  • Tetanus
  • Severe sepsis
  • Muscular dystrophy
  • Prolonged chemical denervation (Mg, long term NMB infusion, clostridial toxin)
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13
Q

how does succs affect serum K+

A

can transiently increase serum K+ by 0.5-1.0 mEq/L for up to 10-15 minutes

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14
Q

why can conditions that increase EJR cause life-threatening hyperkalemia

A

EJRs remain open longer than postjunctional receptors - allows more Na+ to enter & augments K+ leak

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15
Q

how is alpha 7 subunit (pathologic variant of nicotinic receptor) depolarized

A

succs and choline

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16
Q

general rule for avoiding succs with denervation injuries

A
  • avoid for 24-48 hours after injury
  • at least 1 year after

exception - burns (risk can exist for several years)

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17
Q

Primary treatment of succs-induced hyperkalemia

A
  • IV CaCl
  • hyperventilation
  • sodium bicarbonate
  • glucose + insulin
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18
Q

patient response to NDNMBs with increased EJRs

A

resistant

More receptors = more NMB needed to effectively antagonize Nm at NMJ

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19
Q

patient response to NDNMBs with increased EJRs

A

resistant

More receptors = more NMB needed to effectively antagonize Nm at NMJ

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20
Q

what causes fade with TOF

A
  • when a NDNMB competitively antagonizes the presynaptic nicotinic receptor (Nn), ACh mobilization is impaired so only vesciles for immediate release can be used
  • nerve stimulation can quickly exhaust this supply
  • less ACh released with each successive stimulus
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21
Q

2 supplies of ACh at NMJ

A

1) some available for immediate release
2) some that must be mobilized before available for immediate release

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22
Q

what propagates AP along nerve axon

A

Na+ channels

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23
Q

how do ACh vesicles exit nerve

A

via exocytosis
each vesicle releases 5,000-10,000 ACh molecules into synaptic cleft

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24
Q

structure of

A
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24
Q

structure of postsynaptic nicotinic receptor at NMJ

A
  • pentameric ligand-gated Na+ channel in motor endplate at NMJ
  • 5 subunits that align circumferentially around an ion-conducting pore
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25
Q

what happens when ACh activates post-synaptic nicotinic receptor at NMJ

A
  • ACh binds to alpha subunits, which prompts channel to open
  • Na+ and Ca2+ enter cell, K+ leaves
  • Na+ flows down concentration gradient and enters muscle cell
  • voltage-gated Na+ channels activated, muscle cell depolarizes & generates AP
  • myocyte depolarization instructs ER to release Ca2+ into cytoplasm to engage with myofilaments and cause muscle contraction
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26
Q

how is the ACh signal “turned off” at NMJ?

A

AChE positioned around pre- and postsynaptic nicotinic receptors hydrolyzes ACh almost immediately

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27
Q

where are EJRs distributed

A

at NMJ and also throughout sarcolemma

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28
Q

receptors stimulated by succs

A

prejunctional receptors

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29
Q

MOA of nondepolarizing NMBs

A

competitvely antagonize presynaptic Nn receptors

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30
Q

why is there no fade with succs

A
  • succs facilitates mobilization of ACh when it binds to presynaptic Nn receptor
  • there’s always ACh available for immediate release
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31
Q

what distinguishes between a phase 1 and phase 2 block

A

presence or absence of fade

phase 2 - ACh mobilization impaired, nerve terminal can only release imm

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32
Q

NMBs that cause phase 1 block

A

depolarizing NMBs

succs

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33
Q

NMBs that cause phase 2 block

A

nondepolarizers

succs in certain situations

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34
Q

2 situations that can create phase 2 block with succs

A
  1. dose > 7-10 mg/kg
  2. IV gtt
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35
Q

how is phase 2 block characterized

A

fade with tetany, prolonged duration

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36
Q

why can high dose succs cause phase 2 block

A

likely inhibits presynaptic nicotinic receptor, impairs ACh mobilization/release from presynaptic terminal, and/or creates conformational change in postsynaptic receptor

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37
Q

how many twitches will a patient have with succs

A

either 1 or 4

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38
Q

how to reverse a phase 2 block with succs

A

wait it out

(don’t give reversal)

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39
Q

best site to measure NMB onset with TOF

A

orbicularis oculi (closes eyelid) or corrugator supercilia (eyebrow twitch)

CN 7

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40
Q

Relying on flexion of the 5th finger over- or underestimates NMB recovery

A

over

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41
Q

best site to measure NMB recovery

A

adductor pollicis (thumb adduction) or flexor hallucis (big toe flexion)

Nerve = ulnar n. or posterior tibial n.

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42
Q

when is full recovery from NMB assumed

A

TOF ratio is > 0.9 at adductor pollicis

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43
Q

what is residual blockade

A

defined as TOF ratio <0.9

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44
Q

what Vt value suggests NMB recovery

A

5+ mL/kg

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45
Q

max receptors occupied when pt Vt 5+ mL/kg

A

80%

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46
Q

max % receptors occupied when pt reaches no fade with TOF

A

70

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47
Q

vital capacity that suggests NMB recovery & max receptors blocked

A

20+ mL/kg
70%

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48
Q

max % receptors blocked when pt has no fade with 50 Hz tetanus

A

60

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49
Q

inspiratory force that suggests NMB recovery

max % receptors blocked

A

better than -40 (more negative is better)

50%

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50
Q

max % receptors blocked with 5 second headlift

A

50

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51
Q

clinical endpoints of NMB evaluation that suggest max 50% receptors blocked

A
  • head lift > 5 seconds
  • hand grip same as preinduction
  • holding tongue blade in mouth against force
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52
Q

best qualitative test of neuromuscular function

A

holding a tongue blade in the mouth against force

Limitation: can’t be performed with oral ETT in place

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53
Q

structure of succs

A

2 ACh molecules joined together

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54
Q

how can succs cause bradycardia

A

by stimulating M2 receptor in SA node

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55
Q

increases risk of bradycardia with succs admin

A

2nd dose

probably r/t primary metabolite succinylmonocholine

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56
Q

how can succs cause tachycardia

A

by mimicking ACh at sympathetic ganglia

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57
Q

how do adults vs. kids typically respond to succs in terms of HR

A
  • Adults: tachycardia more common than bradycardia
  • Kids: more susceptible to bradycardia d/t higher baseline vagal tone
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58
Q

how does succs affect IOP

A

Transiently ↑ IOP by 5-15 mmHg for up to 10 minutes

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59
Q

how to prevent increased ICP with succs

A

defasciculating dose

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60
Q

how does succs affect intragastric pressure

A

temporarily increases

prevent or minimize with defasciculating dose

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61
Q

how does succs affect barrier pressure

A

net unchanged (increases intragastric pressure, decreases LES tone)

does not increase risk of aspiration

62
Q

how does succs affect barrier pressure

A

net unchanged (increases intragastric pressure, decreases LES tone)

does not increase risk of aspiration

63
Q

side effect of succs that may or may not be related to an MH reaction

A

massetter spasm

64
Q

black box warning of succs

A

risk of cardiac arrest and sudden death 2/2 hyperkalemia in children with undiagnosed skeletal muscle myopathy

65
Q

function of dystrophin

(absence of protein in DMD)

A
  • critical for structure of cytoskeletal on skeletal & cardiac muscle cells
  • helps anchor actin and myosin to cell membrane
66
Q

patho of DMD that results from absence of dystrophin

A
  • sarcomma destabilized
  • allows creatine kinase and myoglobin to enter systemic circulation & cause inflammation, fibrosis, cell death
67
Q

why are patients with DMD predisposed to hyperkalemia with succs

A

Absence of dystrophin alters type and number of postjunctional nicotinic receptors on muscle cell

68
Q

s/s DMD assoc. with dystrophin absence

A
  • skeletal muscle weakness
  • conduction abnormalities
  • cardiomyopathy
  • sometimes cognitive impairment
69
Q

marker of skeletal muscle breakdown

A

Creatine phosphokinase

70
Q

EKG changes with mild hyperkalemia

A

peaked T waves, prolonged PR

71
Q

treatment of cardiac arrest in a child after induction with succs

A

immediately start treating for hyperkalemia:
1. Stabilize myocardium: CaCl 20 mg/kg or CaGluc 60 mg/kg
2. Shift K+ into cells: hyperventilation, glucose + insulin, sodium bicarbonate, albuterol
3. Enhance K+ elimination: Lasix 1 mg/kg, volume resuscitation, dialysis, hemofiltration

72
Q

elemental calcium in 10% CaCl vs. 10% CaGluc

A

10% CaCl = 27.2 mg/mL elemental calcium
10% CaGluc = 9 mg/mL

73
Q

how much 10% glucose to use when treating cardiac arrest from succs

A

0.3-0.5 g/kg 10% glucose solution + 1 unit insulin per 4-5 g IV glucose

74
Q

s/s postoperative myalgia assoc. with succs

A

muscle soreness in neck, shoulders, subcostal region, upper abd/trunk muscles

75
Q

MOA of postop myalgia with succs

A

Believed to be r/t uncoordinated muscle contraction (fasciculations) before paralysis

76
Q

pts at highest risk of postoperative myalgia with succs

A

young adults undergoing ambulatory surgery (women > men), those who don’t routinely engage in strenuous activity

77
Q

do opioids decrease myalgia with succs

A

nope

78
Q

pts with lowest incidence of postop myalgia with succs

A

Children, elderly, and pregnant pts seem to have lowest rates of occurrence

79
Q

methods to decrease risk postop myalgia with succs

A
  • NDNMB pretreatment
  • NSAIDs
  • lidocaine 1.5 mg/kg
  • higher vs lower dose of succs
80
Q

defasciculating dose

A

1/10th ED 95 dose of non-depolarizer

2mg roc, 1.5 mg atracurium, 0.3 vec 3-5 min before succs

81
Q

why is a higher dose of succs needed if defasciculating dose of NDNMB used

A
  • Nondepolarizer will competitively antagonize nicotinic receptor
  • more succs needed to overwhelm effect
82
Q

primary location of AChE

A

NMJ

83
Q

synonyms for AChE

A
  • Acetylcholinesterase
  • Genuine cholinesterase
  • Type 1 cholinesterase
  • True cholinesterase
  • Specific cholinesterase
84
Q

primary location of pseudocholinesterase

A

plasma

85
Q

synonyms for pseudocholinesterase

A
  • Butyrylcholinesterase
  • Pseudocholinesterase
  • Type 2 cholinesterase
  • False cholinesterase
  • Plasma cholinesterase
86
Q

enzyme that metabolizes succs, mivacurium, and ester LAs

A

pseudocholinesterase

87
Q

where is pseudocholinesterase produced

A

liver

88
Q

how does pseudocholinesterase activity serve as an indicator of hepatic function

A

produced in liver

89
Q

reference concentration range of pseudocholinesterase

A

2900-7100 units/L in plasma

90
Q

how does plasma concentration of Pseudocholinesterase affect symptoms

A

Neuromuscular symptoms begin at 60% of normal, prominent at 20% of normal

91
Q

where is pseudocholinesterase located

A

liver, smooth muscle, intestines, white matter, heart, pancreas (not CSF)

92
Q

drugs that reduce Pseudocholinesterase activity

A
  • Metoclopramide
  • Esmolol
  • Neostigmine (not edrophonium)
  • Echothiopate
  • Oral contraceptives/estrogen
  • Cyclophosphamide
  • MAOIs
  • Nitrogen mustard
93
Q

diseases that decrease pseudocholinesterase activity

A
  • Atypical PChE
  • Severe liver disease
  • Chronic renal disease
  • Organophosphate poisoning
  • Burns
  • Neoplasm
  • Advanced age
  • Malnutrition
  • Pregnancy (late stage)
94
Q

definitive diagnosis of atypical acetylcholinesterase

A

dibucaine test

95
Q

what is dibucaine

A

amide LA that inhibits normal plasma cholinesterase (no effect on atypical PChE)

96
Q

what does dibucaine number reflect

A

% of normal enzyme inhibited by dibucaine

97
Q

normal dibucaine no.

A

80 (dibucaine has inhibited 80% of pseudocholinesterase in sample)

98
Q

genotype, dibucaine no., and succs duration assoc. with typical homozygous pseudocholinesterase

A
  • genotype = UU
  • dibucaine no = 70-80
  • succs duration = 5-10 min
99
Q

genotype, incidence, dibucaine no., and succs duration assoc. with typical heterozygous pseudocholinesterase

A
  • genotype = UA
  • incidence = 1/480
  • dibucaine no = 50-60
  • succs duration = 20-30 min
100
Q

genotype, dibucaine no., and succs duration assoc. with atypical homozygous pseudocholinesterase

A
  • genotype = AA
  • incidence = 1/3200
  • dibucaine no = 20-30
  • succs duration = 4-8 hours
101
Q

what is atypical plasma cholinesterase

A

Pseudocholinesterase is produced in sufficient quantity but not functional

qualitative defect

101
Q

what is atypical plasma cholinesterase

A

Pseudocholinesterase is produced in sufficient quantity but not functional

qualitative defect

102
Q

methods to restore levels in atypical pseudocholinesterase

A

Whole blood, FFP, or purified human cholinesterase

103
Q

treatment of choice for atypical pseudocholinesterase

A

postop mechanical ventilation

104
Q

diseases assoc. with hyperkalemia from succs

A
  • DMD
  • Guillain-Barre
  • MS
  • ALS
  • Charcot-Marie-Tooth
  • Hyperkalemic Periodic Paralysis
105
Q

diseases assoc. with nondepolarizing NMB sensitivity

A
  • DMD
  • Guillain Barre
  • MS
  • ALS
  • Huntingdon
  • Myasthenia gravis
  • myotonic dystrophy (may have normal response)
106
Q

what is the ED95 of a non-depolarizing NMB

A

dose at which there’s a 95% decrease in twitch height

107
Q

relationship between ED95 and NDNMB potency

A

inversely related

measure of potency

108
Q

how can ED95 of NDNMB be used to predict onset

A

higher ED95 = lower potency = faster onset

109
Q

mivacurium:
- ED95
- intubation dose
- onset
- duration

A
  • ED95: 0.067 mg/kg
  • intubation dose: 0.15 mg/kg
  • onset: 3.3 min
  • duration: 16.8 min
110
Q

cisatracurium:
- ED95
- intubation dose
- onset
- duration

A
  • ED95: 0.04 mg/kg
  • intubation dose: 0.1 mg/kg
  • onset: 5.2 min
  • duration: 45 min
111
Q

vecuronium:
- ED95
- intubation dose
- onset
- duration

A
  • ED95: 0.043 mg/kg
  • intubation dose: 0.1 mg/kg
  • onset: 2.4 min
  • duration: 45 min
112
Q

atracurium:
- ED95
- intubation dose
- onset
- duration

A
  • ED95: 0.21 mg/kg
  • intubation dose: 0.5 mg/kg
  • onset: 3.2 min
  • duration: 45 min
113
Q

rocuronium:
- ED95
- intubation dose
- onset
- duration

A
  • ED95: 0.305 mg/kg
  • intubation dose: 0.6 mg/kg
  • onset: 1.7 min
  • duration: 35 min
114
Q

pancuronium:
- ED95
- intubation dose
- onset
- duration

A
  • ED95: 0.067 mg/kg
  • intubation dose: 0.08 mg/kg
  • onset: 2.9 min
  • duration: 85 min
115
Q

short-acting NDNMB

A

mivacurium

116
Q

intermediate-acting NDNMBs

A

cisatracurium, vecuronium, atracurium, rocuronium

117
Q

NMBS in benzylisoquinolinium class

A

Atracurium
Cisatracurium
Mivacurium

-curium

118
Q

NMBs in aminosteroid class

A

Rocuronium
Vecuronium
Pancuronium

-ronium

119
Q

are NMBs ionized or unionized

A

ionized

120
Q

which NDNMB class is more affected by renal failure

A

aminosteroids (may prolong duration)

121
Q

metabolism of atracurium

A

Ester hydrolysis 66%
Hofmann 33%

122
Q

elimination of atracurium

A

10-40% renally eliminated
(no liver)

123
Q

metabolite of atracurium & cisatracurium

A

laudanosine

124
Q

metabolism of cisatracurium

A

77% hoffman

125
Q

elimination of cisatracurium

A
  • mostly hofmann
  • renal elim. is 16% of total clearance
  • no liver
126
Q

what is Hofmann elimination

A

base-catalyzed reaction dependent on normal blood pH and temperature

127
Q

how do pH & temp affect Hofmann elimination

A
  • Faster with alkalosis & hyperthermia
  • Slower with acidosis & hypothermia
128
Q

potential adverse effect of laudanosine accumulation

A

seizures

129
Q

metabolism & elimination of roc

A
  • metabolism: none
  • > 70% liver elim
  • 10-25% renal elim
  • no metabolites

primarily eliminated via biliary excretion as unchanged molecule

130
Q

metabolism & elimination of vec

A
  • 30-40% liver metabolism
  • 40-50% hepatic elim.
  • 50-60% renal elim
  • metabolite: 3-OH vecuronium
131
Q

metabolism & elimination of pancuronium

A
  • metabolism: 10-20% liver
  • 15% hepatic elim
  • 85% renal elim
  • metabolite: 3-OH pancuronium
132
Q

how can elim 1/2 times of aminosteroid NDNMBs be prolonged

A
  • hepatic dysfunction
  • renal failure
  • age extremes
133
Q

greatest to least NMB potentiation with volatiles

A

Des > Sevo > Iso > N2O > Propofol

134
Q

antibiotics that potentiate NMB

A

Aminoglycosides, polymyxins, clindamycin, lincomycin, tetracycline

135
Q

antidysrhythmics that potentiate NMBs

A
  • Verapamil
  • amlodipine
  • lidocaine
  • quinidine
136
Q

how does lasix affect NMBs

A

potentiates

137
Q

how does lithium potentiate NMB

A

↑ activates potassium channels

138
Q

how do Mg, Ca, and K affect NMB

A
  • Mg ↑ = ↓ ACh release from presynaptic nerve
  • Ca ↓ = ↓ ACh release from presynaptic nerve
  • K ↓ = ↓ RMP
139
Q

how does hypothermia affect NMB

A

↓ metabolism & clearance

140
Q

how does cyclosporin affect NMB

A

potentiates

141
Q

NMBs that can cause histamine release & how to minimize

A

succinylcholine, atracurium, mivacurium

minimize with slow admin.

142
Q

NMB that can stimulate autonomic ganglia

A

succs

not affected by rate of admin.

143
Q

NMB with slight vagolytic effect

A

pancuronium

144
Q

MOA of vagolytic effect with pancuronium

A

Inhibits M2 receptors in SA node, stimulates catecholamine release, inhibits catecholamine reuptake in adrenergic nerves

↑ HR & CO, minimal effect on SVR

144
Q

MOA of vagolytic effect with pancuronium

A

Inhibits M2 receptors in SA node, stimulates catecholamine release, inhibits catecholamine reuptake in adrenergic nerves

↑ HR & CO, minimal effect on SVR

145
Q

NMB pts with HCOM should not get and why

A

pancuronium - vagolytic effect can cause LVOTO

146
Q

most common cause of periop allergic reactions

A

NMBs

1st - succs
2nd - roc

147
Q

how do NMBs cause allergic reactions

A
  • NMB structures contain 1 or more antigenic quaternary ammonium groups that interact w IgE
  • Causes mast cell and basophil degranulation
148
Q

lab value that reflects allergic reaction to NMB

A

elevated tryptase level (peaks at 15-120 min)

149
Q

assoc. between exposure to soap/cosmetics and NMB allergy

A
  • NMB structures contain 1 or more antigenic quaternary ammonium groups that interact w IgE
  • Possible to develop following exposure to soap or cosmetics (contain quaternary ammonium)
150
Q

What characterizes a phase II block following succs administration?

A

Inhibition of presynaptic nicotinic receptors

151
Q

do NMBs treat bronchospasm

A

No - they relax skeletal muscle, NOT smooth muscle

152
Q

possible explanations for why des potentiates NMB the most of volatiles

A
  • central alpha effect on motor neurons
  • inhibition of postjunctional nicotinic receptors at NMJ
  • increased NMB affinity at postjunctional nicotinic receptors at NMJ

APEX (54 decks)

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