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NMBAs Flashcards

1
Q

What is the resting membrane potential of a neuron? Threshold potential?

A

resting: -90mV
threshold: -45mV

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2
Q

What is the principle effect of NMBAs?

A

to interrupt transmission of nerve impulses at the NMJ in order to optimize surgical conditions and augment patient safety

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3
Q

What types of channels and receptors are found in the membrane of the presynaptic nerve terminal?

A
  • voltage-gated Ca++ channels
  • Nicotinic ACh receptors
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4
Q

Where are nicotinic ACh receptors located?

A

presynaptic and postsynaptic cell membranes

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5
Q

How and where is ACh synthesized?

A

how: acetyl-CoA and choline are catalyzed via choline acetyltransferase (ChAT)
where: cytoplasm

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6
Q

Describe the transportation of ACh throughout the cell:

A

transported from cytoplasm in synaptic vesicles (quanta) containing 1-50K molecules per vesicle. 5-10K ACh molecules are released per vesicle.

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7
Q

What prompts ACh quanta to fuse with the cell membrane?

A
  • motor nerve AP enters, depolarizes nerve terminal
  • voltage-sensitive Ca++ channels open
  • Ca++ diffuses down conc. gradient within nerve terminal (enters the cell)
  • ACh vesicles fuse with nerve cell membrane
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8
Q

What does release of ACh depend on?

A

Ca++ entry into the nerve terminal

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9
Q

How is the amount of ACh in the cell maintained?

A

positive feedback mechanism:
- ACh is released into the synaptic cleft
- ACh diffuses down conc. gradient from pre to postsynaptic cell
- presynaptic nicotinic ACh receptor responds to ACh by increasing synthesis and release

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10
Q

What type and how many subunits of the nicotinic ACh receptor must be activated before anything happens?

A

2 alpha subunits (5 subunits total) must be bound with 2 ACh molecules

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11
Q

Describe what happens when ACh is bound with a nicotinic ACh receptor:

A
  • 2 ACh bind to 2 alpha subunits of nicotinic ACh receptor
  • channels snap open
    • Na+ and Ca++ INTO postsynaptic cell
    • K+ OUT of postsynaptic cell
  • ion shifts cause motor end plate to depolarize and trigger an action potential
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12
Q

How many postsynaptic nicotinic ACh receptors need to be occupied to generate an AP at the motor end plate?

A

250-500K of the 5 million postsynaptic receptors

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13
Q

What happens to ACh when it interacts with acetylcholinesterase?

A
  • AChE splits ACh into choline and acetate
  • choline transported back to nerve terminal for reconversion to ACh
  • acetate diffuses away
  • hydrolyzation happens rapidly d/t high conc of AChE at synapse
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14
Q

Where are nicotinic receptors located (3 places) and what are they responsible for in each location?

A

1) presynaptically: when combined with ACh, further augment ACh release
2) postsynaptically: play a role in initiating depolarization OR blockade by NDMAs
3) extrajunctionally: structurally different from nicotinic receptors @ synapse; proliferate in response to paralysis, dystrophies, motor neuron injury, burns; stay open 4x longer and upregulate K+

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15
Q

Describe the nicotinic receptor at the NMJ:

A
  • ligand-gated ion channel
  • 5 subunits (2 alpha, 1 beta, 1 delta, 1 episilon)
  • both alpha subunits must be occupied by an agonist (ACh) for channel to open
  • when open: Na+ & Ca++ enter; K+ exits
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16
Q

What happens what Na+ and Ca++ enter the cell, and K+ exits the cell?

A

depolarization

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17
Q

Describe how ACh is made:

A

AcetylCoA and choline are combined via choline acetyltransferase to produce ACh

occurs in the presynaptic neuron

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18
Q

Where is ACh stored?

A

vesicles until the neuron fires/depolarizes

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19
Q

Where is acetylcholinesterase stored?

A

synaptic cleft

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20
Q

Give 4 names for AChE:

A

true cholinesterase
specific ‘’
genuine ‘’
type I ‘’

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21
Q

Depolarizing muscle relaxants act as ACh receptor (agonists/antagonists).

A

agonists

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22
Q

NDMAs act as ACh receptor (agonists/antagonists)

A

competitive antagonists

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23
Q

What medication is the only short acting depolarizing muscle relaxant?

A

succinylcholine

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24
Q

Name the long acting NDMRs:

A

pancuronium

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25
Q

Name the intermediate acting NDMRs:

A

atracurium
cisatracurium
rocuronium
vecuronium

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26
Q

Name the short acting NDMRs:

A

mivacurium (no longer available)

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27
Q

How is succinylcholine related structurally to acetylcholine?

A

Succs is 2 ACh molecules bound together

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28
Q

What is the MOA of succinylcholine?

A
  • ACh nicotinic receptor agonist
  • mimics the action of ACh in both presynaptic and postsynaptic neurons
  • presynaptic: mobilizes supplies of ACh in nerve terminal
    postsynaptic: causes ion channels top open, generating a prolonged depolarization of muscle end plate
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29
Q

What does “absolutely refractory period” mean?

A

action potentials cannot be initiated in the skeletal muscle cell until the cell repolarizes; voltage-gated Na+ channels in the membrane adjacent to the motor end plate snap into the inactivated state

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30
Q

What is the dose, onset, and duration of succinylcholine?

A

dose: 0.5-1 mg/kg
onset: 30 seconds
duration: 3-5 minutes

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31
Q

What is the ED95 of succinycholine?

A

0.3mg/kg

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32
Q

Why does succinylcholine have a short DOA?

A

rapid hydrolysis by plasma cholinesterase

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33
Q

What is the metabolite of succinylcholine?

A

succinylmonocholine

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34
Q

List the alternative names for plasma cholinesterase:

A

pseudocholinesterase
butyrylocholinesterase
false cholinesterase
non-specific ‘’
type II ‘’

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35
Q

How much of an injected dose of succinylcholine reaches the NMJ?

A

10%

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36
Q

Where is plasma cholinesterase primarily located?

A

plasma

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37
Q

Give 3 reasons for a prolonged blockade by succinylcholine:

A

1) liver disease (decreased hepatic production of plasma cholinesterase
2) drug-induced decreases in plasma cholinesterase
3) genetically determined presence of atypical plasma cholinesterase

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38
Q

What drugs lower plasma cholinesterase?

A

metoclopramide
esmolol
neostigmine, pyridostigmine
echothiophate
oral contraceptives/estrogen
cyclophosphamide
N2 mustart
MAOIs

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39
Q

What co-existing conditions can lower plasma cholinesterase?

A

atypical plasma cholinesterase
liver disease
renal disease
burns
elderly
organophosphate poisoning
neoplasm
malnutrition
pregnancy

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40
Q

Atypical plasma cholinesterase is a (quantitative/qualitative) defect.

A

qualitative
(pseudocholinesterase produced in sufficient quantity, but it is not functional)

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41
Q

What is the anesthetic implication of atypical plasma cholinesterase?

A
  • cannot hydrolyze succinylcholine
  • prolonged neuromuscular blockade (1-3 hours instead of 3-5 minutes) after normal dose
42
Q

How is atypical plasma cholinesterase dianosed?

A

Dibucaine test (measures the percentage of inhibition of pseudocholinesterase activity)

43
Q

Describe dibucaine and its relevance to plasma cholinesterase:

A

local anesthetic that inhibits normal plasma cholinesterase activity (NO effect on atypical)

44
Q

Give the range of results of a dibucaine test and their implications:

A

80+= normal response to succs (recover 8-10 minutes)
40-60= response to succs prolonged 50-100% (20-30 minutes)
20 and below= response to succs prolonged by 4-8 hours

45
Q

A patient who is heterozygous for atypical plasma cholinesterase will have what response to succs? What about homozygous for atypical?

A

heterozygous = dibucaine # 50-60, 20-30 mins recovery
homozygous atypical = dibucaine # 20-30, 4-8 hour recovery

46
Q

Describe succinylcholine-induced postoperative myalgias:

A
  • typically in neck, back, abdomen
  • last for 24-48 hours
  • common in young muscular adults, women > men
  • minimized with NDMR pretreatment?
  • prevention is to avoid succs, deep intubation
47
Q

List the potential side effects of succinylcholine:

A
  • bradycardia (esp peds)
  • tachycardia and HTN
  • hyperkalemia
  • myalgias
  • myo-globinuria
  • incr intra-gastric pressure, ICP, IOP
  • MH
  • masseter spasm
  • prolonged respiratory paralysis
48
Q

In which population is routine administration of succs contraindicated?

A

peds - risk of cardiac arrest and sudden death d/t hyperkalemia in children with undiagnosed skeletal muscle myopathy

49
Q

List the factors that can alter the depolarizing blockade with succinylcholine:

A
  • antibiotics (esp aminoglycosides)
  • local anesthetics
  • anticholinesterase agents
  • increased extracellular K+
  • increased extracellular Mg+
  • inherited pseudocholinesterase defect
  • lithium
50
Q

Succs can increased K+ in the body - list the potential conditions that can accentuate this side effect:

A
  • muscular dystrophy
  • burns
  • conditions with upregulation of extrajunctional ACh receptors (paraplegia, Guillain-Barre, CVA, spinal cord injury, etc)
  • severe sepsis
51
Q

Describe how extrajunctional nicotinic receptors differ from presynaptic and postsynaptic receptors:

A
  • subunits differ (gamma subunit instead of epsilon, or 5 alphas)
  • response to ACh and succs:
    *increased sensitivity
    *stay open 4x longer
    *increased efflux of K+
52
Q

What is the MOA of non-depolarizing muscle relaxants?

A
  • competitive antagonists at nicotinic ACh receptors
  • presynaptic: inhibit mobilization of ACh to be ready for exocytosis
  • postsynaptic: combine with ACh receptors, competitively block ACh from attaching; channels stay closed, no electrolyte movement
  • no DIRECT effect on the channel (unlike depolarizing agents)
53
Q

Describe the pharmacokinetics of NDMRs:

A
  • highly ionized
  • water soluble
  • limited lipid solubility (do not cross BBB or placenta)
  • renal and hepatic elimination
  • 50% bound to plasma protein
54
Q

What are the steroidal NDMRs?

A

pancuronium (L)
vecuronium (I)
rocuronium (I)

55
Q

What are the benzylisoquinolinium NDMRs?

A

atracurium (I)
cisatracurium (I)
mivacurium (S) - no longer available

56
Q

Which class of NDMRs is not dependent on hepatic or renal function for metabolism/elimination? What happens to them instead?

A

benzylisoquinoliniums (atracuritum & cisatracurium)

instead, they undergo spontaneous degradation in the plasma

57
Q

Describe the metabolism and elimination of atracurium:

A

metabolism: 66% ester hydrolysis, 33% Hoffman
liver elim: NONE
renal elim: 10-40%
metabolite: laudanosine (can cause seizures)

58
Q

Describe the metabolism and elimination of cisatracurium:

A

metab: 77% Hoffman, no ester hydrolysis
liver elim: NONE
renal elim: 16% of total clearance
metabolite: laudanosine (5x less than atracurium)

59
Q

Which class of NDMRs is dependent on hepatic/renal function for metabolism/elimination?

A

aminosteroids

60
Q

Describe the metabolism and elimination of rocuronium:

A

metab: NONE
liver elim: 70%
renal elim: 10-25%
metabolite: NONE

61
Q

Describe the metabolism and elimination of vecuronium:

A

metab: liver 30-40%
liver elim: 40-50% (cleared in bile)
renal elim: 25-30%
metabolite: 3-OH vecuronium (1/2 the potency)

62
Q

Describe the metabolism and elimination of pancuronium:

A

metab: liver 10-20%
liver elim: 15%
renal elim: 85%
metabolite: 3-OH pancuronium (1/2 the potency)

63
Q

Which NDMRs produce a vagal blockade?

A

pancuronium (blocks vagal muscarinic receptors in SA node)
rocuronium (slight effect)

64
Q

List each NDMR’s primary means of elimination:

A

atracurium: ester hydrolysis
cisatracurium: Hoffman
rocuronium: liver
vecuronium: liver
pancuronium: renal

65
Q

Which NDMR is associated with histamine release? What effect can it have?

A

atracurium – may lead to hypotension and tachycardia; dependent on dose and speed of injection

((succs is also associated with histamine release, but is a depolarizing NMBA))

66
Q

List the NMBAs with active metabolites:

A

succs - succinylmonocholine
atracurium - laudanosine
cisatracurium - laudanosine
vecuronium - 3OH vec
pancuronium - 3-OH pan

rocuronium does not have a metabolite

67
Q

Which paralytics are most associated with anaphylaxis?

A

succ > roc > atracurium > cisatracurium > vec

68
Q

Describe how paralytics cause anaphylaxis:

A

chemical structure has an antigenic quaternary NH4+1 group that interacts with IgE causing mast cell and basophil degradation and increasing tryptase

69
Q

What is the dose/onset/duration of pancuronium?

A
  • dose: 0.067 mg/kg
    (intubating 0.1 mg/kg)
    (maintenance 0.01 mg/kg)
  • onset: 3-5 mins
  • duration: 45-90 mins
70
Q

When considering NDMRs, think ______ when you hear “renal elimination”.

A

pancuronium

71
Q

What is the dose/onset/duration of vecuronium?

A
  • dose: 0.043 mg/kg
    (intubating: 0.1 mg/kg)
    (maintenance: 0.01 mg/kg)
  • onset: <3 mins
  • duration: 25-30 mins
72
Q

What is the dose/onset/duration of rocuronium?

A
  • dose: 0.305 mg/kg (LEAST potent)
    (intubating: 1 mg/kg)
    (maintenance: 0.1 mg/kg)
  • onset: 45-90 sec
  • duration: 15-30 mins
73
Q

Which NDMR is ideal for RSI?

A

rocuronium

74
Q

What is the dose/onset/duration of atracurium?

A
  • dose: 0.21 mg/kg
    (intubating: 0.5 mg/kg)
    (maintenance: 0.1 mg/kg)
  • onset: <3 mins
  • duration: 20-35 mins
75
Q

Describe Hoffman elimination:

A

spontaneous non-enzymatic chemical breakdown that occurs at physiologic pH and temp

76
Q

Describe ester hydrolysis:

A

catalyzed by nonspecific esterases (NOT AChE or pseudocholinesterase)

77
Q

Which drug should be avoided in patients sensitive to histamine release? Why?

A

atracurium

  • tachycardia, hypotension, and increased PIP can cause issues
78
Q

What is the dose/onset/duration of cisatracurium?

A
  • dose: 0.04 mg/kg
    (intubating: 0.2 mg/kg)
    (maintenance: 0.01 mg/kg)
  • onset: <3 mins
  • duration: 30-60 mins
79
Q

List the NDMRs in order of potency from least to greatest:

A

roc < atracurium < pan < vec < cisatracurium

80
Q

What is ED95 when it comes to NDMRs?

A

dose where there is a 95% decrease in twitch height
- measure of potency (inversely related)
- dose required for optimal tracheal intubation is 2-3x the ED95

81
Q

List the drugs that potentiate NDMR action:

A
  • aminoglycoside abx
  • antiarrhythmics
  • local anesthetics
  • volatiles (des>SEVO>iso>N2O)
  • MgSO4
  • lithium
  • loop diuretics
82
Q

List the patient factors that potentiate NDMRs:

A
  • hypothermia
  • gender (women are more sensitive)
83
Q

List the electrolyte factors that potentiate NDMRs:

A
  • HYPERmagnesemia
  • HYPOcalcemia
  • HYPOkalemia
84
Q

What effect does chronic anticonvulsant therapy have on NDMRs?

A

decreases the effect of NDMRs; accelerated recovery and increased dosages required (block doesn’t last as long)

85
Q

What electrolyte imbalances decrease the effect of NDMRs?

A
  • hyperparathyroidism
  • hypercalcemia
    (more ACh to compete with NDMRs)
86
Q

How do patients with myasthenia gravis respond to NDMRs?

A
  • increased sensitivity to NDMRs
  • resistant to succs

*fewer functional ACh receptors d/t degradation by antibodies

87
Q

How do patients with muscle denervation injuries respond to NDMRs?

A
  • resistant to NDMRs
  • exaggerated response to succs

*chronic decrease in ACh release with upregulation of postsynaptic ACh receptors; more ACh receptors to be blocked and more being depolarized

88
Q

Which PNS location is best to monitor recovery?

A

nerve: ulnar
muscle: adductor pollicis

89
Q

Which PNS location is best to monitor onset?

A

nerve: facial
muscle: orbicularis oculi or corrugator supercilii

90
Q

What is the pneumonic to list muscles in order from least to most sensitive to NDMRs?

A

Vocal cords
Die (diaphragm)
Out (orbicularis oculi)
After (abdominal rectus)
Adding (adductor pollicis)
Muscle (masseter)
Paralysis (pharyngeal)
Externally (extraocular)

91
Q

What causes fade in PNS signals?

A
  • antagonism of presynaptic nicotinic receptors by NDMRs
  • blocked N receptors cause less release of ACh from vesicles
  • limited supply of ACh in the synaptic cleft
92
Q

What 2 situations may cause a phase II block?

A

1) succs dose > 7-10 mg/kg
2) 30-60 mins of continuous IV infusion of succs

93
Q

Describe a phase I block:

A
  • depolarizing
  • typically preceded by fasciculation
  • decrease in twitch tension
  • NO FADE during repetitive stimulation
  • NO post-tetanic potentiation
94
Q

Describe a phase II block:

A
  • non-depolarizing
  • decrease in twitch tension
  • FADE during repetitive stimulation
  • post-tetanic potentiation
95
Q

What does a TOF ratio indicate?

A

TOF 0.15-0.25 = adequate surgical relaxation
TOF <0.9 = increased aspiration and pharyngeal dysfxn
TOF <8 = impaired inspiratory flow and partial airway obstruction
TOF >0.9 = safe extubation

96
Q

3 twitches corresponds to what percentage of neuromuscular block?

A

75%

97
Q

Which 4 bedside tests indicate a maximum of 50% of receptors remain occupied?

A
  • inspiratory force - better than -40cm H2O
  • head lift >5sec - sustained x5sec
  • handgrip same as preinduction - sustained x5sec
  • sustained jaw clench on tongue blade - sustained x5sec
98
Q

Sustained tetanus x5sec indicates what % of receptors are occupied?

A

60%

99
Q

Vital capacity of >20mL/kg indicates what % of receptors remain occupied?

A

70%

100
Q

4/4 TOF with no fade indicates what % of receptors remain occupied?

A

70-75%

101
Q

A single twitch on the PNS indicates what % of receptors remain occupied?

A

75-80%

102
Q

A tidal volume >5mL/kg indicates what % of receptors remain occupied?

A

80%

Pharm (19 decks)

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