NMBD intro and sux - test 3 Flashcards

1
Q

What is the main effect of NMBDs?

A

Interrupt transmission of nerve impulses at neuromuscular junction

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2
Q

Action of depolarizing NMBD

A

Mimics the action of acetylcholine

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3
Q

Action of non-depolarizing NMBD

A

Interferes with the action of acetylcholine

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4
Q

What is the purpose of NMBD for anesthesia?

A
  1. Decrease airway trauma
    - airway edema
    - hoarseness
    - vocal cord injury
  2. Facilitates surgical exposure
  3. Minimizes injury from patient movement
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5
Q

Classifications of NMBDs:

A
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6
Q

Classification of succinylcholine:

A

Depolarizing

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7
Q

List the long acting NMBDs:

A
  • Pancuronium
  • Doxacurium
  • Pipecuronium
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8
Q

What is the chemical classification of pancuronium?

A

Aminosteroid

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9
Q

What is the classification of Doxacurium?

A

Aminosteroid

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10
Q

What is the classification of Pipecuronium?

A

Aminosteroid

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11
Q

List the intermediate acting NMBDs:

A
  • Atracurium
  • Vecuronium
  • Rocuronium
  • Cisatracurium
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12
Q

What is the chemical classification of Atracurium?

A

Benzylisoquinoline

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13
Q

What is the chemical classification of Vecuronium?

A

Aminosteroid

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14
Q

What is the chemical classification of Rocuronium?

A

Aminosteroid

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15
Q

What is the chemical classification of Cisatracurium?

A

Benzylisoquinoline

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16
Q

What is the clincal and chemical classification of Mivacurium?

A

Short acting; Benzylisoquinoline

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17
Q

What is ED95?

A

Potency of NMBD. Dose that is necessary to produce 95% suppression of a single twitch in the presence of nitrous/barbiturate/opioids

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18
Q

Which nerve is stimulated so that the adductor pollicis muscle will produce 1 twitch at 1Hz

A

Ulnar nerve

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19
Q

What is the order of block dependent on?

A
  • # of presynaptic Ach containing vesicles released
  • # of postsynaptic Ach receptors
  • Blood flow to the area
  • Drug potency
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20
Q

Which muscles block faster, small or large?

A

Small, rapidly moving muscles block faster than large muscles
- onset more rapid, less intense

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21
Q

Larynx effects vs thumb effects:

A

The larynx wasn’t 100% paralyzed before it started wearing off - started wearing off faster than the peripheral
*this is why we watch the larynx for induction but adductor for emergence

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22
Q

What is the preferred central monitoring location for NMBDs?

A

Orbicularis Oculi
- More closely reflects diaphragm and laryngeal muscle blockade
- Underestimate residual paralysis

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23
Q

What is the preferred peripheral monitoring location for NMBDs?

A

Adductor pollicis
- Poor indicator of laryngeal relaxation
- Gold standard for recovery

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24
Q

Ulnar nerve NMBD monitoring:

A
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25
Q

Which muscle is the gold standard to check a twitch on for recovery?

A

Adductor pollicis

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26
Q

A single twitch nerve stimulator starts at _____ Hz/second decreasing to ______ Hz/10 secs.

A

1 Hz/sec to 0.1 Hz/10 secs

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27
Q

With an onset of a block a single twitch will ______ with each stimulus.

A

Fade

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28
Q

What is double burst stimulator?

What Hz?

A
  • 2-3 short twitches followed by 2-3 short twitches
  • Use 50 Hz
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29
Q

Why was the double burst stimulator developed?

A

To improve detection of residual block

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30
Q

Double twitch stimulator will ____ in 2nd response vs 1st

A

Fade; qualitatively better than the TOF

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31
Q

Train of Four is ________ stimuli at _______ Hz with ______ seconds between each burst.

A

4 stimuli at 2 Hz w/ 0.5 seconds between each burst

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32
Q

TOF reflects events at ____ membrane

A

presynaptic

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33
Q

Prior to NMBD what will be your twitches on the TOF?

What will be the TOF ratio (Twitch 4 : Twitch 1)?

A

4/4 twitches

Ratio 1

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34
Q

What happens to the twitches after administration and return of 4 twitches?

A
  • Amplitude of 4th twitch to 1st twitch
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35
Q

What is the TOF ratio if the amplitude of the 4th twitch is 50% of 1st?

A

TOFR = 0.5

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36
Q

Experienced anesthetists are unable to detect fade TOFR > ___

A

0.4
- may choose to not administer reversal - poor choice

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37
Q

There will still be significant residual block if the TOFR is ____

A

0.7-0.9

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38
Q

Tetanic stimulation is very rapid, it will be ________ Hz for _____ seconds.

A

50 Hz; 5 seconds

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39
Q

Tetanic stimulation has a sustained muscle response with which block?

A

Depolarizing

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40
Q

If a _____ NMBD is given, a tetanic stimulation will result in a a non-sustained muscle response (fade).

A

Nondepolarizing NMBD (Roc/Vec)

The fade is a result of presynaptic depletion of ACh or inhibition of release

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41
Q

What is the fade in tetanic stimulation related to?

A
  • Presynaptic depletion of Ach or inhibition of release
  • Frequency and length of stimulation
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42
Q

What is post-tetanic stimulation?

A
  • A single twitch 3 seconds after tetanic stimulation
  • Occurs due to accumulation of calcium during “tetany”
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43
Q

No response in post-tetanic stimulation will mean ______.

A

intense blockade

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44
Q

Characteristics of a presynaptic motor neuron:

A
  • Large, myelinated
  • From spinal cord or medulla
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45
Q

Characteristics of a presynaptic motor nerve ending:

A
  • unmyelinated
  • innervate single muscle mfiber
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46
Q

What is responsible for Ach in the presynaptic NMJ?

A
  • Synthesis and release
  • Reuptake and storage of choline
47
Q

How big is the synaptic cleft?
What does it contain?

A
  • 20-55mm wide with fluid
  • Contains collagen and acetylcholinesterase
48
Q

How many vesicles in the synaptic cleft release Ach?

A

5,000-10,000

49
Q

What electrolyte is Ach release dependent on?

50
Q

What does acetylcholinesterase do to Ach?

A

Hydrolyzes Ach to acetic acid and choline

51
Q

What is the anatomy of the post-synaptic membrane?

A

Membrane with multiple folds

52
Q

Characteristics of the post-synaptic membrane:

A

-90 mV resting membrane potential
- Maintained by sodium/potassium
- nAchR dirrectly opposite

53
Q

nAchR picture:

54
Q

Characteristics of a nAchR subunit:

A
  • Pentameric unit
  • 5 sub pores (2 alpha, beta, gamma, delta)
  • Transmembrane
55
Q

What happens to the nAchR subunit when Ach binds?

A
  • Conformational change
  • Pores open
  • Sodium influx
  • Calcium influx
  • Potassium efflux
56
Q

What happens to the nAchR subunit when an NMBD binds:

A
  • No conformational change
  • No ion flow
  • Probability of binding due to concentration of NMBD vs Ach
57
Q

How is sux different when binding to the nAchR subunit?

A

It only requires binding at 1 alpha subunit
- it can leave one receptor and attach to other nAchRs until hydrolyzed - this is what causes fasiculations

58
Q

What are the two unique characteristics of sux?

A
  • Intense rapid paralysis
  • Offset of effects prior to hypoxia
59
Q

When is sux the most useful?

A

RSI - full stomach, code, trauma, pregnancy, emesis, etc.

60
Q

Does sux release histamine?

61
Q

What is the dose for Sux?
Onset?
Duration?

A

Dose = 1mg/kg IV for actual body weight

Onset: 30-60 seconds

Duration: 3-5 minutes

62
Q

MOA of Sux:

A
  • Attaches to 1 or both alpha subunits
  • Mimics effects of Ach
  • Hydrolysis is slower than Ach - keeps ion channels open (leaks potassium)
63
Q

What is the sux depolarization called?

A

Phase I block

64
Q

Characteristics of a phase I block:

A
  • decreased contraction to single twitch stimulation
  • decreased amplitude to continuous stimulation
  • TOF ratio > 0.7
  • Absence of post-tetanic facilitation
  • Skeletal muscle fasciculations
65
Q

Characteristics of a phase II block:

A
  • Responses typical of non-depolarizing NMBD
  • can be antagonized by anticholinesterase drug
  • abrupt transition
66
Q

How can a phase I block transition to a phase II block?

A
  • Sux dose 2-4 mg/kg
  • Lack of/poorly functioning pseudocholinesterase
  • Relative “overdose” - desensitization
67
Q

How is sux hydrolyzed?

A
  • Butyrylcholinesterase
  • Synthesized in liver
  • terminated by diffusion out of NMJ into plasma
68
Q

What things can effect pseudocholinesterase activity?

A
  • Decreased hepatic function
  • Drug induced decreases (neostigmine, reglan, chemo, insectides)
  • Genetically atypical
  • Chronic disease (renal) - decreased activity
  • Pregnancy (high estrogen levels) = decreased activity
  • Obese = increased activity
69
Q

What is dibucaine?

A
  • Amide local anesthetic
  • inhibits activity of normal variant butyrylcholinesterase
  • % inhibition = dibucaine number
70
Q

What is the dibucaine number?

A
  • Reflects quality not quantity of the enzyme to inhibit butyrylcholinesterase
    20: Sux 1mg/kg lasts 3 hours
71
Q

Dibucaine number:

72
Q

Side effects of Sux:

A
  • Cardiac dysrhythmias
  • Hyperkalemia
  • Myalgia
  • Myoglobinuria
  • increased intragastric pressure
  • increased intraocular pressure
  • Masseter spasm
73
Q

What is pretreatment with non-depolarizing NMBD?

A

Giving a small dose of Roc early on to block the alpha subunit enough that you don’t see fasciculations - prevents an increase in pressures

74
Q

Defasiculating d/t patient symptoms:

A
  • loss of visual focus/blurry
  • mandibular muscle weakness
  • ptosis
  • diplopia
  • dysphagia
  • increased hearing acuity
75
Q

What cardiac dysrhythmias can occur with sux?

A
  • Sinus brady
  • Junctional rhythm
  • Sinus arrest
76
Q

What actions does sux cause at the ANS ganglia?

A
  • increased heart rate and blood pressure
  • mimics action of ach
  • usually occurs with large doses
77
Q

Cardiac dysrhythmias most likely present on ____ dose of Sux.

A

2nd dose - 5 minutes after 1st

78
Q

What patients will have hyperkalemia with sux?
What causes this?

A
  • Unrecognized muscular dystrophy
  • Unhealed 3rd degree burns
  • Denervation of skeletal muscles (atrophy) - 96hrs-6 months
  • Skeletal muscle trauma
  • Upper motor neuron lesions
    *caused by extrajunctional sites
79
Q

Who will experience myalgia with Sch?

Where will the myalgia be located?

A

Young adults;
Neck, back, abdomen

80
Q

What are pediatric patients more at risk for when given sux?

A

Myoglobinuria (damage to skeletal muscles)

81
Q

Inconsistent increases in intragastric and LES pressure are related to:

A
  • intensity of fasciculations
  • direct increase in vagal tone
82
Q

Sch will increase intragastric pressure and LES pressure, this will increase the risk of _______.

A

Aspiration

83
Q

When does maximum increase in intraocular pressure occur after adminstering sux?
How long does it last?

A

Max increase = 2-4 minutes after admin;
Lasts 5-10 minutes

84
Q

Intraocular pressure and sux:

A
  • MOA unknown
  • Contraction of EOM and globe distortion?
  • Resistance to outflow of aqueous humor and dilation of vessels
  • Efficacy of defasciculation controversial
85
Q

Intraocular pressure graph:

86
Q

What eye condition is sux contraindicated?

A

Open anterior chamber injury

87
Q

What patients are at risk for intracranial pressure with sux?

A

Patients with intracranial tumors or or CHI

88
Q

How can you attenuate the increase of ICP with sux?

A

Hyperventilating the patient prior to sux to cause cerebral vasoconstriction and decrease CBF and ICP

89
Q

Sustained skeletal muscle contraction, incomplete jaw relaxation, and/or masseter muscle spasm d/t sux could be an indication of what conditions?

A

Early indicator of Malignant Hyperthermia

Inadequate dosage given in children

90
Q

Definition of malignant hyperthermia:

A

Hereditary rhabdomyolysis associated with anesthetics

91
Q

What can MH lead to if untreated?

A
  • Muscle destruction
  • Hyperkalemia
  • Acidosis
  • Dysrhythmia
  • Renal failure
  • DIC
92
Q

Triggers for MH:

A
  • ALL volatile anesthetics
  • Sux
93
Q

MH causes mutations in what?

A
  • Skeletal muscle calcium release
  • Ryanodine receptor (RyR1) 50-70% of MH patients
94
Q

What population is susceptible to MH?

A

Native americans

95
Q

How is MH diagnosed?

A
  • Skeletal muscle caffeine contracture testing
  • Muscle biopsy
96
Q

Symptoms of MH:

A
  • Acute increased skeletal muscle metabolism
  • Increased oxygen consumption
  • Lactate formation
  • Heat production
  • Rhabdomyolysis
97
Q

Symptoms of rhabdo present in MH:

A

-↑ ETCO2 that you can’t bag fast enough to reverse
- ↑ temp 1 degree C/5 minutes
- Arrhythmias
- Skeletal muscle rigidity

98
Q

What is the A for in Emergency ABCDs of MH?

A
  • Agents: stop all triggering agents
  • Administer non-triggering anesthetics
  • Ask for help
  • Ask for MH cart
99
Q

What is the B for in the Emergency ABCDs of MH?

A

Breathing: hyperventilation with 100% oxygen

100
Q

What is the C for in the Emergency ABCDs of MH?

A

Cooling procedures if patient is >102.2

101
Q

What is the D for in the Emergency ABCDs of MH?

A

Dantrolene: continuous rapid IV push

102
Q

MOA of Dantrolene:

A

CCB: inhibits calcium release into SR
- By affecting the ryanodine receptor

103
Q

How much does Dantrolene decrease mortality?

A

From 80% → 10%

104
Q

What is the dose for dantrolene?

A

2 mg/kg IV
- repeat doses until symptoms subside or 10 mg/kg IV

105
Q

How is dantrolene metabolized?

A
  • In the liver
  • Metabolite = 5-hydroxydantrolene
106
Q

Patients on calcium channel blockers (verapamil, Cardizem) that receive dantrolene as a treatment can result in __________

A

Cardiovascular Collapse (d/t synergistic effects)

107
Q

What are the most common side effects of dantrolene?

A
  • Weakness
  • Phlebitis
  • Respiratory failure
  • GI upset
108
Q

What do 50% of MH patients complain of?

A

Weakness in grip strength - be careful if they’re already on CCB

109
Q

What are the less common side effects of dantrolene?

A
  • Confusion
  • Dizziness
  • Drowiness
110
Q

What autoimmune disease develops Antibodies against the ACh receptor?

A

Myasthenia Gravis

111
Q

Symptoms of Myasthenia gravis:

What is the treatment?

A
  • increasing weakness/fatigue
  • Diplopia
  • Ptosis
  • Extremity and respiratory muscle weakness

Treat with cholinesterase inhibitors

112
Q

Myasthenia Gravis patients are _________ to Succinylcholine? Why?

What is the dose of sux for MG patients?

A

Resistant to Sux. More Sux is needed because the ACh receptors that are left do not function as well.

1.5-2.0 mg/kg

ED95 is 2.5 times higher

113
Q

What is Lambert-Eton (LE) disease?

LE has an increased sensitivity to which type of NMBD?

A

An autoimmune disease that can result from small-cell lung cancers. LE can produce antibodies against calcium channels and decrease the release of ACh pre-junctionally.

LE has a sensitivity to both depolarizing and nondepolarizing NMBD.