Exam 3 - Intro to NMB/Succinylcholine Flashcards

1
Q

Which of the following is the newest NMBD?
A. Atracurium
B. Vecuronium
C. Pancuronium
D. Cistracurium

A

A. Atracurium (1980)
B. Vecuronium (1980)
C. Pancuronium (1960)
D. Cistracurium (1995)

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2
Q

Why was Rapacurium (Raplon) discontinued in 2001?

A

Severe bronchospasm esp. in young men leading to death.

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3
Q

Basic MOA of NDMB and DMB?

A

DMB - mimic ACh
NDMB - antagonize ACh

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4
Q

3 purposes of NMBD for anesthesia?

A
  1. Decrease airway trauma
  2. Facilitate surgical exposure
  3. Minimize injury from patient movement
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5
Q

What classification of NMBD is Succinylcholine (Anectine)?

A

Depolarizing NMBD

Only depolarizing agent used in anesthesia.

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6
Q

What are the 3 long acting NDMB and their chemical classification?

A
  • Pancruonium (Pavulon); Aminosteroid
  • Doxacurium; aminosteroid
  • Pipecuronium; aminosteroid
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7
Q

What are the 4 intermediate acting NDMB and their chemical classification?

A
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8
Q

What is the short-acting NDMB and its chemical classification?

A
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9
Q

What is ED95?

A

The potency of NMBD. The dose that is necessary to produce a 95% supression of a single twitch in the presence of nitrous/ barbiturate/ opioid anesthesia.

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10
Q

What nerve is stimulated so that the adductor pollicis muscle will produce a single twitch at 1 Hz (thumb adduction)?

A

Ulnar nerve

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11
Q

The order of block for NMBD is dependent on what 4 things?

A
  • The number of presynaptic ACh-containing vesicles released.
  • The number of ACh receptors.
  • Blood Flow to the area.
  • Drug potency
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12
Q

What is the order of muscular blockade with NMBD?

A
  • Small moving muscles block faster than large (eyes before diaphragm)
  • Central muscles block faster but a lesser intensity (laryngeal before adductor pollicis)
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13
Q

What does this graph show?

A

Both Muscles experience a dramatic decrease in twitch percent height, but the adductor pollicis is completley blocked while the larynx got down to a twitch height of 20%.

Both muscles recovered at the same rate. Almost 100% twitch response returned by minute 40.

Central muscles have less intense block than peripheral

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14
Q

Checking a twitch in which muscle will assess the diaphragm and laryngeal muscle blockade?

A

Orbicularis Oculi

If there are no twitches to the facial nerve, the diaphragm and laryngeal muscles are adequately blocked. Best indicator of intubating conditions.

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15
Q

The orbicularis oculi underestimates _____________.

A

residual paralysis.

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16
Q

Where should you check twitches to determine recovery from NMBD?

A

Adductor pollicis (Ulnar Nerve)

Gold standard for recovery

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17
Q

What is the proper orientation of electrodes when checking twitches?

A

Postitive (Red) is Proximal

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18
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 (continuous)

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19
Q

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

A

fade

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20
Q

Double burst stimulator is ____ short burst followed by ____ short burst.

The double burst stimulator uses ________ Hz

A

2-3, 2-3

50 Hz (supramaximal current)

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21
Q

Why was the double burst stimulator developed?

A

To improve detection of residual block (fade).
Fade in 2nd response vs 1st response.
Qualitatively better than TOF.

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22
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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23
Q

What is the stimulus for TOF?

A

4 stimuli at 2 Hz in 1/2 second

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24
Q

What is the TOFR if the 4th twitch is 1/2 the height of the 1st twitch?

A

0.5

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25
Q

What can occur at a TOF of 0.7-0.9?

A

It may appear to be 4 equal twitches, but there is still significant paralysis. Need reversal.

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26
Q

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

A

50 Hz for 5 seconds

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27
Q

If a ____ NMBD is given, a tetanic stimulation will result in a sustained muscle response.

A

Depolarizing NMBD (Succinylcholine)

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28
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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29
Q

What is post-tetanic stimulation?
Difference with phase I and phase II block?

A

Single twitch 3 seconds after tetanic stimulation.

The post-tetanic stimulation will occur d/t accumulation of calcium during tetany, the excess calcium will stimulate ACh release.

Phase I = equal amplitude
Phase II = increase amplitude

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30
Q

What kind of NMBD are used in column A, B, and C?

What kind of nerve stimulation is performed in row 1 through 4?

A
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31
Q

Does the use of nerve stimulators accurately tell recovery from NMBD?

A

Yes, a study showed that without use of reversal drugs and only bedside extubation criteria, that 42% of patients had blockade
While only < 4% had blockade with use of NS and reversal agents

32
Q

The presynaptic motor neuron is large and ____ which helps with transmission of nerve impulses.

A

myelinated

33
Q

The motor nerve ending is ____ and innervates single muscle fibers.

A

unmyelinated

34
Q

Transmission down a myelinated neuron occurs at the ____ ?

A

Nodes of Ranvier

35
Q

ACh release is dependent on what electrolyte?

36
Q

What does Acetylcholinesterase do to ACh?

A

Hydrolyze ACh to acetic acid and choline

37
Q

Normal resting membrane potential?
Controlled by what?

A
  • -90 mV
    Na+/K+ levels
38
Q

How many subunits are in a nACh receptor?
How does ACh open the receptor?

A

5
There must be an ACh bound to each ⍺ subunit

39
Q

How does succ affect the nACh receptor?
How does succ cause fasiculations?

A
  • Only requires binding to 1 of the ⍺ subunits
  • Succ “jumps” from one binding site to another causing frequent and non-consistent depolarizations
40
Q

2 unique qualities of succ?
What is it primarily used for?

A
  1. Intense, rapid paralysis
  2. Offsets prior to hypoxia
    Used fo RSI
41
Q

Succ releases ____ and can cause allergic type reactions?

42
Q

What is the dose of Succinylcholine?
Onset:
Duration:

A

Dose: 1 mg/kg IV (actual BW)
Onset: 30-60 seconds
Duration: 3-5 minutes

43
Q

SCh will cause how much increase in serum K+?

44
Q

What is another name given to depolarizing muscle relaxants?

A

Phase I block

45
Q

Twitch characteristics of phase 1 blocks?

A
  • Decrease in amplutude and contraction, no fade
  • TOFR > 0.7
  • No post-tetanic increase
  • Fasiculations
46
Q

Phase II Block are typical of ___________ NMBD.

A

non-depolarizing

47
Q

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

A
  • Large dose of SCh (2-4 mg/kg)
  • Lack of/ poorly functioning pseudocholinesterase
  • Relative “overdose”…. become desensitized → receptors antagonized but channels are closed (not depolarized)
48
Q

Succinylcholine is hydrolyzed by ____ which is made in the ____

A
  • Butyrylcholinesterase (plasma cholinesterase)
  • Liver
49
Q

What factors can decrease pseudocholinesterase activity?
What does this cause?

A
  • Decreased in hepatic production
  • Drug-induced decrease (neostigmine, reglan, chemo)
  • CKD
  • Pregnancy (estrogen cause decrease)
    Prolonged blockade
50
Q

What increases pseudocholinesterase activity?

51
Q

What does dibucaine number mean?

A

The percentage of plasma cholinesterase enzyme inhibitied by dibucaine.

Reflects quality of cholinesterase enzyme (ability to hydrolyze succinylcholine) and not the quantity of the enzyme that is circulating in the plasma - Stoelting p. 1036

52
Q

What is a normal and abnormal dibucaine number?

A

80% = normal
20% = abnormal (normal succ dose will last 3 hours)

53
Q

What is the pre-treatment to the side effects of SCh?

A
  • Pre-treatment with a small dose of non-depolarizing NMBD.
  • The defasciculating dose either decreases, prevents, or masks the side effects of SCh.
54
Q

What should we warn patients about if we pretreat succ?

A
  • Blurry vision
  • Muscle weakness
  • Heavy chest
55
Q

What are the cardiac dysrhythmia of SCh?

A

Sinus Brady
Junctional Rhythm
Sinus Arrest

56
Q

When are effects at cardiac muscarinic and cholinergic seen with succ?

A

Usually on 2nd dose given 5 mins after first

57
Q

What offsets the activation of cardiac ACh-R by succ?

A

Increase in the ANS ganglia → increased HR and BP

58
Q

When are we most concerned with the hyperkalemia caused by succ?

A

When patients have extrajunctional sites (more channels):
Muscular dystrophy
Burns
Atrophy
Muscle trauma
Upper motor neuron lesions

59
Q

Who will experience myalgia with Sch?

Where will the myalgia be located?

A

Young adults

Neck, back, abdomen

60
Q

When do we see myoglobinuria with succ administration?

A

Usually pediatrics who have undiagnosed MH or MD

61
Q

What causes aspiration sometimes seen with succ?

A

Increased intragastic and lower esophageal sphincter pressure

62
Q

What causes increased IOP with succ?
Is this concerning?

A
  • EOM contraction and globe distortion
  • Resistance to outflow of aqueous humour
  • For non-serious eye injuries, the effects only last 5-10 mins
63
Q

What is an absolute contratindicatino to succ?

A

Open anterior eye injury

64
Q

Succ can increase ICP, how can this be attenutated?

A

Hyperventilation prior to administration; although with RSI there is no ventilation

65
Q

What succ side affect mimics and may be a sign of MH?

A

Masseter muscle spasm

66
Q

If MH is untreated what can it lead to?

A

Muscle destruction
Hyperkalemia
Acidosis
Dysrhythmia
Renal Failure
DIC

67
Q

MH is caused by mutations in what receptor to have excessive calcium release from the SR?

A

Ryanodine Receptor (RyR1)

68
Q

What ethnicity of patients are susceptible to MH?

A

Native Americans

69
Q

What are the symptoms of MH?

A
  • An acute increase in skeletal muscle metabolism
  • Increase O2 consumption
  • Lactate formation
  • Heat Production
  • Rhabdomyolysis
  • ↑ EtCO2, cannot be bagged down
70
Q

Emergency ABCD’s of MH

71
Q

What is the dose of dantrolene?

A

2mg/kg IV
Repeat doses until symptoms subside or 10mg/kg IV

72
Q

How does dantrolene work?

A

Inhibits the Ca2+ release from the SR and produces a muscle relaxant effect.

73
Q

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

A

Cardiovascular Collapse (d/t synergistic effects)

74
Q

What autoimmune disease develops Antibodies against the ACh receptor?

Symptoms (Sx)

Treatment (Sx)

A

Myasthenia Gravis (MG)

Sx:
Increasing weakness and fatigue throughout the day
Diplopia
Ptosis
Extremity and Resp muscle weakness

Tx: Cholinesterase Inhibitor

75
Q

Myasthenia Gravis patients are _________ to Succinylcholine? Why?

What is the dose of SCh for MG patients?

A

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

1.5-2.0 mg/kg

76
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.