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Anesthesia Pharm (Spring 2023) Drugs and Doses Only > NMBDs: Physiology/Succinylcholine (Exam III, Andy's Cards) > Flashcards

NMBDs: Physiology/Succinylcholine (Exam III, Andy's Cards) 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

Massive laryngospasm and bronchospasm leading to death.

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3
Q

The effect of NMBD is to interrupt the transmission of nerve impulses at the _____.

A

Neuromuscular Junction (NMJ)

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4
Q

The MOA of NMBD is either depolarizing or non-depolarizing.

Deploarizing NMBD will _________ the action of ACh.
Non-depolarizing NMBD will ______ the action of ACh.

A

Deploarizing NMBD will mimic the action of ACh.
Non-depolarizing NMBD will interfere with the action of ACh.

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5
Q

Purpose of NMBD for anesthesia.

A
  1. Decrease airway trauma
  2. Facilitate surgical exposure
  3. Minimize injury from patient movement
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6
Q

What classification of NMBD is Succinylcholine (Anectine)?

A

Depolarizing NMBD

Only depolarizing agent used in anesthesia.

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7
Q

Name a long-acting non-depolarizing NMBD.

A

Pancuronium (Pavulon)

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8
Q

Name a short-acting non-depolarizing NMBD.

A

Mivacurium (Mivacron)

Move a lot, short-acting

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9
Q

What is the chemical classification of Pancuronium?

A

Aminosteroid

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10
Q

What is the chemical classification of Mivacurium?

A

Benzylisoquinoline

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11
Q

What is the chemical classification of Pancuronium (Pavulon)?

A

Aminosteroid

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12
Q

Which intermediate-acting NMBDs are Benzylisoquinolines?

A

Atracurium (Tracrium)
Cisatracurium (Nimbex)

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13
Q

Which intermediate-acting NMBD are Aminosteroids?

A

Vecuronium (Nocuron)
Rocuronium (Zemuron)

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14
Q

What is ED95 in regards to NMBDs?

A

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

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15
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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16
Q

The order of block for NMBD is dependent on:

A
  • Number of presynaptic ACh-containing vesicles released.
  • Number of ACh receptors.
  • Blood Flow to the area.
  • Drug potency
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17
Q

Low potency NMBD will onset _________ than higher potency NMBD.

A

Faster

Lower potency NMBD will have more molecules than higher potency NMBD. This will create a higher concentration gradient and result in a faster onset.

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18
Q

Small, rapidly moving muscles will be blocked ________ than large muscles.

A

Faster

Eyes will be paralyzed first before diaphragm.

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19
Q

What does this graph show?

A
  1. Both Larynx and Adductor Pollicis muscle received 0.5 mg/kg of Rocuronium.
  2. 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%.
  3. Both muscles recovered at the same rate. Almost 100% twitch response returned by minute 40.
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20
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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21
Q

The orbicularis oculi underestimates _____________.

A

residual paralysis.

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22
Q

Is checking a twitch in the adductor pollicis a good indicator for laryngeal relaxation?

A

No, it is not a good indicator of laryngeal relaxation.

Checking a twitch of the adductor pollicis is a good indicator or peripheral recovery.

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23
Q

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

A

Adductor pollicis (Ulnar Nerve)

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24
Q

What is the placement of electrodes on ulnar nerve?

What will the response be?

A
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25
Q

What is a defasciculating dose of NMBD?

What symptoms will the patient experience with a defasciculating dose?

A

Where 20% of intubating dose is given early (primer) to prevent fasciculation.

Blurred Vision
Mandibular weakness
Ptosis (droopy eyes)
Diplopia (double vision)
Dysphagia
Increased hearing acuity - people need to be quiet

Let patient know they might start to feel week and get blurry vision. Encourage them to close their eyes.

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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 ______.

A

fade with each stimulus

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28
Q

Double burst stimulator is _____ short bursts followed by ______ short bursts.

The double burst stimulator setting uses ________ Hz

A

3, 3

50 Hz (supramaximal current)

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29
Q

Why was the double burst stimulator developed?

A

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

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30
Q

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

A

4 stimuli at 2 Hz with ½ seconds between each burst

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31
Q

TOF reflects events at _________ membrane.

A

Presynaptic

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32
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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33
Q

Experienced anesthetist are unable to qualitatively detect the fade of a TOF < ______.

A

0.4

The twitch will have to go from unblocked to completely blocked in order to tell a difference

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34
Q

There will be significant residual block with a TOF of ______ to _____.

A

0.7 to 0.9

You will not feel a fade, but there will still be blockade at the NMJ. Patient will still need reversal agent.

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35
Q

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

A

50 Hz for 5 seconds

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36
Q

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

A

Depolarizing NMBD (Succinylcholine)

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37
Q

If a _____ NMBD is given, a tetanic stimulation will result in 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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38
Q

What is post-tetanic stimulation?

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.

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39
Q

No response in post-tetanic stimulation will mean ______.

A

intense blockade

40
Q

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

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

A
41
Q

A study performed showed that _____ % of patients that were not given anticholinesterase drugs for NMBD reversal and no use of nerve stimulator had post-op blockade once extubated.

A

42%

42
Q

A study performed showed that less than ____ % of patients that were given anticholinesterase drugs for NMBD reversal and use of nerve stimulator had post-op blockade once extubated.

A

<4%

43
Q

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

A

myelinated

44
Q

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

A

unmyelinated

45
Q

The presynaptic motor neuron is responsible for what three things involving ACh?

A
  • ACh synthesis
  • ACh uptake and storage in vesicles
  • ACh release and uptake of choline
46
Q

The synaptic cleft is _______ nm wide with fluid that contains ________ and _________.

A

20-50 nm
Collagen and acetylcholinesterase (plasma cholinesterase, butyrylcholinesterase)

47
Q

ACh release is dependent on what electrolyte?

A

Calcium

48
Q

What does Acetylcholinesterase do to ACh?

A

Hydrolyze ACh to acetic acid and choline

49
Q

Post-synaptically, the membrane has multiple _______.

Post-synaptically, the resting membrane potential is _______.

Membrane potential is largely maintained by what two electrolytes?

A

folds

-90 mV

Na+ and K+

50
Q

How many subunits are on a transmembrane nicotinic acetylcholine receptor (nAChR)?

Name them.

A

Five subunits. (Pentameric unit)

2 alphas, beta, delta, gamma

51
Q

If NMBD (non-depolarizer) binds to nACh, there will be no __________ change and no ion flow.

A

conformational change

52
Q

Succinylcholine only requires binding at one ________ subunit. It is postulated that this will cause ________ before total blockade.

A

one alpha subunit

fasciculation

53
Q

_________ is the only depolarizing NMBD in clinical practice.

What are two unique characteristics of this drug?

What is this NMBD most useful for?

What is the downside of this NMBD?

A
  • Succinylcholine
  • Provides very intense and rapid paralysis
  • Offsets of effects prior to hypoxia
  • Rapid Sequence Induction
  • Histamine Release (tachycardia, rash, welps)
54
Q

What is the dose of Succinylcholine?
Onset:
Duration:

A

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

55
Q

What is the MOA of succinylcholine (Sch)?

A
  • Attaches to one or both alpha subunits of the nAChR.
  • Mimics the effect of ACh, but has a sustained opening of the receptor channel (hydrolysis is slower than ACh).
56
Q

SCh will cause how much increase in serum K+?

A

0.5 mEq/L

57
Q

What are characteristics of a phase I block?

A

Decrease contraction to single twitch stimulation.
Decrease amplitude to continuous stimulation.
TOF ratio > 0.7 (no fade)
Absence of post-tetanic facilitation
Skeletal muscle fasciculation

58
Q

Phase II Blocks are typical of ___________ NMBD.

A

non-depolarizing

59
Q

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

A

Essentially an overdose

  • Large dose of SCh (2-4 mg/kg)
  • Lack of/ poorly functioning pseudocholinesterase
60
Q

Succinylcholine is hydrolyzed by __________.

A

Butyrylcholinesterase (plasma cholinesterase)

61
Q

What factors can decrease pseudocholinesterase activity?

A
  • Hepatic disease
  • Drugs (neostigmine, reglan, chemo)
  • Genetics
  • CKD
  • Estrogen (think pregnancy)
62
Q

What factor can increase pseudocholinesterase activity?
What does this mean clinically?

A
  • Obesity
  • Higher dosing of succinylcholine is necessary for obese patients.
63
Q

What does dibucaine number mean?

What does it mean in extremely simple terms?

A

Dibucaine number reflects the quality of the enzyme that inhibits the breakdown of butyrylcholinesterase.

  • ↑ Dibucaine number = Fast succinylcholine metabolism
  • ↓ Dibucaine number = Slow succinylcholine metabolism
64
Q

What is normal dibucaine number?

A

80
More butyrylcholinesterase will stick around and break down Sch

65
Q

What will a dibucaine number of 20 mean for Sch?

A

1 mg/kg of SCh will last 3 hours

Less butyrylcholinesterase will stick around

66
Q

What are the side effects of Succinylcholine?

A
  • Cardiac dysrhythmias
  • Hyperkalemia
  • Myalgia
  • Myoglobinuria
  • ↑ Gastric pressure
  • ↑ IOP
  • ↑ ICP
  • Masseter spasm
67
Q

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

A
  • Pre-treatment with non-depolarizing NMBD (5mg of Roc).

This defasciculating dose either decreases, prevents, or mask the side effects of SCh.

68
Q

What dysrhythmias can occur with succinylcholine administration?

A
  • ↓HR
  • Junctional Rhythm
  • Sinus Arrest
69
Q

Cardiac dysrhythmia’s will usually present on the 1st dose of succinylcholine. T/F?

A

False. If dysrhythmias occur, it will be with the 2ⁿᵈ dose.

70
Q

What are succinylcholine’s actions at the ANS ganglia?

A
  • ↑HR
  • mimic ACh

This usually occurs with large doses.

71
Q

Patient’s with _________ sites will have true hyperkalemia when given SCh.

A

Extrajunctional NMJ sites (more ion channels)

72
Q

What patient populations are more susceptible to the hyperkalemic effects of succinylcholine?

A
  • Individuals with unrecognized muscular dystrophy (Duchenne’s)
  • Unhealed 3rd degree burns
  • Denervation of Skeletal Muscles (bed-ridden patients)
  • Upper motor lesions
73
Q

Who will experience myalgia with Sch?

Where will the myalgia be located?

A

Young adults

Neck, back, abdomen

74
Q

Pediatric patients more frequently experience this with succinylcholine administration.

A

Myoglobinuria (damaged to skeletal muscles), usually found later to have MH or muscular dystrophy.

No succinylcholine for children

75
Q

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

A

Aspiration

This is related to the intensity of the fasciculation and the direct increase in vagal tone.

76
Q

Sch will increase intraocular pressure _______ minutes (range) after administration and last _________ minutes (range).

A

2-4 minutes after admin
last 5-10 minutes

77
Q

Sch will be contraindicated in ______________ chamber injury.

A

open anterior

78
Q

Succinylcholine will increase ICP transiently, how can this effect be attenuated?

A

By hyperventilating the patient, the PaCO2 will decrease leading to cerebral vasoconstriction. This will decrease CBF and decrease ICP before Succinylcholine administration.

79
Q

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

A

Early indicator of Malignant Hyperthermia

Inadequate dosage given in children

80
Q

What is the hereditary rhabdomyolysis associated with all volatile anesthetics and SCh?

A

Malignant Hyperthermia (MH)

81
Q

If MH is untreated what can it lead to?

A

Muscle destruction
Hyperkalemia
Acidosis
Dysrhythmia
Renal Failure
DIC

82
Q

MH causes mutations in what receptor that causes excessive calcium release from the SR?

A

Ryanodine Receptor (RyR1)

83
Q

What ethnicity/nationality are susceptible to MH?

A

Native Americans

84
Q

What are the symptoms of MH?

A

An acute increase in skeletal muscle metabolism
Increase O2 consumption
Lactate formation
Heat Production
Rhabdomyolysis (Spiked increase ETCO2, Increase temp 1C/5mins, arrhythmias, rigidity.)

85
Q

What are the emergency ABCDs of malignant hyperthermia?

A
86
Q

Dantrolene has decreased the mortality of MH from 80% to ________%.

A

10%

87
Q

What is the dose of dantrolene?

A

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

88
Q

How does dantrolene work?

How is dantrolene metabolized?

A
  • Inhibits the Ca2+ release from the SR and produces a muscle relaxant effect.
  • Dantrolene is metabolized in the liver to 5-hydroxydantrolene
89
Q

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

A

Cardiovascular Collapse (d/t synergistic effects)

90
Q

What are the most common side effects of dantrolene?

What are less common S/Es?

A

Most Common: Weakness, Phlebitis, Respiratory Failure, GI upset

Less Common: Confusion, Dizziness, Drowsiness

91
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

92
Q

What part of the day would a Myasthenia Gravis patient be scheduled for surgery?

A

Should be the first of the day. When they have the most ACh and their ACh receptors are not worn out.

93
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

94
Q

What is Lambert-Eton (LE) disease?

LE has an increased sensitivity to which type of NMBD?

A

Autoimmune disease: 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.

95
Q

Why does Lambert-Eton disease often develop?

A

Often results from small-cell lung cancers.

Anesthesia Pharm (Spring 2023) Drugs and Doses Only (20 decks)

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