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Spr24 Pharm II > 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. Cisatracurium

A

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

SPACR

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2
Q

Why was Rapacurium (Raplon) discontinued in 2001?

A

Massive bronchospasm leading to death.

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3
Q

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

A

Nerve impulses

Neuromuscular Junction (NMJ)

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4
Q

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

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

A

Depolarizing 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 (pavulon)?

A

Aminosteroid

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10
Q

What is the chemical classification of Mivacurium (mivacron)?

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 (Norcuron)
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

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

A

Faster

Eyes will be paralyzed first before diaphragm.

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18
Q

What does this graph show?

A

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

The larynx recovers quicker.

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19
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 assumed adequately blocked. Best indicator of intubating conditions.

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20
Q

The orbicularis oculi underestimates _____________.

A

residual paralysis.

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21
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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22
Q

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

A

Adductor pollicis (Ulnar Nerve)

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23
Q

What is the placement of electrodes on ulnar nerve?

What will the response be?

A
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24
Q

What is a defasciculating dose of NMBD?

What symptoms will the patient experience with a defasciculating dose? (6)

A

Where small ND-NMB dose is given early to prevent fasciculation with SCh.

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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25
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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26
Q

With an onset of a block, a single twitch will ______.

A

fade with each stimulus

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27
Q

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

The double burst stimulator setting uses ________ Hz

A

2-3, 2-3

50 Hz (supramaximal current)

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28
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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29
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 (4 stimuli over 2 seconds)

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30
Q

TOF reflects events at _________ membrane.

A

Presynaptic

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31
Q

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

What will be the TOFR (Twitch 4 : Twitch 1)?

A

4/4 twitches

Ratio 1

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32
Q

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

A

0.4

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33
Q

There will be significant residual block with a TOFR 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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34
Q

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

A

50 Hz for 5 seconds

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35
Q

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

A

Depolarizing NMBD (Succinylcholine)

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36
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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37
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 ⇒ larger amplitude

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38
Q

No response in post-tetanic stimulation will mean ______.

A

intense blockade

39
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
40
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%

(with bedside criteria alone)

41
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%

(decreased with use of nerve stimulators and reversal)

42
Q

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

A

myelinated

43
Q

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

A

unmyelinated

44
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 reuptake of choline
45
Q

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

A

20-50 nm
Collagen and acetylcholinesterase

46
Q

ACh release is dependent on what electrolyte?

A

Calcium

47
Q

What does Acetylcholinesterase do to ACh?

A

Hydrolyze ACh to acetic acid and choline

48
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 (invaginations)

-90 mV

Na+ and K+

49
Q

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

Name them.

A

Five subunits. (Pentameric unit)

2⍺, β, 𝛿, 𝛾

50
Q

If an ND-NMBD binds to nACh, there will be no ______ ______ and no ion flow.

A

conformational change

51
Q

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

A

one alpha subunit

fasciculation

52
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 a large 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)
53
Q

What is the dose of Succinylcholine?
Onset:
Duration:

A

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

54
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).
55
Q

SCh will cause how much increase in serum K+?

A

0.5 mEq/L

56
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

57
Q

Phase II Blocks are typical of ___________ NMBD.

A

non-depolarizing

58
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
59
Q

Succinylcholine is hydrolyzed by __________.

A

Butyrylcholinesterase (plasma cholinesterase)

60
Q

What factors can decrease pseudocholinesterase activity? (5)

A
  • Hepatic disease
  • Drugs (neostigmine, reglan, chemo)
  • Genetics
  • CKD
  • Estrogen (think pregnancy)
61
Q

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

A
  • Obesity

Higher dosing of succinylcholine is necessary for obese patients.

62
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
63
Q

What is normal dibucaine number?

A

80
More butyrylcholinesterase will stick around and break down Sch

64
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 ⇒ less hydrolysis of Sch

65
Q

What are the side effects of Succinylcholine? (8)

A
  • Cardiac dysrhythmias
  • Hyperkalemia
  • Myalgia
  • Myoglobinuria
  • ↑ Gastric pressure
  • ↑ IOP
  • ↑ ICP
  • Masseter spasm
66
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.

67
Q

What dysrhythmias can occur with succinylcholine administration?

A
  • ↓HR
  • Junctional Rhythm
  • Sinus Arrest
68
Q

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

A

False. dysrhythmias most likely with the 2ⁿᵈ dose.

69
Q

What are succinylcholine’s actions at the ANS ganglia?

A
  • ↑HR and BP
  • mimic ACh

This usually occurs with large doses.

70
Q

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

A

Extrajunctional NMJ sites (more ion channels)

71
Q

What patient populations are more susceptible to the hyperkalemic effects of succinylcholine? (4)

A
  • Individuals with unrecognized muscular dystrophy (Duchenne’s)
  • Unhealed 3rd degree burns
  • Denervation of Skeletal Muscles (bed-ridden patients)
  • Upper motor lesions
72
Q

Who will experience myalgia with Sch?

Where will the myalgia likely be located?

A

Young adults

Neck, back, abdomen

73
Q

Pediatric patients more frequently experience this with succinylcholine administration.

A

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

No succinylcholine for children

74
Q

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

A

Aspiration (may be offset by ↑LES pressure)

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

75
Q

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

A

2-4 minutes after admin
last 5-10 minutes

76
Q

Sch will be contraindicated in ______________ chamber injury.

A

open anterior

77
Q

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

A

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

78
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

79
Q

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

A

Malignant Hyperthermia (MH)

80
Q

What main effects can MH have? (6)

A

Muscle destruction
Hyperkalemia
Acidosis
Dysrhythmia
Renal Failure
DIC

81
Q

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

A

Ryanodine Receptor (RyR1)

82
Q

What ethnicity/nationality are susceptible to MH?

A

Native Americans

83
Q

What are the symptoms of MH?

A
  • Acute ↑ in Sk-M metabolism
  • ↑O2 consumption
  • Lactate formation
  • Rhabdomyolysis (Spiked increase ETCO₂, ↑temp 1ºC/5mins, arrhythmias, rigidity.)
84
Q

What are the emergency ABCDs of malignant hyperthermia?

A
85
Q

Dantrolene has decreased the mortality of MH from ____ to ____%.

A

80% →10%

86
Q

What is the dose of dantrolene?

A

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

87
Q

How does dantrolene work?

How is dantrolene metabolized?

A
  • Inhibits the Ca2+ release from the SR (RyR blocker).
  • Dantrolene is metabolized in the liver to 5-hydroxydantrolene
88
Q

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

A

Cardiovascular Collapse (d/t excess Ca Channel blockade)

89
Q

What are the most common side effects of dantrolene? (4)

What are less common side effects? (3)

A

Most Common:
Weakness
Respiratory Failure
Phlebitis
GI upset

Less Common:
Confusion
Dizziness
Drowsiness

90
Q

What autoimmune disease develops Antibodies against the ACh receptor?

Symptoms (Sx)?

Treatment (Tx)?

A

Myasthenia Gravis (MG)

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

Tx: Cholinesterase Inhibitor

91
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.

92
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

93
Q

What is Lambert-Eton (LE) disease?

LEMS has an increased sensitivity to which type of NMBD?

A

Autoimmune disease: LEMS can produce antibodies against calcium channels (P-type) and decrease the release of ACh presynaptically.

LEMS has a sensitivity to both depolarizing and nondepolarizing NMBD.

94
Q

Why does Lambert-Eton disease often develop?

A

Often results from small-cell lung cancers.

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