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NMBD/R Flashcards

1
Q

What is a clinically acceptable Tidal volume for extubation & what % of receptors may be occupied by a NMB at this endpoint?

A
  • > or equal to 5mL/kg
  • 80% occupied

Nagelhout 7th ed. Ch. 12, pg. 157, Table 12.3

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2
Q

What is a clinically acceptable TOF result for extubation & what % of receptors may be occupied by a NMB at this endpoint?

A
  • No discernable fade
  • 70-75% occupied

Nagelhout 7th ed. Ch. 12, pg. 157, Table 12.3

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3
Q

What is a clinically acceptable Head lift for extubation & what % of receptors may be occupied by a NMB at this endpoint?

A
  • Hold head off bed unassisted for 5 sec
  • 50% occupied

Nagelhout 7th ed. Ch. 12, pg. 157, Table 12.3

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4
Q

What is a clinically acceptable Hand grip for extubation & what % of receptors may be occupied by a NMB at this endpoint?

A
  • Qualitatively = preinduction strength
  • 50% occupied

Nagelhout 7th ed. Ch. 12, pg. 157, Table 12.3

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5
Q

What is a clinically acceptable sustained bite for extubation & what % of receptors may be occupied by a NMB at this endpoint?

A
  • Sustained jaw clench on tongue blade
  • 50% occupied

Nagelhout 7th ed. Ch. 12, pg. 157, Table 12.3

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6
Q

What is a clinically acceptable inspiratory force for extubation & what % of receptors may be occupied by a NMB at this endpoint?

A
  • At least -40cmH2O
  • 50% occupied

Nagelhout 7th ed. Ch. 12, pg. 157, Table 12.3

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7
Q

What is a clinically acceptable vital capacity for extubation & what % of receptors may be occupied by a NMB at this endpoint?

A
  • 20mL/kg
  • 70% occupied

Nagelhout 7th ed. Ch. 12, pg. 157, Table 12.3

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8
Q

What is a clinically acceptable Double-burst for extubation & what % of receptors may be occupied by a NMB at this endpoint?

A
  • No palpable/discernable fade
  • 60-70% occupied

Nagelhout 7th ed. Ch. 12, pg. 157, Table 12.3

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9
Q

What is a clinically acceptable Single-twitch for extubation & what % of receptors may be occupied by a NMB at this endpoint?

A
  • Qualitatively same as preinduction
  • 75-80% occupied

Nagelhout 7th ed. Ch. 12, pg. 157, Table 12.3

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10
Q

What is a clinically acceptable Sustained Tetanus (50Hz) for extubation & what % of receptors may be occupied by a NMB at this endpoint?

A
  • No Fade
  • 70% occupied

NH says at least 20mL/kg but that ain’t make no damn sense.

Nagelhout 7th ed. Ch. 12, pg. 157, Table 12.3

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11
Q

_______ is where the pre-synaptic motor nerve endings meet the post-synaptic membranes of the skeletal muscle.

A

Neuromuscular Junction (NMJ)

Stoelting’s, Ch. 11, pg. 315

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12
Q

What does the pre-synaptic nerve terminal contain?

A

Synaptic vesicles filled with Ach
* at active zones

Stoelting’s, Ch. 11, pg. 315

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13
Q

What are the post-synaptic folds filled with?

A

Nicotinic Ach receptors (nAChRs)
…. seriously

Stoelting’s, Ch. 11, pg. 315

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14
Q

How/where is Ach broken down?

A
  • Acetylcholinesterase (AchE) by hydrolysis
  • located around nAChRs

Stoelting’s, Ch. 11, pg. 315

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15
Q

How many Ach molecules are in a quantum?

A

5,000 - 10,000 per synaptic vesicle

Stoelting’s, Ch. 11, pg. 316

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16
Q

What is a quantum?

A

Amount of Ach within a synaptic vesicle

Stoelting’s, Ch. 11, pg. 316

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17
Q

How/where is Ach synthesized?

A
  • Acetyl coenzyme A + choline by choline acetyltransferase = Ach
  • Cytoplasm of the nerve terminal

Stoelting’s, Ch. 11, pg. 316

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18
Q

nAChRs are pentameric complexes composed of what five things?

A
  • two a subunits
  • one b subunit
  • one d subunit
  • one eipsilon subunit
    Should = 5 idk

Stoelting’s, Ch. 11, pg. 318

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19
Q

What nAChRs subunits does Ach occupy?

A

Two alphas

cuz two

Stoelting’s, Ch. 11, pg. 316

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20
Q

What nAChRs subunits does Succinylcholine occupy?

A

Two alphas

Stoelting’s, Ch. 11, pg. 316

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21
Q

Fetal nAChRs are resistant to what kind of NMBs?

A

Nondepolarizing NMBs

idk man stoelting’s is confusing, I found it on his PPT

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22
Q

Fetal nAChRs are sensitive to what kind of NMBs?

A

Succinylcholine

idk man stoelting’s is confusing, I found it on his PPT

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23
Q

Since active transport calcium pumps move Ca2+ back into the Sarcoplasmic reticulum… what happens if they don’t?

A
  • Sustained contraction
  • Malignant Hyperthermia bruh

Stoelting’s, Ch. 11, pg. 320

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24
Q

What is the most common method for peri-operative monitoring of neuromuscular blockade?

A

Qualitative monitoring
(Peripheral nerve stimulator)

Nagelhout 7th ed. Ch 12, pg. 152

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25
Q

Which muscle/nerve is preferred for monitoring of depth of blockade?

A

Adductor pollicis via ulnar n.

Nagelhout 7th ed. Ch 12, pg. 152

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26
Q

Which muscle/nerve is preferred for monitoring onset of blockade?

A

Orbicularis oculi/corrugator supercili via
Facial n.

Nagelhout 7th ed. Ch 12, pg. 152

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27
Q

In what order are muscles blocked?

by level of sensitivity?

A
  1. Eye muscle
  2. Extremities/Trunk muscles
  3. Abdominal muscles
  4. Diaphragm

Nagelhout 7th ed. Ch 12, pg. 153

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28
Q

In what order do muscles recover after NMB?

A
  1. Diaphragm
  2. Abdominal muscles
  3. Extremities/Trunk muscles
  4. Eye muscle

Nagelhout 7th ed. Ch 12, pg. 153

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29
Q

What are the five clinical tests with a PNS for monitoring NMB?

A
  1. Single twitch
    2. Train-of-Four (TOF)
    3. Double-burst stimulation (DBS)
    4. Tetanus
  2. Post-tetanic count (PTC)

Nagelhout 7th ed. Ch 12, pg. 153

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30
Q

What is the definition and cause of fade?

A
  • Inability to sustain a response
  • Non-depolarizers antagonizing the positive feedback loop of Ach release

Nagelhout 7th ed. Ch 12, pg. 153

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31
Q

What PNS test is this? Definition?

A

Single Twitch
A single supramaximal electrical
stimulus ranging from 0.1–1.0 Hz

Nagelhout 7th ed. Ch 12, pg. 154, Table 12.2

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32
Q

What PNS test is this? Definition?

A

Train of Four
Four twitches at 2 Hz separated by 0.5 sec
(Total of 2 sec)

Nagelhout 7th ed. Ch 12, pg. 154, Table 12.2

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33
Q

What PNS test is this? Definition?

A

Double-Burst Stimulation
Two short bursts of 50 Hz
Separated by 0.75 sec

Nagelhout 7th ed. Ch 12, pg. 154, Table 12.2

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34
Q

What PNS test is this? Definition?

A

Tetany
Rapidly delivery of 30, 50, or 100 Hz stimulus
for 5 sec.

seems rude

Nagelhout 7th ed. Ch 12, pg. 154, Table 12.2

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35
Q

What PNS test is this? Definition?

A

Post-Tetanic count
Single 50 Hz tetanus for 5 sec
followed by single twiches at 1 Hz

Nagelhout 7th ed. Ch 12, pg. 154, Table 12.2

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36
Q

What is the percent blockade with 3 twitches (TOF)?

A

75-80% receptor blockade

Nagelhout 7th ed. Ch 12, pg. 154

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37
Q

What is the percent blockade with 2 twitches (TOF)?

A

80-85% receptor blockade

Nagelhout 7th ed. Ch 12, pg. 154

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38
Q

What is the percent blockade with 1 twitch (TOF)?

A

90-95% receptor blockade

Nagelhout 7th ed. Ch 12, pg. 154

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39
Q

What is the ideal level of NMB with TOF?

A

85-95% blockade

1 or 2 twitches

Nagelhout 7th ed. Ch 12, pg. 154

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40
Q

What does fade with DBS indicate?

A

Significant paralysis
Like a TOF ratio <0.6

you monster

Nagelhout 7th ed. Ch 12, pg. 154

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41
Q

What does fade/no fade mean with Tetany with the PNS?

A

No fade = significant paralysis unlikely
Fade = significant paralysis likely

Fade = bro, chill with the NMB

Nagelhout 7th ed. Ch 12, pg. 154

42
Q

The type of NMB and number of receptors occupied determine the type of response to PNS on presynaptic nerves is the definition for __________ ?

A

Incomplete (partial) neuromuscular block

His ppt, I’m too lazy to look

43
Q

Stimulation of the presynaptic nerve that doesn’t produce a skeletal muscle response is called ___________ ?

A

Complete (full) neuromuscular block

Again… too lazy

44
Q

What are three characteristics of a Non-depolarizing NMB?

A
  • Decrease in twitch tension
  • Fade w/ repeat stimulation
  • Post-tetanic potentiation

Stoelting’s Ch. 12, pg 324

45
Q

What are four characteristics of a Depolarizing NMB?

A
  • Fasiculations during onset
  • Decrease in twitch tension
  • No fade
  • NO post-tetanic potentiation

Stoelting’s Ch. 12, pg 324

46
Q

Neostigmine Mechanism of Action?

A

Inhibits AchE, increases Ach concentration @
nAChRs around NMJ

Anticholinesterase or Cholinesterase inhibitor

Nagelhout 7th ed. Ch 12, pg. 215

47
Q

Anticholinergics are given to attenuate what kind of side effects with AchE inhibitors?

A

Parasympathomimetic side-effects
* Brady/dysrhythmias
* HoTN
* Bronchconstriction
* Hyper-salivation
* N/V/D

Nagelhout 7th ed. Ch 12, pg. 216-217

48
Q

Which anticholinergic is given with each AChE inhibitor?

A
  • Atropine & Edrophonium
  • Glycopyrrolate & Neostigmine

Nagelhout 7th ed. Ch 12, pg. 217

49
Q

All NMB are ______ ______?

A

Quarternary ammoniums
(Similar to Ach)

Except tubocurarine

Stoelting’s Ch. 12. pg. 323

50
Q

Simply, what is the chemical structure of Succinylcholine?

A

Two Ach molecules linked via acetate-methyl groups

Stoelting’s Ch. 12, pg 325

51
Q

What is the ED95 of Succinylcholine?

A

0.3mg/kg

Stoelting’s Ch. 12, pg 325

52
Q

What is the intubating dose of Succinylcholine?

A

1-1.5mg/kg

Stoelting’s Ch. 12, pg 325

53
Q

Succinylcholine is metabolized via _______?

A

Butyrylcholinesterase
or Pseudocholinesterase
or Plasmacholinesterase

Whatever you wanna call it

Stoelting’s Ch. 12, pg 325

54
Q

CV side effects of Succinylcholine?

A
  • Sinus Tachycardia
  • Brady w/ repeat dosing @ muscarinic receptors

Stoelting’s Ch. 12, pg 327 + Nagelhout Ch. 12, pg. 201

55
Q

Other side effects of succinylcholine?

7

A
  • Hyperkalema
  • Increase ICP
  • Increase IOP
  • Increased IGastricP
  • Myoglobinuria
  • Myalgias
  • Masseter spasm

Stoelting’s Ch. 12, pg 327

56
Q

Which drugs are Benzylisoquiniums?

A

-curium
* Atra-curium
* Miva-curium
* Cistra-curium
* Except tubocurarine

Stoelting’s Ch. 12, pg 328-330

57
Q

Which drugs are Aminosteroidals?

A

-curonium
* Pan-curonium
* Ve-curonium
* Ro-curonium

Stoelting’s Ch. 12, pg 331

58
Q

Which aminosteroidal(s) are long acting? >50 min

A

Pancuronium

Stoelting’s Ch. 12, pg 328, table 12-1

59
Q

Which aminosteroidal(s) are medium acting? 20-50 min

A

Vecuronium
Rocuronium

Stoelting’s Ch. 12, pg 328, table 12-1

60
Q

Which Benzylisoquinium(s) are long acting? >50min

A
  • Tubocurarine

Stoelting’s Ch. 12, pg 328, table 12-1

61
Q

Which Benzylisoquinium(s) are medium acting? 20-50min

A
  • Atracurium
  • Cistracurium

Stoelting’s Ch. 12, pg 328, table 12-1

62
Q

Which Benzylisoquinium(s) are short acting? 10-20min

A

Mivacurium

Stoelting’s Ch. 12, pg 328, table 12-1

63
Q

Which NMBs release histamine?

A

Atracurium & Mivacurium

Nagelhout 7th ed, Ch. 12, Box 12.8 & 9

64
Q

What is the ED95/Intubating dose of Cistracurium

A
  • 0.05mg/kg ED95
  • 0.1mg/kg Intubation

Nagelhout 7th ed, Ch. 12, pg 168

65
Q

What is the ED95/Intubating dose of Mivacurium

A
  • 0.08mg/kg ED95
  • 0.25mg/kg Intubation

Nagelhout 7th ed, Ch. 12, pg 168 & 158 table 12.4

66
Q

What is the ED95/Intubating dose of Atracurium

A
  • 0.15mg/kg ED95
  • 0.5mg/kg Intubation

Nagelhout 7th ed, Ch. 12, pg. 158 table 12.4

67
Q

What is the ED95/Intubating dose of Rocuronium

A
  • 0.3 mg/kg ED95
  • 0.6 - 1mg/kg Intubation

Nagelhout 7th ed, Ch. 12, pg. 158 table 12.4

68
Q

What is the ED95/Intubating dose of Vecuronium

A
  • 0.05 mg/kg ED95
  • 0.1mg/kg Intubation

Nagelhout 7th ed, Ch. 12, pg. 158 table 12.4

69
Q

Which drugs undergo Hofmann elimination?

A
  • Atracurium
  • Cistracurium

Nagelhout 7th ed, Ch. 12, pg 169, Table 12.10

70
Q

Which drugs undergo metabolism by Pseudo/Butyl/Plasmacholinesterase?

A
  • Succinylcholine
  • Mivacurium

Nagelhout 7th ed, Ch. 12, pg 168-169, Table 12.10

71
Q

Which drugs undergo metabolism by Hepatic/renal means?

A
  • Rocuronium
  • Vecuronium

Nagelhout 7th ed, Ch. 12, pg 169, Table 12.10

72
Q

Which drug class does Sugammadex reverse?

A

Aminosteroids
* rocuronium > vecuronium»pancuronium

Nagelhout 7th ed, Ch. 12, pg. 175

73
Q

What dose of Sugammadex should you give with a TOF of 2?

You gave roc/vec

A

2mg/kg

Nagelhout 7th ed, Ch. 12, pg. 218

74
Q

What dose of Sugammadex should you give with a TOF of 0 & PTC of 1 to 2?

You gave roc/vec

A

4 mg/kg

Nagelhout 7th ed, Ch. 12, pg. 218

75
Q

You JUST gave 1.2mg/kg Roc and the surgeon is like…. all done here then zips them up. What dose of sugammadex would you give?

A

16 mg/kg

and a piece of your mind

Nagelhout 7th ed, Ch. 12, pg. 218

76
Q

What are a couple of conditions that would prolong NMB?

A
  • Acidosis (metabolic or hypercarbia)
  • Bunch of hypos
  • hypomagnesemia/phosphatemia/kalemia/calcemia/Thermia
  • Trauma
  • Literally a bunch

Nagelhout 7th ed, Ch. 12, pg. 175, Box 12.14

77
Q

Hofmann elimination is based on?

A

pH & temperature

Body’s “alkalosis” & inc. temp initiate Hofmann elim.

Nagelhout 7th ed, Ch. 12, pg. 168

78
Q

What does a dibucaine number of 70 or higher represent?

A
  • Normal butyl/psuedocholinesterase quality
  • Homozygous typical trait

Stoelting’s pg. 326

79
Q

What does a dibucaine number of 40-60 represent?

A

Heterozygous atypical variant

Stoelting’s pg. 326

80
Q

What does a dibucaine number of less than 30 represent?

A

Homozygous atypical variant

Stoelting’s pg. 326

81
Q

You have a patient you want to give Succinylcholine/Mivacurium, and you get a Dibucaine number of 26, what are you concerned for?

A

Prolonged NMB
(4-8 hours)

Stoelting’s pg. 326

82
Q

Your patient has liver/kidney problems, which NMBs would you consider NOT giving?

A
  • Rocuronium > Vecuronium
    Roc eliminated by bile/kidneys
    Vec by bile > kidneys

Nagelhout 7th ed., Ch. 12, pg. 159, Table 12.5

83
Q

You give Neostigmine to reverse your deeply paralyzed patient, what is your concern?

A

Incomplete reversal/Residual NMB

Neostigmine does not reverse deep NMB

Nagelhout 7th ed., Ch. 12, pg. 173

84
Q

What patient population should be counseled prior Sugammadex administration?

A

Women of child-bearing years who take oral contraceptives

Use alternatives for 1 week after exposure

Nagelhout 7th ed., Ch. 12, pg. 176

85
Q

What does Sugammadex do to oral contraceptives?

A

Like aminosteroids, it binds to the oral contraceptive, rendering them inactive

Nagelhout 7th ed., Ch. 12, pg. 176

86
Q

You give neostigmine/edrophonium to reverse NMB, the patient is Bradycardic… why?

A

Because you should have also given glycopyrrolate/atropine to block the parasympathomimetic effects of the AchEs
Atropine > glyco

Nagelhout 7th ed., Ch. 12, pg. 174, table 12.11

87
Q

Why do we use the adductor pollicis to assess diaphragm recovery?

A
  • Muscles of the hand are more sensative to NMB than the diaphragm.
  • Recovery with the AP = recovery at the diaphragm/upper airway muscles

Nagelhout 7th ed., Ch. 12, pg. 153

88
Q

Which subjective measures (including PNS) after NMB indicate the best recovery?

A
  • Double-burst (60-70%)
  • Inspiratory force -40cmH2O (50%)
  • Head lift (Fitty)
  • Hand grip (Fitty)
  • Sustained bite (Fitty)

Nagelhout 7th ed., Ch. 12, pg. 157, table 12.3

89
Q

How do you determine a ToF ratio?

A
  • Compare T4 with T1
  • Very subjective
  • Sensitive between 70-100% blockade

Nagelhout 7th ed., Ch. 12, pg. 154

90
Q

Where do you place the electrodes for an adductor policis PNS?

A
  • Proximal flexor crease of wrist
  • Over/parallel carpi ulnaris tendon

Nagelhout 7th ed., Ch. 12, pg. 152-3 Fig. 12.3

91
Q

Which antibiotics have been associated with prolonged NMB?

A

Aminoglycosides

  • Gentamicin
  • Clindamycin
  • Neomycin

Nagelhout 7th ed., Ch. 55, pg. 1278

92
Q

Which drugs are markedly potentiated in Preeclamptic women?

A

NDNMBs
in women receiving Mag Sulfate

Nagelhout 7th ed., Ch. 51, pg. 1202

93
Q

What concerns would you have with a pt undergoing parathyroidectomy and receiving a NMB?

A

Hypocalcemia potentiates NDNMB

Nagelhout 7th ed., Ch. 37, pg. 865

94
Q

______ and ______ have an inverse relationship

A

Onset and Potency

Nagelhout 7th ed., Ch. 12, pg. 156

95
Q

In order to make a drug with a low potency work you need to _______ ?

A

give a larger dose

achieve a muscle gradient

thus, faster onset

Nagelhout 7th ed., Ch. 12, pg 156

96
Q

You give Miva/atracurium, your patient becomes flush, hypotensive, and tachycardic, why?

A

Modest Histamine release

Nagelhout 7th ed., Ch. 12, pg. 168-169 table 12.10

97
Q

You give Succinylcholine/Rocuronium, your patient becomes flush, hypotensive, and tachycardic, why? What do you give?

A

IgE-mediated Anaphylaxis
* O2, Fluids, epinephrine

Nagelhout 7th ed., Ch. 12, pg. pg. 171

98
Q

You give your patient cis/atracurium and they seize, why?

A
  • Broken down by Hofmann elimination and have Laudanosine as a metabolite
  • Crosses blood brain barrier, causing CNS excitability
  • Potential for seizure, but unlikely

Stoeltings, pg. 343

99
Q

Why would you use a PNS on the facial n. prior to intubation?

A

Relaxation of facial muscles mirrors relaxation in the larynx/diaphragm

Nagelhout 7th ed., Ch. 12, pg. 153

100
Q

How much can Succinylcholine increase serum K+?

A

Intubating dose can increase it 0.5-1 mEq/L

Nagelhout 7th ed., Ch. 12, pg. 158

101
Q

Succinylcholine dose required for a Phase II block?

A

6-8 mg/kg

Nagelhout 7th ed., Ch. 12, pg. 163

Nurs 575 Anesthesia Pharmacology (13 decks)

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