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General Principles > Week 4: NMBAs > Flashcards

Week 4: NMBAs Flashcards

1
Q

Neuromuscular junction consists of (3):

A

Prejunctional motor nerve ending

Synaptic cleft (contains acetylcholinesterase (AChAse))

Highly folded Postjunctional muscle fiber

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2
Q

In nerve stimulation: depolarization reaches nerve terminal and voltage gated __________ channels open and _________ enters the nerve terminal

A

Calcium; calcium

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3
Q

In nerve stimulation: storage quanta Vesicles (presynaptic) release ____________ into the cleft

A

acetylcholine (ACh)

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4
Q

In nerve stimulation: ACh diffuses across the synaptic cleft and binds to the ________________ receptor at the postsynaptic end plate and start of muscle contraction

A

nicotinic cholinergic

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5
Q

The release of ACh quanta is antagonized by _________ and _________.

A

Hypocalcemia ; Hypermagnesimia

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6
Q

1 ACh quanta contains __________ to ___________ ACh molecules.

A

5,000 to 10,000

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7
Q

Post-junctional receptors have ______ subunits.

A

5

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8
Q

Postjunctional receptors with 2 alpha, 1 beta, 1 delta, and 1 epsilon (Fetal or “Adult”)?

A

Adult
** mature - after birth

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9
Q

Postjunctional receptors with 2 alpha, 1 beta, 1 delta, and 1 gamma (Fetal or “Adult”)?

A

Fetal
**immature/fetal-isommer

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10
Q

The two ___ subunits of the receptor contain the ACh-binding sites

A

a ( the a-recognition site )

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11
Q

If both “a” subunits are occupied then a ________ change happens and a _______ channel opens

A

conformational ; central

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12
Q

Sodium (and Calcium) move _________ the cell and Potassium moves __________ the cell. Action potential occurs and a muscle contraction happens.

A

in to ; out of

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13
Q

When a nerve impulse arrives at the neuromuscular junction (NMJ), voltage-gated ion channels open, leading to an influx of __________ within the terminal that causes several hundred vesicles of acetylcholine to fuse with the nerve membrane.

A

Calcium

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14
Q

The acetylcholine within the vesicles is released into the synaptic cleft, combining with and activating _______________ receptors on the motor endplate, the activation of which opens ion channels on the muscle membrane and depolarizes the membrane.

A

nicotinic

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15
Q

The release of ________ from intracellular stores stimulates an interaction between actin and myosin, resulting in muscle contraction.

A

Calcium

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16
Q

Increased Extrajunctional Receptors is called:

A

Upregulation

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17
Q

Upregulation occurs when?

A

When frequency of stimulation of NMJ decreases over days or longer.

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18
Q

What could decrease the frequency of stimulation of NMJ? (6)

A
  • Prolonged use of NMBAs in ICU
  • Immobilization
  • Severe burns
  • CVAs (stroke)
  • Infection
  • Sepsis
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19
Q

In up-regulation, the number of ___________ nAChRs increases

A

immature

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20
Q

In upregulation: The number of immature nAChRs will have increased sensitivity to _______ and _______ and decreased sensitivity to ___________.

A

ACh and SCh ; nondepolarizers

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21
Q

The channel opening time of the immature nAChRs is up to 10-fold longer than that of mature receptors and may allow systemic release of lethal doses of intracellular _______ in response to administration of _________.

A

K+ (Potassium) ; Succinylcholine (SCh)

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22
Q

When does Downregulation of mature nAChRs occur? give example.

A

During periods of sustained agonist stimulation.

Chronic neostigmine use.

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23
Q

In what condition is neogtigmine chronically used?

A

Myasthenia gravis

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24
Q

Sustained agonist stimulation leads to __________ to SCh but __________ sensitivity to nondepolarizing NMBAs.

A

Resistance; extreme .

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25
Q

Uses of muscle relaxants (4):

A
  • Optimize surgical conditions
  • Prevent unwanted movement
  • Facilitate tracheal intubation
  • Improve mechanical ventilation
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26
Q

Primary purpose of muscle relaxants:

A

Primary purpose is to achieve adequate relaxation of the upper airway, vocal cords, and diaphragm to facilitate intubation and surgery

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27
Q

Neuromuscular blocking agents (NMBA) are NOT ________ and DO NOT cause _______.

A

anesthetics ; amnesia.

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28
Q

NMBA do not cause awareness; not enough _________ causes awareness

A

anesthesia

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29
Q

T/F: Complete paralysis is not required for all surgical cases.

A

True :)

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30
Q

Other ways to produce muscle relaxation besides NMBAs?

A
  • Inhalational agents: iso, sevo, des
  • Blocks : regional, spinal
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31
Q

Main site of action of NMBA is on the ________________ receptor at the ________ of the muscle.

A

nicotinic cholinergic ; endplate

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32
Q

median dose that corresponds to 50% twitch reduction

A

ED50

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33
Q

corresponds to 95% block (useful relaxation when twitch abolished)

A

ED95

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34
Q

Characteristics of Neuromuscular Blockers(NMB)

A
  • potency
  • onset of action
  • duration of action
  • recovery index
  • intubating condition
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35
Q

relationship between twitch depression and dose

A

potency

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36
Q

time to maximal blockade

A

Onset of Action

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37
Q

Time of injection to return of 25% twitch height
( Dose dependent )

A

Duration of Action

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38
Q

Time interval between 25% and 75% twitch height
( Speed of recovery )

A

Recovery Index

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39
Q

Two types of Neuromuscular Blocking Agents:

A

Depolarizing & Nondepolarizing

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40
Q

Depolarize at postsynaptic nAChRs

A

Depolarizing NMBAs

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41
Q

Example of depolarizing NMBA:

A

Succinylcholine

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42
Q

Compete for active binding sites on nAChRs

A

Nondepolarizing NMBAs

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43
Q

Two types of nondepolarizing NMBAs

A

Aminosteroid & Benzylisoquinolinium

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44
Q

Aminosteroid - Nondepolarizing NMBAs:

A

Pancuronium
Rocuronium
Vecuronium

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45
Q

Benzylisoquinolinium - Nondepolarizing NMBAs:

A
  • Mivacurium
  • Atracurium
  • Cisatracurium
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46
Q

made up of two ACh molecules joined end to end; acts as a “false transmitter,” mimicking ACh.

A

Succinylcholine

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47
Q

Succinylcholine(SCh) (__________)

A

Anectine

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48
Q

_____________ agent creates an overwhelming persistent stimulation to nAChRs.

A

Depolarizing agent

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49
Q

with ___________ agents membranes become exhausted and unresponsive to ACh. Muscle contraction cannot recur until return of __________ state.

A

depolarizing ; resting

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50
Q

Which drug activates the prejunctional receptors to release ACh and it also mimics ACh.

A

Succinylcholine (SCh) - (Anectine)

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51
Q

Succinylcholine (Anectine) produces sustained depolarization of the __________ membrane and __________ receptors.

A

Postjunctional; extrajunctional

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52
Q

Succinylcholine causes prolonged depolarization of the motor end-plate which inactivates ________ channels and increases influx of ________.

A

Na; Sodium

*** exist of potassium from cell

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53
Q

Succinylcholine(SCh)/Anectine was introduced in what year?

A

1949

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54
Q

How does SCh mimic ACh?

A

it has Two ACh molecules joined end to end

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55
Q

When given may cause fasciculations before total paralysis, specially in patients with a lot of muscle.

A

Succinylcholine(SCh)/Anectine

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56
Q

Succinylcholine IV dose

A

1 -1.5 mg/kg IV

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57
Q

Succinylcholine IM dose in children.

A

4 -5 mg/kg IM

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58
Q

Why give IM succinylcholine?

A

Good for laryngospasm

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59
Q

Succinylcholine IV dose in kids.

A

1.5-2 mg/kg

**children are more resistant.

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60
Q

Succinylcholine IV dose in infants.

A

up to 3 mg/kg

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61
Q

Infants need an increased amount of SCh becaue

A

Not enough muscle and larger volume of distribution.

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62
Q

Onset of Succinylcholine(SCh)/Anectine

A

~ 1 minute ( 30 - 60 seconds).

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63
Q

Duration of Succinylcholine(SCh)/Anectine

A

5-15 minutes (dose dependent)

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64
Q

Infants need an increased amount of SCh becaue

A

Not enough muscle and larger volume of distribution.

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65
Q

Hydrolysis of SCh by ______________ occurs in the plasma, where almost ______% of the IV dose of SCh is hydrolyzed before reaching the NMJ,

A

Butyrylcholinesterase ( AKA Pseudocholinesterase or plasma cholinesterase) ;

90%

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66
Q

Succinylcholine(SCh)/Anectine is broken down by butyrylcholinestarese to :

A
  • Choline
  • Succinylmonocholine
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67
Q

Only _____% of SCh administered reaches the NMJ

A

10%

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68
Q

Recovery occurs when SCh _______ away from the NMJ

A

Diffuses

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69
Q

Butyrylcholinesterase is synthesize in the _________ and found in the __________

A

Liver ; Plasma

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70
Q

Factors that lower Butyrylcholinesterase:

A

Burns
Oral contraceptives
Anticholinesterase
Severe liver disease

Reglan
Advanced age
Malnutrition
Pregnancy

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71
Q

Neostigmine (lesser extent edrophonium) profoundly decreases the pseudocholinesterase activity (at 30 min after administration only 50% normal activity) which means it:

A

Prolongs SCh block.

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72
Q

Abnormal genetic variant of butyrylcholinesterase (over 20 mutations in the coding of the plasma cholinesterase gene) can cause prolonged muscle relaxation after __________ and _____________.

A

succinylcholine and mivacurium

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73
Q

Probably won’t know you have the gene until it happens.

A

Abnormal Plasma Cholinesterase

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74
Q

One way to test for it is to check for Abnormal Plasma Cholinesterase

A

“Dibucaine number”

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75
Q

Dibucaine number

A

The percentage of pseudocholinesterase enzyme activity that is inhibited by Dibucaine

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76
Q

Dibucaine number reflects __________ of cholinesterase enzyme (ability to hydrolyze SCh) not the ___________ that is circulating in plasma

A

quality ; NOT quantity

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77
Q

Types of Butyrylcholinesterase

A

Homozygous Typical
Heterozygous Atypical
Homozygous Atypical

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78
Q

Butyrylcholinesterase: Homozygous Typical

Dibucaine Number

Response to SCh

A

D#: 70- 80

R: Normal

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79
Q

Butyrylcholinesterase: Heterozygous Atypical

Dibucaine Number

Response to SCh

A

D#: 50-60

R: lengthened 50-100%

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80
Q

Butyrylcholinesterase: Homozygous Atypical

Dibucaine Number

Response to SCh

A

D#: 20- 30

R: Prolonged to 4-8 hrs

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81
Q

It is an agonist at the nicotinic receptor of the NMJ and binds with a high affinity, preventing membrane repolarization and thus subsequent action potentials.

A

Succinylcholine Block

(Phase I Block)

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82
Q

With continued dosing of a depolarizing NMBA, a type I block can develop into a:

A

Type II block / nondepolarizing

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83
Q

Cardiovascular Side Effects of SCh

A

Sinus Bradycardia
Junctional Rhythm
Premature ventricular escapes
ASYSTOLE

** treat with atropine

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84
Q

Cardiovascular Side Effects of SCh are more common with

A

redosing and in children ;

** a second dose given within 5 minutes of the first

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85
Q

Cardiovascular side effects reflect the actions of succinylcholine at cardiac ______________ receptors where the drug mimics the physiologic effects of acetylcholine.

A

muscarinic cholinergic

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86
Q

can occur to 80-90 % of patients if not pretreated with nondepolarizer or NSAID before giving SCh.

A

Faciculations

  • Disorganized muscle contractions
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87
Q

In patients given SCh, what is very common 1-2 days postoperatively and can occur in 50-60% of the patients, probably due to fasciculations.

A

Myalgias

** usually big skeletal muscles

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88
Q

SCh administration associated with elevation in the plasma level of potassium of ______mEq/L in healthy patients

A

0.5

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89
Q

Severe hyperkalemia after SCh administration in patients with (4):

A
  • Burns
  • Severe abdominal Infections
  • Severe metabolic acidosis
  • Conditions associated with UPREGULATION of extrajunctional AChR.
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90
Q

Conditions associated with UPREGULATION of extrajunctional AChR.

A

Guillian-Barre syndrome
Hemiplegia
Muscular dystrophies
Burns
Paraplegia

“Guillian & Hemi Must Buy Pasta”

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91
Q

Because of the risk of massive ________, _________ , and ________ in children with undiagnosed muscle disease, succinylcholine is not recommended for use in children except for emergency tracheal intubation

A

rhabdomyolysis ; hyperkalemia;
death

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92
Q

Patients can develop myoglobinuria from muscle damage after ___________ administration.

A

SCh.

** most of the patients with rhabdomyolysis and myoglobinuria were subsequently found to have malignant hyperthermia or muscular dystrophy.

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93
Q

increase in tone of the masseter muscle may be an early indicator of ___________ (especially in children)

A

malignant hyperthermia

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94
Q

It is suggested that the high incidence of masseter spasm in children given succinylcholine may be due to _________ succinylcholine dosage

A

inadequate;

** probably not enough to cause muscle relaxation

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95
Q

Succynylcholine can ________ intragastic pressure and lower esophageal tone (LES).

A

Increase

**maybe dpends on the intensity of fasciculations, pre-dose of NDMR.

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96
Q

Succynylcholine can ________ intraocular pressure.
Peak time:
And return time:

A

Increase

** Peaks at 2-4 min after administration and returns to normal by 6 min

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97
Q

The use of succinylcholine is not widely accepted in open eye injury meaning:

A

when the anterior chamber is open.

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98
Q

SCh can causes __________ in intracranial pressure.

A

Increase

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99
Q

SCh side effects: (12)

A

Sinus Bradycardia
Junctional arrest
Premature ventricular escapes
ASYSTOLE

Fasciculations
Myalgias
Hyperkalemia
Myoglobinuria
Masseter spasm
Increase intragastric pressure and lower esophageal tone (LES).
increased intraocular pressure.
Increased intracranial pressure.

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100
Q

Defasciculating Doses used to be called

A

Curare Dart

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101
Q

A defasciculating dose of ___________ muscle relaxant administered prior succinylcholine decrease its side effects (Including fasciculations and postoperative myalgias).

A

non-depolarizing

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102
Q

Order of meds in a rapid sequence when giving Defasciculating dose:

A
  1. defasciculating dose.
  2. sedation (ex. propofol)
  3. Succynylcholine
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103
Q

__________ after a defasciculating dose

A

Premature muscle weakness

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104
Q

_____________ acts to block ACh receptor sites in an overwhelming, competitive manner.

A

Non-depolarizing

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105
Q

Two classes of ND-NMBA

A
  • aminosteroids
  • Benzylisoquinolinium
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106
Q

Aminosteroids NMDRs

A

Pancuronium
Pipercuronium
Vecuronium
Rocuronium

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107
Q

Benzylisoquinoliium NMDRs

A

Mivacurium
Atracurium
Cisatracurium

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108
Q

Competitively antagonize the presynaptic receptors to decrease release of Ach (fade on TO4)

A

Nondepolarizing Muscle Relaxants

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109
Q

Nondepolarizing Muscle Relaxants compete with ACh for binding on __________ of the alpha subunits of the nAChRs.

A

one or both

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110
Q

NDMR are classified according to:

A

How fast they act:
- long, intermediate, short.

&

Their durationt:
- depending on metabolism, redistribution, elimination and dose given .

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111
Q

Nondepolarizing Muscle Relaxants are almost always given ________

A

Intravenously.

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112
Q

Rocuronium (_________)

A

Zemuron

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113
Q

Rocuronium (Zemuron) ___________ action

A

intermediate

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114
Q

Rocuronium (Zemuron) has RARE histamine release (T/F)?

A

True :)

*could still cause it but RARE!

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115
Q

Rocuronium (Zemuron) has _______ effect of BP and HR

A

NO effect.

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116
Q

can be used to defasciculate with SCh,

A

Rocuronium (Zemuron)

117
Q

Rocuronium (Zemuron) has low potency which means the ________ plasma concentration achieved after a bolus ________ quickly.

A

high ; decreases

118
Q

Rocuronium (Zemuron) has real metabolites (T/F)?

A

False :(…. no real metabolites.

119
Q

Rocuronium has a ______ onset making it good for RSI sequence (can even replace SCh) if dose is doubled.

A

Rapid

*** (Variable onset) prolonged duration at this dose.

120
Q

In laparoscopic procedures, the duration of neuromuscular block produced by rocuronium is increased by approximately ________.

A

25%

** prolongs duration.- attributed to the effects of pneumoperitoneum on hepatic perfusion and blood flow.

121
Q

The most common thing to cause anaphylaxis is said to be NMBAs specially…

A

Rocuronium

122
Q

Rocuronium (Zemuron) Intubating dose:

and duration:

A

0.6 mg/kg

** ~ 30 mins or up to 70 min (after RSI dose)

123
Q

Rocuronium (Zemuron)
RSI dose

Duration:

A

1.2 mg/kg

**up to 70 minutes after RSI dose

124
Q

Rocuronium (Zemuron) comes in a _____ mg vial.

Does it need reconstituing?

A

50

No.

125
Q

Rocuronium (Zemuron) dose for defasciculating dose with SCh.

A

5 mg

126
Q

Rocuronium maintenance/repeat dose :

A

0.1 mg/kg as needed

127
Q

Rocuronium onset:

A

1-2 min depending on dose

128
Q

Rocuronium is ______% eliminated by the liver and _____% by the kidneys.

A

70% and 30%

129
Q

Vecuronium (Norcuron) isn an ________ NMB although it last a little longer than Rocuronium.

A

Intermediate

130
Q

__________ this NMBA would be good to give to an asthmatic patient because it does NOT cause histamine release.

A

Vecuronium (Norcuron)

131
Q

Which NMBA is a very cardiac stable?

A

Vecuronium (Norcuron)

132
Q

Vecuronium (__________)

A

Norcuron

133
Q

Vecuronium (Norcuron) might _________ with Thiopental.

A

precipitate

134
Q

Vecuronium (Norcuron) is ___________ potency.

A

Medium

135
Q

Vecuronium (Norcuron)
intubation/induction dose:

A

0.1 mg/kg

136
Q

Vecuronium (Norcuron)
vial:

Does it need reconstituing?

A

10mg vial

Yes, needs reconstituting into 10mL syringe for 1mg/cc

137
Q

Vecuronium: Pretreatment/priming with ______ of intubation dose given 3-5 min before intubation dose

A

10%

138
Q

Vecuronium - Maintenance dose for surgical relaxation:

A

0.01 mg/kg

139
Q

Vecuronium Onset

Intubating conditions:

Maximal blockade:

A

2-3 minutes - good intubating conditions.

3-5 minutes - maximal blockade

140
Q

T/F: Vecuronoium last longer than Rocuronium?

A

True :)

141
Q

Vecuronium duration for 25% recovery and 95% recovery?

A

25-40 min (25% recovery);

45-60 min(95% recovery).

142
Q

Vecuronium metabolite:

A

3-desacetyl:

** 60% potency of vecuronium

143
Q

Pancuronium (_________)

A

Pavulon

144
Q

Pancuronium (Pavulon) is a _________ acting.

A

Long

145
Q

T/F: Pancuronium (Pavulon) has histamine release.

A

False…. no histamine release

146
Q

Pancuronium (Pavulon) has vagolytic effects causing modest ________ due to antimuscarinic stimulation.

A

tachycardia

** do not give to patient who can’t tolerate changes in HR.

147
Q

Pancuronium (Pavulon) has direct sympathomimetic effects = _________ release and reduced uptake of __________ by adrenergic nerves

A

Norepinephrine ; norepinephrine.

148
Q

With Pancuronium be careful to give to any patient that will not tolerate an increase in ________ and ___________.

A

HR and cardiac output

149
Q

Pancuronium is used in _______________ to counteract the bradycardia associated with high-dose opioid dosing.

A

Cardiac surgery

150
Q

Pancuronium has the potential for significant
_________ ________ blockade, because it last a long time.

A

postoperative residual

151
Q

Pancuronium initial dose and maintenance:

A

0.1 mg/kg - initial

0.02mg/kg - maintenance

152
Q

Pancuronium onset and duration:

A

2-5 minutes.

60 - 100 minutes.

153
Q

Pancuronium hepatic metabolism of ________ % and renal ________%.

A

20%

40-70%

154
Q

Inhalational agents can help speed NMBAs because they cause:

A

muscle relaxation

155
Q

Metabolite (3-OH pancuronium): ______ potency of Pancuronium

A

50%

156
Q

__________ of a drug is determined by the dose required to produce a certain effect. For NMBAs, the effect (response) is depression of normal __________.

A

Potency ; Muscle contraction.

157
Q

relationship between twitch depression and dose

A

potency

158
Q

median dose that corresponds to 50% twitch reduction

A

ED50

159
Q

corresponds to 95% block (useful relaxation when twitch abolished).

A

ED95

160
Q

Hofmann elimination is ________, ___________, __________ chemical breakdown at physiologic temperature and pH.

A

spontaneous,

non-enzymatic,

non-organ dependent.

161
Q

In hofmann elimination
when temperature increases and pH increases……. metabolism ___________.

A

increases.

162
Q

in hofmann elimination
when temperature decreases and pH decreases……. metabolism

A

decreases.

163
Q

Mivacurium (_________)

A

Mivacron

164
Q

Mivacurium (Mivacron) will cause ______________ when given quickly. Pt. may develop bronchospasm.

A

Histamine release

165
Q

Spontaneous recovery from the Mivacurium (Mivacron) block is rapid (T/F)

A

True

**Hofmann elimination

166
Q

Mivacurium (Mivacron) metabolism

A

Hydrolysis by plasma cholinesterase.

167
Q

Mivacurium (Mivacron) intubating dose and infusion?

A

0.2 mg/kg (intubation)

5-8 mcg/kg/min infusion

** “if stupid enough to use as infusion haha.”

168
Q

Mivacurium (Mivacron)
onset and duration:

A

onset: 1 minute

duration: 10-20 minutes

169
Q

Atracurium metabolism is by the same enzymes that degrades ________ and_________.

A

esmolol ; remifentanil.

170
Q

Atracurium (_______)

A

Tracrium

171
Q

Atracurium is ___________ acting?

A

Intermediate acting

172
Q

Atracurium metabolized Hofmann Elimination ______% and ester hydrolysis _______%.

A

30%;

60%

173
Q

Atracurium releases _______ histamine with potential for skin flushing, tachycardia and hypotension

A

SOME

174
Q

Atracurium (Tracrium) dose:

A

0.5 mg/kg

175
Q

Atracurium (Tracrium) onset and duration:

& 95% recovery in:

A

2-3 minutes - onset

20-35 minutes duration.

95% recovery in 60-70 min

176
Q

Atracurium (Tracrium)’s primary metabolite is _________, which can produce rare _______activity.

A

Laudanosine;

Seizure

177
Q

Atracurium (Tracrium) is a _____________ amine which means it can cross BBB and act as a __________.

A

Tertiary;
CNS stimulant.

178
Q

Cisatracurium (_________)

A

Nimbex

179
Q

Cisatracurium is _______ acting , a little longer than Atracurium.

A

intermediate

180
Q

Cisatracurium (Nimbex) is metabolized 30% __________,
and 60%___________.

A

Hofmann elimination;

Ester hydrolysis.

181
Q

Cisatracurium (Nimbex) has ______ histamine release and no changes in ______.

A

NO;

BP & HR

182
Q

Cisatracurium: Potent cis-cis isomer of __________.

A

Atracurium

183
Q

Cisatracurium (Nimbex) dose:

A

0.15-0.2 mg/kg IV

184
Q

Cisatracurium (Nimbex) onset and peak :

A

2-5 min onset; (for intubation)

4-7 min peak

185
Q

Cisatracurium (Nimbex) duration:

A

40-70 min;

20-35 min to begin recovery: up to 93 min for 90% return

186
Q

How to enhance NMBA effects: “SAN -LIAM- HAHA”

A

Streptomycin
Aminoglycoside
Neomycin

Local anesthetics.
Inhalational agents.
Antibiotics.
Magensium

Hypercarbia
Acidosis
Hypothermia
Anticonvulsants (acute administration).

187
Q

Local anesthetics potentiate both ________and _______ by potentiating pre- and postsynaptic effects.

A

NMDA and Depolarizers

188
Q

inhalational agents have a direct effect on __________ receptors.

A

postjunctional

189
Q

Antibiotics that depress the NMJ

A

streptomycin
neomycin
aminoglycosides

190
Q

magnesium is a muscle ________

A

relaxant.

191
Q

Hypothermia prolongs the duration of NMBAs by decreasing receptor _______ and _______ mobilization.

A

sensitivity ; ACh

192
Q

Hypothermia decreases the force of muscle _______. Reduces _______&_______ metabolism. and reduces ___________ elimination.

*altered responses to NMBA

A

contraction;

renal & hepatic

Hofmann

193
Q

Aging results in ________ total body water and serum albumin concentration, reducing the ___________ of NMBAs.

A

Decreased ; volume of distribution

** needing less as opposed to children who large VD and need more.

194
Q

In aging: The decreased ______ function, _______, and __________ decrease the rate of NMBA elimination.

A

CV ;

renal filtration,;

liver blood flow.

195
Q

Hypokalemia: ________ NMBA and can decrease the effectiveness of anticholinesterases (__________) on reversal (antagonizing nondpolarizing block).

A

potentiates;

Neostygmine

196
Q

Hypermagnesemia: prolongs duration of action of NMBA by inhibiting _____ channels

A

calcium

197
Q

Acidosis: interferes with effects of ____________ in reversing
nondepolarizing block.

A

anticholinesterases

198
Q

Hypercarbia: leads to acidosis and interferes with NMBA ______.

A

antagonism

199
Q

All drugs with significant hepatic and renal metabolism (___________) will be affected and their duration of action is prolonged by liver and kidney dysfunction.

A

Aminosteroids

200
Q

_________________- class NMBAs are preferred in patients with organ dysfunction.

A

Benzyllisoquinolinium

*Ex. Atracurium; Cisatracurium

201
Q

Patients with __________ have altered responses to NMBAs; they are already relaxed!! Give less!!

A

Myasthenia Gravis

202
Q

Do not give ___________ to burn patients after the first 24- 40 hours.

A

Succinylcholine

**risk of hyperkalemia leading to cardiac arrest

203
Q

___________ is the enzyme responsible for rapid hydrolysis of released ACh

A

Acetylcholinesterase (AChASe)

204
Q

________% of released ACh is hydrolyzed during its diffusion across the synaptic cleft before reaching the nicotinic receptor.

A

50%

205
Q

AChASe can catalyze ACh at __________ molecules per active site per second

A

4,000

206
Q

Anticholinesterase/Acetylcholinesterase Inhibitors (3):

A

Neostigmine
Edrophonium
Pyridostigmine

207
Q

Selective Relaxant Binding Agent

A

Sugammadex

208
Q

How can NMBAs be reversed? (5)

A

-Diffuse away
-Reversed with an anticholinesterase.
-Excreted
-Encapsulated
-Metabolized

209
Q

Acetylcholinesterase Inhibiting Agents (___________)

A

Anticholinesterase

210
Q

Anticholinesterase Block the breakdown of ACh by __________ whichCauses an increase in ACh at the ___________.

A

Acetylcholinesterase ;

Synaptic cleft

211
Q

Anticholinesterase increase the amount of ________ to compete with NMBA remaining in the _______, causing normal muscle contraction.

A

ACh ;

NMJ

212
Q

Possible side effects of Anticholinesterases: (4)

A
  • Significant parasympathetic effects.
  • Bronchoconstriction
  • Increased salivation
  • Increased bowel motility (will make you poop :) )
213
Q

Significant parasympathetic effects caused by Anticholinesterase are due to stimulation of muscarinic Ach receptors in the _______, ________, ________.

A

heart, lungs, and GI tract.

214
Q

Anticholinesterases are usually given in combination with an ______________.

A

Anticholinergic (Antimuscarinic)

(Ex. glycopyrrolate).

215
Q

Anticholinesterases have a ceiling effect meaning there is maximal inhibition - when _____% of acetylcholinesterase has been inhibited.

A

100

216
Q

Ceiling effect

At maximal inhibition, additional doses of of Anticholinesterases (ex. Neostigmine) will NOT improve recovery and can actually lead to ________________.

A

paradoxical muscle weakness.

**Resultant weakness may be due to desensitization of Ach receptors leading to transmission failure and depolarization block

***occurs with high doses of Neostigmine

217
Q

Neostigmine (_______)

A

Prostigmin

218
Q

Neostigmine inhibits hydrolysis of ACh by AChAsE and blocks AChAse at all cholinergic synapses causing parasympathetic effects such as (3):

A

*Bradycardia
*increased salivation

GI effects

219
Q

Used with _____________ (anticholinergic/antimuscarinic) to decrease muscarinic side effects of Neostigmine

A

glycopyrrolate

220
Q

Neostigmine is a ____________ compound therefore does not penetrate the blood-brain barrier (BBB) very well.

A

Quaternary ammonium

221
Q

Neostigmine has a _________effect and a big dose can cause post - op __________.

A

ceiling;

PONV

222
Q

When to reverse with Neostigmine?

A

Used in deep blocks.

** most effective in moderate blocks but SLOW acting!

223
Q

Neostigmine shouldn’t be given until _________ recovery is evident (TOF).

A

spontaneous (at least one twitch).

224
Q

Neostigmine is more effective with moderate blocks but rapid acting (T/F)

A

False: SLOWWWW acting.

225
Q

Current recommendations for Neostigmine include waiting until 4 tactile TOF counts are visible at the __________ before administering.

A

adductor pollicis

226
Q

T/F: you always have to give a full dose of neostigmine for it to work.

A

False;

ex. pt. who received dose of Roc 4 hours ago does not need a full dose of neostigmine because it is not all there. maybe give half?

227
Q

Neostigmine dose and max dose:

A

0.04-0.08 mg/kg

(max 5mg)

228
Q

For every 1 mg of Neostigmine mix with _______ mg Glycopyrolate.

A

0.2mg/ 1 cc

**sometimes less….. Give glyco first or mixed.

229
Q

Neostigmine onset:

A

starting at 15 minutes (dependent on twitches).

*no twitches takes longeerr.

230
Q

Neostigmine duration:

A

1-2 hours.

231
Q

Neostigmine metabolism and excretion

A

Hepatic and renal excretion.

232
Q

Edrophonium (_________)

A

Enlon

233
Q

Edrophonium is used with ________ (crosses the BBB) due to rapid onset.

A

atropine

***is faster than glyco

234
Q

what is Enlon- Plus?

A

a mixture of Edrophonium and atropine together in the same vial.

235
Q

Edrophonium (Enlon) is mostly INEFFECTIVE when given for DEEP blocks (T/F)

A

TRUE :)

*You are doing great Mik!! haha

236
Q

Edrophonium (Enlon) has a ______onset of _______, and a ________ duration.

A

Rapid; 1-2 mins

Short

237
Q

Edrophonium (Enlon) is a ___________. which crosses or does not cross BBB?

A

Quartenary ammonium ; does NOT cross BBB.

238
Q

Edrophonium (Enlon) dose with atropine dose:

A

0.5-1 mg/kg mixed with atropine 7-10 mcg/kg (0.014 mg/mg of edrophonium)

239
Q

Enlon-plus dose:

A

0.05 - 0.1mg/kg slowly over a minute

240
Q

Sugammadex (__________)

A

Bridion

241
Q

Sugammadex is a __________ that has been developed as an selective relaxant binding agent (SRBA).

A

gamma (y) - cyclodextrin.

242
Q

Sugammadex is an eight sugars arranged in a ring specifically designed to:

A

ENCAPSULATE.

** it does NOT breakdown***

243
Q

Sugammadex is highly water soluble with a hydrophobic cavity large enough to encapsulate _________________ drugs, especially ___________.

A

steroidal intermediate-acting neuromuscular blocking.

**rocuronium > vecuronium

244
Q

This reversal has no real undesirable effects like anticholinesterases.

A

Sugammadex

245
Q

Sugammadex is __________ of depth of neuromuscular blockade.

A

Independent

246
Q

Sugammadex has no effect on ___________ or __________ receptors.

A

Acetylcholinesterase or cholinergic receptors.

247
Q

Sugammadex when injected (over 10 seconds) it immediately captures free molecules of _______ or __________.

A

rocuronium or vecuronium.

248
Q

Sugammadex removes the relaxant from the ______ and moves it into the plasma

A

NMJ

249
Q

The sugammadex-drug complex is filtered out by the:

A

Glomerulus

**not affected by liver disease

250
Q

Sugammadex is eliminated unchanged by the kidneys which is why you should avoid in pt’s with decreased _____________.

A

Createnine clearance.

**can still be used.

251
Q

Sugammadex is not recommended for patients with:

A

End-stage renal disease.

252
Q

Sugammadex vials are available in ______ or _______ .

A

2 mL or 5 mL vials (100mg/ml).

253
Q

Sugammadex elimination:

A

24hr clearance unchaged via kidneys.

254
Q

Dose of sugammadex for routine reversal of moderate block (T2 appearance or 3,4, twitches):

&

Mean recovery time to TOF 0.9:

A

2mg/kg

&

2 minutes

255
Q

Dose of sugammadex for routine reversal of deep neuromuscular block (PTC 1-2):

&

Mean recovery time to TOF 0.9:

A

4mg/kg

&

3 minutes

256
Q

Dose of sugammadex for IMMEDIATE reversal after 1.2mg/kg rocuronium:

&

Mean recovery time to TOF 0.9:

A

16mg/kg

&

1.5 minutes

257
Q

sugammadex has no interaction with succinylcholine or benzylisoquinolines; it only cares about:

A

aminosteroids NMBAs.

258
Q

High does of Sugammadex (16 mg/kg) can possibly cause:

A
  • Bradycardia ( or cardiac arrest).
  • headache
  • hypotension
  • N/V
  • Anaphylaxis
  • Hypersensitivity (pruritus and uticaria).
259
Q

Sugammadex may affect hormonal contraceptives ( for ______ Days) and some antibiotics.

A

7

** tell patient and bracelet is placed on patient to help them remember.

260
Q

Use the lowest dose possible of sugammadex : (requires 4 mg to encapsulate _______mg of rocuronium… usually _____ mg is adequate).

A

1mg;

200 mg.

261
Q

T/F : with Sugammadex most IV infusion solutions are compatible.

A

True :) - (LR,D5,NS) okay!

262
Q

Sugammadex is physically incompatible with what 3 meds?

A
  • Verapamil
  • Ondasetron (Zofran)**
  • Ranitidine (Zantac)
263
Q

Recommended wait time of _______ hours for readmission of Roc/Vec after reversal.

A

24

264
Q

It is recommended to use a ________ or __________ for NMBA redose after reversal with sugammadex.

A

Benzylisoquinolinium ( Nonsteroidal ) or Succinylcholine.

265
Q

If there is nothing else available and you have to redose (< 24 hours ) after giving sugammadex. How much Roc or Vec can you give after:

5-minutes:

4-hours:

A

5 minutes:
1.2mg/kg rocuronium.

4 hours:
0.6 mg/kg rocuronium or
0.1 mg/kg vecuronium.

266
Q

High dose Sugammadex is …..

A

16 mg/kg

267
Q

High dose Sugammadex (16 mg/kg) is associated with increases in ______,______, and _______.

A

aPTT, PT, INR

268
Q

Becareful giving high dose of Sugammadex in patients with (3):

A
  • Coagulopathies
  • treated with therapeutic anticoagulation.
  • Receiving thromboprophylaxis other than heparin and LMWH.
269
Q

High dose Sugammadex can also cause ___________ & __________.

A

Hypersensitivity:
Sneezing, nausea, rash and urticaria

Anaphylaxis.

270
Q

Anaphylaxis with sugammadex is seen more often in higher dosing within ______ minutes of administration. It involves ________,_________, and ___________.

A

5- minutes;

Airway edema, bronchospasm and CV collapse.

271
Q

Treatment for anaphylaxis w/ sugammadex includes small boluses of ______ (10-20 mcg) titrated to response,________, ________ and _________.

A

epinephrine (10-20mcg)

Benadryl

Dexamethasone

Famotidine

272
Q

Physostigmine is a _____________. The ONLY anticholinesterase to do what?

A

tertiary amine;

cross the blood brain barrier.

273
Q

Not used for reversal of muscle relaxants but used to treat anticholinergic toxicity.

A

Physostigmine

274
Q

flushing, dry skin and mucous membranes, mydriasis with loss of accommodation, altered mental status, fever and urinary retention are signs of:

A

anticholinergic toxicity

  • Hot as a hare
  • Dry as a bone
  • Blind as a bat
  • Red as a beat
  • Mad as a hatter
275
Q

Since Physostigmine crosses the BBB it can cause

A

Agitation
Restlessness
Disoriented
Shivers

276
Q

Types of anticholinergics (5):

A

Atropine
Cyclic antidepressants
Antihistamines
Scopolamine
Antipsychotic

277
Q

Excessive use/overdose of cholinesterase inhibitors or organic pesticides.

A

Cholinergic Crisis/Syndrome

278
Q

In Cholinergic Crisis/Syndrome there is excessive _______ peripherally and centrally

A

ACh response

279
Q

S/S: miosis, salivation, bronchoconstriction, bradycardia, abdominal cramping, weakness, lacrimation. CNS: dysphoria, confusion, seizures, coma

A

Cholinergic Crisis/Syndrome

280
Q

Treatment of Cholinergic Crisis/Syndrome

Doses

Atropine:

Pralidoxime:

A

Atropine 35-70 mcg/kg

Pralidoxime 15 mcg/kg every 20 min

  • also Benzos
281
Q

Cholinergic Crisis

Muscarinic Symptoms:

Nicotinic SymptomS:

A

Salivation
Lacrimation
Urination
Defecation
GI cramping
Emesis

Muscle cramps
Tachycardia (Bradycardia in Muscarinic)
Weakness
Twitching
Fasciculations

282
Q

decrease in Ach activity due to auto-reactive antibodies that attack the nicotinic Ach receptors on postsynaptic membranes

A

Myasthenic Crisis

283
Q

How do your differentiate Cholinergic vs Myasthenic Crisis?

A

Give edrophonium - muscle strength will improve if myasthenia gravis.

** if it gets worse it could be cholinergic crisis

284
Q

Cholinergic Crisis S/S (6)

A

Increased cholinergic activity
Increased secretions
Bradycardia
Pupils constricted
Weak or fasiculating muscles
Tensilon test exaggerates symptoms..makes it worse ( edrophonium)

285
Q

Myasthenic Crisis (6) s/s

A

Decreased receptors
Normal secretions
Tachycardia
Pupil normal or dilated
Muscles are weak
Tensilon test relieves symptoms (edrophonium injection)

286
Q

Clinical signs of muscle weakness

A

Blurry vision,
Double vision
Facial weakness,
Facial numbness,
and general weakness

287
Q

Most common signs of Muscle Weakness in the PACU:

A
  • Generalized weakness
  • Patient reported difficulty completing 5-second eye opening
  • Difficulty visually tracking or speaking.

***Indicative of ocular and pharyngeal muscle sensitivity

288
Q

Complications of residual neuromuscular blockade

A
  • Pharyngeal dysfunction
  • Increased risk of aspiration and pneumonia.
  • Need for tracheal reintubation
  • Impaired oxygenation and ventilation (may be blamed on Opioids).
  • Delayed discharge from the PACU
  • Impaired pulmonary function
289
Q

Clinical Signs of Neuromuscular Recovery

A

Tidal volume
Negative inspiratory force
Grip strength
5-second head lift (not a sensitive test for residual block)
Ability to protrude the tongue

**these are unreliable signs of return of muscle strength

General Principles (4 decks)

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