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Pharmacology I > Neuromuscular Blockers > Flashcards

Neuromuscular Blockers Flashcards

1
Q

___________ is a primary neurotransmitter.

A

Acetylcholine (ACh)

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2
Q

Alpha Sub-Units

A
  • “Ligancated (ACh) Ion (Na) Channels”.

- ACh

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3
Q

___ moves in muscle tissue to activate movement.

A

Na

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4
Q

Acetylcholine Structure

A

1 N+ binds to alpha sub-unit

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5
Q

Acetylcholine

A
  • Primary neurotransmitter of parasympathetic system (“Rest and Digest”)
  • Choline acetyltransferase
    ==Ca mediated action potential
  • Deactivated by acetylcholinesterase
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6
Q

What effects do Neuromuscular Blockers have?

A
  • Paralysis ONLY

- No pain relief or sedation

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7
Q

Depolarizing vs Non-depolarizing

A

D: depolarize muscle fiber leaving it constantly stimulated and unable to be affected by ACh.

ND: Competitively block ACh from binding to receptors post-synaptically.

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8
Q

ED95

A
  • Dose necessary to produce 95% suppression of SINGLE twitch response.
  • Greatly < with IA.
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9
Q

Tracheal Intubation Dose is …

A

2x ED95 dose

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10
Q

Order of NMB Effect

A
  • Effected 1st: Small muscles to Large muscles.

- Recovery: Large muscles (>BF) to Small muscles.

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11
Q

Size of Muscle (Sm-Lg) : ____ __ ____

Recovery (< effect) : __ ___

A

: Order of effect

: > BF (Lg muscles - Sm muscles)

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12
Q

NDMB structure is either _______________ or ______________.

(PP slides are different than what was said in lecture)

Difference between Benzyl and Aminosteroid?

A

BENZYLisoquinolinium (>histamine release)or

Aminosteroid

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13
Q

ACh does not just bind to Skeletal Muscle at Nicotinic Receptor, but also…

A

(Not specific)

  • Cardiac muscarinic receptors
  • Autonomic ganglia nicotinic receptors
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14
Q

Do IA interact (PD interaction) with NMB?

A

No.

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15
Q

Succ is ____________.

A

Depolarizing (the only one)

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16
Q

Rocc is __________.

A

Non-Depolarizing (and all others)

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17
Q

“- onium” = ______________

“- curium” = ______________

A

Aminosteroid

BENZYLisoquinolinium

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18
Q

3 long acting NMB

A
  • Pancuronium
  • Doxacurium
  • Pipecuronium
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19
Q

4 intermediate acting NMB

A
  • Atracurium
  • Vecuronium
  • Rocuronium
  • Cisatracurium
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20
Q

1 short acting NMB

A

Mivacurium

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21
Q

Succinylcholine

Onset and Duration

A
  • “looks and smells like ACh”
  • Most rapid onset NMB
  • Onset: 30-60 sec
  • Duration: 3-5 mins
  • The only depolarizing NMB
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22
Q

Succ (Structure)

A

N+ ——-N+ (“one molecule combined to both alpha sub-units”)

  • “Both alpha units must be bound up to cause depolarization”
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23
Q

Succ (Mechanism of Action)

A
  • Slower hydrolysis (“Esterases in the blood can’t recognize the Succ molecule to break down = > duration of action than ACh”)
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24
Q

Succ has _____ presynaptic effects that are “_______ _____”.

Succ has ______ postsynaptic effects.

A

Minor, feedback loops

Important

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25
Q

Hyperdepolarization of Succ causes …

A
  • Leakage of K out of cell (> K by 0.5)

- A lot of Na goes in so K goes out.

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26
Q

Phase I Blockade

A
  • Depolarizing block (Succ)

- Fasciculations at onset (pt is still paralyzed)

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27
Q

Phase II Blockade

A
  • Desensitization: similar to non-depolarizers

- tachyphylaxis

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28
Q

Succ has one or both phases of blockades?

A

Both

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29
Q

DOSE SLIDE 20

A

“Do not memorize”

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30
Q

Plasma Cholinesterase is > or < in obese patients?

A

>

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31
Q

Plasma Cholinesterase is > or < with > estrogen levels?

A

<

meaning > estrogen —> < Plasma Cholinesterase —> > Duration of Succ

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32
Q

Raglan __________ Plasma Cholinesterase.

A

Inhibits

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33
Q

Plasma Cholinesterase

A

Breaks down (hydrolyzes) Succ

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34
Q

Neostigmine ____________ Plasma Cholinesterase

A

Inhibits

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35
Q

Some ppl have atypical cholinesterase which …

A

> duration of Succ to 1-3 hours rather than 5-9 mins.

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36
Q

How to reduce some of the side effects of Succ?

A
  • Prior to giving Succ, give a baby dose of a non-depolarizer
  • Can help reduce all side effects except Hyperkalemia.
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37
Q

Succ (cardiac)

A
  • Sinus Bradycardia
  • Junctional rhythm
  • Sinus arrest

-Cardiac muscarinic receptors
- > risk with 2nd does within 5 mins.
“Rest and Digest”

(Can’t cause > HR and >BP in some ppl).

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38
Q

If pt’s HR < after giving Succ, give Atropine?

A

No, Atropine won’t help (atropine is a muscarinic receptor med).

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39
Q

Pt Hx that > risk for Hyperkalemia with Succ.(4)

A
  • Muscular dystrophy
  • 3rd degree burns
  • Upper motor neuron lesions
  • Muscle atrophy or severe trauma
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40
Q

Is Hyperkalemia an immediate effect?

A

No, up to 96 hours that can last up to 6 months or more.

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41
Q

Pt’s at highest risk of Succ induced hyperkalemia.

A

Male children with undiagnosed myopathy

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42
Q

> rates of Myalgias and where is it found in the body?

A
  • Muscle pain
    Young adults, minor surgical procedures, early ambulation > rates of muscle pain.
  • Found in Neck, Back, Abdomen
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43
Q

In children you could see ___________ from Succ.

A

Myoglobinuria

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44
Q

3 side effect areas caused by Succ.

A
  • Intragastric (> fasiculations —> > aspiration risk)
  • Intraocular (2-4 min post admin)
  • Intracranial (< risk) (article)

“Article-Succ associated with > mortality when used for RSI of severely injured pt’s in ER when compared with Roc).

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45
Q

Succ

A
  • Only depolarizer NMB
  • “Looks and smells like ACh”
  • Parasympathetic NS
  • Short duration of action
  • No reversal agent
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46
Q

ND NMB what receptors do they target?

A

-Compete (antagonism) with ACh for alpha subunits at nicotinic receptors (post junctional)

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47
Q

Sustained muscle contraction does not occur with _______________.

A

ND NMB

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48
Q

Characteristics of ND NMB

A
  • Posttetanic potentiation
  • Potentiation of other nondepolarizers
  • Antagonism by anticholinesterases
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49
Q

What NMB cause histamine release?

A

-Atracurium
-Mivacurium
(

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50
Q

Pancuronium > or < HR?

And other ND NMB?

A

>

- Cardiac muscarinic receptors are blocked, (blocked rest and digest).

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51
Q

ND NMB have a wide _______ __ ______.

A

Margin of safety.

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52
Q

What can long term paralysis for mech ventilation can cause? (>6 days)

A

Critical Myopathy with an unpredictable duration

  • “even if doses are given here and there”
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53
Q

There is > risk for critical myopathy in pts who take _________ and ________.

A

Corticosteroids (highest risk) and aminosteroids.

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54
Q

What groups have the least amount of risk than Succ?

A

Single quaternary ammonium groups

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55
Q

Females have _________ __________ of ___________ ____________.

A

Higher incidence of allergic reactions. (Soaps and cosmetics)

“Case Study not estrogen but soaps” ?

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56
Q

What 6 things enhance NMB

A
  • Volatile anesthetics
  • Aminoglycosides
  • Local anesthetics
  • Antiarrhythmics
  • Diuretics (Lido and quinidine)
  • Mg, Li
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57
Q

What can anticonvulsants and NMB can alter?

A

CYP enzymes

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58
Q

What can cyclosporine and NMB affect?

A

(Poor?) Lung Blockade

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59
Q

What can Corticosteroids and NMB cause?

A

Compound muscle weakness

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60
Q

What can sympathomimetics (epi) and NMB cause?

A

> Onset time due to changes in BF with a faster delivery.

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61
Q

What prolongs duration of NMB?

A

Hypothermia

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62
Q

How does < K effect NMB?

A
  • Resistance to Succ

- Increased sensitivity to ND NMB

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63
Q

How does > K effect NMB?

A

> Succ effects

< ND NMB effects (thermal injury)

64
Q

Is there gender sensitivities with NMB?

A

Yes, Women are more sensitive.

< skeletal muscle?

65
Q

Onset and Duration of Pancuronium

A

Onset: 3-5 min
Duration: 60-90 min

66
Q

ED95 for Pancuronium

A

ED95=70mcg/kg (IDW)

67
Q

Metabolite for Pancuronium

A
  • 3-desacetylpancuronium
  • Renal and hepatic problems > half life. (Aging reduces clearance)
  • 80% eliminated unchanged in urine.
  • Total biliary obstruction, hepatic cirrhosis
68
Q

What is Pancuronium is enhanced by?

A

Respiratory acidosis

69
Q

Does Pancuronium > or < HR, MAP, and CO?

A

>

Anti rest and Digest

70
Q

Mechanism of Pancuronium

A
  • Vagal blockade (CN X)
  • SNS activation
  • Muscarinic interference
71
Q

Can dysrhythmias occur with Pancuronium?

A

Yes, especially in combo with Digoxin.

72
Q

Onset and Duration of Doxacurium

A

Onset: 4-6 mins

Duration 60-90

73
Q

ED95 of Doxacurium

A

ED95 = 30 mcg/kg

74
Q

Do what when using Doxacurium and IA?

A

Reduce Doxacurium dose with IA

75
Q

Doxacurium cardiovascular changes

A

None

“Toxic metabolite that built up esp. with renal failure causing Histamine release”

76
Q

Pipecuronium onset and duration:

A

Onset: 3-5 mins
Duration: 60-90 mins

77
Q

ED95 of Pipecuronium

A

ED95 = 50-60 mcg/kg

78
Q

Pipecuronium

A

Bisquaternary aminosteroid

79
Q

Doxacurium

A

Benzylisoquinolinium, bisquaternary

80
Q

Pancuronium

A

Bisquaternary aminosteroid

81
Q

Cardiovascular issues with Pipecuronium

A

None

82
Q

Infants have __ ______ and __ ______ of effect with Pipecuronium.

A

> potency and < duration

83
Q

Pipecuronium‘s PK is similar to _____________.

No ________ issues

A

Pancuronium

Hepatic

84
Q

Intermediate ND NMB have _________ clearance.

A

Better

85
Q

All Intermediate ND NMB have similar _________.

A

Onset. (Except for Roc) (Roc is faster).

86
Q

Do intermediate ND NMB have a faster or slower recovery rate than long acting ND NMB?

A

Faster (1/3 duration of long acting also)

87
Q

Intermediate NDNMB cardiovascular side effects:

A

None

88
Q

Intermediate ND NMB are _________ reversed by __________________ drugs.

A

Reliably, anticholinesterase (reversal agents)

89
Q

Priming Principle

A
  • Give a small dose of Roc to bind spare receptors (no clinical effect). 4 mins later give the rest. This deepens the neuromuscular blockade rapidly.
  • “or give 4x ED95 of Roc x1 to < onset”.

Goal: to < rate of Roc onset.

90
Q

Atracurium

A

Bisquaternary benzylisoquinolinium

91
Q

Atracurium onset and duration:

A

Onset: 3-5 mins
Duration: 20-35 mins (1/2 hour or less than long acting NMB)

92
Q

Atracurium ED95

A

ED95 = 0.2 mg/kg

93
Q

Atracurium is 82% __________ _________.

A

Protein bound. (Albumin)

94
Q

What are the cumulative effects of Atracurium?

A
  • None
  • Rapid clearance
  • “Predictable offset, no lingering effects”.
95
Q

What is the secondary mechanism of action for both Atracurium and Cisatracurium for metabolism beyond the CYP enzymes?

A
  • Hoffman Elimination

- “So that pts are not sent to the PACU so paralyzed”.

96
Q

Hoffman elimination is ___________ by alkalosis and ___________ by acidosis.

A

Accelerated, slowed

97
Q

Hoffman elimination followed by ___________ followed by another Hoffman elimination.

A

hydrolysis

98
Q

What is Laudanosine?

A
  • Metabolite in Hoffman elimination, independent of renal and hepatic function
  • Safety net of elimination
99
Q

Laudanosine requires an __________ in MAC of IA.

A

Increase

100
Q

Laudanosine is a CNS _________ leading to __________ __________.

A

Stimulant, peripheral vasodilation.

101
Q

What are cardiovascular effects of Atracurium at 3x ED95?

A
  • > HR
  • < MAP
  • Transient
102
Q

Does histamine release with Atracurium?

A

Yes, Block both H1 and H2 receptors to get full effect

103
Q

Elderly vs Infants with Atracurium:

A

Elderly: No effect
Infant: 1/2 dose, > sensitive, > rapid clearance.

104
Q

Cisatracurium

A

Bisquaternary Benzylisoquinolinium

105
Q

Cisatracurium Onset and Duration:

A

Onset: 3-5 mins
Duration: 20-35 mins (> duration in obese pts).

106
Q

Cisatracurium ED95:

A

ED95 = 50 mcg/kg

107
Q

Is it OK to give Cisatracurium to pts with renal and hepatic dysfunction?

A

Yes

108
Q

Cisatracurium has a slight ________ of _________ for elderly pts.

A

Delay, onset

109
Q

How is Cisatracurium different from its “sister” Atracurium?

A

No histamine release

More safe

110
Q

Vecuronium

A

MONOquaternary aminosteroid

111
Q

Vecuronium Onset and Duration:

A

Onset: 3-5 mins
Duration: 20-35 mins

112
Q

Vecuronium ED95

A

ED95 = 50 mcg/kg

113
Q

Aminosteroids love ________.

A

Lipids

114
Q

Vecuronium has a _______ lipid solubility to enter ____________.

A

Higher, hepatocytes

115
Q

Vecuronium‘s lipid solubility allows _________ excretion.

______ metabolism and _________ clearance.

A

Billiary

Hepatic, renal

116
Q

___________ post inject of Vecuronium enhances effects

A

Hypercarbia

117
Q

Large cumulative effect of Vecuronium due to > _____________.

A

Volume of distribution. (Fatty tissues, potential for > duration of action)

118
Q

Does Vecuronium release histamine?

A

No (rarely)

No vagolytic effects

119
Q

Onset is ______ _______ for infants with Vecuronium.

A

More rapid

120
Q

With Vecuronium, duration is longest in __________ and shortest in __________.

A

Infants, children.

121
Q

With Vecuronium, the _________ have a longer recovery rate.

A

Elderly

122
Q

Rocuronium

A

MONOquaternary aminosteroid

123
Q

Rocuronium Onset and Duration:

A

Onset: 1-2 mins
Duration: 20-35 mins

124
Q

Rocuronium ED95

A

ED95 = 0.3 mg/kg

125
Q

Like Vec, Rocuronium is excreted unchanged in the _______.

A

Bile

126
Q

Rocuronium has slight ____________ effects.

A

Vagolytic

127
Q

Does Rocuronium release histamine?

A

No

128
Q

Mivacurium

A

Bisquaternary benzylisoquinolinium

129
Q

Mivacurium Onset and Duration

A

Onset: 2-3 mins
Duration: 12-20 mins

130
Q

Mivacurium ED95

A

ED95 = 80 mcg/kg

131
Q

Mivacurium is rapidly eliminated because it is _________ by _______ ___________.

A

Hydrolyzed by plasma cholinesterase

132
Q

Mivacurium has rapid spontaneous _________

A

Recovery

133
Q

Does Mivacurium release histamine?

A

Yes, transient histamine release

134
Q

Quaternary Ammonium is > _______ and > ______ ______.

A

Ionized and water soluble.

135
Q

What are Quaternary Ammonium CNS effects?

A

None

136
Q

What is volume distribution of Quaternary Ammonium similar to?

A

ECF volume

137
Q

Do Quaternary Ammonium drugs absorb orally?

A

No, all are injectable.

138
Q

Do Quaternary Ammonium drugs cross placenta?

A

No

139
Q

Quaternary Ammonium drugs bind to…

A

Alpha subunit post-synaptically

140
Q

NMB are not …

A

Highly protein bound (Albumin won’t effect med)

141
Q

Mivacurium > or < MAP?

A
141
Q

There is a risk for __________ with Mivacurium.

A

Bronchospasm

142
Q

What NMB is associated with Hoffman Elimination?

A
  • Atracurium

- Cisatracurium

143
Q

What re the NMBs that release histamine?

A
  • Atracurium
  • Mivacurium
    (NOT Cisatracurium eventhough it is a Bis Benzyl)
144
Q

NMB that are urine eliminated?

A
  • Pancuronium
  • Miv (minor)
  • Vecuronium (minor)
145
Q

NMB protein bound to…

A

Atracurium (Hoffman Elimination)

146
Q

What NMB is it ok to give with renal and hepatic dysfunction?

A

Cisatracurium

147
Q

Hepatic Eliminated NMB:

A
  • Vec
148
Q

What NMB is inactive at the NMJ?

A

Cisatracurium

Atracurium

149
Q

What NMB is > risk for Bronchospasm?

A

Miv

150
Q

4 Side Effects of Succ:

A
  • Arrhythmias
  • > K
  • Myalgias
  • > pressure (gastric, ocular, cranial)
151
Q

NMB that have no CV effects:

A

Pip

Dox

152
Q

NMB with slight Vagal effects:

A

Rocc

153
Q

What is TOF for ND NMB?

A

< 0.7.

154
Q

What is TOF with Succ?

A

> 0.7

Pharmacology I (6 decks)

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