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apex > Unit 5 Pharmacology: Neuromuscular Blockers > Flashcards

Unit 5 Pharmacology: Neuromuscular Blockers Flashcards

1
Q

Which subunits must be occupied to open the nicotinic receptor at the motor end plate?

A

Alpha and alpha

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2
Q

What are the 2 types of nicotinic acetylcholine receptors (nAChRs) at the neuromuscular junction?

A
  1. The presynaptic Nn receptor is present on the presynaptic nerve
  2. The postsynaptic Nm receptor is present at the motor end plate on the muscle cell
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3
Q

Describe the postsynaptic Nm receptor including type of channel and subunits.

A

Pentameric ligand-gated ion channel

5 subunits: 2 alpha, 1 beta, 1 delta, and 1 epsilon (a2B1D1E1 subtype)

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4
Q

When 2 Ach molecules simultaneously bind to the 2 alpha receptor on an Nm receptor, what happens?

A

The channel opens, Na+ and Ca+ enter the cell and K+ exits the cell

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5
Q

Why do anions such as chloride not pass through the nicotinic receptor?

A

They are repelled by the strong negative charges situated inside the channel

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6
Q

At rest, the side of the muscle cell is negative relative to the outside, when Nm is activated by Ach what happens?

A

Na+ flows down its concentration gradient and enters the cell, this makes the cell interior more positive, activates voltage-gated sodium channels, depolarizes the muscle cell, and initiates an action potential. Depolarization of the myocyte instructs the endoplasmic reticulum to release Ca+ into the cytoplasm, where it engages the myofilament and initiates muscle contraction.

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7
Q

How is Nm “switched-off”?

A

Acetylcholinesterase is positioned around the pre- and postsynaptic nicotinic receptors, it hydrolyzes Ace almost immediately after it activates these receptors

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8
Q

What are the 2 pathologic variants of the nicotinic receptor?

A

The alpha2, beta1, delta1, gamma1 has a gamma subunit in lieu of an epsilon.
The a7 subtype consists of 5 alpha subunits

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9
Q

What is the term for these pathologic variants of the nicotinic receptor?

A

Extrajunctional Receptors

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10
Q

When are extrajunctional receptors present?

A

Early in fetal development
Denervation
Prolonged immobility

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11
Q

What is the significance of these extrajunctional receptors to Anes?

A

Their presence predisposes a patient to hyperkalemia following succinylcholine administration

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12
Q

What conditions represent contraindications to the use of succinylcholine due to their presence of extrajunctional receptors?

A 
Upper or lower motor neuron injury 
Spinal cord injury
Burns
Skeletal muscle trauma
CVA
Prolonged chemical denervation (Mg, long-term NMB infusion, clostridial toxin)
Tetanus 
Severe sepsis
Muscular dystrophy (muscle atrophy from any cause)
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13
Q

In the absence of extrajunctional receptors, how much can succinylcholine transients increase serum potassium? For how long?

A

0.5 - 1.0 mEq/L

For up to 10 - 15 minutes

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14
Q

How are extrajunctional receptors affected by succinylcholine?

A

They are more sensitive and remain open for a longer period of time

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15
Q

Does succinylcholine have a metabolite?

A

Choline

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16
Q

Does the metabolite of succinylcholine, -choline, cause depolarization?

A

Yes, to the a7 receptor

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17
Q

As a general rule, in the event of denervation injury, succinylcholine is best avoided for how long? Exception?

A

24 - 48 hours following the injury and for at least 1 year after.
Burns may be an exception, the risk of hyperkalmia may persist for several years after the burn (especially with contractures)

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18
Q

What is the treatment for succinylcholine induced hyperkalemia?

A

IV calcium chloride
Hyperventilation
Glucose + insulin

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19
Q

What happens with nondepolarizers in the presence of extrajunctional receptors?

A

Patients with upregulation of extrajunctional receptors are resistant to nondepolarizers - their potency is reduced

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20
Q

Fade during train-of-four stimulation is caused by:

A

Antagonism of presynaptic nicotinic receptors (Nn)

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21
Q

Why does succinylcholine not produce fade?

A

It agonizes the presynaptic nicotinic receptors (Nn)

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22
Q

Acetylcholine is synthesized from what 2 things, in the presence of what?

A

Choline and CoA

Choline acetylcholinesterase

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23
Q

After Ach is synthesized, where is it?

A

It is packaged in vesicles which are anchored by specialized proteins inside the presynaptic nerve terminal

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24
Q

What are the 2 supplies of Ach vesicles?

A
  1. Ach that is available for immediate release

2. Ach that must be mobilized before it can be made available for immediate release (like a stockpile)

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25
Q

What channel opens with an action potential arrives at a nerve terminal in order to release Ach vesicles? Process that occurs?

A

Voltage-gated calcium channels open and calcium enters the nerve terminal, increased intracellular calcium destabilizes the proteins that hold Ach vesicles. The vesicles ext the nerve via exocytosis and each vesicles releases 5,000 - 10,000 Ach molecules into the synaptic cleft. Ach diffuses toward the postsynaptic Nn receptor on the motor endplate, where it depolarizes the motor endplate and initiates skeletal muscle contraction.

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26
Q

When an action potential arrives at a nerve terminal to initiate Ach release not all of the Ach released diffuses toward the motor endplate, where does some of it go and why?

A

A fraction of the Ach molecules bind to prejunctional receptors on the nerve terminal (Nn receptor) and cause mobilization of Ach vesicles inside the presynaptic nerve. This moves part of the “stockpile” to the front line where it is available to immediate release next time the nerve is stimulated.

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27
Q

Nondepolarizers competitively antagonize the presynaptic Nn receptors, what implication does this have?

A

This impairs the mobilization process of Ach, so now only the vesicles that are available for immediate release are able to be used. Since this is a limited quantity, nerve stimulation can quickly exhaust this supply with each successive stimulation less Ach is released, manifesting as a fade with train-of-four, double burst, and tetanus

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28
Q

In contrast to ND-NMB, succinylcholine stimulates the prejuctional receptors, what effect does this have?

A

Succinylcholine has the same effect as Ach, when succinylcholine binds to the presynaptic Nn receptor, it facilitates the mobilization process, so there is always Ach available for immediate release, so no fade is present.

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29
Q

Presence or absence of a fade distinguishes between what 2 types of block?

A

Phase I and Phase II

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30
Q

What type of block does succinylcholine produce? ND-NMB?

A

Sux: Phase I block.
ND: Phase II

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31
Q

How can succinylcholine cause a phase II block?

A
  1. Dose > 7 - 10 mg/kg
  2. 30 - 60 minutes of continuous exposure (IV infusion)f

It likely inhibits the presynaptic nicotinic receptor, impairs Ach mobilization and release from the presynaptic nerve terminal, and/or creates a conformational change in the postsynaptic receptor.

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32
Q

When is post-titanic potential present? When is it not?

A

Present: Normally and with a phase II block

Not present: with a phase I block

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33
Q

What is the most sensitive indicator of recovery from neuromuscular blockade?

A

Inspiratory force better than -40 cm H2O

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34
Q

As a general rule, which group of muscles are paralyzed faster and recover sooner, more central muscles or peripheral muscles?

A

More central muscles are paralyzed faster and recover sooner

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35
Q

What is the best place to measure onset of blockade (intubation conditions)?

A 
Muscle = orbicularis oculi (closes eye) or corrugator supercilii (eyebrow twitch)
Nerve = facial nerve
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36
Q

Best place to measure recovery of blockade (return of upper airway muscle function)?

A 
Muscle = adductor pollicis (thumb adduction) or flexor hallucis (big toe flexion) 
Nerve = ulnar nerve or posterior tibial nerve
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37
Q

Relaying on flexion of what digit overestimates recovery?

A

The fifth finger

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38
Q

What TOF ratio does full recovery occur?

A

> 0.9 at the adductor pollicis

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39
Q

Residual neuromuscular blockade is defined as a TOF ratio of?

A

< 0.9

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40
Q

Recovery from NM blockade Tidal volume:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?

A

5 mL/kg or greater

80%

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41
Q

Recovery from NM blockade TOF:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?

A

No fade

70%

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42
Q

Recovery from NM blockade Vital Capacity:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?

A

20 mL/kg or greater

70%

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43
Q

Recovery from NM blockade Sustained Tetanus (50Hz):
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?

A

No fade

60%

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44
Q

Recovery from NM blockade Double burst stimulation:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?

A

No fade

60%

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45
Q

Recovery from NM blockade Inspiratory force:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?

A

Better than -40 cmH2O (more negative is better)

50%

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46
Q

Recovery from NM blockade Head lift >5 sec:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?

A

Sustained for 5 sec

50%

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47
Q

Recovery from NM blockade Hand grip same as preinduction:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?

A

Sustained for 5 sec

50%

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48
Q

Recovery from NM blockade Holding tongue blade in mouth against force:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?

A

Can’t remove tongue blade against force

50%

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49
Q

What quantitative methods of measuring NMB recovery could solve the insensitivity problem with the bedside assessments?

A

Electromyography or acceleromyography

These are not commonly available

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50
Q

What is the structure of succinylcholine?

A

2 acetylcholine molecules joined together

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51
Q

Succinylcholine side effects (7):

A 
Bradycardia
Tachycardia
K+ release
Increased IOP
Increased ICP
Increased intragastric pressure
Malignant hyperthermia
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52
Q

How can succinylcholine cause bradycardia? What increases this risk? What is probably most responsible for this effect? What may prevent it?

A

By stimulating the M2 receptor on the SA node is can a use bradycardia or asystole.
A second dose increases this risk.
Its primary metabolite succinylmonocholine.
Antimuscarinics may prevent or reverse these bradyarrhythmias

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53
Q

What patient population is more susceptible to bradycardia with succinylcholine? Why? What should be done?

A

Children.
They have a higher vagal tone.
Atropine should always precede a second dose of Sux.

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54
Q

How can succinylcholine cause tachycardia?

A

By mimicking the action of Ach at the sympathetic ganglia it can cause tachycardia and HTN

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55
Q

In adults what is more common with the use of sux, tachycardia or bradycardia?

A

Tachycardia

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56
Q

How does succinylcholine cause potassium release?

A

The Ach causes opening of the nAchR at the neuromuscular junction and increases serum K+ by 0.5 - 1.0 mEq/L for up to 10 - 15 minutes.

57
Q

Hyperkalemia increase the resting membrane potential of excitable tissue, this increases the risk of what?

A

Dysrhythmias

58
Q

Is succinylcholine safe to use in patients with renal failure?

A

Yes as long as K+ level is normal

59
Q

How much does succinylcholine affect IOP?

A

It transiently increases IOP by 5 - 15 mmHg for up to 10 minutes

60
Q

Does pretreatment with a ND-NMB attenuate the risk in IOP from succinylcholine?

A

The text says it’s controversial and/or provides no little benefit

61
Q

What is the debate with succinylcholine in a patient with an open globe injury that needs a TRUE RSI?

A

There is little evidence to support the risk of Sux increased IOP causing extrusion of intraocular contents and permanent blindness. Securing the airway is #1 priority, eye is a close second. Light anesthesia, laryngoscopy, intubation, coughing and/or straining cause a greater rise in IOP than succinylcholine

62
Q

Succinylcholine temporarily increase ICP, what can prevent or minimize this?

A

Defasciculating dose

63
Q

Contraction of the abdominal muscles increases intragastric pressure, what does succinylcholine do that cancels out this increase in risk of aspiration?

A

Raises lower esophageal sphincter tone

64
Q

Does masseter spasm and the absence of other s/sx of MH warrant cancellation of a planned surgical procedure?

A

No

65
Q

What enzyme metabolizes acetylcholine? What are the 5 different names for it?

A 
Type 1 cholinesterase
Acetylcholinesterase 
True cholinesterase
Specific cholinesterase
Genuine cholinesterase
66
Q

What enzyme metabolizes succinylcholine? What are it’s 5 different names?

A 
Type 2 cholinesterase 
Butyrylchoilinesterase 
False cholinesterase 
Plasma cholinesterase 
Pseudocholinesterase
67
Q

Where is pseudocholinesterase produced?

A

In the liver and serves as an indicator of hepatic synthetic function

68
Q

What is the plasma reference concentration of pseudocholinesterase?

A

2900 - 7100 units/L

69
Q

At what level of pseudocholinesterase do neuromuscular symptoms begin? Become serious?

A

60% of normal

Become serious at 20% of normal

70
Q

What other 5 tissues is pseudocholinesterase found?

A 
Smooth muscle
Intestines
White matter of the brain
Heart
Pancreas
71
Q

What 8 drugs reduce pseudocholinesterase activity?

A 
Metoclopramide
Esmolol
Neostigmine
Echothiophate
Oral contraceptives/estrogen
Cyclophosphamide
Monoamine oxidase inhibitiors 
Nitrogen mustard
72
Q

What 9 co-existing conditions reduce pseudocholinesterase activity?

A 
Atypical PChE
Severe liver disease
Chronic renal disease
Organophosphate poisoning 
Burns
Neoplasm
Advanced age
Malnutrition
Pregnancy - late stage
73
Q

What test is used to make the definitive diagnosis of atypical PChE?

A

Dibucaine test

74
Q

What type of drug is Dibucaine and what does it do? What does the result mean?

A

Amide local anesthetic.
It inhibits normal plasma cholinesterase, and has no effect on atypical PChE.
The number reflects the percentage of normal enzyme that is inhibited by dibucaine.

75
Q

What is a normal result for the Dibucaine test? What does it mean?

A

80%. This means that dibucaine has inhibited 80% of the pseudocholinesterase in the sample and suggests that the normal enzyme is present.

76
Q

What is an abnormal Dibucaine test result? What does it mean?

A

20%.

This means that dibucaine did not inhibit the patient’s pseudocholinesterase and that an atypical variant is present.

77
Q 
Typical Homozygous PChE:
Genotype
Incidence
Dibucaine #
Duration of succinylcholine
A

Genotype: UU
Incidence: -
Dibucaine #: 70 - 80%
Duration of succinylcholine: 5 - 10 min

78
Q 
Heterozygous PChE:
Genotype
Incidence
Dibucaine #
Duration of succinylcholine
A

Genotype: UA
Incidence: 1 / 480
Dibucaine #: 50 - 60%
Duration of succinylcholine: 20 - 30 min

79
Q 
Atypical homozygous PChE: 
Genotype
Incidence
Dibucaine #
Duration of succinylcholine
A

Genotype: AA
Incidence: 1 / 3200
Dibucaine #: 20 - 30%
Duration of succinylcholine: 4 - 8 hours

80
Q

What is the treatment of choice for atypical variant PChE? What other treatments are there?

A

Postoperative mechanical ventilation and sedation are the treatment of choice because they are the safest and least expensive.
Whole blood, FFP, and purified human cholinesterase will all restore plasma pseudocholinesterase levels.

81
Q

The routine administration of succinylcholine is contraindicated in young children because of the possibility of?

A

Hyperkalemic rhabdomyolosis

82
Q

What is the black box warning on succinylcholine?

A

Risk of cardiac arrest and death secondary to hyperkalemia in children with undiagnosed skeletal muscle myopathy.

83
Q

What is the most common skeletal muscle myopathy in children?

A

Duchenne muscular dystrophy

84
Q

What is Duchenne muscular dystrophy?

A

X-link, recessive disease that results from the absence of dystrophin protein

85
Q

List 4 skeletal muscle myopathies other than Duchenne’s:

A

Becker
Emery-Dreifuss
Facioscapulohumeral
Limb-girdle muscular dystrophy

86
Q

What EKG changes occur with mild hyperkalemia?

A

Peaked T waves

PR prolongation

87
Q

What EKG changes occur with severe hyperkalemia?

A

Ventricular fibrillation

Asystole

88
Q

If a healthy inflation/child develops cardiac arrest following succinylcholine, particularly a boy < 8 years old, immediate treatment of hyperkalemia should begin. What are the 3 goals and what treatment do they include?

A 
1. Stabilize the myocardium: 
calcium chloride 20 mg/kg
Calcium gluconate 60 mg/kg 
2. Shift potassium into cells
Glucose 0.3 - 0.5 g/kg as 10% solution
Insulin 1 unit per 4 - 5 g of IV glucose
Sodium bicarb 1 - 2 mmol/kg
Hyperventilation 
Albuterol nebulizer
3. Enhance potassium elimination 
Furosemide 1 mg/kg
Volume resuscitation
Hemodialysis
Hemofiltration
89
Q

How much elemental calcium does each contain?
10% Calcium chloride
10% Calcium gluconate

A

10% Calcium chloride: 27.2 mg/mL of elemental Ca

10% Calcium gluconate: 9 mg/mL of elemental Ca

90
Q

In children what situations should succinylcholine be reserved for?

A

Difficult intubation
Laryngospasm
RSI
IM use when IV access is unattainable

91
Q

How long can postoperative myalgia persist for due to succinylcholine? How does it manifest? What is the believed cause of this myalgia?

A

24 - 48 hours
Muscle soreness in the neck, shoulders, subcostal region, upper abdominal muscles, and trunk muscles.
Sux causes uncoordinated muscle contractions before causing flaccid paralysis, these contractions are believed to be the cause of myalgia.

92
Q

List 4 factors that increase the risk of myalgia from succinylcholine:

A

Young adults
Ambulatory surgery
Woman > men
Those that do not routinely engage in strenuous exercise

93
Q

What 3 patient populations seem to have the lowest risk of myalgia from succinylcholine?

A

Children
Elderly
Pregnancy

94
Q

Can pretreatment with ND-NMB decrease or eliminate the myalgia associated with succinylcholine?

A

It might be minimized, but not entirely eliminated

95
Q

What other methods besides ND-NMB may reduce the risk of myalgia with Succinylcholine? (3)

A

NSAIDs
Lidocaine 1.5 mg/kg
A higher dose rather than a lower dose of succinylcholine

96
Q

Do opioids decrease the incidence of myalgia with succinylcholine?

A

No

97
Q

When using a defasciculating dose of a ND-NMB how should the dose of Succinylcholine change? Why?

A

Increase sux dose to 1.5 - 2.0 mg/kg

The ND will competitively antagonize the nicotinic receptor, more sux must be given to overwhelm the ND

98
Q

When should a defasciculating dose NOT be used? Why?

A

Those with pre-existing skeletal muscle weakness, such as myasthenia gravis.
Patient may experience muscle weakness, dyspnea, dysphasia, and diplopia

99
Q 
Diseases with altered responses to NMB: Sux vs ND
Amyotrophic lateral sclerosis
Charcot-Marie-Tooth
Duchenne’s muscular dystrophy
Guillain-Barre
Huntington chorea
Hyperkalemic periodic paralysis
Hypokalemic periodic paralysis 
Malignant hyperthermia
Multiple sclerosis
Myasthenia gravis 
Myotonic dystrophy
Up-regulation of AChRs
A

Amyotrophic lateral sclerosis: Sux hyperkalemia, ND sensitive
Charcot-Marie-Tooth: Sux hyperkalemia, ND normal
Duchenne’s muscular dystrophy: Sux hyperkalemia, rhabdomyolysis; ND sensitive
Guillain-Barre: Sux hyperkalemia; ND sensitive
Huntington chorea: Sux sensitive; ND sensitive
Hyperkalemic periodic paralysis: Sux hyperkalemia; ND normal
Hypokalemic periodic paralysis: Sux normal; ND normal
Malignant hyperthermia: Sux MH; ND normal
Multiple sclerosis: Sux hyperkalemia; ND sensitive
Myasthenia gravis: Sux resistant; ND sesitive
Myotonic dystrophy: Sux muscle contractures; ND normal or sensitive
Up-regulation of AChRs: Sux hyperkalemia; ND resistant or normal depending on timing of injury

100
Q

ED95 is a measure of?

A

Potency

They are inversely related

101
Q

What is ED95 of NMB?

A

The dose at which there is a 95% decrease in twitch height

102
Q

The higher the ED95 the _____ the potency, and the _____ the onset

A

Lower the potency

Faster the onset - because there are more molecules to diffuse from the plasma to the biophase at the NMJ

103
Q

The dose of NMB required to provide optimal conditions for tracheal intubation is ~ _____ times the ED95

A

2 - 3 x ED95

104
Q 
Mivacurium:
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
A

ED95: 0.067 mg/kg
Intubation dose: 0.15 mg/kg
Time to max block (onset): 3.3 min
Time to return to 25% control (~duration): 16.8 min

105
Q 
Cisatracurium:
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
A

ED95: 0.04 mg/kg
Intubation dose: 0.1 mg/kg
Time to max block (onset): 5.2 min
Time to return to 25% control (~duration): 45 min

106
Q 
Vecuronium:
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
A

ED95: 0.043 mg/kg
Intubation dose: 0.1 mg/kg
Time to max block (onset): 2.4 min
Time to return to 25% control (~duration): 45 min

107
Q 
Atracurium :
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
A

ED95: 0.21 mg/kg
Intubation dose: 0.5 mg/kg
Time to max block (onset): 3.2 min
Time to return to 25% control (~duration): 45 min

108
Q 
Rocuronium:
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
A

ED95: 0.305 mg/kg
Intubation dose: 0.6 mg/kg
Time to max block (onset): 1.7 min
Time to return to 25% control (~duration): 35 min

109
Q 
Pancuronium:
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
A

ED95: 0.067 mg/kg
Intubation dose: 0.08 mg/kg
Time to max block (onset): 2.9 min
Time to return to 25% control (~duration): 85 min

110
Q

What are the 2 classes of ND-NMB?

A

Benzylisoquinolinium

Aminosteroid

111
Q

List the benzylisoquinolinium compounds:

A

Atracurium
Cisatracurium
Mivacurium

112
Q

List the Aminosteroid compounds

A

Rocuronium
Vecuronium
Pancuronium

113
Q

Why can renal insufficiency prolong the duration of any of the ND-NMB? Which class is this negligible with?

A

All the ND-NMB are inonized, each other undergoes some degree of renal elimination as unchanged drug.
Benzylisoquinolinium

114
Q

Which ND compounds undergo spontaneous degradation in the plasma and are not dependent on hepatic or renal function for metabolism and elimination?

A

Benzylisoquinolinium compounds (cisatracurium, atracurium, and mivacurium)

115
Q

How is atracurium metabolized?

What other drugs are metabolized by this same method?

A

Hofmann elimination - 33%
Non-specific plasma esterases - 66% : esmolol and remifentanil
Renal elimination 10 - 40%

116
Q

How is cisatracurium metabolized?

A

Hofmann elimination 77%

Renal elimination 16%

117
Q

How is mivacurium metabolized?

A

Pseudocholinesterase

118
Q

What is Hofmann elimination? What does it depend on and how do these 2 things affect it?

A

Base-catalyze reaction
Dependent on normal blood pH and temperature
The reaction is faster with alkalosis and hyperthermia
The reaction is slower with acidosis and hypothermia

119
Q

Which Benzylisoquinolinium compounds have a metabolite? Which produces more of the metabolite?

A

Laudanosine is a metabolite of atracurium and cisatracurium.

Atracurium produces more.

120
Q

What effect does the metabolite laudanosine have?

A

It is a CNS stimulant that is capable of producing seizures. More of a concern with prolonged infusion.

121
Q

How is rocuronium metabolized and eliminated? Does it have a metabolite?

A

Metabolism: none
Liver elimination: > 70%
Renal elimination: 10 - 25%
No metabolite

122
Q

How is vecuronium metabolized and eliminated? Does it have a metabolite?

A

Metabolism: hepatic deacetylation 30 - 40%
Liver elimination: 40 - 50%
Renal elimination: 50 - 60%
Metabolite 3-OH vecuronium - half a potent as its parent, rapidly metabolized into inactive metabolites

123
Q

How is pancuronium metabolized and eliminated? Does it have a metabolite?

A

Metabolism: hepatic deacetylation 10 - 20%
Liver elimination: 15%
Renal elimination: 85%
3-OH pancuronium is half as potent as parent

124
Q

What classes (and drugs) potentiate neuromuscular blockade?

A

VAs: DES > SEVO > ISO > N2O > propofol
ABX: aminoglycosides, polymyxins, clindamycin, lincomycin, tetracycline
Antidysrhythmics: verapamil, amlodipine, lidocaine, quinidine
LAs: probably all of them
Diuretics: furosemide
Other: dantrolene, cyclosporine, tamoxifen

125
Q

What electrolyte disturbances potentiate neuromuscular blockade?

A

Increased lithium activates K+ channels
Increased Mg decreases Ach release from presynaptic nerve
Decreased Ca decreases Ach release from presynaptic nerve
Decrease K decreases RMP

126
Q

What patient factors potentiate neuromuscular blockade?

A

Hypothermia decreases metabolism and clearance

Gender - compared to men, women are more sensitive to the effects of NMBs

127
Q

What NMB cause histamine release? (3)

A

Succinylcholine
Atracurium
Mivacurium

128
Q

What NMB affect autonomic ganglia and how?

A

Succinylcholine stimulates -> tachycardia

129
Q

What NMB affect M2 receptors on the heart? (3)

A

Succinylcholine stimulation -> bradycardia
Pancuronium - moderate blockade
Rocuronium - none to slight blockade

130
Q

How long does the histamine release last from NMB? How can it be minimized? Who should not receive histamine releasing drugs?

A

Generally short lived 1 - 5 min
Can be minimized by slow administration
Those who are sensitive to a higher HR or reduced afterload, unless clinical benefit outweighs the risk

131
Q

What is Pancuronium’s unique effect on the heart?

A

It has a vagolytic effect, it inhibits M2 receptors at the SA node -> stimulates the release of catecholamines, and inhibits catecholamine reuptake in adrenergic nerves -> increase in HR and CO with no or minimal effects on SVR

132
Q

In what specific situation is Pancuronium used in cardiac surgery?

A

To mitigate opioid induced bradycardia in cardiac surgery

133
Q

Patients with what disease should no receive pancuronium? Why?

A 
Hypertrophic cardiomyopathy (idiopathic hypertrophic subaortic stenosis).
Hypertrophied ventricular septum and systolic anterior motion of the anterior leaflet of the mitral valve, when the ventricle contracts forcefully or quickly there is a greater tendency for the anterior leaflet to occlude the LVOT, which reduces flow through the aortic valve -> reduces CO and BP. Pancuronium’s vagolytic effect can be detrimental in this patient
134
Q

In rare instances vecuronium and atracurium have cause what EKG rhythm? Why/how?

A

Asystole

In all cases an opioid was also administered, it’s likely that the vagal effects of the opioid were left unchecked

135
Q

What is the most common cause of perioperative allergic reactions?

A

Neuromuscular blockers

136
Q

Why do NMBs cause anaphylaxis?

A

Their structures contain one of more antigenic quaternary ammonium groups that interact with Ig-E, causing mast cell and basophils degranulation

137
Q

Cross sensitivity may occur in up to ____% of those who have experienced a previous allergic response related to NMBs.

A

70%

138
Q

It is possible that sensitivity to any NMB may develop following exposure to what compounds? Why?

A

Soap or cosmetics

They often contain antigenic quaternary ammonium group

139
Q

Which NMB is most likely to cause anaphylaxis?

A

Succinylcholine
Rocuronium
-multiple choice: choose Sux, if not a choice then pick Roc
-multiple response: sux and roc

apex (46 decks)

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