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2-Anesthesia Pharm Exam 2 > Neuromuscular Blocking Agents Overview/Succinylcholine > Flashcards

Neuromuscular Blocking Agents Overview/Succinylcholine Flashcards

1
Q

Who was the first person to discover neuromuscular blockade?

A

Andrew Griffith

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2
Q

What do neuromuscular blocking agents block?

A

SKELETAL MUSCLE function (not cardiac or smooth muscle)

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3
Q

What is the innervation of skeletal muscles?

A

innervated by large myelinated alpha-motor neurons

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4
Q

Where do the neurons that innervate skeletal muscles originate?

A

from cell bodies located in either the brainstem or the ventral (anterior) horn of the spinal cord

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5
Q

Describe the size and function of B nerve fibers.

A

Size: <3 microns
Function: Pregangolionic, Sympathetic

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6
Q

Describe the size and function of C (unmyelinated) nerve fibers.

A

Size: -.3-1.3 microns
Functions: Temperature, Dull Pain

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7
Q

Describe the size and function of A-delta nerve fibers.

A

Size: 1-4 microns
Function: temperature and sharp pain

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8
Q

Describe the size and function of A-gamma nerve fibers.

A

Size: 3-6 microns
Function: Muscle spindle, muscle tone

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9
Q

Describe the size and function of A-beta nerve fibers.

A

Size: 6-22 microns
Function: Light pressure, touch

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10
Q

Describe the size and function of A-alpha nerve fibers.

A

Size: 6-22 microns
Function: Somatic motor, proprioception

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11
Q

What class of nerve fibers are we concerned with for neuromuscular blocking agents?

A

A-alpha

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12
Q

What are the two components of the neuromuscular junction?

A

Motor neuron and muscle fiber

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13
Q

What synapse occurs at the neuromuscular junction (NMJ)?

A

synapse where PRESYNAPTIC MOTOR NERVE ENDINGS meet the POSTSYNAPTIC MEMBRANES OF SKELETAL MUSCLES (motor end plate)

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14
Q

What is another term for the postsynaptic membranes of the skeletal muscles?

A

Motor end plate

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15
Q

NMJ: What is located at the presynaptic nerve terminal?

A

vesicles filled w/ACh

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16
Q

NMJ: What is located at the postsynaptic muscle membrane?

A

nicotinic ACh receptors (nAChRs)

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17
Q

What are the two types of cholinergic receptors?

A

Muscarinic & Nicotinic receptors

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18
Q

What are targets of nicotinic receptors? (4)

A

Skeletal muscle, cardiac muscle, ganglia and CNS

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19
Q

What is the subunit structure of nicotinic receptors (nAChR)?

A

Two-α’s plus β,δ,ε

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20
Q

Describe normal neuromuscular transmission.

A

two ACh molecules bind to two α subunits located on the postsynaptic muscle membrane nAChR

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21
Q

What happens after two ACh molecules bind to two alpha subunits during normal neuromuscular transmission?

A

This binding initiates conformational changes within the nAChR that opens a channel allowing Na+ and Ca++ ions to move into the skeletal muscle and K+ to move out of the muscle

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22
Q

What ions move out of the skeletal muscle?

A

K+

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23
Q

What happens as a result from the flow of ions in and out of the skeletal muscle? (2)

A

depolarization of the motor endplate and creates the action potential that triggers skeletal muscle contraction

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24
Q

Describe the complete process of neuromuscular transmission.

A

Once the released ACh binds to the α subunits on the nAChR causing conformational change within the receptor and opens the channel so that Na+ flows into the skeletal muscle cell and K+ out of the cell, then depolarization of the skeletal muscle cell occurs with initiation of action potentials across the surface of the muscle membrane and into the transverse tubules of skeletal muscle

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25
Q

What does action potential propagation cause?

A

interaction between 2 types of Ca++ channels within skeletal muscle: dihydropyridine receptor (DHPR) in the T-tubules and ryanodine receptor 1 (RyR1) in the sarcoplasmic reticulum & binds to troponin C causing cross-bridging between myosin and actin (coupling)

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26
Q

What two Ca++ channels within skeletal muscles are a target of action potential propagation?

A

dihydropyridine receptor (DHPR) & ryanodine receptor 1 (RyR1)

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27
Q

Where is the dihydropyridine receptor (DHPR) located?

A

T-tubules

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28
Q

What is the ultimate byproduct of neuromuscular transmission?

A

skeletal muscle contraction

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29
Q

What is the desired onset of an Ideal Neuromuscular Blocking Agent?

A

Rapid, predictable onset of effects with one circulation time to facilitate rapid securing of the airway

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30
Q

What is the desired systemic response of an Ideal Neuromuscular Blocking Agent?

A

Absence of histamine release, influence on heart rate, bronchial tone

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31
Q

What is the desired accumulation of an Ideal Neuromuscular Blocking Agent?

A

Adaptable to long cases, not cumulative

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32
Q

What is the desired non depolarizing side effects of an Ideal Neuromuscular Blocking Agent?

A

Nondepolarizing – does not cause myalgia, or increased ICP, intragastric or ocular pressure

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33
Q

What is the desired blockade level of an Ideal Neuromuscular Blocking Agent?

A

Predictable depth of blockade

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34
Q

What is the desired reversibility of an Ideal Neuromuscular Blocking Agent?

A

Ability to be reversed quickly and completely without residual effects

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35
Q

What is the desired placenta effect of an Ideal Neuromuscular Blocking Agent?

A

Absence of placental transfer when administered to a parturient

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36
Q

What is the desired MH effect of an Ideal Neuromuscular Blocking Agent?

A

Does not trigger malignant hyperthermia

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37
Q

What is the desired clinical byproduct of an Ideal Neuromuscular Blocking Agent?

A

The ability to produce hypnosis and/or amnesia

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38
Q

What are drug characteristics that are important to take into consideration when selecting a neuromuscular blocking agent?

A
  • Duration of action is matched with desired duration effect
  • Drug is not contraindicated
  • Mechanism of metabolism and elimination are compatible with the patient’s comorbidities
  • Any side effects are not contraindicated by the patient’s comorbidities
  • Choice is cost effective for the intended volume/duration used
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39
Q

Define Depolarizing Neuromuscular Blocking Agents.

A

these drugs act as an AGONIST (mimic ACh) at the postsynaptic nAChR causing prolonged membrane depolarization

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40
Q

What is the only Depolarizing Neuromuscular Blocking Agents in clinical use?

A

Succinylcholine

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41
Q

What is the definition of Nondepolarizing Neuromuscular Blocking Agents in clinical use?

A

these drugs COMPETE with ACh for the active binding sites at the postsynaptic nAChR

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42
Q

Nondepolarizing Neuromuscular Blocking Agents are ________ antagonist.

A

Competitive

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43
Q

What properties are NOT associated with NMBDs?

A

NO AMNESTIC OR ANALGESIC PROPERTIES

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44
Q

What is the principle action of non depolarizing NMBDs?

A

binding to one alpha subunit is sufficient to produce neuromuscular blockade (competitive antagonist)

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45
Q

What is the principle action of Succinylcholine (SCh)?

A

binding to nAChR produces prolonged depolarization to the motor endplate desensitization of nAChRs and inactivates voltage-gated Na+ channels at NMJ

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46
Q

What enzyme is present at the NMJ?

A

Acetylcholinesterase

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47
Q

What does Acetylcholinesterase
break ACh into (2)?

A

acetic acid & choline

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48
Q

What does Succinylcholine produce?

A

a depolarizing block also called phase I block

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49
Q

Succinylcholine: Neuromuscular block preceded by _________

A

muscle fasciculations

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50
Q

What is Succinylcholine’s structure similar to?

A

Similar structure to ACh

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51
Q

What is Succinylcholine an agonist or antagonist?

A

Partial agonist at postsynaptic nAChRs

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52
Q

What receptors does Succinylcholine stimulate at the NMJ?

A

Stimulates cholinergic receptors at the nAChRs at the NMJ, ganglionic nicotinic receptors, and muscarinic receptors

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53
Q

What does Succinylcholine cause?

A

prolonged depolarization of the endplate region that results in desensitization of the nicotinic acetylcholine receptors

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54
Q

Where is the prolong depolarization occur in response to Succinylcholine?

A

endplate region

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55
Q

What effect does Succinylcholine have on ions? (2)

A
  • Inactivate voltage gated sodium channels at neuromuscular junction
  • Increases potassium permeability in the surrounding membrane
56
Q

Succinylcholine: Membrane ____________

A

hyperpolarization????

57
Q

What is the structure of Succinylcholine?

A

Two molecules of acetylcholine linked through the acetate methyl groups

58
Q

What does Succinylcholine stimulate?

A

Like acetylcholine, succinylcholine stimulates cholinergic receptors at the neuromuscular junction and at nicotinic (ganglionic) and muscarinic autonomic sites, opening the ionic channels in the acetylcholine receptor

59
Q

What is Succinylcholine permeability to the BBB and placenta? Why characteristic gives it this properties?

A

Contains a quaternary ammonium, does not cross the blood brain barrier OR the placenta

60
Q

What is the usual dose of Succinylcholine for tracheal intubation in adults?

A

Usual dose required for tracheal intubation in adults: 1 – 1.5 mg/kg IV (3x the ED95)

61
Q

What is the usual dose of Succinylcholine for laryngospasm intubation in adults? What is the route and dose commonly used for larygnospasms?

A

0.2-2mg/kg IV or 4-5mg/kg IM

62
Q

What is the onset of Succinylcholine?

A

30-60 seconds (rapid control of airway)

63
Q

What is the duration of action of Succinylcholine?

A

5-15 minutes (ultrashort acting)

64
Q

What is the normal time to recovery for individuals with normal butyrylcholinesterase activity?

A

time to recovery of 90% muscle strength is 9-13 minutes

65
Q

No advantage in using SCh dose larger than _______ in RSI

A

1.5mg/kg

66
Q

What is an important component of Succinylcholine storage?

A

Needs to be refrigerated

67
Q

What causes succinylcholine’s short duration of action?

A

rapid hydrolysis by butyrylcholineterase (plasma cholinesterase/pseudocholinesterase)

68
Q

What does butyrylcholineterase break succinylcholine into?

A

Succinylmonocholine and choline

69
Q

Only _______ of the administered dose of Succinylcholine reaches the neuromuscular junction

A

10%

70
Q

What is succinylmonocholine?

A

weaker neuromuscular blocking agent than succinylcholine and is metabolized slowly to succinic acid and choline

71
Q

What is the concentration of butyrylcholinesterase at the NMJ?

A

There is little to no butyrylcholinesterase at the neuromuscular junction

72
Q

How does butyrylcholinesterase influenc the onset and duration of succinylcholine?

A

controlling the rate at which succinylcholine is hydrolyzed in the plasma before it reaches and after it leaves the neuromuscular junction

73
Q

How does Recovery from succinylcholine-induced blockade occur?

A

as succinylcholine diffuses away from the neuromuscular junction, down a concentration gradient as the plasma concentration decreases

74
Q

What should be check after succinylcholine administration?

A

Always check PNS after succinylcholine administration, prior to administering a nondepolarizing muscle relaxant

75
Q

Where is Butyrylcholinesterase
synthesized and found circulating?

A

Enzyme synthesized in liver & found circulating in plasma

76
Q

What is Butyrylcholinesterase responsible for the metabolism of (7)?

A

SCh, mivacurium, procaine, chloroprocaine, tetracaine, cocaine, & heroin

77
Q

Butyrylcholinesterase: Levels < _____% necessary for prolongation of a SCh-induced block

A

75%

78
Q

What can cause prolonged Neuromuscular block?

A

Butyrylcholinesterase, Neuromuscular block induced by SCh or mivacurium prolonged with significant reduction in concentration or activity of butyrylcholinesterase (plasma cholinesterase/pseudocholinesterase)

79
Q

What are some factors that lower Butyrylcholinesterase activity?

A

advanced liver disease, advanced age, malnutrition, pregnancy, burns, MAO inhibitors, echothiophate, anticholinesterase drugs, metoclopramide, esmolol, organophosphate pesticides

80
Q

What are two important drugs that lower Butyrylcholinesterase activity?

A

echothiophate, anticholinesterase drugs

81
Q

________ and ________ cause a profound decrease in butrylcholinesterase

A

Neostigmine and edrophonium

82
Q

What are the genetic variants of Butyrylcholinesterase referred to?

A

Atypical Plasmacholinesterase

83
Q

Neuromuscular block induced by SCh or mivacurium can be significantly prolonged if patient has __________

A

abnormal genetic variant

84
Q

What are the components of butyrylcholinesterase analysis (2)?

A

Analysis of butyrylcholinesterase involves determination of both the enzyme activity and biochemical phenotypes

85
Q

How is phenotype determined for butyrylcholinesterase analysis?

A

used of enzyme inhibitors: dibucaine or fluoride that produce phenotype-specific patterns of dibucaine or fluoride numbers

86
Q

What is dibucaine?

A

local anesthetic, inhibits the activity of normal butyrylcholinesterase by > 70% compared to only 20% inhibition of the activity of atypical butyrylcholinesterase (atypical plasma cholinesterase) – fluoride also does as well (fluoride number)

87
Q

What does the dibucaine number reflect?

A

quality of the cholinesterase enzyme (ability to hydrolyze SCh), not the quantity of the enzyme that is circulating in the plasma

88
Q

What does the dibucaine number indicate?

A

the percentage of butyrylcholinesterase (plasma cholinesterase/pseudocholinesterase) that is inhibited by dibucaine

89
Q

What is the dibucaine number and response to Normal (Homozygous for the Typical Genotype) butyrylcholinesterase?

A
  • Dibucaine number: 70-80
  • Normal response to SCh or mivacurium
90
Q

What is the dibucaine number and response to Abnormal (Heterozygous for the Atypical Genotype) butyrylcholinesterase?

A
  • Dibucaine number: 50-60
  • Neuromuscular block from SCh/mivacurium prolonged by 50-60%
91
Q

What is the dibucaine number and response to Abnormal (Homozygous for the Atypical Genotype) butyrylcholinesterase?

A
  • Dibucaine number: 20-30
  • Neuromuscular block from SCh/mivacurium prolonged 4-8 hours
92
Q

What is the frequency of Abnormal (Homozygous for the Atypical Genotype) butyrylcholinesterase?

A

1 in 3,500

93
Q

What is the treatment of Abnormal (Homozygous for the Atypical Genotype) butyrylcholinesterase?

A

Requires postop mechanical ventilation/sedation

94
Q

What are the potential rhythm changes associated with succinylcholine? (3)

A

Sinus bradycardia, junctional rhythm, sinus arrest

95
Q

What does the cardiovascular responses from succinylcholine reflect?

A

Reflect SCh actions at cardiac muscarinic cholinergic receptors (mimics physiologic effects of ACh)

96
Q

When are cardiac dysrhythmias most likely occur during succinylcholine administration?

A

cardiac dysrhythmias most likely to occur when 2ND dose of SCh administered approx. 5 minutes after 1st dose

97
Q

What is the most common cardiac dysrhythmias associated with succinylcholine administration in children and adults?

A

Sinus bradycardia freq seen in children and in adults after a repeat dose of SCh

98
Q

What can be effective in treatment of bradycardia associated with succinylcholine?

A

Atropine effective in treating or preventing bradycardia

99
Q

What is the results of ganglionic stimulation in autonomic nervous system?

A

increased HR and SVR (mimics physiologic effects of ACh at these sites)

100
Q

What is a common side effect of Succinylcholine?

A

Hyperkalemia

101
Q

What effect does Succinylcholine have on potassium levels?

A

SCh administration ass. w/approx. 0.5 mEq/dL increase in plasma K+ concentration (well tolerated in healthy indiv’s)

102
Q

What are some patients that associated with severe hyperkalemia when given SCh? (5)?

What effect do these conditions have on K+ release?

A
  • Burns, crush injuries, severe abdominal infections, severe metabolic acidosis, close head injury
  • release of K+ into extracellular space
103
Q

What are the conditions that are associated with upregulation of extrajunctional ACh receptors (3)?

A

hemiplegia/paraplegia, muscular dystrophies, Guillain-Barre҄ syndrome, burns) may lead to development of hyperkalemia

104
Q

Why is SCh not recommended in children?

A

except for emergency tracheal intubation due to undiagnosed muscle disease (causing massive rhabdomyolysis, hyperkalemia, death)

105
Q

What is the relationship between Succinylcholine and Myoglobinuria?

A

Caused by damage to skeletal muscle, especially pediatric patients

106
Q

Unlikely that SCh-induced fasciculations could cause muscle damage resulting in __________

A

myoglobinuria

107
Q

What is true regarding most patients with myoglobinuria and succinylcholine?

A

Most patients with myoglobinuria subsequently found to have malignant hyperthermia or occult muscular dystrophy

108
Q

What effect does succinylcholine have on the eyes?

A

increased intraocular pressure

109
Q

When does increased IOP from succinylcholine peak? When does it return to normal?

A

Peaks at 2-4 minutes, returns to normal by 6 minutes

110
Q

How does succinylcholine cause Increased IOP?

A

Results from contraction of tonic myofibrils and/or transient dilatation of choroidal blood vessels

111
Q

Why should succinylcholine not be used with open injuries?

A

Use of SCh in open eye injuries (open anterior chamber) not widely accepted (avoid)

112
Q

What effect does succinylcholine have on postoperative skeletal muscles?

A

myalgia

113
Q

What is the incidence of myalgia after succinylcholine?

A

0.2% to 89%

114
Q

What is mechanism of mylagia development after succinylcholine?

A
  • May be secondary to fasciculations
  • Possible role of prostaglandins and cyclooxygenases in SCh-induced fasciculations
115
Q

Where is mylagia predominently occur?

A

the skeletal muscles of the neck, back, and abdomen

116
Q

Who is more likely to experience mylagia?

A

Especially in young adults undergoing minor (ambulatory) surgical procedures, especially women

117
Q

What is true about myalgia localized to the neck muscles?

A

can be perceived as a pharyngitis attributed to intubation

118
Q

What is the best prevention for myalgia? (3)

A

muscle relaxants, lidocaine, or NSAIDs

119
Q

What is succinylcholine a known trigger for?

A

malignant hyperthermia

120
Q

What is an early indicator of malignant hyperthermia?

A

Masseter spasm, Increased tone in masseter muscle may be an early indicator of MH

121
Q

What does it mean if their are high incidence of masseter spasm in pediatric patients?

A

may be due to inadequate succinylcholine dosing

122
Q

What are the different blocks associated with succinylcholine?

A

Phase I and Phase II Block

123
Q

What is a phase I block?

A

results from depolarizing neuromuscular block & often preceded by muscle fasciculations

124
Q

What is a phase II Block?

A

results from a depolarizing neuromuscular block with repeated exposure of the NMJ to SCh (i.e., succinylcholine drip)

125
Q

What can abate muscle fasciculations?

A

Precurarization w/small dose nondepolarizing muscle relaxant can often abate muscle fasciculations, but will require a slightly higher SCh intubating dose

126
Q

What does a phase II block resemble?

A

Block resembles a nondepolarizing neuromuscular block (fade observed in a muscle stimulated with peripheral nerve stimulator)

127
Q

What can precurarization prevent? (2)

A

may prevent defasciculations and myalgia associated w/SCh

128
Q

What is precuraization?

A

small dose of nondepolarizing NMBD is given 2-3 minutes before administration of SCh

129
Q

What effect does precurarization have on SCh?

A

Reduces potency of SCh and will require larger dose to produce same effect

130
Q

What is the optimal dose of recuronium for precurarization?

A

(defasciculation) prior to SCh administration: 0.04mg/kg

131
Q

What are some other nondepolarizing NMBDs be used for precurarization?

A

atracurium, vecuronium

132
Q

Where is the location of nicotinic receptors?

A

Skeletal muscle, ganglia, CNS

133
Q

How does SCh cause increased intragrastric pressure?

A
  • The intensity of fasciculations of the abdominal skeletal muscles (can be prevented by prior administration of a nondepolarizing neuromuscular blocker)
  • Direct increases in vagal tone
134
Q

SCh ___________ to regurgitation in patients with an intact lower esophageal sphincter

A

does not predispose

135
Q

What can be done to decreased the ICP effects of SCh?

A

Can be attenuated or prevented by pretreatment with a nondepolarizing neuromuscular blocker

2-Anesthesia Pharm Exam 2 (6 decks)

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