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Lindsays Flashcardlet > RE5: Chapter 12: Neuromuscular Blocking Agents, Reversal Agents, and Their Monitoring > Flashcards

RE5: Chapter 12: Neuromuscular Blocking Agents, Reversal Agents, and Their Monitoring Flashcards

0
Q

Describe neuromuscular depolarization blockade (phase 1 blockade).

A
  1. The motor end plate cannot repolarize until the agent leaves the nicotinic receptor
  2. Because the motor end plate cannot repolarize, it cannot respond to subsequent Ach release
  3. The agent binds to the nicotinic receptor on the motor end plate and causes depolarization
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1
Q

What is the difference between qualitative vs. quantitative neuromuscular blockade monitoring?

A

Qualitative monitoring involves visual or tactile response to evoked electrical stimulus as assessed by the clinician. (MOST COMMON METHOD)

Quantitative monitoring is where the stimulator is coupled with a displacement transducer as a movement measuring device and number value is displayed. (PREFERRED BUT LESS COMMON)

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2
Q

Describe neuromuscular non-depolarizing blockade (phase II blockade).

A
  1. Agent binds to the nicotinic receptor on the motor end plate, but it does NOT cause a conformation change in the receptor.
  2. It does, however, prevent Ach from binding to the receptor rendering the muscle effectively “paralyzed”
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3
Q

What is the preferred method of determining the level of neuromuscular blockade?

A

Contraction of the adductor muscle of the thumb via stimulation of the ulnar nerve.

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4
Q

Where are the electrodes placed to monitor the ulnar nerve?

A

The electrodes are applied over the ulnar nerve. The distal electrode is placed over the proximal flexor crease of the wrist, and the other electrode is placed over and parallel to the carpi ulnaris tendon.

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5
Q

What muscle groups are the most sensitive to neuromuscular blockers?

A

Eye muscles are the most sensitive and are the first group to be affected followed by the extremities, trunk, abdominal muscles and finally the diaphragm.

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6
Q

During recovery, which muscle group recovers first?

A

Diaphragm recovers the first and the eye muscles last!

OPPOSITE DIRECTION!

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7
Q

Which monitoring site is best to measure the onset of neuromuscular blockade? What is the response?

A

Facial nerve - eyelid movement

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8
Q

Which monitoring site is the best to measure recovery from neuromuscular blockade? What is the response?

A

Ulnar nerve - thumb adduction

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9
Q

What does it mean if fade is present?

A

Sign of drug-induced muscle paralysis OR a clinically significant block remains

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10
Q

How does fade occur?

A

Because the nondepolarizing drugs block presynaptic Ach receptors in addition to their classic antagonist effect at postsynaptic Ach neuromuscular junction sites.

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11
Q

What is a single twitch?

A

A single supra-maximal electrical stimulus ranging from 0.1 to 1Hz for 0.1 to 0.2 milliseconds

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12
Q

What monitoring test requires a baseline before drug administration?

A

Single Twitch

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13
Q

What is TOF stimulation?

A

A series of 4 twitches at 2Hz every 1/2 second for 2sec.

Compares the first twitch to the 4th twitch

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14
Q

Which monitoring test reflects blockade from 70% - 100%

A

TOF stimulation

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15
Q

What does it mean if the fourth twitch (T4) disappears OR you have 3 twitches?
Disappearance of the third twitch (T4 and T3 absent)? OR you have 2 twitches?
Disappearance of the second twitch (T4, T3, & T2 absent) OR you have 1 twitch?

A

A block of more than 75%-80%
80%-85%
90%-95%

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16
Q

What is the ideal degree of paralysis?

A

The ideal degree of paralysis necessary for any procedure with sufficient anesthetic depth is 85% to 95%. That correlates with 1 to 2 twitch responses present on TOF stimulation.

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17
Q

What is double-burst simulation?

A

Two short bursts of 50Hz tetanus separated by 0.75 sec

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18
Q

Which is easier to detect fade - TOF or double-burst?

A

Double-burst due to evaluating two twitches rather than four twitches

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19
Q

What indicates significant paralysis with double-burst?

A

Fade of the second impulse is comparable to TOFR of less than 0.6

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20
Q

What is tetanus?

A

Generally consists of rapid delivery of a 30-, 50-, or 100Hz stimulus for 5 seconds

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21
Q

Which degree of hertz is more reliable for detecting fade, but is not always specific?

A

100Hz

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22
Q

What is Posttetanic Count (PTC)?

A

50-Hz tetanus for 5 seconds, a 3 second pause, then single twitch for 1-Hz

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23
Q

A count less than _____ indicates a deep block, and prolonged recovery is likely

A

Eight!

**Used only when TOF and Double-burst stimulation is absent

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24
Q

What is the clinical duration of action of neuromuscular blockade?

A

Time from drug administration to 25% recovery of the twitch response

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25
Q

What is the total duration of action of neuromuscular blockade?

A

Time from drug administration to 90% recovery of twitch response.

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26
Q

What is the recovery index of neuromuscular blockade?

A

Time from 25% to 75% recovery of the twitch response

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27
Q

What is the train-of-four ratio?

A

Compares the 4th twitch of a TOF with the 1st twitch

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28
Q

With TOF, when the 4th twitch is ____% of the 1st twitch, recovery is indicated?

A

90%

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29
Q

What is Posttetanic potentiation?

A

With PTC, the extra Ach will transiently reverse the relaxant by competing for the receptor at the local monitoring site. This augmented response will only last a few seconds until the excess Ach dissipates.

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30
Q

What are some key points related to recovery from neuromuscular blockade?

A 
TV at least 5mL/kg
No palpable fade with TOF or double-burst
Sustained tetanus
VC at least 20mL/kg
Inspiratory force at least -40cm H2O
Head lift x 5 seconds
Adequate hand grip
Sustained bite (corresponds with TOF of 85%)
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31
Q

How does succinylcholine work?

A

Depolarization muscle relaxant.
An agonist at the nicotinic receptor and mimics the actions of Ach by depolarizing the motor end plate, followed by desensitization.

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32
Q

How is succinylcholine metabolized?

A

Hydrolyzed by plasma cholinesterase (pseudocholinesterase) - enzymes found in the plasma, but produced from the liver

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33
Q

How is succ eliminated?

A

Hydrolyzed succinylcholine results in succinylmonocholine and choline, then plasma cholinesterase further reduces it to succinic acid and choline.

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34
Q

What can a prolonged neuromuscular blockade result from?

A

Excessive doses of succ in patients with atypical, inhibited or deficient levels of plasma cholinesterase.

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35
Q

What is the ED95 of succ?
Intubating dose?
Time of onset?
Duration of action?

A

ED95: 0.3mg/kg
Intubating dose: 1-1.5mg/kg
Time to onset: 30-60sec
DOA: 5-15 minutes

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36
Q

What does ED95 stand for?

A

The dose necessary to provide the desired effect in 95% of the population

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37
Q

What is the onset of action at the larynx of succ?

A

34 seconds for a 1mg/kg dose

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38
Q

What % of the injected dose actually reaches the neuromuscular junction?

A

10%

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39
Q

What is the plasma 1/2 life of succ?

A

2-4 minutes

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40
Q

All muscle relaxants including succ contain?

A

Quaternary ammonium - this structure renders it WATER SOLUBLE in the body.

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41
Q

Does succ cross the BBB and has direct CNS effects?

A

FALSE!

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42
Q

How much does succ indirectly increase ICP?

A

Small and transient rise of 10 to 15 mmHg for 5 to 8 minutes after administration

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43
Q

How does succ effect the CV system?

A

Slight tachycardia and sudden abrupt bradycardia may result in repeated doses in adults and any dosing in children.

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44
Q

What does the bradycardia result from?

A

Autonomic ganglia and parasympathetic muscarinic receptor stimulation

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45
Q

How much does an incubating dose of succinylcholine increase serum potassium level?

A

0.5 - 1 mEq

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46
Q

What may prolong the effects of succ?

A

Certain types of liver damage since cholinesterase substrates are produced by the liver

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47
Q

What can serve as a sensitive measure of the synthetic capacity of the liver?

A

pseudocholinesterase (PChE) activity

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48
Q

What other diseases might decrease levels of PChE be found in?

A

Pts with acute infections, pulmonary embolism, muscular dystrophy, myocardial infarction, pregnancy, and after surgical procedures.

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49
Q

What test can be done to determine whether an atypical enzyme is present and the cause of prolonged apnea experienced in pts after being given succ?

A

Dibucaine inhibition test - Dibucaine is an AMIDE local anesthetic that inhibits typical or usual PChE, but NOT atypical PChE.

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50
Q

What is a normal dibucaine number?

What does it mean?

A

80
Means 80% of the PChE activity was inhibited by dibucaine. If a 20 was obtained, the patient has atypical enzyme because dibucaine did not inhibit the patients enzyme activity.

KNOW BOX 12-3

51
Q

Atypical PChE has an increased or decreased enzyme activity and what is the associated dibucaine #?

A

Enzyme activity is decreased by 70% or more

The duration of succ is significantly prolonged with a dibucaine # 16-30

52
Q

What types of patients may have a markedly decreased PChE activity, but normal enzymes?

A

Pts with acute or chronic liver disease, organophosphate poisoning, CRD, patients in late stages of pregnancy and patients undergoing estrogen therapy

53
Q

Can succ by used with renal patients?

A

As long as serum K+ is WNL (usually renal failure Pts are dialyzed prior to surgery)

54
Q

How is the onset of succ effected in the elderly?

A

The onset may be slightly prolonged d/t slower circulation time, but clinical relevance is minimal.

55
Q

What types of drugs, commonly taken by the elderly, inhibit cholinesterase and may prolong the actions of succ?

A 
Anticholinesterase drugs used to treat Alzheimer's disease which include: 
Tacrine (Cognex)
Donepezil (Aricept)
Rivastigmine (Exelon)
Galantamine (Razadyne)

They increase acetylcholine levels in the CNS and are referred to as cognitive enhancers.

56
Q

What is the recommended dose of succ in obese patients?

A

1.0mg/kg based on TOTAL body weight

57
Q

Why should succ be reserved for only emergencies in pediatrics?

A

Severe hyperkalemia and rhabdomyolysis d/t undiagnosed duchenne muscular dystrophy (onset of symptoms usually present around 5yo)

58
Q

How does succ cause increases in serum K+?

A

As the action potential traverses the neuron, an influx of sodium and release of potassium occurs.

59
Q

Why might Pts with upper or lower motor denervation, infection, direct muscle trauma, muscle tumor, muscle inflammation, burn injury, immobilization, and prolonged chemical denervation by muscle relaxants, drugs, or toxins cause HYPERKALEMIA?

A

Up-regulation of AChRs spreading throughout the muscle membrane

60
Q

How long after a burn is it considered unsafe to administer succ?

A

More than 24hrs after the burn

61
Q

What is the treatment for succ induced hyperkalemia?

A

Drugs that promote cellular uptake of K+ including insulin with glucose, catecholamines and sodium bicarbonate

62
Q

What are some contraindications to the use of succ?

A

Hyperkalemia
Burn patients (injuries over 35% of total BSA)
Severe muscle trauma
Neurologic injury
Severe sepsis
Muscle wasting or prolonged immobilization
MH
Duchenne muscular dystrophy
Genetic variants of pseudocholinesterase
Allergy

BOX 12-5

63
Q

What are S/S of MH?

A 
Muscle rigidity
Rhabdomyolysis 
Increased CO2 production
Convulsions
Metabolic acidosis
Tachycardia
Rapid increase in temp
64
Q

What can reduce the fasciculations and myalgia caused by succ?

A

Small doses of nondepolarizing muscle relaxants (10-30% of ED95). Also pretreatments with sodium channel blockers (lidocaine) or NSAIDS may also work.
Opioids do NOT have any impact!

65
Q

Name the SEs of succinylcholine.

A 
Hyperkalemia 
Dysrhythmias
Myalgia
Myoglobinemia
Elevated ICP
Elevated IOP
MH
Masseter spasm
66
Q

What is a phase II block?

A

When large does of succ are given causing changes that resemble more of a nondepolarizing block as evidenced by FADE in response to tetanic stimuli, TOF and DBS and theoretically, antagonism with drugs such as neostigmine

67
Q

What are characteristics of a Depolarizing (Phase I) Block?

A
  1. Muscle fasciculations precedes onset of neuromuscular blockade
  2. Sustained response to tetanic stimulation
  3. Absence of Posttetanic potentiation, stimulation or facilitation
  4. Lack of fade to tetanus, TOF, or DBS
  5. Block potentiated by anticholinesterase drugs
68
Q

What are the characteristics of a Nondepolarizing (Phase II) Block?

A
  1. Absence of muscle fasciculations
  2. Appearance of tetanic fade and Posttetanic potentiation, stimulation or facilitation
  3. TOF or DBS fade
  4. Reversal with anticholinesterase drugs
69
Q

What drugs are used for RSI?

A

Succ

Roc

70
Q

What percent of Roc is protein bound?

What does this cause?

A

46%

A more rapid onset b/c more unbound drug is readily available at the neuronal binding sites

71
Q

What is the intubating dose for Roc?

How long does onset of action take?

A

0.6 - 1.2mg/kg

45-90 seconds

72
Q

What is the onset of the agent related to?

A

It’s potency. (the less potent the agent, the faster the onset)

73
Q

How long does an intubation dose of 0.6 - 1.0mg/kg last?

A

30-90 minutes

74
Q

Define priming.

A

Priming involves giving 10% of the calculated intubating dose prior to inducing anesthesia - this speeds on the onset by seconds

75
Q

How is roc metabolized?

A

Both hepatic and renal elimination. Renal accounts for 33% of elimination

76
Q

What is the elimination half-life of roc?

A

60-120 minutes

77
Q

What is an intubating dose of vec?

A

0.1mg/kg with the maximum suppression of muscle twitch occurs within 3 minutes of administration

78
Q

How does the lipid solubility of vec compare to pancuronium?

A

Vec is more lipophilic than pancuronium, but is still predominantly a hydrophilic compound

79
Q

How is vec eliminated?

A

Hepatic and renal mechanisms

Because vec is more lipophilic than other agents in its class, it doesn’t solely depend on the kidneys for elimination.

80
Q

Is vec more or less potent than pancuronium?

A

1.5x more potent

81
Q

what is the mean duration of blockade of pancuronium?

A

109 minutes - one of the longest acting nondepolarizing

82
Q

What is the main SE of pancuronium?

A

Tachycardia

83
Q

How is pancuronium eliminated?

A

Via the kidney through glomerular filtration and small amts released in the bile.

84
Q

What % protein bound is atracurium?

A

82% and is ionized so it doesn’t distribute into fat

85
Q

What is the onset of atracurium?

A

Inversely proportional to the dose in the range of 1.2 - 2.8 minutes

86
Q

How is atracurium metabolized?

A
  1. Hoffman elimination
  2. Nonspecific ester hydrolysis

(organ independent)

87
Q

What is Hoffman elimination dependent on?

A

Temperature

pH

88
Q

In what types of states is laudanosine released?

A

Mild alkaline states

89
Q

What are the advantages of cisatracurium?

A

CV stability
Non-organ dependent elimination
Lack of histamine release

90
Q

How does the potency of cis compare to atracurium?

How does the potency of cis compare to roc?

A

Cis is 3x more potent than atracurium but with a slower onset of action.

Cis is 5x more potent than roc, but with a slower onset of action, longer duration and slower spontaneous recovery.

91
Q

How is cis metabolized / eliminated?

A 
Hoffmann elimination in the plasma and tissues (77%) and 
Nonspecific esterases (23%)
92
Q

What is the half life of cis?

A

26-36 minutes

93
Q

What is a metabolite of cisatracurium and atracurium?

A

Laudanosine

94
Q

How does the metabolite of cis compare to atracurium?

A

Cis liberates 1/5 as much laudanosine as atracurium

95
Q

What is the chemical structure of all muscle relaxants?

Water or lipid soluble?

A

Quaternary ammonium compound

Water soluble at physiologic pH

96
Q

How do NMBAs effect the CV system?

A

**NMBAs have NO DIRECT EFFECT on the CV system, only INDIRECT actions such as histamine release!

Atracurium: increased HR & decreased BP at high doses (0.5mg/kg) b/c of histamine release

Pancuronium: tachycardia d/t vaguely tic and indirect sympathomimetic actions

97
Q

Which muscle relaxants are affected by changes in hepatic and renal status?

A

Roc
Vec
Pan

All are primarily eliminated by liver, biliary, and renal excretion.

98
Q

What are the NMBAs agents of choice for patients with liver disease?

A

Atracurium and cisatracurium; however, cis is preferred due to is lack of histamine release

99
Q

Which NMB is most effected by renal function?

A

Pancuronium (80-85% dependent on renal elimination)

100
Q

How are the onset times of NMBAs effected in the elderly?

A

Onset times are generally delayed in the elderly due to slower circulation times.

101
Q

How should NMBAs be dosed in obese patients?

A

Dosed at IDEAL body weight (EXCEPTION: Succ dosed at TOTAL body weight)

102
Q

How are NMBAs effected in neonate compared to adults?

A

Neonates/infants have a higher volume of distribution and differences in redistribution, elimination, and metabolic rates.

The onset of action of relaxants tends to be FASTER in children.

The DOA of intermediate NMBAs is LONGER in infants than children and the recovery is FASTER in children than adults.

103
Q

How does hypothermia effect NMBA DOA?

A

Prolongs DOA (due to decreased metabolism and delayed hepatic and renal clearance)

104
Q

What are the main components of the allergenic reactions to NMBAs?

A

Quaternary and tertiary ammonium ions in the relaxant molecules

105
Q

How do cholinesterase inhibitors (edrophonium, pyridostigmine, and neostigmine) work?

A

By inhibiting AChE, thereby increasing the concentration of endogenous ACh around the cholinoreceptors.

106
Q

Are cholinesterase inhibitors lipid soluble?

A

Poorly. Minimal crossing through lipid barriers

107
Q

Define recurarization.

A

Adequate reversal was obtained, but the drug effect was reestablished

108
Q

How does edrophonium work?

A

It is a simple alcohol that contains a quaternary ammonium group. It a reversible inhibitors of cholinesterase because it electrostatically attaches to the binding site of AChE and is stabilized by hydrogen bonding.

Since a true chemical bond is NOT formed, ACh competes with edrophonium for the binding site of AChE leading to a shorter duration of action!

109
Q

How does neostigmine and pryidostigmine work?

A

They are carbamic acid esters of alcohols and contain a quaternary or tertiary ammonium group.

They are INDIRECT-ACTING Cholinesterase Inhibitors by inhibiting AChE and increasing the concentration of ACh around the cholinoreceptors.

110
Q

What is the onset of action and DOA of neostigmine vs. edrophonium vs. pyridostigimine?

A

Neostigmine: most commonly used, may increase PONV
Onset of action: 5-15 minutes
DOA: 45-90 min

Edrophonium: rapid onset, short duration
Onset of action: 5-10 minutes
DOA: 30-60 min

Pyridostigime: slow onset, long DOA, rarely used
Onset of action: 10-20 minutes
DOA: 60-120 minutes

111
Q

How is neostigmine metabolized / eliminated?

A

Renal excretion 50% by glomerular filtration and the remaining 50% is hydrolyzed by plasma esterases and hepatic metabolism.

112
Q

Why are anticholinergics given with anticholinesterases?

A

To prevent the parasympathetic / muscarinic SEs of the anticholinesterase drugs such as vagal SEs d/t systemic buildup of Ach. SEs include: bradycardia, hypotension, bronchoconstriction, hypersalivation, diarrhea, and increase in PONV.

113
Q

What is the chemical makeup of glyco?

A

Quaternary ammonium compound - ionization limits GI absorption, BBB and placental penetration.

114
Q

What is glyco used most often?

A

It produces less initial tachycardia and has NO CNS effects

115
Q

What chemical compounds are atropine and scopolamine?

A

Tertiary amines

116
Q

Which anticholinergics cross the BBB?

A

Atropine and scopolamine? crosses the BBB and the placental barrier

Glyco unable to cross the BBB, placental barrier and limits GI absorption due to its ionization. Qua ternary ammonium derivatives often have potent peripheral effects WITHOUT CNS activity.

117
Q

What is the onset of IV glyco?
Onset of IM glyco?
DOA?

A

IV: 1 min
IM: 15-30 minutes
DOA: 2-3 hrs

118
Q

How is glyco metabolized / excreted?

A

Excreted in the feces and urine, primarily as an unchanged drug

119
Q

What is the normal dose of neostigmine and robinal?

What is the normal dose of edrophonium and atropine?

A

Neostigmine: 0.05mg/kg
Robinal: 0.01mg/kg

Edrophonium: 0.5-1mg/kg
Atropine: 0.15mg per 10mg of endrophonium

120
Q

What is sugammadex?

A

First selective binding agent (SRBA)

It is a modified gamma-cyclodextrin that works by encapsulating and forming very tight water-soluble complexes at a 1:1 ratio with steroidal neuromuscular blocking drugs.

121
Q

What is the clinical dosage range of sugammadex?

A

2 to 16 mg/kg according to the depth of the block

16mg/kg dose is also used immediate rescue situations.

122
Q

What are some reported adverse drug reactions of sugammadex?

A

Dry mouth, dysgeusia, nausea, vomiting, allergy, chills, and postural HTN

123
Q

How much is the drug is eliminated in the urine within 24 hours of administration?

A

80%

124
Q

Does sugammadex affect bezylisoquinolones such as atracurium and cisatracurium?

A

No, thus if neuromuscular blockade needs to be reestablished after the administration of sugammadex, these drugs may be given.

Lindsays Flashcardlet (27 decks)

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