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Top Drawer > Muscle Relaxants > Flashcards

Muscle Relaxants Flashcards

1
Q

What are 3 ways to cause muscle relaxation?

A
  1. increase volatile anesthetic
  2. regional anesthesia
  3. NMBA
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2
Q

Classes of NMBAs

A
  • depolarizing
  • nondepolarizing (aminosteroids & benzylisoquinolines)
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3
Q

What drug(s) are depolarizing NMBAs?

A

succinylcholine

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4
Q

What drug(s) are nondepolarizing aminosteroids?

A
  • rocuronium
  • vecuronium
  • pancuronium
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5
Q

What drug(s) are nondepolarizing benzylisoquinolines?

A
  • mivacurium
  • atracurium
  • cisastracurium
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6
Q

How does succinylcholine work?

A

binds to 2 alpha subunits of nicotinic cholinergic receptors (like ACh), allowing Na+ and Ca++ to flow in, K+ to flow out, and causing depolarization of the muscle

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7
Q

Succinylcholine mimics the action of __________

A

acetylcholine

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8
Q

When administered succinylcholine, the muscle remains depolarized until ________________

A

succinylcholine diffuses away from the receptor

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9
Q

When is succinylcholine used?

A
  • rapid muscle relaxation
  • routine intubation
  • very short cases
  • OB
  • RSI
  • laryngospasm
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10
Q

T/F: There is a reversal agent for succinylcholine

A

false
there is no reversal agent for succinylcholine; just has to diffuse away

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11
Q

Which NMBA has the potential to trigger malignant hyperthermia?

A

succinylincholine

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12
Q

Succinylcholine has potential to __________ HR due to _____________ stimulation

A
  • decrease HR
  • muscarinic stimulation
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13
Q

What is Phase I of succinylcholine administration?

A

normal expected phase from proper dosing; no fade on TOF

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14
Q

What is Phase II of succinylcholine administration?

A

happens from large or repeated doses of SCh; fade will be seen on TOF

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15
Q

The most common side effect of succinylcholine

A

fasciculations

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16
Q

Fasciculations can cause _____________

A

myalgia (muscle pain)

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17
Q

T/F: Succinylcholine has minimal histamine release

A

true

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18
Q

What are the potential side effects in children when given succinylcholine?

A
  • hyperkalemia
  • bradycardia
  • cardiac arrest
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19
Q

How is succinylcholine metabolized?

A

hydrolyzed in plasma by buyrylcholinesterase aka plasma cholinesterase aka psuedocholinesterase

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20
Q

Succinylcholine Dosing

A

1 - 1.5 mg/kg for RSI
20 mg for laryngospasm

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21
Q

Succinylcholine onset and duration

A

Onset: 30-60 sec
Duration: < 10 min

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22
Q

Succinylcholine IM Dosing

A

3-5 mg/kg

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23
Q

Succinylcholine IM onset and duration

A

Onset: 2-5 min
Duration: 10-30 min

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24
Q

____________ is a weak active metabolite of succinylcholine

A

succinylmonocholine

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25
Q

What can prolong blocking effects of succinylcholine?

A

anything that can cause decreased levels of pseudocholinesterase (pregnancy, liver disease) and pseudocholinesterase abnormality

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26
Q

T/F: Pregnancy can prolong blocking effects of succinylcholine

A

true
pregnancy decreases pseudocholinesterase levels, causing decreased metabolism of SCh

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27
Q

What are the triggers for MH?

A
  • succinylcholine
  • volatile inhalational agents
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28
Q

T/F: Nitrous oxide can trigger MH

A

false

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29
Q

What are the first signs of MH?

A
  • unexplained increase in CO2
  • unexplained increase in temp
  • masseter spasm/rigidity
  • unexplained sudden tachycardia
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30
Q

How do nondepolarizing NMBAs work?

A

compete with and block ACh at the alpha subunits of the nicotinic receptors on the motor endplate, inhibiting depolarization

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31
Q

When are nondepolarizing relaxants used?

A

muscle relaxation for surgery or for intubation

32
Q

How are aminosteroid nondepolarizing NMBAs metabolized and excreted?

A
  • primarily liver breakdown
  • kidney excretion
33
Q

T/F: nondepolarizing NMBAs have the most reported allergic reactions

A

true
nondepolarizing relaxants have potential for allergic reactions

34
Q

What is the most commonly used NMBA?

A

rocuronium

35
Q

Rocuronium Dosing

A

Routine induction: 0.6 mg/kg
RSI: 1.2 mg/kg

36
Q

_____ mg of rocuronium can be used as a _______________ dose for succinylcholine

A
  • 5 mg
  • defasciculating dose
37
Q

What is the maintenance/repeat dose for rocuronium?

A

0.1 - 0.2 mg/kg

38
Q

Rocuronium onset and duration

A

Onset: 1-2 min
Duration: 30 min

39
Q

Rocuronium is primarily eliminated/metabolized by _______________

A

the liver

40
Q

Vecuronium Dosing

A

0.08 - 0.1 mg/kg

41
Q

What is the maintenance/repeat dose for vecuronium?

A

0.01 mg/kg

42
Q

Which agent can you pretreat with 10% of the intubation dose 3 minutes before intubation?

A

vecuronium

43
Q

T/F: vecuronium has minimal histamine release

A

false
vecuronium has NO histamine release

44
Q

Vecuronium onset

A
  • good intubating conditions: 2-3 min
  • maximal blockade: 3-5 min
45
Q

Vecuronium has potential to precipitate with _____________

A

thiopental

46
Q

Does vecuronium have great cardiac effects?

A

no
vecuronium is fairly cardiac stable

47
Q

Pancuronium Dosing

A

0.08 - 0.12 mg/kg

48
Q

Pancuronium maintenance dose

A

0.01 mg/kg

49
Q

Pancuronium onset and duration

A

Onset: 2-3 min
Duuration: 60-100 min

50
Q

Pancuronium is a __________ acting NMBA

A

long acting

51
Q

T/F: there is NO histamine release with pancuronium

A

true

52
Q

What are the CV effects from pancuronium?

A
  • increased HR (tachycardia)
  • increased BP
  • incrased CO
53
Q

Must be careful in administering pancuronium in _________ patients

A

cardiac
may not be able to tolerate increase in HR, BP, and CO

54
Q

When is pancuronium used?

A

in situations where patient can be paralyzed for extended period of time due to long acting duration. not typically used for surgery, unless going to ICU intubated

55
Q

How does pancuronium cause tachycardia and high BP?

A

antimuscarinic stimulation –> norepinephrine release and reduced uptake of norepi by adrenergic nerves

56
Q

How are benzylisoquinoline NMBAs metabolized?

A
  • Hofmann Elimination
  • ester hydrolysis
  • plasma cholinesterase
57
Q

What is Hofmann Elimination?

A

spontaneous, non-enzymatic, non-organ dependent chemical breakdown; dependent on temperature and pH

58
Q

In regards to Hofmann elimination, what factors increase metabolism?

A
  • increased temp
  • increased pH (alkalosis)
59
Q

In regards to Hofmann elimination, what factors decrease metabolism?

A
  • decreased temp
  • decreased pH (acidosis)
60
Q

Which NMBAs are associated with histamine release?

A
  • rocuronium
  • mivacurium
  • atracurium
  • succinylcholine
61
Q

Which NMBAs have NO histamine release?

A
  • vecuronium
  • pancuronium
  • cisastracurium
62
Q

Mivacurium Dosing

A

Induction: 0.15 - 0.2 mg/kg
Infusion: 4-10 mcg/kg/min

63
Q

Mivacurium onset and duration

A

Onset: 1 min
Duration: 10-20 min

64
Q

Mivacurium is associated with ____________ when given quickly and can cause ____________

A
  • HISTAMINE RELEASE
  • flushing, hives
65
Q

Spontaneous recovery from mivacurium is rapid or slow?

A

rapid

66
Q

How is mivacurium metabolized?

A

plasma cholinesterase

67
Q

Mivacurium has the same mechanism of metabolism as which agent? What is this mechanism of metabolism?

A
  • Succinylcholine
  • plasma cholinesterase
68
Q

Atracurium Dosing

A

0.3 - 0.6 mg/kg

69
Q

Atracurium onset and duration

A

Onset: 2-3 min
Duration: 20-35 min (25%), or 60-70 (95%)

70
Q

How is atracurium metabolized?

A
  • Hofmann elimination
  • nonspecific ester hydrolysis
71
Q

What is the effect of atracurium on BP?

A

small decrease in BP

72
Q

What is the primary metabolite of atracurium?

A

laudanosine

73
Q

____________ is the primary metabolite of atracurium and has potential to cause ___________ since it can ______________

A

Laudanosine is the primary metabolite of atracurium and has potentail to cause seizures since it can cross the BBB

74
Q

Cisatricurim Dosing

A

0.1-0.15 mg/kg

75
Q

Cisatrcurium onset, peak, and duration

A

Onset: 2-3 min
Peak: 3-5 min
Duraiton: 40-70 min (25%); 20-35 min to begin recovery; 93 min (90%)

76
Q

What are the top 5 drugs that cause anaphylaxis during surgery?

A
  1. sugammadex
  2. rocuronium
  3. antibiotics
  4. local anesthetics
  5. propofol

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