NMBAs Flashcards

1
Q

Other names for succinylcholine

A
  • annectine
  • SCh
  • Quelicin
  • Suxamethonium
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2
Q

Doses for SCH

RSI:
Small children:
IM:
Laryngospasm:

A

RSI: 1-1.5 mg/kg

Small children: 2 mg/kg (peds often give 1 mg/kg with atropine in same syringe)

IM: 3-5 mg/kg

Laryngospasm: 20 mg (1 cc)

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3
Q

Indication for annectine (6)

A
  • rapid muscle relaxation
  • routine intubation
  • very short cases
  • OB
  • RSI (full stomachs)
  • laryngospasm
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4
Q

Contraindication for Quelicin

A
  • MH
  • kids have increased risk for hyperK and cardiac arrest from undiagnosed myopathies
  • prolonged block with pseudo cholinesterase abnormality/deficiency (pregnancy/liver disease)
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5
Q

MOA of Annectine

A

Bind to 2 alpha subunits of nicotinic cholinergic receptors

Allow Na and Ca influx, K efflux—> depolarizes cell and remains depolarized until diffuses away from receptors

Mimics ACh

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6
Q

CV and Respiratory effects of suxamethonium

A

CV: Muscarinic stimulation —> can decrease HR

**esp in peds

Resp: apnea

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7
Q

Neuro effects of SCh

A

Questionable increase in IOP and intragastric pressure, increases ICP

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8
Q

SCh could interact with what drug groups

A

Drugs used to treat Myesthenia Gravis and chemo drugs can prolong effects

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9
Q

Clinical implications of SCh

A
  • used frequently in OB
  • avoid in pts whose K is already high— burns, trauma, renal failure — immobilization and stroke causes extra receptors which can cause a profound increase in K
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10
Q

Onset and duration of Quelicin

A

O: 30-60 seconds IV; 2-5 min IM
D: < 10 IV; 10-30 min IM

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11
Q

Metabolism of SCh

A

Plasma cholinesterase (PCE); diffuses from NMJ, hydrolyzed in the plasma and liver by PCE

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12
Q

T or F: the weak active metabolite of SCh is succynltricholine

A

F- weak active: succinylmonocholine

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13
Q

T or F: there is severe histamine release from succyinlcholine

A

F- minimal Release of histamines

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14
Q

What can large or repeated doses of SCh cause

A

Phase II block

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15
Q

If a patient has pseudocholinesterase deficiency, what test will tell you severity of deficiency

A

Dibucaine number

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16
Q

Why is there no reversal of SCh

A

Only 10% of the drug administered reaches the NMJ

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17
Q

What can cause postop muscle pain after SCh administration

A

Fasciculation

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18
Q

Rocuronium (___)

is ________ acting

A

Zemuron

intermediate

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19
Q

Dosing of Zemuron

Intubation/surgical relaxation

Maintenance/repeated dose

RSI

Defasiculations

A

Intubation/surgical relaxation: 0.6 mg/kg

Maintenance/repeated dose: 0.1-0.2 mg/kg prn

RSI: 1.2 mg/kg

Defasiculations: 5 mg (0.03 mg/kg)

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20
Q

Indications for Zemuron

A
  • routine induction
  • surgical relaxation
  • RSI
  • defasiculation
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21
Q

CV effects of Zemuron

Histamine release?

A
  • none
  • rare histamine release
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22
Q

Clinical implications to keep in mind with OB patients & SCh:

A

Don’t defacisulate them… you will see eyes flutter but they don’t need it

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23
Q

rocuronium

  • onset
  • duration
  • elimination
A

O: 1-2 min (dose dependent, large dose can mimic SCh)
D: ~ 30 mins (variable) (up to 70 min with RSI)
E: hepatic 70% renal 30%

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24
Q

Sequence for Zemuron use for defasicuations

A

A. Give 5-10 mg Roc, wait a minute
B. follow with inductions agent
C. Administer SCh

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25
Q

Special considerations for Roc (3)

A
  • lack hormonal activity
  • volatile anesthetics can enhance NMB activity
  • burns may require higher doses
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26
Q

Vecuronium (___)

A

Norcuron

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27
Q

Dosage of Norcuron

Induction/intubation:

Priming:

Maintenance:

A

Induction/intubation: 0.08-0.1 mg/kg

Priming: 10% given 3-5 min prior

Maintenance: 0.01 mg/kg

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28
Q

CV effects of Vecuronium and is there histamine release?

A

CV = stable

Histamine = no histamine release

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29
Q

T or F: Vecuronium is very fast acting so it would be better for short cases

A

F: intermediate acting, best for long cases

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30
Q

Which NMBA is typically used for open heart surgeries

A

Vecuronium

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31
Q

Norcuron

Onset:

Duration:

A

O = 2-3 min (good intubating conditions) & 3-5 min (max blockade)

D = 25- 40 min (25% recovery) & 45-60 min (95% recovery)

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32
Q

Metabolite of Vec and potency:

A

3-desacetyl

60% potency of vec

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33
Q

Vec can precipitate with ________

A

Thiopental

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34
Q

T or F: Norcuron lacks hormonal activity

A

T

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35
Q

T or F: volatile anesthetics can enhance NMB activity

A

T

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36
Q

Pancuronium (___)

A

Pavulon

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37
Q

Pancuronium intubation and maintenance dose

A

I: 0.08- 0.12 mg/kg

Maintenance: 0.01 mg/kg

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38
Q

Caution for pancuronium in:

A

Caution in renal patients

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39
Q

CV effects of Pancuronium and is there histamine release? (5)

A
  • CV = atropine like effect in SA node (antimuscarinic effects)
  • tachycardia & increased CO due to antimuscarinic stimulation (it is a vagolytic)
  • causes norepinephrine release and decreased reuptake by adrenergic nerves
  • can be used in cardiac surgery to counteract bradycardia from high-dose opioid usage
  • increases BP

No histamine release

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40
Q

Cautiously use PAncuronium in what patients

A
  • pt who will not tolerate HR & CO increase —> poor choice in unstable cardiac patients
  • renal patients
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41
Q

Pancuronium-

Onset

DOA

Metabolism

Excretion

A

O: 2-3 min
DOA: 60-100 min
Metabolism: hepatic 20%
E: renal 40-70%

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42
Q

Active metabolite of pancuronium

A

3-OH- pancuronium

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43
Q

NMBAs:

A. Amino steroids

B. Benzylquinolone

A

A. Rocuronium, vecuronium, pancuronium

B. Atracurium, cisatricurium, mivacurium

44
Q

Atracurium (___)

A

Tracrium

45
Q

Atracurium

Dose
Onset
DOA

A

0.3-0.6 mg/kg
2-3 mins
20-35 mins (begin recovery) & 60-70 mins (95% recovery)

46
Q

System effects of tracrium

A

CV= minimal decrease in BP
Histamine= small
Other = in hyper parathyroidism, hypercalcemia decreases sensitivity, thus shorter DOA

47
Q

T or F: Atricurium is a good choice for renal patients

A

T

48
Q

Metabolism of atricurium

A

60% nonspecific ester hydrolysis
30% Hofmann elimination
10% renal

49
Q

Active metabolite of atricurium

A

Laudanosine = can produce rare seizure activity (tertiary amine crosses BBB)

50
Q

Onset and DOA of atricurium

A

O: 2-3 min
DOA: 20-35 min; 95% recovery in 60-70 min

51
Q

Cisatracurium (___)

A

Nimbex

52
Q

Dose for nimbex

A

0.1-0.15 mg/kg IV

53
Q

CV effects and histamine release of nimbex

A

CV= NO changes HR or BP
Histamine = none

54
Q

T or F: Nimbex is a good choice for NMBA in a renal transplant patient

A

T

55
Q

Nimbex:

Metabolism
Onset
Peak
Duration

A

Metabolism: Hoffman elimination, metabolite breakdown by nonspecific esterase metabolism
Onset: 2-3 min
Peak: 3-5 min
Duration: 40-70 min; 20-35 min to begin recovery; up to 93 min for 90% return

56
Q

Cisatracurium is the potent ___ isomer of ___.

A

cis-cis; atracurium

57
Q

Rate each of the following as Short acting (SA), Intermediate acting (IA), or long acting (LA)

  • Roc
  • Vec
  • Pancuronium
  • atracurium
  • Nimbex
  • mivacurium
A
  • Roc = IA
  • Vec = IA
  • Pancuronium = very LA
  • atracurium = IA
  • Nimbex = IA/LA
  • mivacurium = SA
58
Q

Mivacurium (_______)

A

Mivacron

59
Q

Doses for mivacurium

Intubation
Infusions

A

Intubation: 0.15-0.2 mg/kg
Infusions: 4-10 mcg/kg/min

60
Q

Contraindication for mivacurium

A

Asthma and low BP due to large histamine release

61
Q

T or F: there is a small histamine release with rapid administration of mivacurium

A

F- LARGE histamine release

62
Q

Onset, DOA, and metabolism of mivacurium

A

O: 1 min
DOA: 10-20 min
M: hydrolysis by plasma cholinesterase

63
Q

3 ways to cause muscle relaxation

A
  • muscle relaxants
  • IAs
  • blocks
64
Q

Succinylcholine C/I:

A
  • Severe hyperkalemia (burns, severe abdominal infections, metabolic acidosis)
  • MH history
  • Upregulation (burns, hemiplegia, long ICU stays, CVA)
65
Q

Anaphylaxis under GA presents as:

A

increased PIP on vent (have to look for different signs than awake patients)

66
Q

Which three drugs are the most likely to cause anaphylaxis in the perioperative period?

A

32% Sugammadex
27% Rocuronium
23% Antibiotics

*we typically give all three together so it can be difficult to determine the cause of anaphylaxis

67
Q

Cisatracurium metabolism:

A

nonspecific ester hydrolysis & Hofmann elimination

68
Q

What side effects does histamine release cause?

A

Skin flushing, tachycardia, hypotesion

69
Q

Which of the NMBs produces the active metabolite Laudanosine?

A

Atracurium and Cisatracurium (Hofmann elimination is what produces this)<br></br>However, Cisatracurium is a much more potent drug than Atracurium, so because we are able to give a much smaller dose of Cisatracurium, there is extremely minimal risk of Laudanosine.

70
Q

Which of the benzylisoquinolinium NMBs has an active metabolite that we worry about?

A

Atracurium – Laudanosine (tertiary amine which can produce seizure activity)

71
Q

Which of the benzylisoquinolinium NMBs has an active metabolite that we worry about?

A

Atracurium – Laudanosine (tertiary amine which can produce seizure activity)

72
Q

Which of the benzylisoquinolinium NMBs has an active metabolite that we worry about?

A

Atracurium – Laudanosine (tertiary amine which can produce seizure activity)

73
Q

Which of the nondepolarizing NMBs may cause changes to BP?

A

Mivacurium and Atracurium (due to histamine release)

74
Q

Panc metabolism

A

70% renal
20% hepatic

75
Q

vec metabolism

A

~ 50/50 hepatic/renal

76
Q

How do we know when a patient is ready for intubation?

A
  • TOF, but BEST mode is single twitch, so you can see when it starts to fade (meaning patient is ready)
  • time (agent-dependent)
  • patient becomes easier to ventilate
77
Q

Aminosteroid NMBs:(small/large) volume of distribution (limited/high) lipid solubility

A

small

limited

78
Q

Aminosteroid NMBs:
highly (unionized/ionized) at physiological pH

A

ionized

79
Q

Aminosteroid NMBs:
_____ histamine release

A

minimal

80
Q

Aminosteroid NMBs:
primarily ___ breakdown and ___ excretion

A

primarily liver breakdown,
kidney excretion

81
Q

Nondepolarizing NMB MOA:

A

compete with/block ACh at the nicotinic receptor alpha subunits on motor endplate – inhibits depolarization

82
Q

MH occurs more commonly in:

(peds/adults)
(males/females)

A

peds (1 in 15,000) … vs 1 in 10,000 to 50,000 in adults

males

83
Q

How do you reconstitute Ryanodex?

A

Reconstitute 250 mg vial with 5 cc of STERILE WATER - (50 mg/cc)
Administer 2.5 mg/kg rapidly through large bore IV

84
Q

How do you reconstitute Dantrolene?

A

Reconstitute the 20 mg vial with 60 cc of STERILE WATER

85
Q

Dantrolene dose:

A

2.5 mg/kg

86
Q

How do we administer GA to patients with a history of MH?

A

Propofol TIVA, O2, N2O, regional?

87
Q

What are the first signs of MH?

A

rapidly increasing EtCO2
tachycardia
generalized muscle rigidity

88
Q

Can we use N2O in patients with MH history?

A

YES! It is a gas, not a volatile agent

89
Q

What are the top triggers for MH?

A

Volatile agents and SCh

90
Q

What four drugs are most often involved in drug errors?

A

(17.1%) Succinylcholine
(13.2%) Inhalational Agents
(11.7%) Opioids
(9.3%) Local anesthetics

91
Q

Succinylcholine dose:
(laryngospasm)
conc:

A

20 mg
(20 mg/cc)- give 1 cc

92
Q

Succinylcholine
dose: (IM adults)
conc:
onset:
duration:

A

3-5 mg/kg IM
(20 mg/cc)
2-5 mins
10-30 mins

93
Q

Succinylcholine
dose: (IV peds)
conc:
onset:
duration:

A

2 mg/kg (d/t larger volume of distribution and faster total clearance)
(20 mg/cc)
30-60 sec
10 mins

94
Q

Succinylcholine metabolite:

A

Succinylmonocholine is a weak, active metabolite

95
Q

Aside from a genetic deficiency of pseudocholinesterase, what else may cause a deficiency?

A

Pregnancy and liver disease (it is synthesized in the liver)

96
Q

Succinylcholine metabolism:

A

Butyrylcholinesterase (pseudo/plasma cholinesterase) –> synthesized by the liver and found in the plasma —-> hydrolyzes SCh in the plasma after it diffuses away from the NMJ

97
Q

Why do we only administer Succinylcholine in Peds for emergency situations?

A

Peds are at increased risk for fatal hyperkalemia and cardiac arrest (d/t undiagnosed myopathies)

98
Q

What does a Dibucaine number measure?

A

Measures QUALITY pseudocholinesterase

99
Q

Prolonged apnea after administration of Succinylcholine might be related to what?

A

Pseudocholinesterase abnormality;
check Dibucaine number

100
Q

Succinylcholine (decreases/increases) intraocular pressure.

A

increases (peaks 2-4 mins; returns to normal by 6 mins)

101
Q

Succinylcholine (decreases/increases) ICP.

A

increases (increased ICP more likely d/t lack of adequate anesthesia)

102
Q

Succinylcholine (decreases/increases) intragastric and LES tone

A

increases (these two effects negate increased risk for aspiration)

103
Q

Succinylcholine causes ___ histamine release.

A

minimal

104
Q

Which of the NMBs normally causes a Phase I (no fade) TOF?

A

SCh, with large or repeated doses a Phase II (fade) TOF can result

105
Q

For what reason is rapid sequence induction performed?

A

Aspiration risk!!

106
Q

How do you determine which muscle relaxant to use?

A

Pre-existing conditions
Procedure length
Type of procedure

107
Q

What are three ways to cause muscle relaxation?

A

Volatile anesthetics
NMBs
regional anesthesia