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General Principles > Exam 2- NMBAs > Flashcards

Exam 2- NMBAs Flashcards

1
Q

where are lower motor neuron cell bodies located?

A

in the ventral horn of the spinal cord and the motor nuclei of cranial nerves

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2
Q

how do lower motor neurons project their axons?

A

via the ventral roots to control effector organs

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3
Q

what are effector organs?

A

muscles and glands

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4
Q

what are the characteristics of somatic motor neurons (3)

A

large diameter, myelinated, and fast conducting

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5
Q

what happens to an axon as it approaches its ending?

A

they lose their myelin sheaths before branching into terminal fibers

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6
Q

where does each terminal fiber supply a muscle fiber via a specialized connection?

A

the NMJ

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7
Q

what does the NMJ consist of?

A

the presynaptic motor neuron, the postsynaptic muscle fiber, and the senaptic cleft

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8
Q

what contains the enzyme acetylcholinesterase?

A

the synaptic cleft

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9
Q

what does the NMJ convert

A

the electrical signal of the motor nerve into a chemical signal which in turn is converted into an electrical event leading to a mechanical response

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10
Q

what does the motor unit consist of?

A

the motor neuron and the muscle fiber it innervates

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11
Q

what subunits are capable of binding ACh?

A

only the 2 alpha subunits

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12
Q

what kind of receptors for acetylcholine?

A

nicotinic

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13
Q

what is the primary purpose of muscle relaxation?

A

to achieve adequate relaxation of the upper airway, vocal cords, and diaphragm to facilitate intubation and surgery

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14
Q

NMBAs are NOT

A

anesthetics

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15
Q

do NMBAs cause amnesia?

A

no

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16
Q

is complete paralysis required for all surgical cases?

A

no

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17
Q

main site of action of NMBA is on what receptor?

A

the nicotinic cholinergic receptor

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18
Q

what is the twitch monitor?

A

a device used to measure how much muscle relaxation is caused by the dose of a muscle relaxant

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19
Q

only depolarizer used in anesthesia?

A

succinylcholine

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20
Q

ACh mediates transmission of

A

an impulse from nerve to muscle

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21
Q

what happens when depolarization of the motor nerve reaches the nerve terminal?

A

voltage-gated Ca2+ channels open, and the vesicles (quanta) that contain ACh are released
by exocytosis from the nerve terminal into the cleft

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22
Q

K+ channels in the nerve terminal area limit

A

the extent of Ca2+ entry into the terminal, and regulate the transmitter quantal release, initiating nerve membrane repolarization

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23
Q

the release of ACh quanta is antagonized by (2)

A

hypocalcemia and hypermagnesemia

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24
Q

where is ACh synthesized?

A

in the presynaptic nerve terminal

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25
Q

what is ACh synthesized from?

A

acetate and choline

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26
Q

where is most of the ACh contained?

A

in the reserve pool

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27
Q

Once nerve depolarization occurs and the intracellular
Ca2+ concentration increases, ACh quanta are released into

A

the synaptic cleft

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28
Q

what is ED50

A

what dose corresponds to a 50% twitch reduction

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29
Q

what is ED95?

A

corresponds to 95% block

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30
Q

anesthesia focuses on ED50 or ED95?

A

ED95

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31
Q

duration of action related to muscle blockers?

A

time of injection to return of 25% twitch height

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32
Q

what is the recovery index?

A

time interval between 25% and 75% twitch height

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33
Q

is rocuronium a depolarizer?

A

no, it is a nondepolarizer

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34
Q

where does a depolarizer work?

A

at the postsynaptic nAChRs

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35
Q

provide an example of a depolarizer

A

succinylcholine

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36
Q

define nondepolarizing drugs

A

competes for active binding sites on nAChRsp

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37
Q

examples of nondepolarizing

A

everything except succinylcholine

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38
Q

what does succinylcholine activate?

A

the prejunctional receptors to release ACh

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39
Q

what does succinylcholine mimic?

A

ACh

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40
Q

what does succinylcholine do to the postjunctional membrane and extrajunctional receptors?

A

produces sustained depolarization

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41
Q

what does prolonged depolarization of the motor end-plate do?

A

inactivates Na channels & increases influx of K

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42
Q

what drug may cause fasiculations before total paralysis?

A

succinylcholine

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43
Q

what is the typical IV dose for succinylcholine?

A

1-1.5 mg/kg

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44
Q

what is succinylcholine onset?

A

about 1 minute

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45
Q

what is succinylcholine duration?

A

5-15 minutes, dose dependent

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46
Q

almost 90% of SCh is…

A

hydrolyzed in the plasma before reaching the myoneural junction

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47
Q

where does hydrolysis of SCh occur?

A

in the plasma

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48
Q

what hydrolyzes SCh?

A

butyrylcholinesterase (pseudocholinesterase or plasma cholinesterase)

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49
Q

what is SCh broken down into?

A

succinylmonocholine and choline

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50
Q

how much of SCh releases the NMJ?

A

only 10%

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51
Q

where is Butyrylcholinesterase/Pseudocholinesterase/Plasmacholinesterase sythesized?

A

in the liver

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52
Q

where are Butyrylcholinesterase/Pseudocholinesterase/Plasmacholinesterase found?

A

in the plasma

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53
Q

what factors lower pseudocholinesterase?

A

severe liver disease, advanced age, pregnancy, malnutrition, burns, anticholinesterase drugs and Reglan, oral contraceptives

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54
Q

what does neostigmine do to pseudocholinesterase activity?

A

profoundly decrases activity

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55
Q

what can cause prolonged muscle relaxation after succinylcholine and mivacurium?

A

abnormal genetic variant of butyrylcholinesterase mutation

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56
Q

how do you test for abnormal genetic variant of butyrylcholinesterase?

A

check the dibucaine number

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57
Q

dibucaine number

A

results can help to identify individuals at risk for prolonged paralysis following the administration of succinylcholine.

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58
Q

Phase 1 block

A

expected w succinylcholine

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59
Q

with continued dosing of a depolarizing NMBA what can occur?

A

a phase I block can develop into a phase II block

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60
Q

what can cause a phase 2 block?

A

repeated SCh doses or an IV continuous infusion

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61
Q

phase 2 block

A

muscles are no longer receptive to acetylcholine released by the motor neurons

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62
Q

cardiovascular side effects of SCh

A

Sinus bradycardia, junctional and arrest PARTICULARLY IN CHILDREN

Premature ventricular contractions

reflect the actions of succinylcholine at cardiac muscarinic cholinergic (M2) receptors where the drug mimics the physiologic effects of acetylcholine

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63
Q

when is arrest common with SCh?

A

more common if a second dose is given within 5 minutes of first dose and in children

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64
Q

what do you treat SCh arrest with?

A

atropine

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65
Q

what can SCh do to plasma levels of potassium?

A

increase potassium by 0.5 mEq/dL in healthy patient

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66
Q

renal patients should avoid

A

Succinylcholine

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67
Q

SCh can cause severe hyperkalemia in what patients?

A

pts with burns, severe abd infections, severe metabolic acidosis

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68
Q

risk of SCh in children?

A

severe rhabdo, hyperkalemia, and death

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69
Q

what pre treatment can you give a patient to reduce cardiac effects

A

anticholinergics

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70
Q

Myoglobinuria

A

from muscle damage after SCh (most of the patients with rhabdomyolysis and myoglobinuria were subsequently found to have malignant hyperthermia or muscular dystrophy)

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71
Q

malignant hyperthermia can be caused by

A

SCh

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72
Q

masseter spasm

A

increase in tone of the masseter muscle may be an early indicator of malignant hyperthermia (especially in children)

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73
Q

what can SCh do to intragastric pressure?

A

increase intragastric pressure and lower esophageal tone (LES)

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74
Q

when does SCh increase intraocular pressure? (time)

A

2-4 min after administration

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75
Q

what drug is a contraindication a open eye injury?

A

SCh

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76
Q

malignant hyperthermia receptor

A

ryanodine

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77
Q

what activates the ryanodine receptor

A

halogenated agents & succinylcholine

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78
Q

what does MH cause release of?

A

massive uncontrolled release of Ca ++ from the sarcoplasmic reticulum

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79
Q

2 classes of nondepolarizing muscle relaxants

A

aminosteroids and benzylisoquinolinium

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80
Q

aminosteroids

A

pancuronium, pipercuronnium, vecuronium, rocuronium

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81
Q

benzylisoquinolinium examples

A

atracurium and cisatracurium

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82
Q

nondepolarizing muscle relaxants mechanism of action

A

Competitively antagonize the presynaptic receptors to decrease release of Ach (fade on TO4)

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83
Q

what do non depolarizing muscle relaxants compete with?

A

ACh for binding on one or both of the alpha subunits

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84
Q

rocuronium action

A

intermediate dose dependent

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85
Q

rocuronium histamine release?

A

rare

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86
Q

rocuronium effects on BP or HR?

A

none

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87
Q

what can be used to defasiculate with SCh?

A

rocuronium

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88
Q

rocuronium potency (low or high)

A

low

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89
Q

rocuronium intubating dose

A

0.6 mg/kg

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90
Q

highest anaphylaxis drug

A

rocuronium

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91
Q

rocuronium onset

A

good for RSI, variable onset

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92
Q

rocuronium metabolites

A

no real metabolites

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93
Q

rocuronium RSI dose

A

1.2 mg/kg

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94
Q

rocuronium comes in a ______. vial

A

50 mg

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95
Q

maintenance/repeat dose of rocuronium

A

0.1 mg/kg

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96
Q

rocuronium defasiculating dose with SCh?

A

5 mg

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97
Q

where is rocuronium mostly eliminated?

A

by the liver

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98
Q

vecuronium induction dose

A

0.1 mg/kg

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99
Q

vecuronium comes in a ______ mg vial

A

10

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100
Q

pretreatment of vecuronium for intubation dose is given when?

A

3 to 5 min before intubation dose

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101
Q

vecuronium maintenance dose for surgical relaxation

A

0.01 mg/kg

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102
Q

pancuronium acting time

A

long acting

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103
Q

pancuronium histamine release?

A

none

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104
Q

pancuronium vagolytic effects

A

modest tachycardia due to antimuscarinic stimulation

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105
Q

pancuronium direct sympathomimetic effects

A

norepinephrine release and reduced uptake of norepinephrine by adrenergic nerves

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106
Q

what drug has potential for significant postoperative residual blockade?

A

pancuronium

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107
Q

pancuronium initial dose

A

0.06-0.1 mg/kg

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108
Q

pancuronium maintenance dose

A

0.02 mg/kg

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109
Q

pancuronium onset

A

2-5 min

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110
Q

pancuronium duration

A

60-100 min

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111
Q

what drugs undergo hoffmann elimination?

A

Benzylisoquinolines

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112
Q

what is Hofmann elimination

A

Spontaneous, non-enzymatic, non-organ dependent chemical breakdown at physiologic temperature and pH

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113
Q

does mivacurium have histamine release?

A

yes when given quickly

114
Q

mivacurium recovery

A

spontaneous recovery from the block is rapid

115
Q

mivacurium metabolism

A

hydrolysis by plasma cholinesterase

116
Q

mivacurium intubation dose

A

0.2 mg/kg

117
Q

mivacurium infusion dose

A

5-8 mcg/kg/min

118
Q

mivacurium onset and duration

A

1 min onset, 20 to 30 min duration

119
Q

atracurium: short/intermediate/long acting

A

intermediate acting

120
Q

atracurium histamine release?

A

yes

121
Q

atracurium cardiovascular effects

A

skin flushing, tachycardia, and hypotension

122
Q

atracurium metabolism

A

hofmann elimination and ester hydrolysis

123
Q

atracurium dose

A

0.5 mg/kg

124
Q

atracurium onset

A

2-3 min

125
Q

atracurium duration

A

20 to 25 min

126
Q

atracurium primary metabolite

A

laudanosine

127
Q

what can laudanosine produce?

A

rare seizure activity

128
Q

cisatracurium: short/intermediate/long acting

A

intermediate

129
Q

cisatracurium metabolism

A

30% hofmann elimination

130
Q

cisatracurium histamine release

A

no

131
Q

cisatricurium cardiovascular changes

A

none

132
Q

what is a potent cis-cis isomer of atracurium

A

cisatracurium

133
Q

cisatricurium dose

A

0.15-0.2 mg/kg IV

134
Q

Cisatracurium onset

A

2-3 min

135
Q

Cisatracurium peak

A

4-7 min

136
Q

Cisatracurium duration

A

40-70 min

137
Q

what does hypothermia do the NMBA?

A

prolongs the duration by decreasing receptor sensitivity and ACh mobilization

138
Q

what happens to renal and hepatic metabolism w hypothermia?

A

renal and hepatic metabolism are reducesd

139
Q

what does hypothermia do to Hofmann elimination?

A

reduces Hofmann elimination

140
Q

what does aging do to the volume of distribution of NMBA

A

reduced volume of distribution due to decreased total body water and serum albumin

141
Q

what potentiates NMBAs

A

hypokalemia

142
Q

AChASe can catalyze ACh at _____ molecules per active site per second

A

4,000

143
Q

Anticholinesterase/Acetylcholinesterase Inhibitors

A

neostigmine, edrophonium, pyridostigmine

144
Q

Selective Relaxant Binding Agent

A

sugammadex

145
Q

what blocks the breakdown of ACh by AChAse

A

Acetylcholinesterase Inhibiting Agents/Anticholinesterase

146
Q

high dose of neostigmine

A

maximal inhibition

147
Q

Edrophonium: short/ intermediate/ long acting

A

short duration

148
Q

what drug is endrophonium used with?

A

atropine

149
Q

Enlon-Plus

A

is a mixture of Edrophonium and atropine together in the same vial

150
Q

edrophonium is mostly ineffective when?

A

given for deep blocks

151
Q

edrophonium onset

A

rapid, 1-2 minutes

152
Q

Edrophonium dose

A

.5-1 mg/kg mixed with atropine 7-10 mcg/kg (0.014 mg/mg of edrophonium)

153
Q

enlon-plus dose

A

Enlon-plus: .05-.1 mg/kg slowly over a minute

154
Q

endrophonium given without atropine

A

causes bradycardia

155
Q

what conditions are associated with upregulation of extrajunctional AChR

A

hemiplegia, paraplegia, muscular dystrophies, Guillian-barre syndrome, and burns

155
Q

is sugammadex water soluble

A

yes, highly

156
Q

what drug can encapsulate steroidal NBMA drugs

A

suggamadex

157
Q

what drug has 8 sugars arranged in a ring

A

sugammadex

158
Q

what are undesireable affects of sugammadex

A

nothing really

159
Q

does sugammadex effect acetylcholinesterase or cholinergic receptors?

A

no

160
Q

what drug when injected over 10s immediately captures free molecules of rocuronium or vecuronium?

A

sugammadex

161
Q

where is sugammadex filtered out

A

by the glomerulus

162
Q

when should you avoid sugammadex

A

patients with decreased creatinine clearance

163
Q

what drug should be avoided in ESRD?

A

sugammadex

164
Q

sugammadex routine reversal of modertate block dosing

A

2mg/kg

165
Q

sugammadex routine reversal of deep neuromuscular block dose

A

4mg/kg

166
Q

sugammadex dose for immediate reversal after rocuronium

A

16 mg/kg

167
Q

sugammadex and hormonal contraceptives

A

decreased effectiveness of birth ocontrol

168
Q

sugammadex hypersensitivity reactions

A

sneezing, nausea, rash and urticaria

169
Q

which reversal agent has a risk of anaphylaxis

A

sugammadex- airway edema, bronchospasm and CV collapse

170
Q

when is sugammadex anaphylaxis seen most often?

A

higher dosing

171
Q

when does sugammadex anaphylaxis occur?

A

within 5 min of admin

172
Q

how to treat sugammadex reactions?

A

small boluses of epinephrine (10-20 mcg) titrated to response, Benadryl, dexamethasone and famotidine

173
Q

what is the only anticholinesterase that crosses the BBB?

A

physostigmine

174
Q

what is not used for the reversal of muscle relaxants

A

physostigmine

175
Q

what are fasiculations

A

involuntary rapid muscle twitches that are too weak to move a limb but are easily felt by patients and seen or palpated by clinicians

176
Q

fasiculations with SCh

A

80-90% if not pretreated w non-depolarizer or NSAIDs for myalgias

177
Q

myalgias with SCh

A

usually big skeletal muscles; 50-60% for 1-2 days

178
Q

a defasiculating dose of _________________ administered prior to succinylcholine decreases its side effects

A

non-depolarizing muscle relaxant

179
Q

what is the onset of rocuronium

A

1-2 min depending on dose

180
Q

what is the duration of rocuronium

A

about 30-70 min after RSI dose

181
Q

what is rocuronium elimination

A

primarily by the liver (70%)/ 30% renal

182
Q

vecuronium: short/intermediate/long

A

intermediate NMB

183
Q

vecuronium histamine release

A

none

184
Q

vecuronium cardiac implications

A

cardiac stable

185
Q

what drug might precipitate with thiopental

A

vecuronium

186
Q

what kind of potency does vecuronium have

A

medium potency

187
Q

what is vecuronium onset

A

2-3 min for good intubating conditions
3-5 min for maximal blockade

188
Q

what is vecuronium duration

A

25-40 min you will see 25% recovery; 45-60 min you will see 95% recovery

189
Q

vecuronium metabolite

A

3-desacetyl (60% potency of vecuronium)

190
Q

pancuronium direct sympathomimetic effects

A

norepinephrine release and reduced uptake of norepinephrine by adrenergic nerves

191
Q

pancuronium cautions

A

in any patient that will not tolerate increased HR and cardiac output

192
Q

what drug poses the potential for significant postoperative residual blockade?

A

pancuronium

192
Q

what drug is used in cardiac surgery to counteract the bradycardia associated with high-dose opioid dosing

A

pancuronium

192
Q

what is the primary metabolite of atracurium

A

laudanosine

192
Q

patients with what condition might have an altered response to NMBAs?

A

myasthenia gravis

192
Q

what can laudanosine produce

A

rare seizure activity

193
Q

acidosis interferes with

A

effects of anticholinesterases

194
Q

hypercarbia leads to _______ and interferes with _________

A

acidosis; antagonism

195
Q

hypermagnesemia prolongs NMBA duration of action by

A

inhibiting calcium channels

196
Q

hypokalemia potentiates ___________ and can __________ the effectiveness of anticholinesterases on reversal

A

NMBAs; decrease

197
Q

what drugs can cause bronchoconstriction, increased salivation, increased bowel motility

A

Acetylcholinesterase Inhibiting Agents/Anticholinesterase

198
Q

Acetylcholinesterase Inhibiting Agents/Anticholinesterase drugs are usually given in combination with

A

an anticholinergic / antimuscarininc

199
Q

what drugs can cause significant parasympathetic effects

A

Acetylcholinesterase Inhibiting Agents/Anticholinesterase

200
Q

maximal inhibition occurs when

A

100% of acetylcholinesterase has been inhibited

201
Q

at maximal inhibiton

A
  • Additional doses of acetylcholinesterases will not improve recovery
  • Can lead to paradoxical muscle weakness
  • Resultant weakness may be due to desensitization of Ach receptors leading to transmission failure and depolarization block
202
Q

what does neostigmine inhibit

A

hydrolysis of ACh by AChAsE

203
Q

neostigmine is used with

A

glycopyrrolate

204
Q

what does using glycopyrrolate with neostigmine do ?

A

decreases muscarinic side effects of neostigmine

205
Q

does neostigmine penetrate the BBB?

A

not very well

206
Q

when to reverse with neostigmine

A

recommendations include waiting until 4 tactile TOF counts are visible at the adductor pollicis before administering

shouldn’t be given until spontaneous recovery evident (TOF)

207
Q

neostimine is more effective in

A

moderate blocks but it is slow acting

208
Q

neostigmine dose

A

0.04-0.08 mg/kg

209
Q

max neostigmine dose

A

5 mg

210
Q

for every 1 mg of neostigmine,

A

mix with 0.2 mg glyco

211
Q

neostigmine onset

A

15 min, dependent on twitches

212
Q

neostigmine duration

A

1-2 hours

213
Q

neostigmine metabolism

A

hepatic, urinary excretion

214
Q

sugammadex removes

A

the relaxant from the NMJ and moves it into the plasma

215
Q

high dose of sugammadex (16mg/kg) has the potential for

A

bradycardia/ cardiac arrest, headache, hypotension, N/V, anaphylaxis and hypersensitivity (pruritus and urticaria)

216
Q

how many mg of sugammadex is required to encapsulate 1mg of rocuronium

A

4 mg

217
Q

what is sugammadex physically incompatible with

A

verapamil, ondansetron and ranitidine

218
Q

how long should you wait after sugammadex administration before readministering Roc or Vec?

A

24 hours after reversal

219
Q

high dose (16mg/kg) sugammadex coagulation affects

A

increased aPTT, PT and INR

220
Q

high dose sugammadex caution in patients (3)

A

with coagulopathies

treated with therapeutic anticoagulation

receiving thromboprophylaxis other than heparin and LMWH

221
Q

is physostigmine used for reversal of muscle relaxants?

A

no

222
Q

what is physostigmine used to treat

A

anticholinergic toxicity

223
Q

S&S anticholinergic toxicity

A

flushing, dry skin and mucous membranes, mydriasis with loss of accommodation, altered mental status, fever and urinary retention

224
Q

CNS symptoms anticholinergic toxicity

A

restless, shivers, agitation, disoriented

225
Q

provide examples of anticholinergics

A

atropine, scopolamine, antihistamines, antipsychotics, cyclic antidepressants

226
Q

anticholinergic drug side effects

A
227
Q

treatment for cholinergic crisis

A

Atropine 35-70 mcg/kg
Pralidoxime 15 mcg/kg every 20 min
Benzos

228
Q

S&S cholinergic crisis

A

miosis, salivation, bronchoconstriction, bradycardia, abdominal cramping, weakness, lacrimation,

229
Q

CNS effects of cholinergic crisis

A

dysphoria, confusion, seizures, coma

230
Q

cholinergic crisis muscarinic symptoms

A
231
Q

cholinergic crisis nicotinic symptoms

A
232
Q

cholinergic crisis vs. myasthenic crisis

A

Cholinergic crisis: excess activity of Ach

Myasthenia Gravis: decrease in Ach activity due to auto-reactive antibodies that attack the nicotinic Ach receptors on postsynaptic membranes

233
Q

how do you differentiate between cholinergic crisis and myasthenic crisis

A

Give edrophonium… muscle strength will improve if myasthenic crisis

more strength = myasthenia (M&M)

234
Q

muscle strength will improve with endrophonium in?

A

myasthenia gravis

235
Q

does edrophonium cross the BBB?

A

no

236
Q

cholinergic crisis has _________ secretions while myasthenic crisis has __________ secretions

A

increased; normal

237
Q

cholinegic crisis: bradycardia or tachycardia?

A

bradycardia

238
Q

myasthenic crisis: bradycardia or tachycardia?

A

tachycardia

239
Q

what test relieves myasthenic crisis symptoms?

A

tensilon test

240
Q

pupils are constricted in

A

cholinergic crisis

constriction = cholinergic

241
Q

pupils are normal or dilated in

A

myasthenic crisis

242
Q

increased cholinergic activity

A

cholinergic crisis

243
Q

decreased cholinergic receptors

A

myasthenic crisis

244
Q

tensilon test makes symptoms worse in

A

cholinergic crisis

245
Q

clinical signs of muscle weakness

A

Blurry vision, double vision

Facial weakness, facial numbness, and general weakness

Most common signs in the PACU:
Generalized weakness
Patient reported difficulty completing 5-second eye opening
Difficulty visually tracking or speaking
Indicative of ocular and pharyngeal muscle sensitivity

246
Q

complications of residual neuromuscular blockade

A

Need for tracheal reintubation

Impaired oxygenation and ventilation (may be blamed on Opioids)

Impaired pulmonary function

Increased risk of aspiration and pneumonia

Pharyngeal dysfunction

Delayed discharge from the PACU

247
Q

clinical signs of neuromuscular recovery

A

Tidal volume

Negative inspiratory force

Grip strength

5-second head lift (not a sensitive test for residual block)

Ability to protrude the tongue

Take home: these are unreliable signs of the return of muscle strength

248
Q

depolarizing NBMAS produce muscle relaxation by

A

directly depolarizing the nAChRs

249
Q

SCh acts as a __________, mimicking ___________

A

false transmitter; ACh

250
Q

Nondepolarizing NMBAs compete with

A

ACh for the two α-subunits

251
Q

define onset of action for an NMBA

A

the time from administration (usually intravenously, IV) until maximal neuromuscular block (disappearance of ST).

252
Q

onset time is _________ related to dose

A

inversely

253
Q

is the only depolarizing NMBA available clinically

A

succinylcholine

254
Q

succinylcholine has the fastest _________, shortest __________, and greatest ________ of any NMBA

A

fastest onset, shortest duration, and greatest reliability

255
Q

SCh has molecular similarity to

A

ACh

256
Q

is SCh degrated by acetylcholinesterases?

A

no

257
Q

is SCh fade or no fade

A

no fade because of progressive but equivalent decrease in the force of contractions

258
Q

when may spontaneous breathing resume after 1mg/kg SCh dose

A

may resume as fast as 5 minutes after 1 mg/kg SCh administration

259
Q

characteristics of depolarizing block

A

decrease in train-of-four (TOF) amplitude without fade in response to depolarizing agent administration

260
Q

what can be given to decrease the incidence of postoperative myalgia?

A

lidocaine and rocuronium, but carry a risk of heavy side-effects

261
Q

what drugs can attenuate IOP increase if given pre-treatment?

A

lidocaine and sufentanil

262
Q

treatment of hyperkalemia

A

hyperventilation, IV calcium chloride, and glucose/insulin to shift potassium intracellularly.

263
Q

drug with a black box warning in the pediatric population

A

Succinylcholine

264
Q

patients receiving ____________ (drug) may be particularly susceptible to muscle injury from administration of SCh

A

statin therapy

265
Q

In obese individuals who need RSI, the dose of SCh should be calculated on

A

the basis of actual body weight rather than ideal body weight.

266
Q

when is the use of SCh contraindicated

A

hx or family hx of malignant hyperthermia

267
Q

where are nondepolarizing NMBAs distributed mostly

A

in the ECF

268
Q

larger nondepolarizing NMBAs may need to be administered in patients with

A

renal/hepatic failure, and in burn patients

269
Q

vecuronium recovery time may be prolonged significantly in the patient with

A

diabetes mellitus

270
Q

Adding depolarizing and nondepolarizing NMBAs results in

A

mutual antagonism

271
Q

what does the dibucaine number reflect?

A

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

272
Q

what is a normal dibucaine number range?

A

70-80

273
Q

which NMBA is associated with an increase in potassium?

A

succinylcholine

274
Q

which 2 NMBAs are associated with histamine release

A

mivacurium and atracurium (less in atracurium)

275
Q

what does neostigmine inhibit

A

acetylcholinesterase

276
Q

what is used to treat myasthenia gravis

A

neostigmine

277
Q

what is the function of neostigmine in anesthesia

A

reversal of effects of non-depolarizing NMBA drugs after surgery

General Principles (6 decks)

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