NMB- COMPLETED Flashcards
(266 cards)
1
Q
Depolarizing neuromuscular blocking drugs
A
Mimics acetylcholine; Competitive agonists, and generating action potentials
2
Q
Non-depolarizing neuromuscular blocking drugs
A
Interferes with actions of acetylcholine
3
Q
2 types on Non-depolarizing MB
A
Benzylisoquinolinium compounds
Aminosteroid compounds
4
Q
The Main neurotransmitter is
A
Acetylcholine
5
Q
Anticholinergic agent only work at
A
MUSCARINIC receptors
6
Q
ACh in high concentration acts as an
A
inhibitor to vesicle release
7
Q
Agonist will ______muscle contraction while antagonists _______muscle contraction
A
activate muscle contraction
Antagonist will prevent muscle contraction (NDNMB)
8
Q
Patient who suffer from stroke have extra
A
EXTRAjunctional receptors
9
Q
Nicotinic receptor at motor end plate
A
acetylchonisterase (true) metabolize ACW
10
Q
Before succinylcholine starts working
A
you see fasciculations, Cell can’t repolarize, no new depolarization
11
Q
Acetylcholine can’t break down
A
Succinylcholine (PSEUDOCHOLINESTERASE in plasma)
12
Q
ACH has how many subunits
A
5
13
Q
Ach must occupy both ______ for a conformotional change to occur
A
Alpha subunit , capable of binding Ach
14
Q
Depolarizing Agents
A
Mimic the action of Ach but remain attached longer than ACh
15
Q
Competitive Agents
A
Benzylisoquinoliniums
Aminosteroids
16
Q
90% suppression of a single twitch response
A
is considered evidence of adequate drug-induced skeletal muscle relaxation
17
Q
Laryngeal spasms associated with
A
can be treated with doses of 0.1mg/kg of succinylcholine
18
Q
Used to measure the speed of onset and duration of NM blockade
A
• Adductor pollicis, orbicularis oculi
19
Q
What TOF IS CONSIDERED evidence of return?
A
Traditionally TOF >0.7 has been considered evidence of return of adequate skeletal muscle strength to allow spontaneous
ventilationon
20
Q
• Pharyngeal dysfunction and risk of aspiration exist when TOF
A
<0.9
21
Q
Benzylisoquinoliniums NMB are
A
Cisatracurium
Atracurium
22
Q
Aminosteroids NMB are
A
Rocuronium
Vecuronium
23
Q
Reversal agent for aminosteroids ONLY is
A
SUGAMMADEX
24
Q
At the neuromuscular Junction, the receptor is Nicotinic or muscarinic
A
Nicotinic
25
ACh binds to nicotinic or muscarinic
Nicotinic (only one at NMJ anyway)
26
Nicotinic are
Sodium channels and some voltage gated channels
27
ACh binds to ACh receptors --->
action potential of fibers and muscle movement occur
28
Presynaptic receptor are located on the
A-alpha motor neuron
29
Postsynaptic receptor are located on the
Skeletal muscle
30
After succinylcholine binds to the 2 alpha subunits, conformational change of channel allow channel to open what cations flows in and out?
Sodium and calcium flow in
Potassium flow OUT
Generating an end plate potential
31
Nicotinic receptors are
ion channels
32
When there is a voltage change Na channels
open and then the resultant action potential travels through muscle then open sodium channels and release CA from the SR --> The calcium allows actin and myosin to interact leading to muscle contraction
33
What is Ach broken down by ? located where ?
Acetylcholinesterase , at the motor end plate, adjacent to the receptor
34
ACh is broken down into
Acetyl and choline
35
What happens after ACh is broken down?
ion channels eventually close, allowing the end plate to repolarize. Calcium then return to the SR allowing the muscle to relax.
36
Succinylcholine is different in agonist of Ach receptors because
it remains attached longer , prolongs the depolarization state and the CELL CANNOT REPOLARIZE (cell cannot start over the cascade require to be repolarized)
37
What dose of the ED95 is required to facilitate the Endotracheal intubation ?
2 times ED95
38
What is considered evidence of adequate drug-induced skeletal muscle relaxation?
90% suppression of a single twitch response
39
Does NMB have any CNS depressant or analgesic properties?
NO
40
What can laryngeal spasms be treated with
0.1mg/kg of Succinylcholine
41
What does the nerve stimulators do?
Measure the speed of onset and duration of NMB
42
2 major muscles use to measure
Adductor pollicis
| Orbicularis Oculi
43
What is evidence of return of ADEQUATE skeletal muscle strength to allow SPONTANEOUS VENTILATION
TOF > 0.7
44
What is the patient at risk for when TOF ratio is <0.9?
Pharyngeal dysfunction
| Risk of aspiration
45
TOF assessment: TOF 0/4 means ______blockade, receptor occupancy is ____%.
Intense ; > or equal to 95%
46
TOF assessment: TOF 1/4 means ______blockade, receptor occupancy is ____%.
Moderate/ surgical block; 90%
47
TOF assessment: TOF 2/4 means ______blockade, receptor occupancy is ____%.
Moderate/surgical block; 85%
48
TOF assessment: TOF 3/4 means ______blockade, receptor occupancy is ____%.
Recovery; 80%
49
TOF assessment: TOF 4/4 means ______blockade, receptor occupancy is ____%.
Recovery; 75%
50
Faster to block : large muscle ________than fast moving muscles
HARDER
51
From most difficult to easier to block DAOL
Diaphram
Adductor Policis (open-slow)
Orbicularis Oculi
Laryngeal muscles (Thyroarythenoid muscles close gottis fast)
52
VA and NMB what effect do they have on NMB
Potentiate action of NMB
53
What is the charge of quarternary ammonium?
They are permanently charged
54
What is water soluble and HIGHLY IONIZED at physiologic pH?
Quaternary ammonium
55
Quaternary ammonium does not penetrate?
BBB, GI tract, placenta and undergo small tubular reabsorption
56
NMB will NOT affect VA but will VA affect NMB ?
Yes
57
Does NMB affect VA
No
58
What terminates the action of NMB
Redistribution
59
Factors affecting clearance, VD and half time
Age, volatile anesthetics, Hepatic or renal disease.
60
Are NMB highly bound to proteins
NO
61
Rate of disapperance of NMB from blood is rapid why?
due to distribution to tissue
62
What is potency when defining NMB?
The effective dose necessary to depress a single twitch depression 95%.
63
What is Duration of action when defining NMB?
Time from injection to onset of maximal single twitch depression
64
What is Recovery of index when defining NMB?
Time from 25% return of single twitch height to 75% return of single twitch height.
65
What is Clinical duration when defining NMB?
Time from injection to recovery of the TOF ratio to >0.7 or >0.9
66
What is the MOA mechanism of action Succinylcholine?
Mimics Ach and binds Ach receptor generating a muscle action potential
67
Depolarizing NMB are not metabolized by acetylcholinestrase so there is ?
prolonged depolarization of the motor end plate
68
Depolarizing NMB acts as AGONIST or ANTAGONIST?
AGONIST
69
The only DEPOLARIZING agent in clinical use is?
Succinylcholine
70
Low dose of succinylcholine is
0.5 - 1 mg/kg IV
71
Onset of low dose of Succinylcholine
30-60 seconds
72
What are the effects seen with PHASE I BLOCKADE? Return to function ____
Extensive Fasciculations (return to function in 5 mins)
73
What are the effects seen with PHASE II BLOCKADE? renal to function ____
NO FASCICULATIONS; 10-15 minutes
74
High dose of Succinylcholine is
2-4 mg/kg
75
High doses goes right to phase ____blockade
II
76
Less postop myalgia is associated with
High dose and phase II blockade
77
Metabolism of Succ is ____Compared to Ach
Low
78
Succinylcholine on ion channel effect
keep them open longer(depolarization )
79
NMB occurs because a ______post junctional junction cannot respond to subsequent release of Ach
Depolarized
80
Depolarizing muscular relaxant aka
PHASE I blockade (prolonged depolarization)
81
Explain the Phase I Block?
After initial excitation , sodium channel close on the cytosolic side but outer door remains open
membrane return to its RESTING STATE --> resulting in muscle relaxation and a phase I block
82
Absence of Post tetanic stimulation
Phase I Block
83
NO Fade with this type of Block
Phase I block
84
With Phase I block what happens to the Block when an Anticholinesterase Inhibitors are given?
Augmentation of block
85
TOF ratio > 0.7 in Phase I block
Can't see fade
86
Decrease contraction with a single twitch stimulation? which Phase?
Phase I Block
87
Decrease in AMPLITUDE but sustained response to continuous stimulation? which Phase?
Phase I Block
88
The onset of Phase I block is accompanied by what?
Presence of Fasciculations
89
Pre and postsynaptic binding with this block?
Phase II Block
90
Phase II block main action is
Inhibits release of Ach vacuoles
| Inhibits Ach receptor
91
Phase II block resemble
Response of nerve stimulator that is considered to be characteristic of non-depolarizing NMB
92
Succ induced phase II Block occurs with (CHR)
Higher doses 2-4 mg/kg
Repeated doses
Continuous infusions
93
Phase II Block occurs
Rapidly
94
Varying degree of phase I and II may be present how do you know PHASE I is predominant?
Given a reversal agent such as ANTICHOLINESTERASE will INTENSIFY THE BLOCK
95
So which agent do you given and how do you determine the block present?
Small dose of Anticholinesterase (Edrophonium 0.1-0.2 mg/kg ). If the small dose antagonizes the block, subsequent higher doses will further antagonize the effects/.
96
The onset of PHASE II Block is manifested initially as _______. What may be needed______
Tachyphylaxis ; increased dose
97
T/F majority of Succ metabolized before reaching NMJ
True
98
The brief duration of action of succ is due to
Hydrolysis by PLASMA CHOLINESTERASE (pseudocholinesterase)
99
Where is plasma cholinesterase metabolized?
in the liver
100
Pseudocholinesterase efficiency?
has enormous ability to hydrolyze Sch at a rapid rate , so only a small fraction reach the NMJ
101
Because plasma cholinesterase are not present at high concentration at the NMJ, what is the metabolism of SCH dependent on?
Diffusion away from the NMJ
102
What can decrease plasma cholinesterase activity?
Decrease hepatic production--> prolong effect
| Atypical cholinesterase --> slower metabolism
103
2 ethnicities with decrease plasma cholinesterase activity?
Persian Jewish
| Alaska natives
104
Neogstimine on plasma cholinesterase activity
Profound effect on plasma cholinesterase activity (30 mns after administration, activity still reduced by 50%)
105
Decrease plasma cholinesterase activity by 40% but not prolong block
High estrogen levels.
106
Myasthenia gravis on plasma cholinesterase
Decrease plasma cholinesterase and prolong block
107
What test is done to diagnose genetic disease Atypical plasma cholinesterase?
Dibucaine
108
Atypical plasma cholinesterase usually diagnosed how>
when a patient experience prolonged block after admin of Succ.
109
_______gene is responsible for Atypical PC
single gene
110
A normal dibucaine test number is
#80
111
Dibucaine is a
LA
112
Dubicaine usuallly inhibits ____% of plasma cholinesterase activity compared to _________% in the atypical enzyme
80%; 20%
113
Dubicaine homozygous number is
#20
114
What is the significance of homozygous number 20 in dubicaine test? How many abnormal gene?
EXTREME: Very long blockade 6-8 hours due to presence of 2 abnormal genes
115
Dubicaine heterozygous number is
#40-60
116
What is the significance of heterozygous number 40-60 in dubicaine test?How many abnormal gene?
Slighly prolonged block 20-30 mns
| 1 abnormal gene
117
Resistant to Succ means
Increase plasma cholinesterase activity
118
How does myasthenia gravis dose of succ different?
required 2.6 times the ED95 because of the DESTRUCTION OF ACH receptor
119
Adverse effects of Succinylcholine CHIMMMS
```
Cardiac arrhythmias
Hyperkalemia
Increased IOP, IGastricP, ICP
Malignant Hyperthermia
Myalgia
Myoglobinuria
Susttained skeletal muscle contractions
```
120
What attenuates the or PREVENT the occurance of cardiac arrhythmias, myalgia, increase Intragastric pressure and increase ICP
Administration of a NON-PARALYZING dose of a NON-DEPOLARIZING NMB drug
121
Doest the administration of a nondepolarizing NMB drug influence the magnitude of POTASSIUM RELEASE EVOKED?
NO
122
Cardiac Dysrhythmias associated with Succ
Sinus brady, junctional, 'sinus arrest (action of muscarinic cholinergic receptor)
123
Risk of cardiac dysrhythmias increased with
2nd dose is given 5 minutes after initial dose.
124
Atropine dose of _______ Does NOT PREVENT BRADYCARDIA to response of 2nd dose of Succ
<6mcg/kg
125
Succinylcholine contraindicated in
Muscular dystrophy
126
Denervation injury effect on nicotinic receptors?
INCREASED
127
Denervation injury leading to skeletal muscle atrophy
MS and GBS, spinal cord and CVA (UMN lesions)
128
MS , GBS, spinal cord injury and CVA and SUCC may cause
HYPERKALEMIC ARREST due to UPREGULATION of receptors and INCREASED POTASSIUM RELEASE
129
Myalgia occurs with Phase ____ and may be perceived as ________
I; sore throat
130
Myalgia prevented by going straight to ______block with a _____dose
Larger dose of succ , goes straight to PHASE II block,
131
What dose myoglobinuria relfects?
Muscle damage damage due to fasciculations
132
Intragastric pressure prevented by ________ and increase IGP increase risk of
Administering small dose of NDNMB ; aspiration
133
Avoid Sch in patients with this eye injury although not proven______because SUCC increases ____
Open eye injury; IOP
134
Succ and intracranial tumors safe?
yes , although succ increases ICP no contraindications
135
Sustained skeletal muscle contraction represented by
MASSETER rigidity (may be hard to differentiate from MH)
136
2 conditions associated with increased skeletal muscle contraction
Myotonia congenita and dystrophica
137
Strong inductor of Malignant Hyperthermia
Succinylcholine
138
Decision of what agent to use is determined by
```
DDRMCC
Difference in onset
Difference in duration
Rate of recovery
Metabolism
Clearance
Cost
```
139
Clinical classification of NDNMB
Short, intermediate, and long acting.
140
Classification based on their molecular structures (2)
Benzylisoquinolinium
| Aminosteroids
141
Drugs similar to curare
Benzylisoquinolinium
142
Benzylisoquinolinium identified with ______in the word
-acurium
143
Aminosteroids has ______in the word
Curonium
144
2 intermediate acting aminosteroids
Vecuronium
| Rocuronium
145
Non-depolarizing (ND) NMB MOA acts as
COMPETITIVE ANTAGONIST at the alpha subunits of the PJ nicotinic receptors
146
Do NDNMB have prejunctional nicotinic receptor site? significant
yes; not significant
147
When does NEUROMUSCULAR BLOCKADE occur?
When 80-90% of the RECEPTORS ARE BLOCKED
148
Decreased twitch response to a single stimulus?
NDNMB
149
FADE with continuous stimulation with NDNMB or DNMB
NDNMB
150
Antagonism of NDNMB
by anticholinesterase agents
151
Do NDNMB cause fasciculations?
NO
152
Does NDNMB active MH??
No
153
NDNMB characteristics
Fade (unstained response) to continous stimulation , TOF ratio <0.7
154
Benzylisoquinolinium cause drug induced________
Release of histamine and vasoactive substances
155
Narrow autonomic MARGIN of safety
PANCURONIUM
156
Critical care myopathy occurs when drug given for _____occur more with the ______NDNMB agenst
> 6 days; Aminosteroids
157
What INCREASE THE incidence of critical care myopathy of NDNMB?
Administration of GLUCOCORTICOIDS prior to the administration of NMB
158
Drugs that enhance NMB Agents? VAL CDM LGC
```
Volatile
Antibiotics -Aminoglycosides
Local anesthetics
Cardiac dysrhythmic drugs Quinidine, Lidocaine
Diuretics
Magnesium
Lithium
Ganglionic Blockers
Cyclosporins
```
159
Dose dependent increase in NMB effects with those agents?
DIES (Des, Iso, En, Sevo)
160
Least effect on increase in NMB with that agents
Nitrous
161
Enhanced effect of NMB with this Antibiotics?
Aminoglycosides (may decrease release of Ach)
162
Antibiotics with NO EFFECT on NMB
PCN and cephalosporins
163
Small LA doses and NMB
Small doses enhance NMB produced by NDNMB
164
Large doses of LA on NMB
Block NEURAL transmission
165
ESTER local anesthetics compete with
Succ for plasma anticholinesterase
166
How does Lidocaine and quinidine augment preexisting block?
via Na channel inhibition
167
Diurectics dose that enhance NMB?
Furosemide 1mg/kg
168
Does MANNITOL affect the degree of NMB by NMB agents
NO
169
Chronic hypokalemia ______Dose requirements for pancuronium but __________ the dose of ________ needed to antagonize the block
Decrease; Increases ; NEOGSTIMINE
170
How does mag affect NMB
Enhances NMB produced by NDNMB ( more with VEC) due to prejunctional release
171
Patients clinically treated with Phenytoin are
resistant to the effects of NMB due to upregulations of receptors ; need HIGHER doses
172
ABT; May prolong duration o f block of NDNMB
Cyclosporine
173
Decrease the onset of action (Faster)of NMB ND
Hypotension Ephedrine(shunts blood to skeletal muscle)
174
NDNMB Esmolol decreases CO meaning ____
DELAYS ONSET
175
Hypothermia and NDNMB, 2 drugs
hypothermia prolongs the duration of NMB of pancuronium and vecuronium
176
Hypothermia on atracurium?
Prolong effects of atracurium and decrease the continuous dose necesarry to maintain the block
177
Hypokalemia and succinylcholine
Resistance to Succ, increase sensitivity to NDNMB
178
Hypokalemia -_________ the transmembrane potential causing __________ of cell membrane
Increases, Hyperpolarization
179
Hyperkalemia _________The transmembrane potential partially ______cell membrane
decreases, POLARIZING,
180
Hyperkalemia and succinylcholine
INCREASE sensitivity to succ,
| RESISTANCE TO to NDNMB
181
Burns and NDNMB
Resistance to NDNMB
182
Monitoring NM blockade with a nerve stimulator on the side effected by CVA reveals a
Decreased sensitivity to NMB drugs (up-regulation of nicotinic receptors)
183
Monitoring NM blockade with a nerve stimulator on the CVA patient
may underestimate the degree NMB present at the muscles of ventilation
184
Drugs class LESS LIKELY and LESS CROSS REACTIVE
Drugs with a SINGLE Quaternary ammonium
| Roc, Pan, Vec
185
Enhance effects of NDNMB______Therefore always check ____ prior to givin ND
Sch ; TOF
186
MEN vs WOMEN which is more sensitive to NMB
WOMEN more sensitive (men have more skeletal mass)
187
Does NDNMB agents metabolized by either acetylcholinesterase or pseudocholinesterases?
No
188
ED 95 dose of Pancuronium
70mcg/kg
189
Dose of ______provide adequate relaxation for intubation for 3 minutes
0.08 to 0.12 mg/kg
190
Onset of pancuronium
3-5 minutes
191
Long acting AMINOSTEROID
Pancuronium
192
Duration of action of Pancuronium
60-90 mns
193
Enhances pancuronium induce blockade
Respiratory acidosis
| also OPPOSES ANTAGONISM with neogstimine
194
Avoid in RENAL FAILURE (aminosteroid)
PANCURONIUM (decrease clearance)
195
Need higher initial dose to have same effect of pancuronium in those patients? what about the effect?
Hepatic patients : effect may last longer
196
Aminosteroid with modest increase in HR MAP and CO
Pancuronium (vagal effect
197
Pancuronium and digitalis
Increase risk dysrhythmias
198
With this drug the increase in HR may offset opiods induce bradycardia
Pancuronium
199
Intermediate acting NDNMBS are
ACVR
| Atracurium, Cisatracurium, Rocuronium, Vecuronium
200
What makes intermediate NDNMBs different?
Efficience Clearance that minimize the likelihood of cumulative effects of continuous infusion
201
1/3 the duration of Long acting NDNMBs
Intermediate acting; 20-35 mins
202
Characteristics of intermediate acting NDNMBs
Absent cumulative effects and cardiac effets.
203
Characteristics of intermediate acting NDNMBs as far as REVERSAL? time frame?
Reliably blocked by anticholinesterase drugs often within 20 mins
204
A benzylisoquinolinium which is a mixture of 10 isomers
Atracurium
205
Atracurium ED95 dose is
0.2mg/kg
206
Intubation dose of Atracurium is
0.5 mg/kg
207
Atracurium onset of action
3-5 minutes
208
Duration of action of Atracurium
20-35 mins
209
Maintenance dose of Atracurium
0.1mg/kg
210
Metabolism of Atracurium
1/3 Undergoes HOFFMAN elimination (spontaneous degradation at physiologic temp and pH)
211
Safety net drug for patient with IMPAIRED RENAL and HEPATIC (Benzoisoquinolinium)
ATRACURIUM
212
Other metabolism mechanism of Atracurium
Hydrolysis 2/3
213
T/ F both metabolism routes of Atracurium are independent of hepatic or renal ?
True
214
Does Atracurium have a metabolites if yes what is it?
LAUDANOSINE (may lead to CNS stimulation, increase MAC and VA
215
Side effects of ATRACURIUM
Hypotension and tachycardia (fall SVR , increase in CI)
216
Atracurium: histamine release
NO
217
Should be AVOIDED In ASTHMATICS (THINK AAA)
ATRACURIUM (ATRACURIUM AVOIDED ASTHMATICS)
218
Should not be mixed with Barbiturates, or alkaline pH
ATRACURIUM
219
Monoquarternary aminosteroids NDNMB
Vecuronium
220
Intubating dose of Vecuronium
0.08 - 0.12 mg/kg
221
ED95 dose of Vecuronium
50mcg/kg
222
Packaged as a powder and unstable in solution
VECURONIUM
223
Vecuronium Onset of action
3-5 minutes
224
Duration of action
20-30 minutes
225
More lipid soluble due to
monoquartery structure
226
_______undergoes both Renal and hepatic excretion
Vecuronium
227
Elimination prolonged in renal failure with this drug
VECURONIUM
228
Slower onset of action of VECURONIUM with those patients
Renal failure patients
229
Prolonged duration of action of VECURONIUM
Hepatic Cirrhosis
230
Hypoventilation /Hyperventilation which one enhances Neuromuscular blockade
Hypoventilation
231
This Aminosteroids has a large Vd
Vecuronium
232
Cumulative effects of AMINOSTEROIDS from most to least? PVA
Pancuronium > Vecuronium > Atracurium
233
Aminosteroid devoids of Cardiac effects even with RAPID amdinistration
Vecuronium
234
Lack VAGOLYTICS and histamine (aminosteroids)
Vecuronium
235
What should vecuronium be administered with and why?
Incidence of bradycardia (vagotonic effect)
236
Decreased in clearance with elderly patients? and why?
VECURONIUM
Decrease hepatic and renal flow
Decrease hepatic enzyme activity
237
Vecuronium in the immediate post partum period duration of action is _________
DOA prolonged
238
Duration increase in OBESE patients
Vecuronium (lg Vd)
239
Does Atracurium duration increase in obese patient?
NO
240
Monoquaternary aminosteroids
Rocuronium
241
ED95 dose of Rocuronium
0.3mg/kg
242
Onset of action of Rocuronium
1-2 minutes
243
Intubatind dose of Rocuronium
0.6 - 1 mg/kg
244
The lack of potency of Rocuronium compared to Vecuronium
Vecuronium faster onset ( occupy more receptor faster)
245
Potency and onset of action are
Inversely proportional?
246
After the administration of ______times the ED95 the onset of Rocuronium resembles the onset of 1mg/kg of Succ
3-4 times
| 1mg/kg of Sch
247
What is the ONLY non-depolarizing NMB that may be used as an alternative to Succinylcholine due to rapid onset?
ROCURONIUM
248
Muscle more resistant to the effects of Rocuronium
laryngeal muscles more than Adductor POLLICIS
249
large doses of Rocuronium May be delayed at the laryngeal muscles even though the
adductor policis appear blocked --> may cause difficult intubation .
250
2 muscles for Rocuronium more resistant to blockade
Laryngeal adductor
| Diaphram
251
What does not confirm paralysis of the diaphragm and laryngeal muscles with ROC?
Complete suppression of single twitch response at ADDUCTOR POLICCIS
252
What can cause paralysis?
Initiating laryngocopy at the time of peak laryngeal muscle paralysis
253
ROC Renal and hepatic effects
modestly increase DOA
| Liver disease longer DOA
254
CV Rocuronium
no CV or release of histamine
255
What is consistent with ND aminosteroid NMB agents?
NO HISTAMINE RELEASE
256
Useful in opthtalmic procedures associated with vagal stimulation?
ROCURONIUM
257
Bisquaternary BENZYLISOQUINOLINIUM
Cisatracurium
258
ED95 dose of Cisatracurium
50mcg/kg
259
Onset of duration of Cisatracurium
3-5 mns
260
Duration of action of Cisatracurium
20-35 mins
261
Prolonged Cisatracurium infusions are not associated
with prolonged effects
262
Clearance of Cisatracurium
Hoffman Elimination
263
Is nonspecific plasma esterase involved in Cisatracurium?
NO
264
Nonplasma clearance of Cisatracurium means
Can be given to Renal and liver disease
265
Potency Cisatracurium vs Atracurium
Cisatracurium because less LAUDANOSINE with cisatracurium
266
Devoid of histamine and CV effects even with rapid admini Benzoisoquinoilnium
Cisatracurium
