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Dr. Ni Putu Wardani Residen Anestesiologi Reanimasi Om Awighnam Astu Namo Siddham
Page 1
Nondepolarizing
Short-acting
Short-acting
Succinylcholine
Mivacurium
Intermediate-acting
Atracurium
Cisatracurium
Vecuronium
Rocuronium
Long-acting
Doxacurium
Pancuronium
Pipecuronium
Metaboli Primary
sm
Excretion
Vagal
Blockade5
Atracurium B
+++
Insignificant
++
++
Cisatracuri
um
+++
Insignificant
++
++
Mivacurium B
+++
Insignificant
++
Doxacuriu
m
Insignifica Renal
nt
+++
Pancuroniu S
m
Renal
++
+++
++
Pipecuroniu S
m
Renal
++
+++
Vecuronium S
Biliary
++
++
Rocuronium S
Insignifica Biliary
nt
+++ ++
1.
2.
3.
4.
5.
Chemical
Structure1
B, benzylisoquinolone; S, steroidal.
Onset: +, slow; ++, moderately rapid; +++, rapid.
3
Duration: +, short; ++, intermediate; +++, long.
4
Histamine release: 0, no effect; +, slight effect; ++, moderate effect; +++, marked effect.
5
Vagal blockade: 0, no effect; +, slight effect; ++, moderate effect.
2
Dr. Ni Putu Wardani Residen Anestesiologi Reanimasi Om Awighnam Astu Namo Siddham
Page 2
ED95 for
Adductor
Pollicis
During N2/O2
Anesthesia
(mg/kg)
Intubatio Onset of
n Dose
Action for
(mg/kg)
Intubating
Dose (min)
Duration
of
Intubating
Dose (min)
Maintenance
Dosing by
Boluses
(mg/kg)
Maintenance
Dosing by
Infusion
(g/kg/min)
Succinylcholi 0.5
ne
1.0
0.5
510
0.15
215 mg/min
Rocuronium
0.3
0.8
1.5
3575
0.15
912
Mivacurium
0.08
0.2
2.53.0
1520
0.05
415
Atracurium
0.2
0.5
2.53.0
3045
0.1
512
Cisatracuriu
m
0.05
0.2
2.03.0
4075
0.02
12
Vecuronium
0.05
0.12
2.03.0
4590
0.01
12
Pancuronium 0.07
0.12
2.03.0
60120
0.01
Pipecuroniu
m
0.05
0.1
2.03.0
80120
0.01
Doxacurium
0.025
0.07
4.05.0
90150
0.05
Patient Is
Somnolent
ANESTHESIA SECRET
1. Describe the anatomy of the neuromuscular junction (NMJ)
A motor nerve branches near its terminus to contact many muscle cells, losing myelin
to branch further and come into closer contact with the junctional area of the muscle
surface. Within the most distal aspect of the motor neuron, vesicles containing the
neurotransmitter acetylcholine (ACh) can be found. The terminal neuron and muscle
surface are loosely approximated with protein filaments, and this intervening space is
known as the junctional cleft. Also contained within the cleft is extracellular fluid and
acetylcholinesterase, the enzyme responsible for metabolizing ACh. The postjunctional
motor membrane is highly specialized and invaginated and the shoulders of these
folds are rich in ACh receptor
Dr. Ni Putu Wardani Residen Anestesiologi Reanimasi Om Awighnam Astu Namo Siddham
Page 6
SCH increases intraocular pressure (IOP). There is a theoretical risk for the use
of SCH in patients with open eye injury, that being extrusion of extraocular
contents. However, the increases in IOP are modest and from a clinical
perspective, extrusion of ocular contents has not been observed. Certainly if a
nondepolarizing agent is administered instead of SCH, and the patient is
intubated prior to optimal intubating conditions, coughing on the endotracheal
tube (called "bucking") increases IOP significantly and puts the patient at risk for
extruding ocular contents.
characterizes it. When added to the serum under study, dibucaine inhibits normal
plasma cholinesterase by 80%, while the atypical plasma cholinesterase is inhibited
by only 20%. Hence, a patient with normal pseudocholinesterase is assigned a
dibucaine number of 80. If a patient has a dibucaine number of 40-60, then that
patient is heterozygous for this atypical pseudocholinesterase and will have a
moderately prolonged and usually clinically insignificant block with SCH. If a patient
has a dibucaine number of 20, the patient is homozygous for atypical plasma
cholinesterase and will have an extremely prolonged block with SCH.
Short-acting
Mivacurium
Rocuronium
Intermediate-acting
Rocuronium
Vecuronium
Atracurium
Cisatracurium
Long-acting
Pancuronium
Pipecuronium
Doxacurium
ED95*
(mg/kg
)
Intubating Dose
(mg/kg)
Duration
(minutes)
0.08
0.3
0.2
0.6
1-1.5
2-3
15-20
30
0.3
0.05
0.23
0.05
1.2
0.15-0.2
0.75
0.2
1.0
1.5
1-1.5
2
60
60
45-60
60-90
0.07
0.05
0.025
0.08-0.12
0.07-0.85
0.05-0.08
4-5
3-5
3-5
90
80-90
90-120
Dr. Ni Putu Wardani Residen Anestesiologi Reanimasi Om Awighnam Astu Namo Siddham
Page 8
Calcium channel and -adrenergic blockers impair ion transport but the clinical
significance at the NMJ is probably not important.
Magnesium inhibits the release as well as the depolarizing effect of ACh and
decreases muscle fiber excitability. Lithium also potentiates neuromuscular
blockade.
Long-term use of steroids results in a myopathy and also has some affect on the
NMJ, particularly when muscle relaxants have been used for a prolonged period.
Dr. Ni Putu Wardani Residen Anestesiologi Reanimasi Om Awighnam Astu Namo Siddham
Page 9
Single stimulus
TOF stimulation
Tetanic stimulation
Double-burst stimulation
receptors are occupied, the third twitch disappears at 85% occupancy, the second
twitch disappears at 85-90% occupancy, and the first twitch disappears at 90-95%
occupancy. However, there is accumulating evidence that visual or tactile evaluation
of the TOF response is inadequate for evaluating neuromuscular function because it
has been demonstrated repeatedly that even with experienced practitioners,
subjective TOF estimations correlate poorly with true TOF fade. There has recently
been a call for more objective measures of return of motor function, such as
accelomyography, strain-gauge monitoring, and electromyography.
Dr. Ni Putu Wardani Residen Anestesiologi Reanimasi Om Awighnam Astu Namo Siddham
Page 11
DB stimulation appears to be more sensitive than TOF stimulation for detecting small
degrees of residual neuromuscular blockade. DB involves the application of an initial
burst of three 0.2-millisecond impulses at 50 Hz followed by an identical stimulation in
750 milliseconds. The magnitude of the responses to double burst is approximately
three times greater than that of TOF stimulation, thus making it easier to assess
degree of fade present.
However, volatile anesthetics, other medications, and the patient's underlying health
also affect strength and, under these conditions, lighter levels of blockade may be
satisfactory.
26. Discuss the appropriate time to reverse neuromuscular
blockade, based on nerve stimulation
The best method of terminating the relaxant effect is to dose sparingly and allow the
relaxant to be metabolized. Recall that only one of the alpha subunits of the
postjunctional receptor need be occupied by a relaxant molecule to inhibit function,
whereas two molecules of ACh are necessary to stimulate the receptor, so, even
though the nondepolarizing relaxants are competitive antagonists, the receptor
dynamics favor the relaxants. With these caveats, neuromuscular blockade can be
reversed when there is at least one twitch with TOF stimulation. However, this still
reflects a very deep level of blockade and the clinician should monitor the patient
closely for clinical signs of inadequate return of strength. The greater the TOF when
reversed, the better. It is also important to remember that recent tetanic stimuli will
result in overestimating the TOF.
27. Review the drugs and doses commonly used to antagonize
nondepolarizing blockade
Acetylcholinesterase inhibitors prevent the breakdown of acetylcholinesterase,
increasing the amount of ACh available at the NMJ. Neostigmine 25-70 g/kg and
edrophonium 0.5-1 mg/kg are commonly used for this purpose perioperatively.
Edrophonium also stimulates the prejunctional membrane, increasing release of ACh.
These medications contain positively charged quaternary ammonium groups, are
water soluble, and are renally excreted.
28. Review important side effects of acetylcholinesterase
administration
Increasing the available acetylcholine at the NMJ (a nicotinic receptor) will also
stimulate muscarinic cholinergic receptors. Of particular concern is the effect on
cardiac conduction. Unopposed muscarinic effects will impair sinus-node conduction,
resulting in sinus bradycardia, junctional rhythms, and in the extreme, asystole. To
prevent this, anticholinergics are administered in concert with the
acetylcholinesterase. Glycopyrrolate 7-15 g/kg is coadministered with neostigmine
and atropine 7-10 g/kg with edrophonium so that the onset of anticholinergic activity
is appropriately timed with the onset of acetylcholinesterase inhibition.
29. Should all patients who receive nondepolarizing relaxants be
reversed?
There is mounting evidence that residual neuromuscular blockade and clinical
weakness occur with disturbing frequency, even when the patient has received only
one dose of an intermediate-duration nondepolarizing relaxant. These residual effects
have been noted even 2 hours after a single dose. Part of the problem appears to be
Dr. Ni Putu Wardani Residen Anestesiologi Reanimasi Om Awighnam Astu Namo Siddham
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Dr. Ni Putu Wardani Residen Anestesiologi Reanimasi Om Awighnam Astu Namo Siddham
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