M100s Conote for Block P.

Introduction ____________________________________________________________ 2
History________________________________________________________________ 2
Mechanism _____________________________________________________________ 3
Indications ______________________________________________________________ 6
_____________________________________________________ 7
Mechanism of Action _____________________________________ 7
Nondepolarizing Neuromuscular Blockade ______________ 7
Characteristics of Nondepolarizing Neuromuscular Blockade _________________ 7
Nondepolarizing Muscle Relaxants _______________________________ 10
Nondepolarizing Muscle Relaxants structure _________________ 10
d-Tubocurarine _________________________________________________________ 10
Pancuronium Bromide(1972) ______________________________________________ 10
Atracurium and Vencuronium______________________________________________ 12
Cisatracuroum besylate (Nimbex)___________________________________________ 16
Rocuronium____________________________________________________________ 19
Mivacurium ____________________________________________________________ 23
Reversals() - Anticholinesterase Drugs _______________________________ 26
Reversals() - Anticholinesterase Drugs ___________________________________ 26
Onset ________________________________________________________ 27
drug _____________________________________________________________ 27
Characteristics of cholinergic receptors and Muscarinic effect ____________________ 28
___________________________________________________________ 29
Complete Reversal of Neuromuscular Blockade _______________________________ 29
Factors affecting depth/duration of neuromuscular blockade ______________________ 30
What should be done if antagonize a nondepolarizing neuromuscular block is fail? ____ 31
Reversals ()Sugammadex (Bridion ) ________________________________ 31
Encapsulation of Rocuronium by Sugammadex(Bridion ) _______________________ 31
Bridions Mechanism of Action Is Unlike Traditional Reversal Agents _____________ 32
What happens when Bridion is injected? _____________________________________ 33
Sugammadex (Bridion ) Pharmacokinetics ___________________________________ 34
Increased Flexibility in the Time of Reversal __________________________________ 34
Practical bridion use _____________________________________________________ 35
Faster Reversal from Rocuronium at Reappearance of 2 Counts ___________________ 36
Rapid Dose-Dependent Reversal From T2 in Children and Adolescents Following
M100s Conote for Block P.1

Rocuronium 0.6 mg/kg _______________________________________________________ 36

No Dose Adjustment Required With Increasing Age ____________________________ 37
Depolarizing Neuromuscular Blockade _____________________________________ 37
Mechanism of action act as Ach receptor agonists ___________________________ 37
Characteristic of Depolarizing Neuromuscular Blockade ____ 38
Succinylcholine _________________________________________________________ 39
Disadvantages of Succinylcholine _____________________________________ 41
Conditions causing susceptibility to succinylcholine-induced hyperkalemia __________ 42
Depolarizing and non-depolarizing muscle relaxants _________________________ 43
Monitoring of Neuromuscular Function ___________________________________ 44
Introduction ____________________________________________________________ 44
The Datex Relaxograph __________________________________________________ 44
Electromyography _______________________________________________________ 45
Clinical Application ______________________________________ 45
Clinical Application of Nerve Stimulator _____________________________________ 46

P1~P5 P6~P10 P11~P18 P18~P25

P26~P33 P33~P36 P37~P43 P43~P51

e-mail
A
3121101 70 - siwach@kmu.ed
2
5; u.tw
(A )
()

()

~@@

P.50 ~
M100s Conote for Block P.2

Muscle Relaxants and Their Antagonists

Introduction
BY
History
1. History of Neuromuscular Blockades(Muscle Relaxants)

1942, Harold Griffith reported the first use of a curare (a South American
arrow poison) preparation in clinical anesthesia
Muscle relaxants produce paralysis, not anesthesia
not ensure unconsciousness, amnesia & analgesia

(1) 1942 Harold Griffith

(curare)

(2)
(3) (
)
2. Non-depolarized muscle relaxant

(1) Aminosteroids
Benzylisoquinoline
(2) Aminosteroids Benzylisoquinoline
M100s Conote for Block P.3

Mechanism

( GABA)(
3.
Botulism)()

1. Neuromuscular Junction

(1) motor end plate

Acetylcholine vesiclesvesicles
Acetylcholine
(2) motor end plate Acetylcholine receptor
Acetylcholine Acetylcholine receptor
2. Ach Receptor
(1) Ach receptor
(2) (A )Ach receptor subunitsAch subunits
(central channal)(B )

M100s Conote for Block P.4

3. Summary of Neuromuscular Transmission

(1) Ach vesicles
(2) Ach receptor
(3) Motor end plate
(4)

4.
(1) ( 26-5) Ach
receptor(resting end-plate)
Ach vesiclespost junction membrane

M100s Conote for Block P.5

(2) ( 26-7)Nerve impluse Ach receptor

(depolarization)(

(3) ( 26-9) Ach receptor Ach
esterase()

(4) ( 26-10) Ach Ach esterase

M100s Conote for Block P.6

Indications
1. Indications of Muscle relaxant

To facilitate intubation
To reduce the amount of inhalational anesthetic
To produce relaxation
To overcome laryngospasm

(1)
(2)
stage3stage4


(3) laryngospasm

2. Take Notice

Induce apnea enough dosage, IM or IV

Prepare instruments for ventilation support before injection

(1) IM IV
ventilation support
(2)
M100s Conote for Block P.7

Mechanism of Action By

Nondepolarizing Neuromuscular Blockade

1. Compete with neurotransmitter Ach at postjunctional receptor
2. D-tubocurarine, pancuronium, vecuronium, atracurium, rocuronium etc.
Depolarizing Neuromuscular Blockade
1. Act as Ach receptor agonists
2. Succinylcholine, decamethonium

1.
2. postjunctional receptor Ach

3. Ach agonist duration Ach
( phase I phase II)

Nondepolarizing Neuromuscular Blockade

1. (
d-tubocurarine ) IV IM
neuromuscular junction post-
Junctional receptor nerveimpulse
Ach receptor

Characteristics of Nondepolarizing Neuromuscular Blockade

1. Fade(+)
2. Post-tetanic facilitation or potentiation (+)
3. Can be antagonized with anticholinesterase agents
4. Antagonized by depolarizing agents
M100s Conote for Block P.8

1. Fade
2. Post-tetanic facilitation or potentiation
3. anticholinesterase ()
4. Antagonized by depolarizing agents
5. fade post-tetanic facilitation or potentiation
( PPT )

(1) nerve stimulator ulnar nerve

A. Patterns of Electrical Stimulation

TwitchA single pulse 0.2 ms in duration.

TetanyA sustained stimulus of 50-100 Hz, usually lasting 5 s.
Train-of-fourA series of four twitches in 2 s(2-Hz frequency), each 0.2 ms
long.

a. Twitch 0.2
b. Tetany 5 50-100 Hz
c. Train-of-four twitch( 0.2
)
B.
fading
M100s Conote for Block P.9

(2) Fade

May be due to a prejunctional effect

of nondepolarizing relaxants that
reduces the amount of Ach in the
nerve terminal available for release
during stimulation (blockade of Ach
mobilization)

A. Ach
B. nondepolarizing neuromuscular block fade
depolzrizing neuromuscular block
C. () nondepolarizing neuromuscular blockade
(A)(B)
(fade)B/A TOF ratio TOF ratio
muscle relaxants
(3) Posttetanic potentiation

May relate to a compensatory increase

in Ach mobilization following tetanic
stimulation

A.
nondepolarizing muscle relaxant

tetanic
stimulation
tetanic stimulation
fade
depolzrizing muscle relaxant
B. Ach
M100s Conote for Block P.10

Nondepolarizing Muscle Relaxants

Nondepolarizing Muscle Relaxants structure
Benzylisoquinolines Aminosteroids
d-Tubocurarine Pancuronium
Atracurium Vercuronium
Cisatracurium Rocuronium
Mivacurium Pipecuronium
()

d-Tubocurarine

1. Adult: 10-30mg IV
2. Onset: 3 min
3. Duration : 45-60 min
4. 40-60% renal elimination ( renal disease)
5. Histamine release (+) (Bronchial asthma)
6. Placental transfer: poorly

1. onset time
2. 40-60(
!!!)
3. Histamine
4.

Pancuronium Bromide(1972)

1. Reduced histamine release

2. Few undesirable C-V effects
3. Provided stable intra-op course
4. Widely adopted for intermediate or long procedures
5. Succinylcholine used for intubation brief procedures

1.
2. Histamine release Histamine Bronchial asthma
M100s Conote for Block P.11

Histamine ()
3.
4. Succinylcholine
Pancuronium Bromide
5. () (2hr)
<1hr intubation surgeon
(Intubation polarizing muscle relaxant succinylcholine
intubation pancuronium)
6. d-Tubocurarine Pancuronium Bromide
(1) Pancuronium Bromide
d-Tubocurarine
(2)
d-Tubocurarine
M100s Conote for Block P.12

BY
Atracurium and Vencuronium

1. Vecuronium Atracurium muscle relaxant(

30-40 ) muscle relaxant
side effect

Atracurium
1. Side effects depended on dose and speed of injection
2. Use with caution in cardiovascular disease
3. Avoid in patients with history of hypersensitivity, anaphylactoid reactions,
asthma
4. 3 times safer than curare
Vecurouium
1. First surgical muscle relaxant with no clinically significant cardiovascular
effects

2.
Atracurium Vecuronium
Pancuronium
histamine release
allergy
---
Cisatracurium Rocuronium
M100s Conote for Block P.13

(1) Atracurium CV
vecuronium
Cardiovascular Effects of Atracurium

1.2 x ED 90 under Halothane Anesthesia: above normally recommended doses.

3. Vencuronium

4. Infusion Dose

1. Appropriate with long procedures, when it is desirable to avoid the C - V

effects of long-acting drugs.
2. Atracurium: 6 g/Kg/min; Vecuronium: 1-1.5 g/Kg/min
3. Monitoring is required because individual patient variability

(1) Atracurium Vecuronium IV injection

infusion
neuromuscular monitor
M100s Conote for Block P.14

5.
(1) Atracurium

A. Atracurium ester hydrolysis

Hoffman elimination liver enzyme
a. Hoffman elimination PH
atracurium base
electron
M100s Conote for Block P.15

(2) Vecuronium

Metabolism: Main metabolite only 2% as potent as parent drug

Excretion:
(1) Biliary: 46%
(2) Renal: 7 %

A. Vecuronium 2%

B. Biliary tract 7%
6. &
(1) Vecuronium liver
function
(hepatic impairment)recovery

(2) liver disease Atracurium
Vecuronium Atracurium Hoffmann eliminaiton Vecuronium
hepatic impairment Atracurium
M100s Conote for Block P.16

(3) .

According to Dependence on Renal Excretion for Their Elimination

1. Greater than 90 percent: Decamethonium
- 60-80 percent: Pancuronium
2. 40-60 percent: d-Tubocurarine, Metocurine
- Less than 20 percent: Atracurium, Succinylcholine, Vecuronium,
cisatracurium
**Percent of injected dose dependent on the kidney for its elimination.

A. Decamethonium90%

B. Pancuronium d-Tubocurarine ;
AtracuriumVecuronium
renal function
Cisatracuroum besylate (Nimbex)
1.

Isomers of atracurium besylate

ED95: (adult)
- cisatracuronium : 0.05mg/kg
- atracurium: 0.17mg/kg
Potency: threefold of atracurium
Similar to atracurium except slow onset, very little histamine, 1/5 less
laudanosine (cerebral excitatory)
Stable hemodynamics
77% Hofmann degradation at normal pH ; 17% renal clearance

(1) Cisatracurium atracurium (isomer)

(potency) atracurium onset
atracurium duration
(2) Cisatracurium Atracurium histamine release

(3) Atracurium Cisatracurium Hofmann degradation liver
M100s Conote for Block P.17

function atracurium Cisatracurium

(4) Atracurium Hofmann elimination
laudanosine(cerebral excitatory)
cisatracurium 1/5(
side-effect )
(5) ~
(6) ~

2.

Opiod/N2O/O2,
Propofol/O2,
Propofol/N2O/O2
* Dosage: 0.15 0.2 mg/kg
* Intubation in 2 3 min
* Maximum block in 3 4 min
* Clinical duration ~ 55 min

(1) intubation ( propofol) drug

interaction intubation duration 5-10mins
50
M100s Conote for Block P.18

3.
(1) ( 65 yro)

Plasma clearances of cisatracurium were not affected by age; however, the

volumes of distribution were slightly larger in elderly patients than in young
patients resulting in slightly longer t1/2 values for cisatracurium.

A. 18
clearance
(2)

Children (2 12 years)
1. lower ED95 (0.04mg/kg, halothane/N2O/O2) than in adults
2. faster onset and shorter duration of action (0.1mg/kg, opioid
anesthesia) than in adults
Infants (1 23 months)
1. faster onset & longer clinically effective duration of action (0.15
mg/kg, opioid anesthesia) than children

A. 2~12 Cisatracurium halothaneN2O

dose onset duration
B. 1~23 Cisatracurium onset duration

(3)

There were no differences in EC50, and t1/2 between patient groups.

The t1/2 values if metabolites are longer in patients with hepatic disease
and concentrations may be higher after long- term administration.

A. atracurium cisatracurium liver

transplant atracurium
cisatracurium Hofmann degradation
M100s Conote for Block P.19

(4) (ESRD)

There were no clinically significant alternation in the recovery profile of

Nimbex in patients with renal dysfunction.
The recovery profile of Nimbex is unchanged in the presence of renal or
hepatic failure, which is consistent with predominantly organ-
independent elimination.

A. cisatracurium 17%
ESRD
(5) Cisatracurium
8 Hofmann degradation half-life

Rocuronium BY

1. Rocuronium vecuronium (
) side chain
2. Rocuronium

Intubation condition at 1 minute after Succinylcholine Chloride (1.0 mg/kg)

and Rocuronium Bromide (0.6 mg/kg)
M100s Conote for Block P.20

(1) Rocuronium onset 1 onset

tubocurarineatracuriumvecuronium 2,3 onset
(2) onset Succinylcholine 95%neuromuscular
block
3. onset rocuronium (1min)
atracurium (2.5~3min) vecuronium (3min)

4. Rocuronium (histamine release)

(histamine release) atracurium mivacurium

M100s Conote for Block P.21

(1) [][][]
(2) Rocuronium vecuronium ()
atracuriummivacurium d-tubocurium

(3) bronchospasm cardiovascular system

(HR oxygen consumption )
rocuronium() vecuronium ()
5. infusion Rocuronium maintain dose

Recommended Infusion Rate (adults) to maintain twitch response at 10% of

control
1. 0.3-0.6mg/kg/hr(5-10ugkg/min), initiated after recovery from an intubating
dose.
2. Upon receiving the desired level of neuromuscular block, the infusion rate of
rocuronium bromide should be individualized for each patient.

(1) initiate intubation Rocuronium 0.6mg/Kg

6. Rocuronium onset recovery ( onset recovery
) Rocuronium ( intermittent
duration ) 25% 90% (TOF) 14
5% 25%
M100s Conote for Block P.22

7.

Biliary excretion is the main elimination route

Up to 30% of the total dose administered is eliminated unchanged by the
kidneys in the first 12 hours

(1) Rocuronium elimination vecuronium (

1.
) Rocuronium
dosage
(2) 12 30%(
)
(3) Rocuronium Bromide(0.6 mg/kg)
Effects of Renal Failure on Onset of Neuromuscular Blockade Under Steady
State Isoflurane Anesthesia

A. rocuronium
Rocuronium
(4) Rocuronium
Rocuronium
M100s Conote for Block P.23

8. Rocuronium bromide conclusions

Aminosteroid drug
Onset approximately twice as fast as vecuronium bromide or atracurium
besylate
Clinically acceptable intubation condition in 60 seconds at normal
intubation dose
Clinical duration and recovery characteristics similar to vecuronium bromide
and atracurium besylate
Favorable cardiovascular profile and virtually free from histamine release
For use in outpatient or inpatient procedures of varying length
Stable in aqueous solution

:
(1) Rouronium
(2) Onset time vecuronium atacurium recovery
time
(3) intubation
(4)
(5)
Mivacurium

Short-acting
Hydrolyzed by plasma cholinesterase
Intubation dose: at least 0.2 mg/kg
time: at least 2 min before
Cardiovascular response
1. 2-3X ED95: minimal
2. > 3 X ED95 histamine release decrease mean arterial BP

1. (duration15-20 ) Micarurium Onset time 2

2. (m99) Micarurium
M100s Conote for Block P.24

3. Micarurium
plasma (serum) cholinesterase cholinesterase

4. : histamine

5. micarurium

6. miracurium (duration 15-20 )

7. (Recovery)
Pancuromium Atracurlum Mivacurium
M100s Conote for Block P.25

8. muscle relaxant metabolism

(1) Mivacurium plasma cholinesterase liver

liver function metabolism
succinylcholine
M100s Conote for Block P.26

Reversals() - Anticholinesterase Drugs BY

Reversals() - Anticholinesterase Drugs

70 kg adult
1. Edrophonium 35mg (0.5mg/Kg)
2. Neostigmine 2.5-3mg
3. Pyridostigmine 20mg
Plus anticholinergic
1. Atropine 1mg
2. Glycopyrrolate 0.4mg

1. (Nondepolarizing) muscle relaxant

Anticholinesterase reverse
2. Nondepolarizing muscle relaxants
Relaxant Reversals

3. anticholinesterase (Edrophonium, Neostigmine,
Pyridostigmine) Neostigmine Edrophonium
onset time

Ps. :(Edro)
(Neo)(Pyrido)
4. Anticholinesterase Drug Muscarinic side effect()
anticholinergic (Atropine Glycopyrrolate)
M100s Conote for Block P.27

Onset

Figure16-28 Onset of action of edrophonium, neostigmine, and

Pyridostigmine in the reversal of 90% pancuronium block.(Data from
Ferguson A,Egerszegi P,Bevan DR,Neostigmine,pyridostigmine, edrophonium
as antagonists of pancuronium.Anesthesiology53:390.1980)

1. anticholinesterase onset Edrophonium

drug

1. Anticholinesterase Drugs

M100s Conote for Block P.28

Characteristics of cholinergic receptors and Muscarinic effect

1. Anticholinesterase Drug Muscarinic effect atropine

2. Muscarinic effect
(1) : arrhythmia
(2) : (bronchospasm) secretion (
)
(3) GI: secretion
(4) :
M100s Conote for Block P.29

Complete Reversal of Neuromuscular Blockade

Train-of-four with fourth and first twitches essentially equal

Sustained head lift, hand grasp & tongue protrusion for 5 seconds
Able to cough & clear secretions
Vital capacity between 10-20 ml/kg
Inspiratory force at least 25 cm H2O
Respiratory rate 25-30/min

1.
(1) peripheral nerve stimulator ulnar nerve train-of-four
( 90%)
tongue drop, airway

ps. train-of-four:
(2) 5
5

(3) secretion
(4) vital capacity

Hello kitty :Hello ~

M100s Conote for Block P.30

Factors affecting depth/duration of neuromuscular blockade

Temperature
Hypothermia: prolong the effect
Acid-base status:
Respiratory & metabolic acidosis
augment the N-M blockade
Inhalational anesthetic conc.
depth & duration of N-M blockade
Electrolyte imbalance
Hypokalemia,hypocalcemia
enhance the N-M blockade
Concomitant medications
Verapamil (calcium channel blocker) potentiate the effect
Antibiotics (aminoglycoside, polypeptide classes) deepen the N-M blockade

1. (heat loss) metabolism

muscle
relaxant prolong
2. Acid-base status muscle relaxation

3. Inhalational anesthetic : muscle relaxant
interaction ( muscle relax )
4. Electrolyte imbalance N-M blockade
5. Concomitant medications
Calcium Channel Blocker

M100s Conote for Block P.31

What should be done if antagonize a nondepolarizing neuromuscular block is

fail?

Has enough time been allowed for the neostigmine to act fully?
Is the neuromuscular blockade too intense to be antagonized?
What is the acid-base & electrolyte status of the patient?
What is the patients temperature?
Is the patient receiving any drug that might interfere with reversal?

relaxant reversal ?(!)

1. muscle relaxant antagonist
muscle relaxant Ach
receptor muscle relaxant free receptors
antagonist
2. anticholinesterase drug motor
end plate

3. acid-base electrolyte imbalance
4.
5.

Reversals ()Sugammadex (Bridion)

Encapsulation of Rocuronium by Sugammadex(Bridion)

1. Sugammadex non-depolarization neuromuscular blockades agent

2. Bridion
3. Sugammadex Rocuronium
M100s Conote for Block P.32

encapsulate ()
4. Sugammadex binding agent Rocuronium complex
receptor

hello ?
!!!
~

Bridions Mechanism of Action Is Unlike Traditional Reversal Agents

1. NMB(neuromuscular blockade)

2. Conventional NMB reversa()AchE inhibitor Ach AchE

receptor

3. Reversal with Bridion()Sugammadex Rocuronium

M100s Conote for Block P.33

complex

BY
What happens when Bridion is injected?
A. Esmeron Rocuronium

B. Esmeron() IV

C. neuromuscular
junction
A. Bridion Sugammadex

B.

Bridion()IV

C.

A. Rocuronium Sugammadex
Bridion-Esmeron complex
B. Rocuronium

M100s Conote for Block P.34

A. Sugammadex

A. Sugammadex
Rocuronium complex
B. Rocuronium
Ach receptor

Sugammadex (Bridion) Pharmacokinetics

Vss 11 to 14 L
T elimination 1.8 hours
Cl estimated to be ~88 mL/min
Major route of elimination: renal
1. 96% of the dose excreted in urine, of which
at least 95% could be attributed to
unchanged Bridion

1.

2. reverse Sugammadex

3. Vss (volume of distribution at steady state) 11~14L
4. T (half-life) 1.8
5. Cl (clearance) 88 ml/min
6. 96%95%

Increased Flexibility in the Time of Reversal
M100s Conote for Block P.35

Immediate Reversal*
1. Within 3 min following administration of rocuronium, 16 mg/kg
Routine Reversal
1. 4 mg/kg if recovery has reached 12 PTC (deep blockade)
2. 2 mg/kg if spontaneous recovery has reached the reappearance of T2
(moderate blockade)
Bridion allows full relaxation until the end of surgical procedures
Only recommended with rocuronium-induced blockade.
Ps. PTCpost tetanic count.

1. Immediate Reversal Rocuronium3 16mg/kg Sugammadex

reversal reverse
2.
muscle tone
reverse
3. Sugammadex Rocuronium non-depolarization NMB

4. ()deep blockade(1-2 PTC) reversal 4mg/kgmoderate
blockade(T2,80% block) 2mg/kg
Practical bridion use

Vial 2 ml, 100 mg/ml 200 mg per vial

1. 2 mg/kg in a 70 kg person: 140 mg one vial

1. 2ml 200mg (1ml 100mg)

2. ()70
M100s Conote for Block P.36

Faster Reversal from Rocuronium at Reappearance of 2 Counts

1. neostigmine
TOF(Train-of-four) reverse 50min(
49min)
2. Sugammadex (Bridion) reverse 3min( 2.7min)
reverse~
Rapid Dose-Dependent Reversal From T2 in Children and Adolescents Following
Rocuronium 0.6 mg/kg

1. Sugammadex (Bridion) reverse

M100s Conote for Block P.37

(1)
(2) receptor

No Dose Adjustment Required With Increasing Age

1.

2. Sugammadex (Bridion) muscarinic effect
cholinergic agent( atropine )
Depolarizing Neuromuscular Blockade BY
Mechanism of action act as Ach receptor agonists
1.
(1) 2 Phase I II block
2. Phase I block

Resemble Ach bind to Ach receptors

not metabolized by acetylcholine esterase
muscle end-plate prolonged & continuous depolarization
muscle relaxation (because opening of lower gate in perijunctional sodium
channels is time limited. Sodium channels close and cannot reopen until the
end-plate repolarizes)
(1) Ach AchR
M100s Conote for Block P.38

(2) AchE
(3) () 2 gate(&)
(voltage-dependent)
(time-dependent)
A
B Na+C

3. Phase II block

After a period of prolonged end-plate depolarization

ionic and conformational changes in Ach receptor
clinically resembles non-depolarizing muscle relaxants

(1) (dosage repeat ) depolarizing muscle

relaxants AchR Phase II block
non-depolarizing muscle relaxants
(2) Phase I Phase II
non-depolarizing muscle relaxants

Characteristic of Depolarizing Neuromuscular Blockade

M100s Conote for Block P.39

Muscle fasciculation preceding the onset of the block may by associated

with postoperative myalgia or muscle stiffness
Initial absence of fade at slow and fast rates of motor nerve stimulation
Absence of posttetanic potentiation
Potentiation of the block by anticholinesterases
Antagonism of block by previous administration of nondepolarizing relaxant
Succinylcholine (SCh), decamethonium
1. ( block
metabolism lactate
)
2. fade posttetanic potentiation
3. reverse reverse action
4. Anticholinesterase block
5. Succinylcholine (SCh), decamethonium

peripheral nerve stimulation test Phase I Phase II
Phase I anticholinesterases fasciculation
muscle relaxion

Succinylcholine

Adult: 60-80 mg IV (1.0

mg/kg )
Onset: within 1 min
Duration: 5-10 min
Fate in the body by plasma or
pseudocholinesterase
Placental transfer: not cross
placenta even in large (300
mg) does

1. acetylcholine
diacetylcholine
M100s Conote for Block P.40

2. Onset (<1min)duration (5-10min)

3. macarurium plasma (metabolism)
pseudocholinesterase (elimination)
4. Cesarean section(C/S)
succinylcholine(99 )
5.
6. Succinylcholine receptor

Na+ lower gate
Na+ lower gate
Na+

7. fade

8. ( 99 )

(1) Succinylcholine pesudocholinesterase

cholinesterase ()
M100s Conote for Block P.41

(2) plasma pesudocholinesterasecholinesterase

Succinylcholine
(3) atypical cholinesterase Succinylcholine
()
Disadvantages of Succinylcholine

Morbidity
1. Muscle pain
Unpredictability
1. Atypical pesudocholinesterase
2. Tachyphylaxis(:A rapid decrease in the response to a drug
after repeated doses over a short period of time)
3. Phase II block
Contraindications
1. Possible malignant hyperthermia
2. Myotonia()
3. Possible hyperkalemic response
Other side effects
1. Cardiac dysrhythmias()
2. Increased intraocular pressure
3. Increased intragastric pressure
Interaction with neuromuscular diseases, e.g., myasthenia gravis, muscular
dystrophies

1.
2. pesudocholinesterase succinylcholine
duration
3. duration
( Tachyphylaxis)
Phase II Block
4. Contracindication
(1) malignant hyperthermia
(2) Myotonia()muscle tone
(3) depolarization
hyperkalemia arrhythmia
M100s Conote for Block P.42

5. Other side effects
(1) Cardiac dysrhythmias()
(2) Increased intraocular pressure () eyeball injury

(3) Increased intragastric pressure () NPO()
succinylcholine

aspiration pneumonitis
6. neuromuscular diseases ( myasthenia gravis, muscular
dystrophies)
Conditions causing susceptibility to succinylcholine-induced hyperkalemia

Burn injury
Massive trauma
Severe intra-abdominal infection
Spinal cord injury
Encephalitis
Stroke
Guillain-Barre syndrome
Severe Parkinsons diseases
Tetanus
Prolonged total body immobilization
Ruptured cerebral aneurysm
Polyneuropathy
Closed head injury
Near drowning
Hemorrhagic shock with metabolic acidosis
Myopathies (eg. Duchennes dystrophy)
1. PPT succinylcholine

(1) Bum injury massive trauma
succinylcholine

M100s Conote for Block P.43

(2) Guillain-Barre syndrome acute infection

(3) :spinal cord injury CNS injury
(4) polyneuropathy head injury plasma
hyperkalemia
BY
Depolarizing and non-depolarizing muscle relaxants

1. Muscle relaxants depolarizing non-depolarizing

(1) Depolarizing succinylcholine
(2) Non-depolarizing
A. long-acting()
B. intermediate-acting( 30-40 )
C. short-acting( 15 ) short-acting
Mivacurium succinylcholine onset time

M100s Conote for Block P.44

Monitoring of Neuromuscular Function

Introduction

Visual assessment: (non-invasive method)

1. open eyes, head lift, hand grip, protrude tongue, tidal volume
Peripheral nerve stimulation: (employing evoked response)
1. Mechanomyography (MMG, MG)
2. Electromyography (EMG)
Respiration:
1. blood gas analysis

1. muscle relaxants 3 muscle

(1) Visual assessment

(2) Peripheral nerve stimulation
A. EMG
B. relaxation
neuromuscular disease
()
C. Respiration blood gas analysis PaO2 PaCO2

The Datex Relaxograph
The Datex RelaxographTM neuromuscular transmission (NMT) monitor is
designed for monitoring neuromuscular block by electrically stimulating a
peripheral nerve and display in the resulting integrated EMG response.
The monitor employs the Train-of-Four (TOF) principle and features an
automatic search for supramaximal stimulation current level. (20 sec.)
Disposable surface electrodes (order code 57268) for both stimulation and
measurement of the EMG response are available. The RelaxographTM is
delivered complete with all necessary accessories

1. peripheral nerve stimulation Datex RelaxographTM

Train-of-four(TOF, )

M100s Conote for Block P.45

Electromyography

1. Electromyography
2. atracurium 15
atracurium muscle muscle
relax muscle
recovering
3. 75% blocking recovering 25%
muscle relaxants
4. () muscle recovering 90-100%
recover
5.
()
Clinical Application
Monitoring onset
1. to determine the optimum time for tracheal intubation
Surgical Relaxation
1. working range during anesthesia: 75-95% blocking
Monitoring recovery
T4 ratio of 90% correlated well with adequate clinical recovery

1.

2. 75%-95% 75%

M100s Conote for Block P.46

3. train-of-four
ICU T4/T1>90%
Clinical Application of Nerve Stimulator
Ulnar nerve at the wrist
1. adductor pollicis and flexor digitorium
Median nerve at the wrist
1. Thenar muscle
Lateral popliteal nerve
1. Dorsal flexion of the foot
Facial nerve

1.
ulnar nerve() adductor pollicis flexor digitorium
median nerve()thenar muscle

2. Position of electrodes and measuring site alternative
()
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Ulnar n. Median n.

1. Abductor digital minimi 1. Abductor pollicis brevis

2. Dorsal interosseous (I-IV) muscle
3. Adductor pollicis brevis
muscle
:
3.

The Five electrode are placed as show in figure 4.1(alternative electrode site
aregiven in Appendix I): The ground electrode (black) and the two
stimulationelectrode (brown, white) over the ulnar nerve. Two recording
electrodes (res, green)on the hypothenar muscle.

(1)
A. x2(REDGREEN)
B. x1(BLACK)
C. x2(BROWNWHITE)
(2)
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4. Response to Peripheral Nerve Stimulation Patterns of Electrical Stimulation

Tetany: A sustained stimulus of 50-100Hz, usually lasting 5 sec.

Twitch: A single pulse 0.2 msec. in duration
Train-of-four: a series of 4 twitches in 2 sec (2-Hz frequency), each 0.2 msec
long

(1)
1. Tetany() 500-100Hz
5

2. Twitch()
0.2 depolarizing
blockade
3. Twitch

4. Train-of-four

twitch T1-T4
5.
fade T1
T4
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5. train-of-four(TOF) )

Effects of single twitch, tetanus, and train-of-four (TOF) assessed by a force

transducer recording contraction of the adductor pollicis muscle.

(1) A ( muscle relaxants) ulnar nerve

(2) B muscle relaxants total paralysis

(3) C depolarizing muscle relaxants
fade TOF
(4) D nondepolarizing muscle relaxants tetany
fade TOF
()
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6. train-of-four(TOF)()*****

(1) 75%-95% TOF

(2)

twitch () 25%
75%

(3) T4 ratio (T4)(T1)

T4 T1
T4 ratio 100%
M100s Conote for Block P.51

7. Various depths of blockade

Intense block: no response to either TOF or PTC stimulation

Deep block: response to PTC but not to TOF stimulation
Moderate block: reappearance of response to TOF stimulation
Superficial block: reappearance of T4 T4/T1 ratio > 1%
No block: T4/T1 ratio > 90 %
(1)
A. Superficial block superficial block
B. Moderate blockTOF 1-3
4
C. Deep blockintense block
PTC count 0 0 deep block 0 intense block
PTCposttetanic count TOF