NEUROMUSCULAR

BLOCKING AGENTS

BY: DR. JOHNNY S. VILLANUEVA

QUEZON CITY GENERAL
HOSPITAL MEDICAL CENTER
•BRIEF HISTORY NEUROMUSCULAR DRUGS
•PHYSIOLOGY AND PHARMACOLOGY
•PHARMACOLOGICAL CHARACTERISTIC OF NEUROMUSCULAR
BLOCKING AGENTS
•DEPOLARIZING DRUGS: SUCCINYLCHOLINE
•NON DEPOLARIZING DRUGS
•DRUG INTERACTIONS
•ALTERED RESPONSE TO NEUROMUSCULAR BLOCKING AGENTS
•MONITORING OF NEUROMUSCULAR BLOCKADE
•ANTAGONSM OF NEUROMUSCULAR BLOCK
Strychnos toxifera (Curare) from
Koehler's Medicinal-Plants 1887
1954: Beecher & Todd
showed 6 fold increase in
mortality when muscle
relaxant were used
History
•1596: Sir Walter Raleigh - Arrow
poison
curare from creepers
•
•
•
•
•1811: Sir Benjamin Brodie - Curare’s
paralysing effects
•
 History

•1942: Curare •1970’s: Fazadinium

•1947: Gallamine •1980: Atracurium
•1949: d- •1992: Mivacurium
Tubocurarine •1994: Rocuronium
•1951: SCh •1995: Cis-
•1960: Pancuronium atracurium
•1964: Alcuronium •2000: Rapacuronium
 Events
POSTSYNAPTIC
1. Activation of the postsynaptic nicotinic
receptor requires simultaneous occupation
of the receptors two alpha subunits by Ach.
2. Propagation of the action potential
initiate release of calcium from the
sarcoplasmic reticulum.
2.
3. Ach is hydrolyzed(milliseconds to
prevent prolong depolarization) by
acetylcholinesterase (true cholinesterase)
to choline (reused for synthesis of new
ACh) and acetate
 Events
PRESYNAPTIC
1. The release of Ach normally decreases
during high frequency stimulation under
physiologic condition. In the presence of
muscle relaxant this decreased release of
Ach produces a progressive decrease in
skeletal muscle response (fade) with each
stimulus .
2. Fade is an important property of non
depolarizing neuromuscular blockade and is
useful for monitoring purposes.
Nicotinic Receptor at adult NMJ
A
C
h
Epsilon / Gamma Alpha

Ion Channel
Alpha
Beta

ACh
Delta

In fetal & denervated receptors: Gamma replaces Epsilon

 Ach Receptors
• Immature • Mature
 Spread  Localized
 Unstable  Stable
 ½ life 24 hrs  ½ life 2 weeks
 Longer burst duration  Burst activity
 Smaller conductance  Normal conductance
 2-10 times longer  Channel opens for 0.5
channel opening millisecond
(slow closing) 
 •
 A. Pharmacological Characteristics of
neuromuscular blocking agents.
•The effect of NMBDs is measured as the
depression of adductor muscle
contractions (twitch) following electrical
stimulation of the ulnar nerve.
•
B. Potencyis determined by constructing the
dose response curves, which describe the
relationship between twitch depression and
dose.

C. Onset time or time to maximum blockade can

be shortened if the dose is increased.
 D. Duration of action is the time from
injection of the NMBD to return of 25%
twitch height (comparisons are usually
made at 2x ED 95) categories of NMBDs may
be based on the duration of action.

E. Recovery index is the time between 25

and 75% twitch heights (reflects speed of
recovery once return of twitch is
manifest) . The adductor pollicis is the
most commonly monitored muslce for
determining onset and duration of action
of NMBDs.
100
T
w
i
80 t
c
h
d
e
60 p
r
e
s
s
i
40 o
n
ED 50 ED 95

20
(%)

O 0.1 0.2 0.3 0.4

Dose (mg/kg)
Sodium channel
Resting Active Inactive

= V
= T
Sodium channel
Resting Active Inactive

Na
= V
= T
Sodium channel
Resting Active Inactive

Na
= V

= T
 Classification of Muscle Relaxants
According to Onset and Duration of Block at adductor pollicis

Onset to Maximum Block

Ultrarapid (< 1min) Succinylchholine

Rapid (1-2min) Rocuronium

Intermediate (2-4min) Atracurium

Mivacurium
Vecoronium
Pancoronium

Long (>4min) Cisatracurium

Doxacurium
Adductor Pollicis
Duration to 25% recovery of T1

Ultra-Short(<8min) Short(8-20mins) Intermediate(20-50mins ) Long

(>50mins)
Succinylcholine Mivacurium
Vecuronium Pancuronium
Atracurium Doxacurium
Rocuronium
Cis-atracurium
Classification of Muscle Relaxants
According to Mechanism of Action

Depolarizing Non
, depolarizing ,
Non Competitive ,
competitive , antagonist .
agonist .
Tubocurarine
Succinylcholi
ne
Structure / Activity Relationship
• Bis quaternary amines
 Succinylcholine, Pancuronium, Atracurium
 steroids block postganglionic muscarinic
ACh receptors
• Mono quaternary amines
 D-Tubocurarine, Vecuronium, Rocuronium
 In acidosis, Tertiary amine protonated  +
charge  increased potency
 Benzylisoquinolines are histaminergic
 Bridging structure in between two amines
is lipophilic and determines potency
•
Pharmacokinetics

• Potency
 Low affinity – high dose – quick onset
 High affinity – small dose – slow onset
• Speed of onset
 Fast injection – high gradient – quick
onset
• Perfusion
 Delayed onset with reduced cardiac
output
 Onset  diaphragm < larynx <
orbicularis oculi < adductor pollicis
Pharmacokinetics

• Obesity
 +ve charge prevents fat absorption
 Vd / kg and clearance markedly
reduced
 Unaltered elimination half life
• Temperature
 Prolonged action with hypothermia
 Temp. independent degradation of
Mivacr.
Pharmacokinetics
Age
• Children:
 Larger Vd (more dose required)
 Sensitive NMJ (prolonged action)
 Higher HR (faster onset)
• Aged:
 Widening of NMJ & reduced no. of
receptors
 Delayed distribution & elimination
 Organ-dependent metabolism &
elimination of steroid relaxants are
affected
Pharmacokinetics

• Pregnancy
 Unaltered
 Magnesium – increased potency &
duration of action
 Ionized state – minimal placental
transfer (except prolonged use in
ICU)
 May have reduced plasma
cholinesterase activity
Pharmacokinetics

• Burns
 Up-regulation of receptors (at least 30%
burns)
 Resistance to non-depolarizers (starts
at10 – peaks at 40 – declines at 60
days.)
 Altered affinity no increase in extra
junctional
• receptors
 Sensitive to Succinylcholine
(hyperkalemia)

Pharmacokinetics

Gender
•

 Women require 22% less Vecuronium


 Women 30% more sensitive to Roc

 Probably due to differences in body
composition, % of skeletal muscle
mass, Vd & Plasma protein
composition
Succinylcholine
1951
 The only depolarizing NMBA currently
used
 Only NMBA with short onset (< 1 min) &
short duration (5 – 10 min)
 Both N2 atoms are quaternary (+ ve)
 Almost exclusively used for RSI or to
counteract laryngospasm (0.1 mg/kg)
 IV injection – small fraction reaches NMJ
 ED 95 is 0.35 – 0.5 mg/kg (dose =
1mg/kg)
 Depolarizing effect within 20-40 sec
 Depolarizing Agents / structure :

 Only member = succinylcholine (suxamethonium/

Anectine ®)
 succinylcholine
•resembles two

•acetylcholine

•molecules linked end to end ,it has two quaternary

ammonium cations which interact with the anionic

sites on the muscle end plate receptors.

Dr. Med. Khaled Radaideh06/01/11 35

 Depolarizing Agents / MOA & Termination

This continuous stimulation of receptors lead to receptors desensetization (unresp

continuous stimulation of receptors
h ,it resists the hydrolysis by Ach-estrase leadsoto
enzyme repeated
remains action
attached potentials
to receptors & initial
for longer time phase of
s at end plate lead to depolarization of muscle fibers (so called depolarizing)

termination
Drughydrolysis
undergo spontaneous remains bybinding to Ach
endogenous receptors
plasma causing(pseudocholieesterase),
cholinesterase desensatization till no
 Depolarizing Agents /
Pharmacodynamics
CNS : MSS :
effect on consciousness , pain threshold & cerebral fnx -skeletal muscles paralysis
intra -ocular pressure -myalagia
intracranial pressure -myoglobinemia , myoglobinurea
-messeter muscle spasm

Dynamics

CVS : GU :
-Bradycardia -Coz metabolites excreted by kidneys, pts with RF may
-Dysarrythmia -
-Sinus arrest

Resp :
-respiratory muscles paralysis

Dr. Med. Khaled Radaideh06/01/11 37

Hyperkalemia following suxamethonium

 Usually there’s transient & brief increase in serum K+ of

about 0.5 meq/L following succinylcholine.

 Pts with K+ >=5.5 meq/L should not receive it.

 Pts having acute disruption of nerve activity of the skeletal
muscles if they take this drug they’ll have acute rise in
serum K+ to level as high as 13 meq/L  cardiac arrest.

Dr. Med. Khaled Radaideh06/01/11 38

Hyperkalemia following suxamethonium
continue

•Those pts who are at high risk of this dangerous

hyperkalemic response include :
- Extensive 3rd degree burns
- Severe intra-abdominal infx
- Severe closed head injury
- UMN lesions
- Pts with nerve damage or neuromuscular diseases
like muscular dystrophy
- Pts with traumatic paralysis

Dr. Med. Khaled Radaideh06/01/11 39

Suxamethonium : indications

•1- Non Fasting Patients :i.e. Emergency, cesarean

section….., (full stomach)
•2- predicted difficult intubation

•3- prior to ECT

•4- Operations of short duration where muscle

relaxation is needed.
•

Dr. Med. Khaled Radaideh06/01/11 40

Succinylcholine
contraindications
 Neuromuscular disease
 Denervation (after 2 days)
 Immobilization (after 3 days)
 Burns (after 2 days)
 MH susceptibility
 Basal sr. K > 5.5
 Sepsis / infection
 Allergy to SCh
 Characteristics of Nondepolarizing
Neuromuscular Blockade

•Decreased twitch amplitude

•Fade with continuous (tetanic) stimulation
•Train of four ratio <0.7
•Post tetanic potentiation
•Absence of fasciculations
•Antagonism by anticholinesterase drugs
•Augmentation by other non depolarizing muscle
relaxant
Mechanism of action of non depolarizing drugs

• These drugs combine with nicotinic

receptors and prevent binding of
acetylcholine so prevent depolarization of
the muscle cell membrane so inhibiting
muscle contraction.

Dr. Med. Khaled Radaideh06/01/11 43

 Mechanism of action of
non depolarizing drugs continue

these drugs competitively block the

•

receptors this means that you can

overcome their action by increase Ach
concentration by giving Ach esterase
inhibitors such as pyridostigmine or
neostigmine .

Dr. Med. Khaled Radaideh06/01/11 44

The sequence of skeletal muscle paralysis

•Skeletal muscles are paralyzed as follow:

•Small rapidly contracting muscles of face and eyes

,fingers, limbs, neck and trunk, intercostals and

lastly diaphragm.
•Recovery is in reverse.

Dr. Med. Khaled Radaideh06/01/11 45

Pharmacokinetics

 All neuromuscular junction blocker are given

intravenously because oral absorption is poor
as they are highly polar.
•

 Don’t cross BBB or placenta.

Dr. Med. Khaled Radaideh06/01/11 46

Factors that affect their duration of action:
• 1-PH: changes metabolic acidosis and to a lesser extent
respiratory acidosis extend the blockage duration
•

• 2-body temperature: Hypothermia potentiate the blockage

duration.
•

• 3-age: Older patients have prolonged effect also.

•

•4-electrolytes changes: Decrease in serum potassium conc.

potentiate the blockage. Decrease in ionized calcium
conc. also potentiate the blockage
•Note:

•Concomitant administration of potent inhalational agents

potentiate the duration of blockage esp. with isoflurane,

enflurane and sevoflurane.

Dr. Med. Khaled Radaideh06/01/11 47

Non-depolarizing agents

 Bind to one or both Alpha units of AChRs

 Competitive antagonism of Ach
 No conformational change in AChR
 Dynamic binding (repeated association
& dissociation) – competition
 Presynaptic receptors also blocked
 70 – 80 % receptor occupancy - twitch
depression
 92 % receptor block: complete block
Non-depolarizing agents

• Aminosteroids • Benzylisoquinolines
 
 Pancuronium  Atracurium
 Vecuronium  Cis-atracurium
 Rocuronium  Mivacurium
 Rapacuronium  d - Tubocurarine
Non depolarizing drugs:

1.Pancuronium bromide
2.Atracurium
3.Cisatracurium
4.Vecuronium bromide
5.Rocuronium bromide
6.Mivacurium
7.Alcuronium
8.Others
Dr. Med. Khaled Radaideh06/01/11 50
Classification according to duration of action:

1. Short acting duration: Mivacurium (Mivacron)

•

• 2. Intermediate:
•Vecuronium (Norcuron)

•Rocuronium (Zemuron)

•Cisatracurium (Nimbex)
•

• 3. long acting: Pancuronium (Pavulon)

•

Dr. Med. Khaled Radaideh06/01/11 51

 Nondepolarizing muscle relaxants
ED95 Priming Intubatin Onset Dur25 TOF>0. Recover
g dose 9 y

Rapac 1-1.2 1.5 1-1.5 15-20 25-50

u
Roc. 0.3 -- 0.6-1 1.5-2.5 35-50 55-80 60-120

Vec. 0.06 0.01 0.15-2 2-3 30-40 50-80 90-180

Pan. 0.07 3.5-6 70-120 130-220

Miva 0.08 0.02 0.25 2.5-4.5 15-20 25-40 25-40

Atra. 0.25 0.05 .7-.8 2-3 35-50 55-80 60-90

Cis- 0.05 0.01 .2-.4 3-6 40-55 60-90 75-120

atra.
Non-depolarizing agents
Altered response
• Volatile Anesthetics
 CNS depression  reduced
s eletal tone
 Decreased sensitivit
of post  unctional
memb to
depolari ation
 No effect on ch
release or on
receptors
 hange in
pharmacodynamics
Non-depolarizing agents
Altered response
• Antibiotics
 Aminoglycosides: pre junctional
effects like magnesium (decreased
release of Ach)
 Stabilize post junctional memb.
 Calcium improves Ach release but
stabilize pos tjunctional memb, so
unpredictable effect
Non-depolarizing agents
Altered response
• Local Anesthetics
 Enhance the block by interfering Ach
release, stabilizing memb &
depressing skeletal muscle fibres.

 Esters compete with SCh for plasma
cholinesterase activity
Non-depolarizing agents
Altered response
• Anti dysrhythmic drugs
 IV lidocaine & quinidine potentiate the
block
• Diuretics
 Furosemide 1 mg/kg enhances the block
(reduced cAMP production)
 Hypokalemia decreases doses of
Pancuronium
 No effect of Mannitol
Non-depolarizing agents
Altered response
• Magnesium
 Enhanced block by reduced Ach release
and stabilizing the memb.
• Lithium
 Enhanced block
• Phenytoin
 Resistance to non-depolarizing NMBA
Non-depolarizing agents
Altered response
• Steroids
 IV steroids -- no effect
 In myasthenia, ACTH or cortisol
improve NM function
• Hypothermia
 Prolonged duration of action (Panc,
Vec)
 Reduced hepatic, renal & Hoffman
clearance
Non-depolarizing agents
Altered response
• Potassium
 Acute fall in extra cellular K+ 
 ncreased trans memb
potential  hyper
polariyation 
increased
sensitivit to non
depolari ing 
resistance to  h
• Paresis / Hemiplegia
 Resistance to non-depolarizers plegic
limb > healthy limb > normal
individual (Proliferation of extra
SCh followed by a non-
depolarizing NMB agent
 Enhanced twitch suppression with
intubating dose of SCh (not with 0.5
mg/kg)
 Desensitized post junctional memb.
by SCh
 Duration of action of subsequent
doses is not prolonged
Combination of Non
depolarizing NMB agents
 Additive effects with drugs having
same site of action (dTc +
Metocurine)
 Synergistic effects with drugs having
different sites of action
(Pancuronium + dTc or Metocurine)
o Shorter duration of action
o Fewer side effects
Drug Metabolism Renal Biliary

Succinylcholine 98 - 99 % <2% --
Mivacurium 95 – 99 % <5% --
Atracurium 70 – 90 % 10 – 30 % Laudanosin
Cis-atracurium 70 – 90 % 10 – 30 % Laudanosin
Vecuronium 30 – 40 % 40 % 10 – 20 %
(Hepatic) (metabolites) (metabolites)

Pancuronium 10 – 20 % 60 – 80 % 10 %
(Hepatic)
Rocuronium Minimal 30 – 40 % 60 %
(Hepatic)
Elimination

 Single dose: primarily redistribution

 Multiple doses: primarily by elimination
 Renal
 All agents can be eliminated
 Normal renal function: 1-2 ml/kg/min of
drug elimination (= normal GFR)
 No re-absorption
 Poor renal function: Prolonged
elimination ½ life of renal dependent
drugs (Panc, Alcuronium)
 Non enzymatic Decay
Hofmann elimination
 Atracurium & cis-atracurium
 Spontaneous degradation
 Inactive metabolites: Laudanosine and
Monocrylate
 Atracurium: ester hydrolysis
Hepatic elimination

 Hepatic elimination imp. in renal

failure

 Steroids: Rocuronium, Pancr, Vecr.

 Deacetylation causes active
metabolites (Accumulation with
prolonged use)

Rocuronium
Mono quaternary amminosteroid
 ED95 = 0.3 mg/kg, onset = 1 - 2 min and
• duration 20 - 35 min
 Resembles Vec but less potent (fast
onset)
 3-4 X ED 95 onset comparable with SCh
(@ adductor pollicis & not @ larynx)
 Largely excreted unchanged (upto 50%)
in bile in 2 hrs (>30% renal excretion
in 24 hrs)
 Prolonged action in renal, hepatic
diseases and old age
 Absence of histamine release
 Slight vagolytic action
Cis-atracurium
benzylisoquinolinium
 Purified form of one of 10 steroisomers of
atracurium, 5 times more potent
 Similar to atracurium except slow onset,
very little histamine & 1/5th less
laudanosine (cerebral excitatory)
 ED95 = 50 mcg/kg, onset 3 - 5 min &
duration 20 – 35 min
 77% Hoffman degradation at normal pH to
inactive laudanosine + alcohol (again
Hoffman)
 17% renal clearance (non specific
esterases not involved)
 Stable hemodynamics, organ independent
clearance
Mivacurium
Benzylisoquinoline
 Only non-depolarizer with short duration
 ED95 80 mcg/kg, onset 2 – 3 min,
duration 12 – 20 min
 2 X ED95 ok but 3 X ED95 
histamine release and
h potension
 Hydrolyzed by plasma cholinesterase
(88 % rate of SCh) 7% unchanged in
urine
 Inactive metabolites
 Antagonism: Spontaneous recovery, ?
Reversal with neostigmine,
Rapacurium

 Introduced in USA in 2000

 Less potent  more dose 
rapid onset
 yhort duration
 Histamine release 
bronchospasm
hypotensiony
tachycardia
 Withdrawn in 2001
Doxacurium

 Benzylisoquinoline
 Most recent
 Available in the USA
 Intubating dose = 0.5 mg / kg
 Long onset & prolonged duration
 No histamine release
 No cardiovascular effects
 Excreted mainly in the urine & the
bile
Newer Agents

• ORG 9487
 Aminosteroid
 Low potency, ED 90 = 1.15 mg/kg
 Rapid onset (similar to SCh @
add.pollicis but vocal cords are
resistant)
 Duration longer than SCh
• BW 785 U
 Benzylisoquinolin, onset 60 – 90 sec,
duration 10 – 15 min
 Histamine release 
hypotension
•
Newer Agents
Gantacurium (GW 280430 A)
 By GSK, similar to Mivacurium
 ED 95 = 0.18 mg/kg
 3 x ED 95 (0.54 mg/kg): Onset 1.2 -
1.8 min & duration of 15 min
 Higher doses cause histamine release
without change in onset time
 Alkaline hydrolysis in plasma +
spontaneous formation of cysteine
adducts
 Very little genetic variability
Newer agents

• 51W89
 One of 10 isomers of Atracurium
 Onset & duration like Atracurium
 Minimum CV effects, Hofmann
elimination
 “Nearly ideal” relaxant with
intermediate duration
• Future possibilities
 Incorporation of reversing molecule
 Reversal by complex formation (Poly
anions)
 Reversal by enzymatic hydrolysis
ANTAGONISM OF NEUROMUSCULAR BLOCKADE

Inhibition of acetylcholinesterase by
anticholinesterase drugs. (neostigmine, pyridostigmine,
edrophonium)

Dosage of 0.04-0.07 mg/kg/iv in neostigmine and 0.25-

0.5mg/kg/iv in edrophonium.
Monitoring

 Time of intubation
 Degree of relaxation
 Time to reverse
 Time for extubation
 Residual curarization
Monitoring
Indications
 Long interventions
 Changed pharmacokinetics /
dynamics
 No moving / straining allowed
 No reversal preferred
 Disturbed electrolyte balance
 Expected drug interactions
Monitoring
Features
 Increased safety
 Cost effective
 Easy documentation
• Techniques
 Peripheral nerve stimulation (PNS)
 Mechanomyograph (MMG)
 Electromyograph (EMG)
 Acceleromyography (AMG)
Monitoring
Peripheral nerve stimulus
• Subjective monitoring:
 Visual & / or tactile
 Muscle monitored should be in sight
 Lacks accuracy & reliability
 Acceptable TOF ratio of > 70% for
extubation (only 10% correct
observations)
 Double burst stimulus (DBS): Only 40 %
of anesthesiologists are able to
recognize a fade

Stimulating patterns
Single twitch (ST)
 Reflects events at post junctional
membrane
 Single supra maximal electrical stimuli
applied to peripheral motor nerve
 Frequency every second (1 Hz) or every
10 seconds (0.1 Hz)
 Used for monitoring onset of block
 Same response to both groups of NMBAs
 Response influenced by position of
muscle, muscle temp.
 Calibration required before relaxation
(not suitable for day-to day clinical
practice)
Stimulating patterns
Tetanus
 Normally 50 Hz for 5 sec
 Fade with non-depolarizing block
 Post-tetanic facilitation
 Painful
 May produce lasting antagonism
Stimulating patterns
Train of four (TOF)
 Reflects events at pre synaptic
membrane
 Used successfully for onset,
maintenance & recovery of block
 Four supra maximal stimuli q 0.5
seconds (2 Hz). May be repeated q
12 – 15 seconds
 Advantage: relative ratio of 4th to 1st
response remains the same despite
changes in absolute responses
Train of four (TOF)

No. of responses Neuromuscular Muscle power

block
1 95 % 5%
2 90 % 10 %
3 85 % 15 %
4 75 % 25 %
Stimulating patterns
Post-tetanic count (PTC)

 If no response with ST or TOF: block
can’t be assessed. PTC assesses the
intensity of deep block (due to
facilitation).
 50 Hz tetanus for 5 sec.   sec
later single twitch
at  H and count the
no of responses
 hould not be repeated
for  min (possible
antagonism in the
muscle
Stimulating patterns
Double burst stimulation
 Two short (0.2 milliseconds) bursts of
50 Hz tetanic stimuli separated by
750 milliseconds
 DBS with 3 impulses in each of bursts
(3,3) most commonly used
 Ratio of second response to the first
is equivalent to TOF ratio
 Easily seen or felt by the
anesthesiologist

Monitoring
Mechano-myograph
 Isometric measurement of force of
contraction with a force
displacement transducer.
 Simple, accurate & reliable.
 Sensitive to external physical
influences and limb has to be fixed
in one position.
 Used for scientific studies
Monitoring
Electromyography
 Measures evoked compound muscle
action potential
 Correct positioning of electrodes very
imp.
 Extensive & sensitive equipment
 Diathermy interference
 Seems to underestimate block during
recovery
 Scientific use but not popular for
routine clinical use
Monitoring
Influencing factors
• Choice of muscle
 Diaphragm (most resistant) > other
resp, upper airway & facial muscles >
peripheral & abdominal (least
resistant)
 Adductor pollicis (hand) & Flexor hallucis
brevis (leg): sensitive (may be
unreliable for intubation), less chance
of overdosing,
 Orbicularis oculi: Onset, duration &
sensitivity same as resp. muscles
 Other: Laryngeal, masseter, other facial
muscles (research purposes only)
Monitoring
Clinical applications
 Onset: Orbicularis oculi  y
T or
T F
 urgical relaxation 
or  responses to T F =
sufficient blocyy
 hen intense bloc
required   T
 Recoveryy TyF ratioyDyy
 Reversaly yhen y or
more TyF responses
 xtubation hen TF
reaches  –  
Choice of muscle relaxants:
•Consideration for choosing a muscle relaxant
include:
•* Duration of action required
•* Route of excretion
•* Tendency to release histamine
•* Cardiopulmonary side effects
•* The ability to reverse the blockage
•* Contraindication to any specific muscle relaxant.
•*Cost

Dr. Med. Khaled Radaideh06/01/11 89