SURG ANES NEUROMUSCULAR BLOCKING DRUGS

NEUROMUSCULAR BLOCKING DRUGS  Succinylcholine

 Muscle relaxant  Decamethonium
 Interferes with physiologic sequence of B. Non – Depolarizers
neuromuscular transmission Long acting
 Not anesthetics  D – tubocorarine
Uses:  Metocurine
 Provides skeletal muscle relaxation to  Pancuronium
facilitate intubation  Gallamine
 Provide optimal surgical working  Piperonium
condition  Devacurium
 Note: lacks CNS depressant and Intermediate Acting
analgesic effects  Atracurium
 Vecuronium
3 WAYS TO SUPRESS MUSCLE TONE  Mivacurium
1. Giving muscle relaxant
2. Giving anesthestia  can result to ACETYLCHOLINE
overdose  Quarternary ammonium ester
3. Epidural or spinal anesthesia  block  Excitatory neurotransmitter at the
signals as they traverse the vertebral synapse in autonomic ganglia
canal  Synthesis:
o Acetylation
SEQUENCE OF ONSET OF NEUROMUSCULAR o Storage
BLOCKADE o Release into the post synaptic
1. Small rapidly moving muscle: eyes, cleft
digits o Binds to the post synaptic
2. Trunk, abdomen receptor
3. Intercostal muscle  Change in the permeability of ions
4. Diaphragm
 Decrease in transmembrane potential
 Recovery occurs in the Reverse order
from 90 MV to 45 MV  Action
potential  Muscle Contraction
IV INJECTION OF NONDEPOLARIZER TO A
PERSON WHO IS AWAKE
DEPOLARIZERS
1. Difficulty focusing
SUCCINYLCHOLINE
2. Weakness in mandibular muscles
 Onset: 30-60 sec
3. Ptosis
 Duration:3-5 mins
4. Diplopia
 Mechanism of action:
5. Dysphagia
Mimics action of Ach
6. Relaxation of small muscles of the ears

Persistent Depolarization
TYPES OF NEUROMUSCULAR BLOCKING DRUGS
d/t
A. Depolarizers

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SURG ANES NEUROMUSCULAR BLOCKING DRUGS

Sustained opening of the  UMN lesion

channels  Severe intra-
Abdominal
Prevents propagation of AP infection
 Closed head injury
Muscle paralysis  Renal failure
 Sustained opening of the channels o Myalgia (pain)
o Myoglobinuria
Depolarization associated with o Increased intragastric
leakage of K ions from interior of pressure
the cell o Increased intraocular
*succinylcholine can cause pressure
hyperkalemia  Contraction of tonic
myofibrils
0.5mEq/ L increase in K serum  Dilatation of
choroidal blood
 Metabolism: vessels
Succinylcholine o Increased intracranial
Plasma cholinesterase pressure
Succinylmonocholine + Choline o Sustained skeletal muscle
Plasma Cholinesterase contration
Succinyl Acid + Choline  Myotonia

 Conditions that has low NON DEPOLARIZERS

cholinesterase activity INTERMEDIATE ACTING
o Severe liver dse  Atracurium
o Pregnancy  Vecuronium
o Anticholinesterase drugs  Mivacurium
 There would be prolonged
cholinesterase activity 2 mechanism of action:
 Binds to postsynaptic receptos
 Adverse Side effects:
o Cardiac Dysrythmias Prevents Ach from activation
 Sinus bradycardia Na channel
 Junctional rhythm
 Sinus arrest Depolarization cannot occur
o Hyperkalemia
 Unhealed tertiary  May also act at presynaptic site
wounds to block Na channels
 Denervation 
atrophy Impaired release of Ach

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SURG ANES NEUROMUSCULAR BLOCKING DRUGS

to renal or hepatic dse

MIVACURIUM patients
 Short acting Benzylquinolium
compound LONG ACTING
 Metabolism: PANCURONIUM
o Only non-depolarizers  Causes increase in
that is rapidly o Heart rate
hydrolyzed by plasma o Mean arterial
cholinesterase pressure
 Clinical uses: o Cardiac output
o Rapid onset  CVS effects are attributed
o Rapid delivery to:
o Adaptable to short o Selective cardiac
acting procedure vagal blockade
(ambulatory care o Activation of
surgery) sympatheric
nervous system
ATRACURIUM  Increase heart rate may be
 Metabolism: undesirable in:
o Hoffman elimination o Hypovolemia
o Ester hydrolysis o Valvular heart
 Laudanosine : metabolite : CNS disease
stimulation o CAD
 + histamine release  Excreted principally in
o Contraindicated in kidneys
asthmatic patients  There should be reduced
o Can cause decrease in BP by dosage given to patients
20% with hepatic or renal dse 
 Renal or hepatic dse prolong the duration

VECURONIUM PIPECURONIUM
 Monoquarternary steroidal  Non depolarizers
analogue of Pancuronium  Main advantage: no adverse side
 Devoid of vagolytic effects effects
 No histamine release  Devoid of histamine, CVS effects
 If with opioids  Bradycardia  Similar structure to pancuronium
 15-25% is excreted to kidneys and  Elimination: renal
bile  Clinical use:
 Importance: o Replacement for
o Reduced doses of pancuronium where
vecuronium should be given increased HR is avoided

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SURG ANES NEUROMUSCULAR BLOCKING DRUGS

o Ishemic heart dse

o Long term mechanical
ventilation

SUMMARY

NICOTINIC RECEPTORS MUSCARINIC HISTAMINE RELEASE

RECEPTORS
SUCCINYLCHOLINE Stimulates Stimulates -

PANCURONIUM No effect Block -

PIPECURONIUM No effect No effect -

VECURONIUM

ATRACURIUM No effect No effect +

MIVACURIUM

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