Neuromuscular Blocking Agents
Submitted by – Amandeep
Department Of Veterinary Medicine
L2013V40M
INTRODUCTION
• Agents that interfere with transmission of
nerve impulse from somatic nerve ending to
skeletal muscle fibres
• Profound muscle relaxation & even paralysis
of skeletal muscles
Muscle Relaxants
Peripheral acting muscle
relaxant
Centrally acting muscle relaxant
Peripheral Acting Muscle Relaxant
Neuromuscular blocking agents
Directly acting drugs
Why?
• Inhalant anesthetics(IA) are complete anesthetics
• Fulfill triad-unconsciousness, analgesia & muscle
relaxation- of anesthesia
• Light planes- good loss of consciousness
• Deeper planes- analgesia & M. relaxation
• Cardiovascular compromise
Balanced Anesthesia
• Low concentration of IA to provide unconsciousness
• Analgesic to inhibit nociceptive processing
• NMBA to relax skeletal muscle
Physiology
At Microscopic Level
• Protruded circular area- binding site for Ach
• Pit- extracellular opening for ion channel
• Ach binds to one R• R composed of alpha,
beta, gamma & delta• 2 molecules of Ach bind
to 2 alpha subunits• Protein rotates into new
conformation
Uses of NMBA
• Adequate surgical muscle relaxation without compromising
recovery
Absolute relaxation, eg : intra-ocular procedures, microsurgery
Specific muscle relaxation, eg : laparotomy , Caesarean
section, some orthopaedic surgery (reduction of dislocations),
diaphragm surgery
Uses of NMBA
• Reduction of anaesthetic dose
• Preservation of cardiopulmonary function
• Reduced operating times in 'high risk' patients
• Where positive pressure ventilation (PPV) required
• Where spinal reflexes need to be suppressed, eg: ear canal
surgery
Non – Depolarizing Depolarizing
• Act by competitively
blocking the binding of ACh
to its receptors / directly
block the ionotropic activity
of the ACh receptors
• Bind to Ach receptors but no
activation occurs
• Act by depolarizing the
plasma membrane of the
skeletal muscle fibre similar
to Ach
• Bind to Ach receptors
causing activation
Muscle paralysis
Neuromuscular Blocking Agents
• Non depolarising-
1. Long acting e.g tubocurarine
2. Intermediate acting e.g vecuronium, atracurium
3. Short acting e.g mivacurium
• Depolarising eg suxamethonium & decamethonium
Dose rates
• Pancuronium –
• In cattle - 0.04mg/kg, slow I/V(initial dose),
followed by increments of 0.008mg/kg
• In horse – 0.06mg/kg, , slow I/V(initial dose),
followed by increments of 0.001mg/kg
Dose rates
Doxacurium- usually not used
Atracurium –
Horse@ 0.15mg/kg, slow I/V(initial dose), then
increments of 0.06 mg/kg
Vecuronium- Horses@ 0.1 mg/kg slow I/V initial dose,
then increment of 0.02mg/kg
Mivacurium- it does not need reversal
Drug ( Depolarizing NMB)
Horse(mg/kg)
Cattle(mg/kg)
Succinyl choline(Scoline ®)
0.12-0.15 0.01-0.02
Non Neuromuscular effect
• Cardiovascular effect
• Histamine release
• Placental transfer
• CNS effects
• Protein binding
Non Neuromuscular Effect Of Succinylcholine
• Hyperkalemia
• Intraocular pressure
• Intragastric pressure
• Intracranial pressure
• Muscle soreness
Reversal Of NM Blockade
Achieved by establishing high concentration of acetylcholine at the
binding site
Atropine (0.04 mg/kg S/C)
Glycopyrrolate (0.01 mg/kg I/M) administered intravenously atleast
one minute prior to the administration of reversal agent to block the
muscarinic effects of acetylcholine
Reversal Of NM Blockade
• Neostigmine 0.1 mg/kg I.V
• Edrophonium 1.0 mg/kg I.V
Cholinesterase Reversal
Cholinesterase reversal by increasing ACh and
displacing NMBA from receptors
Sugammadex MOA
• Modified cyclodextrin
• Cavity created by ring
is lipophilic, exterior is
hydrophilic
• Encapsulate lipophilic
drugs yet remain soluble
in water
Sugammadex MOA
• Resultant sugammadex bound NMBA (inclusion
complex) is then excreted by the kidneys
• Renal clearance of the NMBA has been found to be
enhanced by sugammadex encapsulation
Thanks
