BY
Dr Oyedepo O. O. (B.Sc.; MBBS; FMCA)
Dept. of Anaesthesia,
College of Health Sciences,
University of Ilorin. Ilorin.
Ni...
OUTLINE
ANATOMY OF NEUROMUSCULAR JUNCTION
 PHYSIOLOGY OF NEUROMUSCULAR
TRANSMISSION
 FACTORS THAT MAY AFFECT NMT&NMB
 C...
ANATOMY OF NMJ
Each motor nerve sends processes to each
muscle fiber in the motor unit
 Forming a highly organized and sp...
THE NEUROMUSCULAR JUNCTION
PHYSIOLOGY OF NEUROMUSCULAR
TRANSMISSION
FACTORS AFFECTING NMT
Muscle relaxants are potentiated by various factors: Drugs Most of the inhalational anaesthetic age...
Muscle contraction is controlled by motor
neurons that release the neurotransmitter
acetylcholine at neuromuscular junctio...
DEPOLARIZING NEUROMUSCULAR
BLOCKADE
ACETYLCHOLINE ANALOGUES INTERACT
WITH POSTJXNAL CHOLINERGIC-NICOTINIC
RECEPTOR
 DEPOL...
NON-DEPOLARIZING
NEUROMUSCULAR BLOCKADE
COMBINE REVERSIBLY WITH PJXNAL
CHOLINERGIC-NICOTINIC RECEPTORS
WITHOUT OPENING SOD...
CHARACTERISTICS OF IDEAL
MUSCLE RELAXANT
NON DEPOLARZING
 FAST ONSET
 FREE OF CVS SIDE EFFECT
 EASILY ANTAGONISED
 STA...
CLASIFICATIONS
DEPOLARIZING-SUCCINYLCHOLINE,
DECAMETHONIUM(SHORT ACTING)
 NON DEPOLARIZING
-AMINOSTEROIDS(VAGOLYSIS)
.PAN...
CLASSIFICATION OF NON-DEPOLARIZERS


LONG ACTING

D-TUBOCURARINE
METOCURINE
DOXACURIUM
PANCURONIUM
GALLAMINE
PIPECURONIUM...
DIFFERENCES BTW DEPOLARISERS AND NON
DEPOLARIZERS
EVOKE STIMULUS

DEPOLARIZING

NON-DEPOLARIZING

TRAIN OF FOUR

CONSTANT ...
SUXAMETHONIUM
Chemical structure:- 2 molecules of Acetyl Choline
linked together with 2 quaternary amine groups.
 Physica...
SIDE-EFFECTS
Cardiac arrhythmias-sinus bradycardia, ventricular
premature beats
 Hyperkalaemia esp-massive burns, muscle
...
CAUSES OF PROLONGATION OF ACTION IN
PLASMACHOLINESTERASE DEFFICIENCY


PHYSIOLOGICAL



PREGNANCY



CONTRACEPTIVE PILL...
D- TUBOCURARINE
FIRST NMB AGENT USEDD IN ANESTHESIA
 IT CAUSES MS PARALYSIS WITHIN 3 MINS
 DURATION= 30-40 MINS (LONG AC...
PANCURONIUM











IS AN AMINOSTEROID MS RELAXATION WITHIN 2
MIN
RECOMMENDED LOADING DOSE WITHING 0.060.08 MG/...
GALLAMINE


SOLELY EXCRETED BY THE KIDNEY HENCE
ABSOLATELYCONTRAINDICATED IN RENAL
DISEASE



CROSSES THE PLACENTA HENCE...
ATRACURIUM










Dose
0.3-0.4 mg kg-1 or 30 mg increment 0.080.1mg kg-1
Amps 2.5 ml = 25 mg
Cardiovascularly sta...
CIS-ATRACURIUM



Dose

0,15 mg kg-1 or 10 mg

Amps



5 ml = 10 mg

Features Similar to Atracurium without the
histamin...
MIVACURIUM
Dose 0.15 mg kg-1 or 10 mg
Amps 5 ml = 10 mg and 10 ml = 20 mg
 New on the market
 Much shorter acting than t...
VECURONIUM
Dose 0.1 mg kg-1 or 6 mg
Amps 2 ml = 4 mg and 10 ml = 20 mg as a dry
powder needing reconstituting with sterile...
ROCURONIUM










Dose
0,3 - 0,9 mg kg-1 or 20 - 50 mg
Amps 5 ml = 50 mg and 10 ml = 100 mg
New on the market
Lo...
ALCURONIUM
0,25 mg kg-1 or 15 mg
Amps 2 ml = 10 mg
 Cardiovascularly more stable, with
occasional tachycardia
 Histamine...
DOXACURIUM
Benzylisoquinoline compound closely related to
mivacurium and atracurium
 MOST POTENT CURRENTLY




ONSET-10...
METOCURINE
BIS-QUARTERNARY AMINE

DERVATIVE OF DTC
PHARMACOLOGY SIMILAR
TO DTC
PIPECURONIUM
Elimination depends on renal (70%)

and secondarily biliary (20%).
principal advantage over
pancuronium is ...
REVERSAL OF NMB








Acetyl Choline is normally degraded in milliseconds by Cholinesterases.
The degradation of Ace...
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Muscle relaxants   neuromuscular blocking drugs 2
Upcoming SlideShare
Loading in …5
×

Muscle relaxants neuromuscular blocking drugs 2

1,261
-1

Published on

Published in: Sports, Automotive
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total Views
1,261
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
133
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide

Muscle relaxants neuromuscular blocking drugs 2

  1. 1. BY Dr Oyedepo O. O. (B.Sc.; MBBS; FMCA) Dept. of Anaesthesia, College of Health Sciences, University of Ilorin. Ilorin. Nigeria.
  2. 2. OUTLINE ANATOMY OF NEUROMUSCULAR JUNCTION  PHYSIOLOGY OF NEUROMUSCULAR TRANSMISSION  FACTORS THAT MAY AFFECT NMT&NMB  CHARACTERISTICS OF IDEAL MUSCLE RELAXANT  CLASSIFICATION OF NMB & DISTINCTION BTW DMR&NDMR  INDIVIDUAL AGENT  REVERSAL OF NMB 
  3. 3. ANATOMY OF NMJ Each motor nerve sends processes to each muscle fiber in the motor unit  Forming a highly organized and specialized structure neuromuscular junction, or motor endplate  The invagination of the muscle fiber sarcolemma forms the synaptic trough  The space between the axon terminal and invaginated sarcolemma is called the synaptic cleft 
  4. 4. THE NEUROMUSCULAR JUNCTION
  5. 5. PHYSIOLOGY OF NEUROMUSCULAR TRANSMISSION
  6. 6. FACTORS AFFECTING NMT Muscle relaxants are potentiated by various factors: Drugs Most of the inhalational anaesthetic agents. Aminoglycoside antibiotics esp. Gentamycin, Kanamycin. β-Blockers Ca-channel blockers  Electrolytes Depressed Ca++ Raised Mg++ Raised K+  Acidosis  Temperature -If T° depressed then Suxamethonium is potentiated. -If T° raised then Non-depolarisers are potentiated  Myasthenia gravis and other inherited muscle abnormalities e.g. dystrophies, dystonias
  7. 7. Muscle contraction is controlled by motor neurons that release the neurotransmitter acetylcholine at neuromuscular junctions.  Acetylcholine then diffuses across the narrow synaptic cleft and binds to acetylcholine receptors on the membrane of the muscle cell.  Opening of ion channels within the receptor molecules, in such a way that a depolarizing, synaptic ion current can flow. This current triggers an all-or-nothing response in the form of an action potential across the plasma membrane of the muscle cells.  The action potential moves out in all directions from the neuromuscular junctions, resulting in stimulation of the entire muscle fiber within a few milliseconds, the contractile mechanism responds and the fiber contracts 
  8. 8. DEPOLARIZING NEUROMUSCULAR BLOCKADE ACETYLCHOLINE ANALOGUES INTERACT WITH POSTJXNAL CHOLINERGIC-NICOTINIC RECEPTOR  DEPOLARIZATION OF ENDPLATE AND MUSCLE FIBRE THEN MUSCLE CONTRACTS  CONTRACTION IS NOT SUSTAINED  PERSISTENT OCCUPATION OF RECEPTORS, DEPOLARIZATION, INTERUPTION OF NEUROMUSCULAR TRANSMISSION  END RESULT IS MUSCLE PARALYSIS 
  9. 9. NON-DEPOLARIZING NEUROMUSCULAR BLOCKADE COMBINE REVERSIBLY WITH PJXNAL CHOLINERGIC-NICOTINIC RECEPTORS WITHOUT OPENING SODIUM CHANNELS  COMPETING WITH ACETYLCHOLINE REDUCING THE RECEPTORS AVAILABLE FOR ACH  70% OCCUPANCY BLOCK RESPONSE OF END-PLATE POTENTIAL IN RESPONSE TO A SINGLE NV IMPULSE -MSC REMAIN INERT  90-95% OCCUPANCY RESULTS IN COMPLETE 
  10. 10. CHARACTERISTICS OF IDEAL MUSCLE RELAXANT NON DEPOLARZING  FAST ONSET  FREE OF CVS SIDE EFFECT  EASILY ANTAGONISED  STABLE PHARMACOKINETIC & PHARCODYNAMIC IN PRESENCE HEPATIC AND RENAL DISEASES  NO SUCH DRUG YET
  11. 11. CLASIFICATIONS DEPOLARIZING-SUCCINYLCHOLINE, DECAMETHONIUM(SHORT ACTING)  NON DEPOLARIZING -AMINOSTEROIDS(VAGOLYSIS) .PANCURONIUM .VECURONIUM .PIPECURONIUM .ROCURONIUM .RAPACURONIUM -BENZYLISOQUINOLINIUM .D-TUBOCURARINE .ATRACURIUM .DOXACURIUM .MIVACURIUM .CIS-ATRACURIUM .METOCURINE .GALLAMINE 
  12. 12. CLASSIFICATION OF NON-DEPOLARIZERS  LONG ACTING D-TUBOCURARINE METOCURINE DOXACURIUM PANCURONIUM GALLAMINE PIPECURONIUM  INTERMEDIATE ACTING ATRACURIUM CIS-ATRACURIUM VECURONIUM ROCURONIUM  SHORT ACTING MIVACURIUM RAPACURONIUM
  13. 13. DIFFERENCES BTW DEPOLARISERS AND NON DEPOLARIZERS EVOKE STIMULUS DEPOLARIZING NON-DEPOLARIZING TRAIN OF FOUR CONSTANT BUT DIMINISHED FADE TETANY CONSTANT BUT DIMINISHED FADE DOUBLE BURST STIMULATION CONSTANT BUT DIMINISHED FADE POSTTETANIC POTENTIATION ABSENT PRESENT NEED NO REVERSAL OF BLOCK NEED REVERSAL OF BLOCK FASCULATION PRESENT FASCULATION ABSENT
  14. 14. SUXAMETHONIUM Chemical structure:- 2 molecules of Acetyl Choline linked together with 2 quaternary amine groups.  Physical properties:- It is available in 2 forms: Succinylcholine chloride-Aqeous-Temperate Succinylcholine bromide-Powder-Tropic  Rapid onset, short duration(3-5mins)  Indications-To facilitate ETT placement  Dose-Intubating dose in adult is 1mg/kg -Xren esp infants is 1.5-2.0mg/kg  Rapidly hydrolysed by plasma cholinesterase 
  15. 15. SIDE-EFFECTS Cardiac arrhythmias-sinus bradycardia, ventricular premature beats  Hyperkalaemia esp-massive burns, muscle trauma, UMNL&LMNL, renal dx and severe abd infx  Raised IOP  Raised ICP  Raised IGP  Scoline pain-ambulant and muscular pts  Anaphylactoid rxn  Masseter spasm-could erald MH 
  16. 16. CAUSES OF PROLONGATION OF ACTION IN PLASMACHOLINESTERASE DEFFICIENCY  PHYSIOLOGICAL  PREGNANCY  CONTRACEPTIVE PILLS  MALNUTRITION  LIVER DX CIRRHOSIS  HEMODIALYSIS  ECHOTHIOPATE (AN EYE DROP)
  17. 17. D- TUBOCURARINE FIRST NMB AGENT USEDD IN ANESTHESIA  IT CAUSES MS PARALYSIS WITHIN 3 MINS  DURATION= 30-40 MINS (LONG ACTING)  CAUSES HYPOTENSION BY 2 MECH 1.SYMPATHETIC GANGLIONIC BLOKAGE 2.HISTAMINE RELEASE  METABOLISED IN LIVER & EXCRETED BY KIDNEY 
  18. 18. PANCURONIUM         IS AN AMINOSTEROID MS RELAXATION WITHIN 2 MIN RECOMMENDED LOADING DOSE WITHING 0.060.08 MG/KG INCREMENT OF 0.01-0.02 MG/KG LARGE AMOUNT BOUND TO PLASMA PROTEIN DEPENDENT ON RENAL EXCRETION 80% METABOLISED AND EXCRETED BY THE LIVER DOES NOT RELEASE HISTAMINE CVS- INCR BP DUE TO NOR ADRENALINE RELEASE - SINUS TACHYCARDA DUE TO ITS
  19. 19. GALLAMINE  SOLELY EXCRETED BY THE KIDNEY HENCE ABSOLATELYCONTRAINDICATED IN RENAL DISEASE  CROSSES THE PLACENTA HENCE CONTRAINDICATED IN OBST  Vagolytic, causing early, severe tachycardias
  20. 20. ATRACURIUM       Dose 0.3-0.4 mg kg-1 or 30 mg increment 0.080.1mg kg-1 Amps 2.5 ml = 25 mg Cardiovascularly stable, but larger doses release histamine with mild hypotension Breakdown occurs spontaneously and is dependent on pH and T° (Hoffman degradation). Hepatic degradation also occurs resulting in the formation of Laudanosine Laudanosine is a convulsant in high doses, but clinically has not been a problem It is safe in hepatic & renal failure Non-cumulative, even after prolonged infusions Similar duration of action to Vecuronium Expensive
  21. 21. CIS-ATRACURIUM  Dose 0,15 mg kg-1 or 10 mg Amps  5 ml = 10 mg Features Similar to Atracurium without the histamine release.
  22. 22. MIVACURIUM Dose 0.15 mg kg-1 or 10 mg Amps 5 ml = 10 mg and 10 ml = 20 mg  New on the market  Much shorter acting than the previous 2 agents (± 10 minutes), with rapid recovery It will not replace Suxamethonium  Degraded by plasma cholinesterase (competing with Suxamethonium) and thus contraindicated in patients with “Scoline Apnoea”.  May be used as an infusion  Expensive 
  23. 23. VECURONIUM Dose 0.1 mg kg-1 or 6 mg Amps 2 ml = 4 mg and 10 ml = 20 mg as a dry powder needing reconstituting with sterile water  Cardiovascularly very stable, with occasional bradycardia  No histamine release  Shorter acting (± ½ the duration of the preceding drugs)  Hepato-biliary excretion and can thus be used in renal failure  Expensive 
  24. 24. ROCURONIUM        Dose 0,3 - 0,9 mg kg-1 or 20 - 50 mg Amps 5 ml = 50 mg and 10 ml = 100 mg New on the market Low dose provides slow intubation and short duration (± 15 min) High dose provides very fast intubation (± 60 - 90 sec) and long duration Cardiovascularly stable with a mild increases in heart rate and blood pressure Very rapid onset (similar to, but not as predictable as Suxamethonium), but has an intermediate to long duration of action. Undergoes no metabolism and 10ly eliminated by d liver & slightly by d kidney Expensive.
  25. 25. ALCURONIUM 0,25 mg kg-1 or 15 mg Amps 2 ml = 10 mg  Cardiovascularly more stable, with occasional tachycardia  Histamine release with possible mild hypotension.  Dose
  26. 26. DOXACURIUM Benzylisoquinoline compound closely related to mivacurium and atracurium  MOST POTENT CURRENTLY   ONSET-10MIN  DURATION 3HOURS  ELIMINATED UNCHANGED BY THE KIDNEY  SLIGHTLY METABOLISED BY PLASMA CHOLINESTERASE
  27. 27. METOCURINE BIS-QUARTERNARY AMINE DERVATIVE OF DTC PHARMACOLOGY SIMILAR TO DTC
  28. 28. PIPECURONIUM Elimination depends on renal (70%) and secondarily biliary (20%). principal advantage over pancuronium is its lack of cardiovascular side effects due to a decreased binding to cardiac muscarinic receptors
  29. 29. REVERSAL OF NMB     Acetyl Choline is normally degraded in milliseconds by Cholinesterases. The degradation of Acetyl Choline may be inhibited by the use of an Acetyl Cholinesterase inhibitors e.g Edrophonium Pyridostigmine Neostigmine Physiostigmine Acetyl Choline is the neuro-transmitter at numerous receptors and the use of an Acetyl Cholinesterase inhibitor will result in an increase in Acetyl Choline at all cholinergic receptors (pre- and post-ganglionic Parasympathetic nerves, as well as pre-ganglionic Sympathetic nerves). The effects of relative overactivity of Acetyl Choline that would result if a Muscarinic blocker were not given at the same time, includes the following severe bradycardia bronchospasm copious secretions other parasympathetic effects e.g. increased gut motility, pupil constriction, etc. The standard reversal "cocktail" for an adult is therefore a mixture of:Neostigmine 2,5 mg plus Atropine 1,0 - 1,2 mg or Neostigmine 2,5 mg plus Glycopyrrolate 0,4 - 0,6 mg mixed in the same syringe.
  1. A particular slide catching your eye?

    Clipping is a handy way to collect important slides you want to go back to later.

×