Overview Of Neuromuscular Blockade & Specific NMDRs Flashcards Preview

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1

The Neuromuscular Junction (NMJ) in Skeletal Muscle

Excitation-contraction coupling: Nervous impulse is converted into a skeletal muscle contraction at the NMJ

2

Acetylcholine (Ach)

Key neurotransmitter at the NMJ
Formed from ACETYL CoA + CHOLINE
Stored in pre-synaptic vesicles
Binds to NICOTINIC cholinergic receptors on post-junctional membrane
Broken down by Acetylcholinesterase (AChE)

3

Ach release blockers (BAM)

Botox
Aminoglycoside
Magnesium
(tubocurarine= block NMJ from binding to ACH receptor)

4

How is Muscle Relaxation Achieved

Blocking Motor Nerves= local anaesthetics
Blocking The NMJ= IV muscle relaxants (neuromuscular blockers
Blocking receptors inside cells= Dantrolene

5

Classification of Neuromuscular Blockers

A) Depolarising=> Suxamethonium
B) Non-depolarising=> all other muscle relaxants

6

Depolarising agent

Non-competitive action
Cannot be reversed… wear off / are metabolised over time

7

Non-depolarisers

Competitive inhibition
Compete with Ach for nicotinic receptors
Require reversal

8

ED95

"Effective Dose”
Dose of muscle relaxant that will paralyse 95% of normal people
Usual intubating does: 2 x ED95

9

Adequate paralysis

Adequate dose of muscle relaxant will result in:
Inability to breathe
Inability to maintain an airway
Loss of protective reflexes
Consciousness is completely unimpaired!!!

10

Factors that potentiate muscle relaxants

Drugs= inhalation agents and aminoglycosides antibiotics
Electrolytes: low Calcium, high magnesium and low potassium.
pH: Acidosis
Temperature: cold; warm (non-depolarisers)
Diseases: myasthenia gravis; muscular dystrophy, dytonia and myopathies and renal failure

11

Some clinical examples where muscle relaxants are used

Improved surgical access (abdominal surgery)
Facilitate intubation or bronchoscopy
Prevention of movement in microsurgery
Manipulation of fractures
Preventing / mitigating physical effects of convulsions
ICU=Tetanus; Respiratory failure; Severe ↑ ICP

12

Before administering muscle relaxant it is essential to:

Assess the airway
Be competent in airway management
Have necessary equipment

13

Suxamethonium

Physical properties: 2 ACH molecules, dose 1-2mg/ml and stored in fridge (Ampoules 100mg/2ml)

14

What does Suxamethonium do?

Profound paralysis (60s)
Ultra-short acting
Causes fasciculations
Lasts 5 minutes

15

How is Suxamethonium metabolized?

Metabolised by pseudocholinesterase aka plasma cholinesterase
synthesised in liver
Found freely in plasma
Markedly decreased in SCOLINE APNOEA
No reversal

16

SCOLINE APNOEA

Inherited homozygous or heterozygous
Prolonged paralysis
Supportive treatment with ventilation + sedation
FFPs

17

Suxamethonium Side-Effects "BATH MASH"

Bradycardia
Anaphylaxis
Triggers MH
Histamine release
Muscle pain
Arrhythmia
Scoline Apnoea
Hyperkalemia

18

Suxamethonium Contra-indication R-MUD

Drug allergy
Scoline apnoea
MH
Unknown myopathies
Risk of hyperkalaemia (Renal failure
Paralysis
Crush / Burn injury)

19

Non-depolarising agents

Benzylisoquinolines
Curare-based: atracurium, cisatracurium

Aminosteroids
Pancuronium, vecuronium, and rocuronium

Doses: based on lean body mass
Physical properties:
2 – 5ml ampoules
May require refrigeration

20

Pharmacology of non-depolarisers
1)Clinical Effects
2)Metabolism
3)Excretion

Clinical effects:
Marked paralysis in 1 – 5 minutes (take longer to act)
No fasciculations
Duration is variable
Short-acting
Intermediate-acting
Long-acting

Metabolism:
Hepatic
Hoffman degradation

Excretion:
Renal
Hepatobiliary

21

Vecuronium

Powder that must be mixed with water
Cardiovascularly stable
No histamine release
Intermediate-acting
Largely hepato-biliary excretion therefore safe in renal failure, but avoid in hepatic disease.

22

Rocuronium

Most commonly used non-depolariser
Solution kept in fridge (50mg in 5mL)
Cardiovascularly stable
High dose: 1mg/kg can provide intubating conditions within 1 minute
Modified RSI
Intermediate duration of action
The higher the dose, the longer the paralysis

23

Atracurium

Kept in Fridge
Histamine releasing
Increased risk of anaphylaxis
Hoffman degradation=
Spontaneous degradation=> breaks up into inactive molecules
Dependent on pH and temperature
Potentially toxic metabolite: laudanosine
Safe in renal and liver failure
Intermediate duration of action

24

Reversal of non-depolarising agents

ALL NMDR's should be reversed even if it has worn-off clinically.
NMDRs compete with Ach
So to reverse NMDR, increase Ach, so inhibit AchE.

25

Drugs used for reversal
AchE inhibitor/
Anticholinergic inhibitor AND their doses

Neostigmine=
Acetylcholinesterase inhibitor
Increases Ach concentration in synaptic cleft
Ach COMPETES with NDMR
But Ach ↑es at both nicotinic and muscarinic receptors which can cause side-effects
Anticholinergic agent=
Specifically an ANTI-MUSCARINIC agent
Atropine or glycopyrrolate
Given to prevent muscarinic effects (the B’s)
Bronchial secretions
Bronchospasm
Bradycardia
“B”eristalsis (peristalsis)

Neostigmine 2.5 mg + Glycopyrrolate 0.4–0.6 mg
Neostigmine 2.5 mg + Atropine 1 mg

26

When is it safe to reverse?

Check readiness with a peripheral nerve stimulator (TRAIN OF FOUR)
At least 3 twitches should be present
If a patient is already breathing adequately, it is generally safe to administer muscle relaxant

Beware the patient with compromised liver or kidney function

27

Signs of inadequate reversal

Jerky respiration
Reduced VT
Tracheal tug
Restlessness, may be worsened by hypoxia
Inability to raise head from pillow
Weak hand grip
Poor ability to cough
Ptosis

28

Management of Inadequate Reversal

Exclude another cause
Anaesthetic agents, analgesia, hypo or hypercarbia, CVA
Maintain ventilation
Reverse any potentiators
Warm patient
Check Mg, K, Ca
Use PNS
Repeat dose neostigmine (max: 5mg)
(Neostigmine in bigger doses can may cause weakness)

29

Sugammadex

Reverse rocuronium
Selective Relaxant Binding Agent
NO muscarinic side-effects
VERY EXPENSIVE