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Anaesthesia > Overview Of Neuromuscular Blockade & Specific NMDRs > Flashcards

Overview Of Neuromuscular Blockade & Specific NMDRs Flashcards

1
Q

The Neuromuscular Junction (NMJ) in Skeletal Muscle

A

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

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2
Q

Acetylcholine (Ach)

A

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)

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3
Q

Ach release blockers (BAM)

A

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

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4
Q

How is Muscle Relaxation Achieved

A

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

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5
Q

Classification of Neuromuscular Blockers

A

A) Depolarising=> Suxamethonium

B) Non-depolarising=> all other muscle relaxants

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6
Q

Depolarising agent

A

Non-competitive action

Cannot be reversed… wear off / are metabolised over time

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7
Q

Non-depolarisers

A

Competitive inhibition
Compete with Ach for nicotinic receptors
Require reversal

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8
Q

ED95

A

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

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9
Q

Adequate paralysis

A

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

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10
Q

Factors that potentiate muscle relaxants

A

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

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11
Q

Some clinical examples where muscle relaxants are used

A

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

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12
Q

Before administering muscle relaxant it is essential to:

A

Assess the airway
Be competent in airway management
Have necessary equipment

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13
Q

Suxamethonium

A

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

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14
Q

What does Suxamethonium do?

A

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

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15
Q

How is Suxamethonium metabolized?

A 
Metabolised by pseudocholinesterase aka plasma cholinesterase
synthesised in liver
Found freely in plasma
Markedly decreased in   SCOLINE APNOEA
No reversal
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16
Q

SCOLINE APNOEA

A

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

17
Q

Suxamethonium Side-Effects “BATH MASH”

A 
Bradycardia
Anaphylaxis
Triggers MH
Histamine release
Muscle pain
Arrhythmia
Scoline Apnoea
Hyperkalemia
18
Q

Suxamethonium Contra-indication R-MUD

A 
Drug allergy
Scoline apnoea
MH
Unknown myopathies
Risk of hyperkalaemia (Renal failure 
Paralysis
Crush / Burn injury)
19
Q

Non-depolarising agents

A

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
Q

Pharmacology of non-depolarisers

1) Clinical Effects
2) Metabolism
3) Excretion

A 
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
Q

Vecuronium

A 
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
Q

Rocuronium

A

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
Q

Atracurium

A 
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
Q

Reversal of non-depolarising agents

A

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
Q

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

A 
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
Q

When is it safe to reverse?

A

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
Q

Signs of inadequate reversal

A 
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
Q

Management of Inadequate Reversal

A 
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
Q

Sugammadex

A

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

Anaesthesia (15 decks)

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