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Anaesthesiology > Neuromuscular Blockers > Flashcards

Neuromuscular Blockers Flashcards

1
Q

Name the depolarising (noncompetitive) blocker

A

Suxamethonium (scolene)
Ultra short acting

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2
Q

Name 7 contraindications to suxamethonium

A
  1. History or family history of malignant hyperthermia or Scoline apnea (pseudocholinesterase def )
  2. Hyperkalaemia in major trauma
  3. Severe burns. 24h - 9 months (hyperk)
  4. Muscular dystrophy (eg duchenne) and other myopathies
  5. Known hypersensitivity to suxamethonium
  6. Muscle degeneration as in paraplegia or severe chronic sepsis
  7. Acute narrow angle glaucoma or penetrating eye injuries (increase IOP )
  8. Demyelinating injuries 48h - 9 months
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3
Q

What is the moa of Scoline?

A

Depolarising (noncompetitive) blocker that initially activates (agonist) acetylcholine receptors causing depolarisation, but in doing so block further activation. Repeated administration results in drug action becoming more characteristic of nondepolarising drugs (phase 2 ) by receptor desensitisation.

Agonism of post synaptic nicotinic acetylcholine Rs lead to sodium influx, potassium efflux, remains bound longer, preventing repolarisation or binding of Ach thus no propagation of action potential.

Binds to 2 units of nachR so also called diacetylcholine

Not broken down by acetylcholinesterase but by pseudocholinesterase in plasma.

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4
Q

What is the benefit of using depolarising over nondepolarising postsynaptic neuromuscular blockers? (3)

A

• Rapid onset (30-60S)
• short duration of action ( 5 to 10 minutes)
• broken down by pseudocholinesterase (not acetylcholinesterase as with non depolarisers) so result in prolonged blockade at the muscle end plate.

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5
Q

Name 10 adverse effects or complications of suxamethonium

A
  1. Myalgia! or even fractures post-op due to initial spasms /fasciculation’s pre-paralysis
  2. Masseter spasm (can be warning of malignant hyperthermia )
  3. Increase intraocular, intracranial and intragastic pressure due to fasciculation’s
  4. Anaphylaxis, bronchospasms (histamine release)
  5. Av node dysrhythmias- ventricular arrhythmia
  6. Bradycardia due to muscarinic receptor activation. Can be prevented by giving atropine.
  7. Hyperkalaemia due to potassium release from muscle (foetal type Nachr)
    8.scolene apnea
  8. Malignant Hyperthermia
  9. Secretions ( muscarinic side effect)
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6
Q

What causes scoline apnea? (And mivacurium apnea)

A

Inherited disorder (autosomal recessive) of pseudocholinesterase resulting in decreased metabolism of suxamethonium resulting in prolonged paralysis.

Variations: heterozygous 30-60 min, homozygous 3-6 hours

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7
Q

What is malignant hyperthermia and pathophysiology?

A

Rare Genetic (chromosome 17 aut dom or king-denborough syndrome aut recessive ) hypermetabolic disease triggered by exposure to inhalational agents and suxamethonium. Caused by defect in receptor on endoplasmic reticulum called the ryanodine receptor (RYR 1) (calcium channel r), causing it to stay open and flood cell with calcium with resultant persistent contractile state.

Increase use ATP, ATP demand exceeds supply, multi organ failure and death.

Exertion, heat stroke and porcine stress syndrome trigger it.

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8
Q

Name 6 early signs of malignant hyperthermia

A
  1. Masseter spasm
  2. Generalized muscular rigidity! (Specific sign)
  3. Tachycardia!
  4. Hypercapnia (specific and first sign)
  5. Hypoxia
  6. Combined metabolic respiratory acidosis
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9
Q

Name 6 late signs of malignant hyperthermia

A
  1. Hyperthermia >38 (specific sign)
  2. Rhabdomyolysis (specific sign)
  3. Acute renal failure
  4. Cardiac arrhythmia
  5. Hypotension
  6. Circulatory failure
    Increased serum creatine phosphate and serum myoglobin!
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10
Q

What is the antidote for malignant hyperthermia?

A

Dantrolene 2.5 mg/kg max 10mg/kg/24h
Mix with 60 ml water. Poorly soluble in water so administer through blood administration set to filter precipitants.

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11
Q

Name the 7 treatment steps for malignant hyperthermia

A
  1. Get help, stop offending agent, hyperventilate with 100% oxygen. New breathingcircuit with no residual vapour. Keep asleep with propofol.
  2. Dantrolene 2.5mg/kg rapidly iv large bore! Mix 20mg vile from fridge with 60 ml water
    Maintain anaesthesia with propofol TIVA
  3. Bicarbonate for metabolic acidosis
  4. Cool patient - gastric lavage, cold fluids etc
  5. Treat dysrhythmias . usually resolve with treatment of acidosis and hyperkalaemia. Use standard drug therapy except calcium channel blockers! May cause hyperk or cardiac arrest used with dantrolene.
  6. Treat hyperkalaemia with hyperventilation, bicarbonate, glucose/insulin, calcium if life threatening
    Treat myoglobinaemia with forced alkaline diuresis (furosemide, mannitol and fluid)
    Treat DIC with FFP, cryoprecipitate, platelets
  7. Follow ETCO2, electrolytes, blood gas, ck, core temp, urine output and colour, coagulation studies. Admit to ICU.
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12
Q

Name the 2 classes of non-depolarising muscle relaxants with 3 examples each

A

Benzylisoquinolines:
• mivacurium (short acting),
• atracurium (intermediate)
• cys-atracurium (intermediate)

Steroids:
• vecuronium (intermed)
•Rocuronium (intermed)
• pancuronium (long acting)

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13
Q

What is the preferred muscle relaxant in RSI?

A

Suxamethonium

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14
Q

What is the preferred muscle relaxant in patients with no risk aspiration but need ETT?

A

Non-depolarising

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15
Q

What is the preferred muscle relaxant in surgeries needing muscle relaxants eg ECT, joint reduction?

A

Suxamethonium

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16
Q

Name 3 indications suxamethonium

A

• RSI (risk aspiration)
• very short procedures needing muscle relax eg ECT, reductions dislocations
• emergency drug to treat laryngospasm

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17
Q

Moa non-depolarizing muscle relaxants?

A

• Competitive antagonists ach at nachr
• prevent ach binding therefore no depolirazation possible, causing muscle relaxation

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18
Q

How reverse non-depolarizing muscle relaxants?

A

Neostigmine (with glycopyrolate/atropine)

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19
Q

Where are steroid muscle relaxants metabolised?

A

Liver
(Vecuronium most, rocoronium least)

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20
Q

Where are steroid muscle relaxants excreted?

A

Kidneys (pan and rocuronium also biliary)

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21
Q

Where are benzylisoquinolone muscle relaxants metabolised?

A

Organ independent
Mivacurium: pseudocholinesterase
Atracurium and cis-atracurium: Hoffman elimination and ester hydrolysis
Not excreted

Therefore best in liver and renal impairment!

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22
Q

Name an adverse effect mivacurium

A

Prolonged apnoea if decreased pseudocholinesterase

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23
Q

Name an adverse effect atracurium

A

Release histamine so avoid in asthmatics
Cis-atracurium not.

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24
Q

Name an adverse effect pancuronium

A

Vagolytic: cause tachycardia. Avoid in ihd.

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25
Q

Which 4 muscle relaxants must be stored in fridge?

A

•Atracurium
• cis-atracurium
•Rocuronium
• pancuronium

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26
Q

Name 4 drugs that may prolong the action of suxamethonium

A

MELC.

• Lithium
• ecothiopate eye drops
• cyclophosphamide
• metoclopramide

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27
Q

Name 6 factors that may prolong the action of non-depolarizing agents

A

HHHAMM

• Metabolic acidosis
• hypothermia
• hypokalaemia
• hypermagneseMia!
• antibiotics especially aminoglycosides
•Myasthenia gravis, myasthenia syndrome (lambert Eaton), muscular dystrophies

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28
Q

Name 9 conditions predisposing to upregulation of NachR (nicotine acetylcholine receptors) and consequence thereof

A

I Molest Giant PLUMBS

Found in states of functional denervation. Characterised by foetal type receptors at extra functional sites. Result in increased requirements nondepolarising muscle relaxants (resistance) and hyperkalaemia after suxamethonium admin
• umn lesions
• LMN lesions
• muscle injury
• burn injury!
• immobilisation
• sepsis or infection
• prolonged exposure to NMB
• multiple sclerosis
• guillan barre

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29
Q

Name 6 acquired causes of decreased pseudocholinesterase activity that prolong suxamethonium action slightly (can appear like sux apnea) NB

A

• Pregnancy ( dilution effect)
• newborns (dilutional effect and immature liver, thus decreased pcE synthesis)
• liver diseases
•Malnutrition
• severe hypothyroidism
• plasmapheresis

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30
Q

Treatment scolene apnoea? (5)

A

• Treat apnoea:mechanical ventilation until normal muscle strength returns
• prevent awareness: continue anaesthesia with inhalant or sedate well with benzo
• exclude differential diagnosis
• confirm scolene apnoea: PCE activity. With Dibucaine (local anaesthetic that inhib activity PCE) or fluoride number. If confirmed counsel and test family and medic alert bracelet
• options: ffp/whole blood contain PCE and will speed recovery but risk infections high so not recommended. Also recombinant PCE but very expensive.

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31
Q

Name 2 ways a patient is tested for malignant hyperthermia gene

A

• Gold standard: halothane/caffeine contraction tests on fresh muscle biopsy
• genetic studies on blood samples but lower sensitivity but not in sa.

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32
Q

How should patients with history malignant hyperthermia be anaesthetised?

A

Propofol tiva

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33
Q

Name 2 causes downregulation NAchR and consequence

A

Decreased requirement nondepolarizing muscle relaxants, increase sensitivity
• myasthenia gravis
• organophosphate poisoning

34
Q

Neostigmine moa?

A

Acetyl Cholinesterase inhibitor non-selective
Increase acetylcholine at ach R and muscarinia

35
Q

Side effects neostigmine and how to prevent? (6)

A

Muscarinic side effects
• bronchospasm
• secretions
• bradycardia
• diarrhoea
• hypersalivation

Add anti-cholinergic eg atropine, glycopyrrolate

Can’t use in myotonia

36
Q

Which anticholinergic is preferred for co-administration with neostigmine to prevent muscarinic side effects? (6)

A

Glycopyrrolate over atropine
• No CNS side effects because doesn’t cross BBB because quarternary amine
• No central effects so can use in elderly
• longer duration
• more effective as antisialogogue (decreased saliva)
• less tachycardia so can use in cardiac patients

37
Q

Which anticholinergic preferred for treatment emergency bradycardia?

A

Atropine because faster onset than glycopyrrolate

38
Q

Train of four monitor normal vs depolarising vs non-depolarising?

A

• Normal all same height and long
• depolarising all same height and short until disappear
• non-depolarising fade, gradual decrease in height until disappear

39
Q

According to train of four, when can non depolarising muscle relaxants be reversed?

A

At least third twitch. Not before.

40
Q

What is ed95?

A

Dose required to decrease amplitude of a single twitch (with a nerve stimulator) by 95%
Indicate potency of muscle relaxant

41
Q

How much muscle relaxant should be given for induction surgery?

A

1-2 times ED95

42
Q

How much muscle relaxant should be given for intubation?

A

3 times ED95

43
Q

How calculate train of four ratio?

A

Twitch 4÷1
So if only 3 counts, can’t work out ratio.
Can’t describe ratio for sux (will always be 1)

44
Q

What does TOF count o mean?

A

Deep block. Can intubate, do neurosurgery etc.

45
Q

What does TOF count 0-3 mean?

A

Can perform abdominal surgery
Can’t admin neostigmine yet

46
Q

What does TOF count 4 mean in terms of surgical stim?

A

Need more muscle relaxant to perform abdominal surgery

47
Q

What does TOF count 4 with ratio <90% mean?

A

Patient should not yet be extubabed

48
Q

What does TOF count 4 with ratio > 90% mean?

A

Patient can now be extubated

49
Q

Name 7 signs suggesting adequate reversal of muscle relaxant and ready to be extubated

A

• Normal tidal volume, no paradoxical breathing or tracheal tug
• effective cough
• strong grip with hand
• ability to keep eyes open, no ptosis
• ability to lift head off pillow 5 seconds (best sign)
• presence masseter muscle tone
• satisfying response measured with nerve stimulator (gold standard)

50
Q

Alternative newer drug to reverse rocuronium and vecuronium?

A

Sugammadex (cyclodextrin)
Reverse immediately unlike neostigmine

51
Q

How does myasthenia gravis respond to muscle relaxants?

A

• Depolarising: resistant to small dose, phase 2 block in large dose
• nondepolarizers: overly sensitive

52
Q

How does myasthenia syndrome (lambert Eaton) respond to muscle relaxants?

A

Overly sensitive to all

53
Q

How does burns patient respond to muscle relaxants?

A

• Depolariser: hyperkalaemia
• non-depolariser: resistant

54
Q

How does myotonia respond to muscle relaxants?

A

• Depolariser: myotonic response (also can’t use neostigmine)
• non-depolariser: must reduce dose, muscle wasting

55
Q

How does muscle dystrophies respond to muscle relaxants?

A

• Depolariser: hyperk, hyperthermia
• non depolarising: overly sensitive if myopathy

56
Q

Adverse effect cis-atracurium?

A

Broken down slower in acidosis

57
Q

Which is the longest acting muscle relaxant?

A

Pancuronium

58
Q

Which muscle relaxant is the only one in powder form?

A

Vecuronium

59
Q

Which drugs used in theatre have highest propensity to elicit allergic reactions?

A

Nondepolarising muscle relaxants

60
Q

Onset action of suxamethonium?

A

30-60 seconds

61
Q

Atropine chemical structure?

A

Tertiary amine

62
Q

NMB agent of choice for trauma patients with gross hypovolaemia?

A

Scolene followed by atracurium

63
Q

A patient can be regarded as fully reversed when TOF ratio is?

A

97%

64
Q

Label picture 69

A

A: normal evoked stimulus without nmb
B: phase 1 depolarising block
C and D: phase 2 depolarising block (dose too high) or nondepolarising block

65
Q

Name an ultra short acting muscle relaxant

A

Suxamethonium

66
Q

Name an short acting muscle relaxant

A

Mivacurium (benzylisoquinolines)

67
Q

How long does sux last?

A

About 5 minutes

68
Q

Name intermediate acting muscle relaxants (4)

A

Benzylisoquinolones
• atracurium
• cys-atracurium

Steroids
• vecuronium
• rocuronium (about 30-40 min)

69
Q

Name long acting muscle relaxants

A

Pancuronium: about 3 hours

70
Q

Indication pancuronium

A

• Want long paralysis of about 3 hours
• tachycardia is acceptable
Eg cardiac surgery

71
Q

Indications and advantages rocaronium and vecuronium (5)

A

• Routine surgery with healthy patient
• cardiac stable drugs,!
• release very little histamine so can be safely used in asthmatics!
• fast onset, last 30-40 minutes
• modified RSI if suxamethonium contraindicated

72
Q

Indication atracurium and cysatracurium?

A

Organ pathology eg renal/liver failure: benzylisoquinolines have organ independent metabolism
No effect on CVS

73
Q

What and when is the first muscle to regain function after paralysis?

A

Diaphragm at train of four count 2.

74
Q

How’s suxamethonium action terminated?

A

Diffuses away from nach R and broken down in plasma by pseudocholineslerase ( no pharms reversal)

75
Q

NB Name 9 differences between atropine and glycopyrrolate (structure, BBB, central effects, absorption, onset, duration, effect on secretions, HR, cost, placenta)

A

• Tertiary vs quaternary amine
• crosses BBB (cns side effects) vs not
• central effects eg confusion (avoid in elderly) vs not
• oral absorption (good premed for antisialogogue) vs not
. Fast (emergency) vs slower onset
• shorter duration vs longer
• effective antisialogogue vs 4x more effective (better iv before fibre-optic intubation)
• most tachycardia (avoid in IHD or fixed co ) vs slight
• cheap vs expensive
Crosses pLacenta completely (lipid-soluble) vs not completely (fully ionised)

76
Q

At what train of 4 count can neostigmine be administered to reverse block?

A

3-4

77
Q

Name 5 signs inadequate reversal of muscle relaxant

A

• Tracheal tug (very reliable)
• jerky movements of limbs- “ floppy fish “
• ineffective cough
• ptosis
• paradoxical breathing.

78
Q

Name 9 differential diagnoses for malignant hyperthermia

A

• Sepsis (hyperthermia, hypercarbia, acidosis )
• hypoventilation (hypercarbia, acidosis )
• iatrogenic overheating (hyperthermia, tachycardia )
• thyrotoxicosis (hyperthermia, hypercarbia, tachycardia )
• pheochromocytoma (ht, tachycardia, fever )
• neuroleptic malignant syndrome (hyperthermia, muscle rigidity, rhabdomyolysis, acidosis )
• transfusion related reactions ( tachycardia, hypercarbia, acidosis )
• anaphylaxis ( shock, tachycardia, acidosis )
• defected anaesthetic circuit ( tachycardia, hypercarbia, acidosis )

79
Q

Dantrolene moa?

A

Blocks calcium release from sarcoplasmic reticulum, therefore depressing excitation contraction coupling in skeletal muscle → muscle relaxation
= hydantoin derivative muscle relaxant

80
Q

If patient has scalene apnea, what other drug should be avoided?

A

Mivacurium

81
Q

What is dubucaine? Uses?

A

• Amide local anaesthetic
• diagnose scolene apnoea
•40% = heterozygous gene abnormality, 20%= homozygous

Anaesthesiology (24 decks)

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