Muscle Relaxants Flashcards by Iseoluwa Ojo

Acetylcholine

Neurotransmitter at NMJ

Formation
 ________ + ________ ( enyzme
_________________ ) → Ach

Destruction
 Action of ________ present in ________

Choline + acetyl co A

choline acetyl transferase

acetyl cholinesterase

synaptic cleft

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Neuromuscular Transmission :

Depolarisation of motor nerve→ ____ propagated to _______→↑permeability to ________ & ________ of vesicles→Ach release

Ach cross synaptic cleft & bind to receptors →Dep. of _________________ & generation of AP →_____ channels open→_____ release→ _______ + _________ coupling → CONTRACTION

AP; NMJ; calcium; exocytosis

muscle end plate; Na; Ca

actin + myosin

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Factors which influence NMT

Prevent Ach SYNTHESIS
_______________

Prevent Ach RELEASE
_______________, _______________, ____________, _______________

Deplete Ach STORES

______________

Hemicholinium

↓calcium, ↑magnesium Botulism Aminoglycosides

Tetanus

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Factors which influence NMT

Block Ach RECEPTORS
_______,________________

Block action of acetyl- cholinesterase
_______________,______________

Muscle relaxants Myasthenia gravis

Anticholinesterases

Organophosphorus

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What are Muscle Relaxants?

Drugs used to impair _______________ and used to provide skeletal muscle _________ during anaesthesia or critical care.

neuromuscular transmission

relaxation

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Indications for Muscle Relaxants :

To Facilitate :
_________
__________
____________

Tracheal intubation
Ventilation
Surgical access

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Classification

DEPOLARISING MR ( Competitive or Non-Competitive?))

Resemble Ach →bind to receptors → _____________ (_____________)

Not metabolised by _____________.

Concentration in synaptic cleft remains high.
Reversal by _____________ from ________ & ___________ by _____________ Phase ___ block
No ___________
No _____________

Non-Competitive

initial depolarisation ; fasiculations

acetylcholinesterase ; diffusion ; NMJ

Hydrolysis ; pseudocholinesterase Phase I

fade; post tetanic potentiation

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Depolarizing Block

Because _______ resembles Ach it stimulates the receptors first causing _________

•It then stays fixed on receptors as it is not metabolised by ____________.

•It therefore prevents Ach from reacting with the receptors and allowing NMT.

suxamethonium; fasiculations

acetylcholinesterase

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NON DEPOLARISING MR(Competitive or Non-Competitive?)

Bind to Ach receptors (with or without?) initial depolarisation; (fasciculation or no fasiculations?) .
Phase ___ block

Exhibit ______
Exhibit _______________

Competitive ; without

II; fade; post tetanic potentiation

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Non-Depolarising MR

Reversal- redistribution, metabolism, excretion.

_______________ - inhibits ______________→ ↑ Ach.

Potentiated by __________,__________ agents, (alkalosis or acidosis?) , ↓ K, ↑ Mg, ↓ Ca.

Anti cholinesterase; acetyl cholisterase

aminoglycosides ; volatile

Acidosis

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Monitoring the NMJ Peripheral nerve stimulator
Assess _______ , _______, _______ or _______ response to electrical stimulus.

Use _______, _______ or _______ nerve

visual, tactile, mechanical or EMG

ulnar, facial or tibial nerve

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Monitoring the
Patterns of stimulation.

Single twitch (_____ – ______ Hz).

Tetanic stimulation (____ - ____ Hz. x ______ s)

Post tetanic stimulation using single twitches
Train of four —____ twitches at ____ hz.

0.1 – 1.0 Hz

50 - 100 Hz. x 3- 5s

4 twitches at 2 hz.

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Train of Four (TOF) twitches:

Only 3 twitches → ____% block
Only 2 twitches → ____%
Only 1 twitch → ____%
No twitch →____%

75% ; 80% ; 90% ; 100%

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Train of Four (TOF) twitches:

____ % reqd for intubation
____ –____% for maintenance
___ –____% before attempting reversal

100
90-100
75-80

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Train of Four (TOF) twitches:

100 % reqd for __________
90 –100% for __________
75 –80% before __________

intubation
for maintenance
before attempting reversal

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BefORE MR(NO BLOCK)

No MR given, Ach crosses NMJ and stimulates the receptors causing NMT •Nerve stimulator produces ______ twitches
•Also applicable to ________ of ________

full

reversal of NDMR

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After MR (Complete block)

•NDMR blocks the Ach receptors and prevents further NMT
•Nerve stimulator produces ______ twitches on stimulation
•__________ can be carried out.

no; Intubation

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Partial Block

•NDMR gets ______________ and few Ach molecules can now stimulate the receptors •Nerve stimulator produces __________ amplitude.

metabolised

reduced twitch

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FADE

With a partial block- _____ MR show a _________↓ amplitude – No fade

•With a partial block- ________ MR show a __________ ↓ in amplitude from the 1st to the 4th twitch in a TOF - Fade

Dep; uniform

non-dep; gradual

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Post-Tetanic Facilitation

With a partial _______ block, tetanic stimulation recruits Ach molecules to
the synaptic cleft
•Subsequent twitches have __________ – Post tetanic facilitation/stimulation

non-dep; ↑amplitude

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Suxamethonium

Clinical Practice in 1951
____ Ach molecules

Dose
_______ mg/kg ____
____ mg/kg ___/____

Onset: __________
Indicated in (slow or rapid?) sequence induction
Duration ________________

1–2; I.v
2; I.m/s.c

30-45 secs; rapid

2 –5 mins

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Suxamethonium

Best for anticipated ________________

difficult intubation

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Suxamethonium

CVS - _____cardia
More frequent in (children or adults?)and with a ______ dose given within ________.

MSS - ________ → Postoperative __________

↑ ————-,______,__________ pressures

Hyperkalaemia-↑K by 0.5meq/L x3–5 mins
↑with _________ injuries , ______

Brady; children; 2nd ; 5 mins

Fasiculations; myalgia

Intragastric, intraoccular, intracranial

Denervation; burns

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Suxamethonium

Can cause ________________, a
Premonitory sign of ________________

Myoclonus
Adverse drug reaction

Malignant hyperthermia

masseter spasm

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Suxamethonium is metabolised by ______________ which has a reduced Conc in : ?????(list 4)

pseudo- cholinesterase Pregnancy - Liver disease, - Malnutrition, - ↓ protein states

Pseudocholinesterase Inhibitors - ___________ - ___________ - ___________ Results in ____________

- Ecothiopate - Phenelzine - Trimetaphan prolonged apnoea

Dibucaine Number Normal DN ____-____% Heterozygous DN ______% -apnoea x _________ min Homozygous DN _________% - apnoea x _________

75–85 40-60; 10 – 20 15-25; 6-8 hours

Non-depolarising MR CLASSIFICATION ________________ _____________________

Benzylisoquinolines Aminosteroids -Vagolytic

Non-depolarising MR CLASSIFICATION Benzylisoquinolines -Release __________ Examples : __________ , __________, __________ __________

Histamine Atracurium ,Cis-atracurium, Mivacurium Doxacurium

Non-depolarizing MR Aminosteroids -Vagolytic _____________ , _____________, _____________, _____________

Pancuronium, Vecuronium Pipecuronium, Rocuronium

Non-depolarizing MR There’s a _________ dose for intubation , and ____________ dose (which is ________ of _________ dose)

Loading; intubation Maintenance; 1⁄3 -1⁄4 loading

Atracurium : 1980 Solution stored at _______oC Dose Loading dose -____mg/kg Maintenance- _____-______ Infusion ___-____ mcg/kg/min Onset ____-_____ mins Duration ________ mins

2 – 8 0.5 ; 1/3 – 1⁄4 5-10 1.5 – 2 20 - 30

Atracurium Effects _____________ _______________

CV stability Bronchospasm

Atracurium Metabolism •____________ degradation 50-60% (____________ dependent, ____________ but ________ and _________ dependent) • _________________

Hoffman’s degradation ; Non organ dependent Non enzymatic ; pH and temp dependent Ester hydrolysis

Laudanosine - Product of ____________, can cause _______________ & _________ especially in ________ failure.

Hoffman metab. CNS excitability ; Seizures; liver

Cis-Atracurium ___________ of atracurium DOSE - ____-_____mg/kg ONSET - _____-______ DURATION – _____-______

Isomer 0.1 – 0.2 1.5 –2 mins 30 – 40 mins

Cis-Atracurium EFFECTS ____________ release ____________ METAB -70 – 80 % __________ (More or Less?) ____________ produced as less total dose used.

No histamine; CV stability Hoffmans; less laudanosine

Mivacurium 1993 Mivacurium DOSE - _____ – _____ mg/kg ONSET –_____ –_____ mins DURATION –_____ – _____ mins

DOSE - 0.15 – 0.2 mg/kg ONSET –1.5 –2 mins DURATION –10 – 20 mins

Mivacurium EFFECTS _____________ (Small or Large?) dose given rapidly → ________ release. METAB - _______________________.

CV stability Large histamine Plasma cholinesterase

Alternative to suxamethonium especially in paeds is ???

Mivacurium

Doxacurium : 1991 DOSE - _______ mg/kg ONSET – ______ mins. DURATION - _____________.

1991 DOSE - 0.05 mg/kg ONSET – 4- 5 mins. DURATION - 1-3 hours.

Doxacurium : EFFECTS ____________ release. _____________ METAB (Slow or Fast?) hydrolysis by _____________. Excreted (changed or unchanged?) by liver and kidneys. USES - ____________ surgery-neuro, cardio.

No histamine; CV stability Slow ; plasma cholinesterase Unchanged; Prolonged

Pancuronium : 1967 ________________ compound. DOSE – _____ – _____ mgkg ONSET – _____ –_____ mins. DURATION – _____ – _____ mins.

Bisquartenary amino- steroid DOSE – 0.08 – 0.1mgkg ONSET – 2 – 3 mins. DURATION – 40 – 60 mins.

Pancuronium EFFECTS ___________ / ___________ ↑ ____, _____, _____. Useful in _______ Caution in ___________ or ___________ dx

Vagolytic / Sympathomimetic ↑ HR, BP, CO. shock hypertension ; Ishaemic Heart dx

Pancuronium METAB By the ______ with _______ excretion Presence of __________________, so caution in ________________

Liver; renal Active metabolites renal dysfxn.

Vecuronium 1983 Comes as _________ DOSE -____ – ____mg/kg ONSET - _____ mins. DURATION -_________ mins EFFECTS - ________________ METAB – 75% _______. 25% _______ . ______ admin.

powder 0.08; 0.12 ; 1.5; 20 – 30 CV stability; biliary; renal ICU

Pipecuronium : 1990 DOSE – ______ – ______ mg/kg ONSET – ______ – ______ mins. DURATION - ______ – ______ mins.

0.06 – 0.1mg/kg 2.5 – 3 mins. 90 – 120 mins.

Pipecuronium EFFECTS - ___________ METAB - 70% _______ . 30% _______.

CV stability Renal Biliary

Rocuronium : 1994 DOSE – ______ – _____ mgkg ONSET - _______. DURATION – _____ – ____ mins.

DOSE – 0.45 – 0.6 mgkg ONSET - 60 secs. DURATION – 30 – 40 mins.

Rocuronium METAB. – Eliminated _________ by liver. Reversed by __________

unchanged Sugammadex

_______________ Can replace suxamethonium for rapid sequence induction

Rocuronium

Sugammadex can be given immediately after rocuronium T/F. With scenario

T 16mg/kg e.g in cases of failed intubation

Further classification of MRs ONSET Rapid – ___________,___________ Intermediate- ______,______,________,________,__________ Delayed – ____________.

Suxamethonium (30s), Rocuronium (60s) Atracurium, Mivacurium, Pancuronium, Pipecuronium,Vecuronium. Doxacurium

Further Classification of MRs DURATION Ultra- short - ___________ Short acting – ____________. Intermediate – __________, __________, __________. Long - __________, __________, __________.

Ultra- short - Suxamethonium Short acting – Mivacurium. Intermediate – Atracurium, Vecuronium, Rocuronium. Long - Pancuronium, Doxa, Pipe.

Reversal : ________________/________________  Reversibly bind to enzyme leading to deactivation → ↑ Ach conc at NMJ → ↑ Ach at Nicotinic and Muscarinic Sites.  ______________

Acetylcholinesterase Inhibitors /Anti Cholinesterase. Neostigmine

_______________- can reverse rocuronium

Sugammadex

Effects Of Anticholinesterase: ______cardia ______________ ↑ __________ CNS ________ ↑ _________ ↑ Glandular secretions. Muscarinic effects antagonised by _____________

Brady; Bronchospasm Secretions; agitation Peristalsis; anticholinergics

Muscarinic effects antagonised by anticholinergics - _________,________.

Atropine Glycopyrrolate

Effects Of Anticholinesterase: Neostigmine- ______ mg/kg. _____-_____ mg max. Atropine - ____mg/ 1 mg neostigmine. Glycopyrrolate -_____ mg/ 1 mg neostigmine.

0.04 2.5 – 5 0.5 ; 0.25

In reversal, Anticholinergics given after neostigmine T/F

F Anticholinergics given before or with Neostigmine BUT never after

Clinical Assessment of Reversal: Sustained _________ x ____ secs → < 30% blk Ability to ___________ ___________ ___________ Maintain sustained ___________. Achieve adequate ______ - look at the reservoir bag Achieve adequate ______- 15mls/kg. Achieve inspiratory press _____cmH2O

head lift x 5 secs Open mouth. Protrude tongue. Cough hand grip. VT VC 20cmH2O

D-Tubocurarine : 1935 _____________ compound. Dose _____ – _____mg/kg. Onset ___-____ mins. Duration – ____-____mins.

Dose 0.5 – 0.6 mg/kg. Onset 3 – 5 mins. Duration – 30 - 50 mins.

D-Tubocurarine : Effects – Histamine release +++ →Broncho______ - Vaso________. - ____tension ________ blockade. Severe _______________. Metabolism. - Excreted unchanged by _______. Uses - ______________ anaesthesia.

spasm.; dilatation; Hypo Ganglion; anaphylaxis kidneys Hypotensive