Muscle Relaxants Flashcards
(30 cards)
What is the name of the neurotransmitter at the NMJ of skeletal muscle?
Acetylcholine
How is ACh broken down?
By acetylcholinesterase - done rapidly, ACh acts for a short duration
ACh release is blocked by?
Magnesium, Aminoglycosides (antibiotics) and Botox.
Describe the different paths in which muscle relaxation can be achieved?
- Blockade of motor nerves (local anaesthetic) - no downstream electrical activity will occur, therefore sensory and motor loss.
- Blockade of NMJ (IV muscle relaxants) - prevent ACh binding to nicotinic receptors,therefore function not performed.
- Blockade of receptors inside muscle cells (dantrolene)
Name the two types of neuromuscular blockers.
Depolarising agents - e.g. suxamethonium
Non-depolarising agents - all other muscle relaxants
Outline the difference in MOA between the different types of neuromuscular blockers.
Depolarising - non competitive action, cannot be reversed, wears off or is metabolised over time
Non depolarising - competitive inhibition, competes with ACh for nicotinic receptors and requires reversal
What does ED95 mean?
Effective dose - dose of muscle relaxant that will paralyse 95% of normal people
Usually intubating dose = 2xED95
Adequate dose of muscle relaxant will result in?
Inability to breathe
Inability to maintain airway
Loss of protective reflexes
List some factors which potentiate muscle relaxants.
Drugs - inhalational agents, amino-glycoside (gentamicin)
Electrolytes - low Ca, high Mg, low K
PH - acidosis
Temperature - cold, warm (with non depolarisers)
Disease - myasthenia gravies, muscular dystrophies, dystonias, myopathies, renal failure
List the indications for muscle relaxation.
Surgical factors - facilitate surgical access, immobile field required
Anaesthetic factors - intubation/protection of airway required, controlled ventilation required, prone/abnormal positioning
Patient factors - critical illness
Before administering muscle relaxant, it is essential to?
Assess the airway
Be competent in airway management
Have necessary equipment
What are the clinical effects of suxamethonium?
Profound paralysis within 60 seconds
Causes fasciculations
Ultra short acting - lasts 5 minutes
Explain how suxamethonium is excreted.
Metabolised by pseudocholinesterase (plasma cholinesterase) which is synthesised in the liver and found freely in plasma.
What is meant by scoline apnoea and how is it treated?
Inherited homozygous/heterozygous conditions which presents with prolonged paralysis due to markedly reduced pseudocholinesterase (faulty enzymes that are unable to break down Sux)
Supportive treatment with ventilation + sedation, give FFP (will contain healthy pseudocholinesterase from donors)
List the side effects of suxamethonium.
Muscle pains (myalgia)
Bradycardia
Hyerkalaemia and arrhythmias, even cardiac arrest
Triggers malignant hyperthermia
Scoline apnoea
Histamine release
Anaphylaxis
What are the contraindication for suxamethonium.
Drug allergy
Scoline apnoea
MH
Unknown myopathies
Risk of hyperK (renal failure, paralysis, crush/burn injury)
Name the two categories of non depolarising agents, and provide example of drugs within each category.
Benzylisoquinolines
- atracurium, cisatracurium
Aminosteroids
- pancuronium, vecuronium, rocuronoum
Outline the clinical effects of non-depolarisers.
Marked paralysis in 1-5 minutes (take longer to act)
No fasciculations
Duration is variable (short, intermediate, long)
How are non-depolarisers metabolised and excreted?
Metabolism: Hepatic + Hoffman degradation
Excretion: Renal + hepatobiliary
Comment on the following things regarding vecuronium:
- duration of action
- physical properties
- impact on CVS
- excretion
- histamine release
Intermediate acting
Powder + mixed with water
CVS stable
Hepatobiliary excretion, safe in renal failure but avoid in liver disease
No histamine release
Comment on the following things regarding rocuronium:
- duration of action
- impact on CVS
Intermediate acting (30 minutes), in higher dose causes longer paralysis but can provide intubation within 1 minutes (rapid sequence induction)
CVS stable
Comment on the following things regarding atracurium:
- duration of action
- excretion
- histamine release
Intermediate acting
Hoffman degradation (spontaneous degradation, breaks up into inactive molecules), depends on pH and temp, potentially toxic metabolite (laudanosine) can cause convulsion and CNS toxicity, safe in renal + liver failure
Histamine releasing, increased risk of anaphylaxis
Comment on the following things regarding cisatracurium:
- duration of action
- physical properties
- excretion
- histamine release
Intermediate acting, slower onset of action
Isomer of atracurium
Hoffman degradation, safe in renal failure, no toxic metabolites
No histamine release
Explain how the drugs used for reversal of non-depolarising muscle relaxants work.
Neostigmine
- acetylcholinesterase inhibitor
- increased ACh concentration in synaptic cleft which competes with NMDR but ACh increase at both nicotinic and muscarinic rectors which can cause side effects
Anticholinergic agent - atropine/glycopyrrolate
- specifically an anti muscarinic agent
- given to prevent muscarinic effects (bronchial secretions, brochospasm, bradycardia, B-eristalis (peristalsis)
