Muscle Relaxants Flashcards
What are the 2 classes of muscle relaxants?
Depolarisers
Non-depolarisers
MoA of depolarisers?
Physically resemble ACh and bind to ACh receptors
Generates a muscle action potential
ACh receptor agonists
What is the name of the depolarising muscle relaxant?
Suxamethonium/”Sux”
MoA of non-depolarisers?
Bind ACh receptors
Unable to induce required receptor changes for depolarisation to occur
ACh receptor antagonists (competitive antagonists)
Can be reversed by increasing ACh concentration at post-junctional membrane
List the names of the non-depolarising muscle relaxants?
Short-acting:
Mivacurium (Mivacron)
Intermediate acting: Vecuronium (Norcuron) Rocuronium (Esmeron) Atracurium (Tracrium) Cisatracurium (Nimbex)
Long-acting:
Pancuronium (Pavulon)
Alcuronium (Alloferin)
Clinical effects of Sux?
1 mg/kg = profound paralysis in 60s (preceded by vasiculations - scoline pains 3 days post administration)
Effects last 5 minutes
Increases plasma K+ levels (beware use in those with high pre-op K+ levels e.g. renal failure, burns, muscle disuse)
Bradycardia (an occasional S/E - may lead to cardiac arrest, ensure vagolytic drug on hand, such as Atropine)
Scoline Apnoea - what is it and how is it managed?
Apnoea caused by administration of Sux
Inherited disorder
Pseudocholinesterase (breaks down Sux) enzyme is chemically different to the norm, with varying degrees of activity
Prolonged paralysis due to non-breakdown/slow breakdown of Sux
Management:
Supportive
Ensure adequate sedation
Ventilate mechanically until muscle power returns
FFP may be tranfused to accelerate Sux degradation
Metabolism and excretion of muscle relaxants?
Longer-acting agents (i.e. Pancuronium): renal excretion Intermiate agents (i.e. Rocuronium, vecuronium): predominantly hepato-biliary excretion Atracurium and Cisatracurium (Nimbex): do NOT rely on organ function for metabolism and excretion, but rather Hoffman degradation (somewhat related to temperature and pH)
Agents used in the reversal of non-depolarisers?
NEOSTIGMINE (acetyl-chonlinesterase inhibitors), together with GLYCOPYROLLATE or ATROPINE (anti-cholinergic drugs that blocks muscarinic receptors to prevent neostigmine effect on heart nodes, smooth muscle and glands)
When is it safe to administer a reversal agent?
Clinical signs indicating that the patient is ready for reversal and also exhibiting signs of spontaneous recovery: Gag reflex Breathing Coughing Eye opening Sustained head lift 5-10s Sustained hand squeeze Sustained jaw grip of tongue depressor
Use of a peripheral nerve stimulator to assess reversibility:
Train-of-four stimulation (>3 twitches present)
How PNS works and how to use it?
Supra-maximal stimuli used to stimulate a peripheral nerve (15-40mA) with each impulse duration
Types of stimuli from a PNS?
Twitch (one impulse of short duration given every 10s to ensure patient paralysed before intubation)
Train-of-four (to monitor the degree of the neuro-muscular block and assess for reversibility)
Tetanus (sustained burst of impulses given - to detect any residual block or kick-start the nerve under deep paralysis)
Double-burst stimulation (used under light paralysis where TOF difficult to distinguish
Post-tetanic potentiation (5s tetanus followed by 20 impulses - shows fade response earlier than TOF, and used under deep paralysis to estimate time to recovery)
Signs of inadequate reversal?
Jerky respiration Poor chest expansion with low TV Tracheal tug Restlessness Inability to raise head Weak hand grip Poor ability to cough Ptosis (drooping eyelid)
Factors that potentiate and prolong the action of muscle relaxants?
A,E,I,O,U
Acidosis
Electrolytes (K+, low calcium, high magnesium)
Inherited muscle abnormalities (myasthenia gravis, dystrophies, dystonias)
Other: inhalational agents, gentamycin
Under/over warming (hypo/hyperthermia)
What is the dose for Sux?
1 mg/kg
