Muscle relaxants Flashcards by Michael Nel

What are the indications for muscle relaxants?

Patient (risk of regurg) - Obese, pregnant, hx of reflux, hiatus hernia, unstarved, bowel obstruction, delayed gastric emptying.
Anaesthetic - ability to control gasses required (ventilation), resp disease, abnormal positioning required, ETT placement is easier.
Surgical - microsurgery (NB no movement), muscle relaxation required (eg laparotomy, ortho), ECT therapy

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What must be given before any general muscle relaxant?

A hyponotic agent (avoid awareness!)

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Apart from muscle relaxants, how else can muscle relaxation be acheived?

Regional anaesthesia (spinal, epidural, nerve block)

2. High dose volatile

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What are the two categories of neuromuscular blockers?

Depolarising

Non-depolarising

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Three sites at which action potential can be blocked to achieve muscle relaxation

Nerve membrane
Neuromuscular junction
Muscle membrane

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How do depolarising NMBs work?

Similar structure to ACh. Non-competitive binder of ACh receptors. These agents act by depolarizing the sarcolemma of the skeletal muscle fiber. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh. There are two phases to the depolarizing block. During phase I (depolarizing phase), they cause muscular fasciculations (muscle twitches) while they are depolarizing the muscle fibers. Eventually, after sufficient depolarization has occurred, phase II (desensitizing phase) sets in and the muscle is no longer responsive to acetylcholine released by the motoneurons. Not reversible.

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How do non-depolarising NMBs work?

Competitive binding of ACh receptors. DO NOT depolarise membrane simply prevent ACh from binding. Reversed by giving high dose of ACh.

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What is ED(95) for NMBs?

The dose of NMB required to paralyse 95% of normal poeple.

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What is the intubating dose of NMBs?

2 x ED(95)

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Intubating dose of NMBs leads to…

Loss of muscle tone (cannot maintain airway)
Inability to breath or cough
Loss of protective reflexes (esp. laryngeal)

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What factors potentiate/prolong the action of muscle relaxants?

Drugs (Aminoglycosides[eg. Genta] and inhalational anaesthetics)
Electrolytes (decreased Ca, increased Mg, and change in K)
Acidosis
Temperature (Hypothermia = depolarisers, hyperthermia = non-depolarisers)
Inherited muscle abnormalities (Myasthenia gravis, dystrophies etc)

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Most common NMB depolariser

Suxamethonium (ultrashort-acting)

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NMB used in very short cases (short acting)

Mivacurium

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Most commonly used NMBs in healthy patients

Vecuronium (intermediate acting)

Rocuronium (intermediate acting)

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Best NMB to use in patients with renal failure

Cisatracurium (intermediate acting)

[can use atracurium but it can cause histamine release and hypotension]

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Long acting NMB used in cardiacs and long cases

Pancuronium

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When is suxamethonium contraindicated?

Any condition with high potassium as it causes K to be released from cells.
1. Renal failure
2. Massive tissue injury (burn or crush injury)
3. Disuse of muscle (paraplegic, stroke, end stage AIDS)
Careful in conditions with decreased pseudocholiesterase activity:
1. Hypothermia
2. Liver disease
3. Pregnant women
4. Certain drugs

Possible side effects of suxamethonium

Scoline pains
Hyperkaleamia (an increase of about 0.5 is seen)
Bradycardia (ACh-like structure increases parasympathetic tone)
Malignant hyperthermia
Scoline apnoea (different pseudocholineesterase structure)

What are the treatment options for scoline apnoea?

Give FFP. This will contain the enzymes needed to degrade suxamethonium. However, risk of infection and transfusion related acute lung injury (TRALI)

Therefore, sedating and ventilating for several hours waiting for spontaneous resolution is preferential.

How is suxamethonium metabolised?

By plasma- or psuedocholinesterases (synthesised by the liver) present in the plasma.

Two different structure of non-depolarising NMBs

benzyl-isoquinolines

amino-steroids

Why do non-depolarisers have no CNS effect?

They are highly ionised and water soluble. Tightly bound to plasma protiens.
Therefore, no penetration of lipid barriers.

When choosing intubation dose of non-depolarising NMB what must be taken into account?

Patients lean body mass

What is the likely cause of a sudden deterioration in a patient’s haemodynamic status following administration of a NMB?

Anaphylaxis

What is Hofmann degradation?

Spontaneous non-enzymatic chemical breakdown occuring at physiological pH and temperature.

Why is Cisatracurium preferred over atracurium?

Far less histamine release

What is the basic mechanism of action for drugs that reverse the action of non-depolarising muscle relaxants?

They block ACh esterase. Therefore, less ACh is broken down leaving more to out compete the NMB.

Where is ACh released in the nervous system?

1. Entire parasympathetic system 2. Some sypathetic (ganglia, adrenal medulla, sweat glands) 3. CNS 4. Skeletal muscle

Which receptors specifically do muscle relaxants bind?

Nicotinic cholinergic receptors (autonomic ganglia and skeletal muscle)

Which specific receptors do anticholinergic drugs (eg. atropine and glycopyrrolate) bind?

Muscarinic choliergic receptors (heart, SM, glands)

What would happen if ACh esterase inhibitor was given alone?

Build up of ACh at all sites (nicotinic and muscarinic). Therefore, increased ACh would cause bradycardia, bronchospasm, bronchosecretion, peristalsis, pupillary constriction.

Why is ACh esterase inhibitor (neostigmine) given with anticholinergic drugs (atropine or glycopyrrolate)?

To reverse the muscle relaxant by maximising nicotinic transmission whilst minimising autonomic side effects.

Which clinical signs suggest a patient is ready for NMB reversal?

``` Gag reflex Breathing Coughing Eye opening Sustained [5-10s] headlift, hand squeeze, jaw grip ```

What is the best way to determine if a patient is ready for NMB reversal?

Peripheral nerve stimulation

Using PNS when is a patient ready for NMB reversal?

>/= 3 twitches | >30 mins since last dose of muscle relaxant

Which nerves can be used for PNS monitoring?

``` Ulnar Facial Posterior tibial Common peroneal (All superficial nerves) ```

Eight signs of inadequate muscle relaxant reversal

1. Jerky respiration 2. Low tidal volume / poor chest expansion 3. Tracheal tug 4. Restlessness (hypoxia) 5. Unable to raise head 6. Weak hand grip 7. Poor cough 8. Ptosis

Types of PNS stimuli

1. Twitch 2. Train-of-four (TOF) 3. Tetanus (fade = residual block) 4. Double burst stimulation (emphasises TOF result) 5. Post-tetanic facilitation/ potentiation (deep paralysis for estimation of time to recovery)

Approach to post-operative weakness / hypoventilation

1. A B C 2. Exclude central cause (opiods, CO2, anaethesia) 3. Reverse/correct potentiators of NMBs (eg temp, acidosis) 4. Use PNS to determine if persistent NMB 5. If thought due to NMB give one more dose of reversal agent 6. Continue A B C and be patient

What dose must not be exceeded with neostigmine?

5mg (causes weakness itself)

What must you look at before drawing up a drug?

Name Dates Concentrations

What new NMB reversal drug may be available soon?

Sugammadex. Effective against amino-steroids (roc- vec- and pan- curonium). Encapsulates amino-steroids and can reverse deep neuromuscular block. Excreted renally.