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The science and use of muscle relaxants

Neuromuscular blocking drugs

Neuromuscular blocking drugs, or ‘muscle relaxants’, produce skeletal muscle relaxation, allowing easier intubation of the trachea, easier mechanical ventilation and improved operating conditions. Always remember that a neuromuscular blocking drug is not an anaesthetic agent. Muscle relaxants must not be given instead of analgesics or hypnotics to prevent movement in response to surgical stimuli. They have no effect on consciousness and must never be given to a conscious patient.

Neuromuscular blocking drugs will stop the patient’s breathing. They must never be given to a patient unless the doctor is certain they can ventilate the patient (either by mask or endotracheal intubation).

Mechanism of action

Peripheral motor nerves innervate skeletal muscle at the neuromuscular junction. Each motor nerve synapses on several muscle fibres forming a motor unit. Activation of a motor nerve causes release of acetylcholine (Ach) from the nerve ending. Ach is synthesised in the motor nerve and stored in vesicles. Each vesicle contains approximately 5 x 10³ molecules of Ach. The nerve ending and adjacent muscle are called the motor end plate. Electrical depolarisation of the motor nerve causes increased permeability to calcium ions, which causes release of Ach. The space between the nerve ending and the muscle is called the synaptic cleft. The Ach crosses from the nerve ending to receptors on the muscle, binding to the what is called the post-synaptic membrane. Activation of these Ach receptors causes muscle contraction by altering the ion permeability of the post-synaptic membrane and causing depolarisation of this membrane.

Depolarisation refers to the change in electrical charge that exists across a cell membrane, where the charge inside a cell changes to become more similar to the charge outside of a cell. A moving wave of such depolarisation is termed an action potential and is the basis for the conduction of impulses along a nerve, within muscle or other excitable tissue. An electrical charge exists across cell membranes because the difference concentrations of ions between the intracellular (inside a cell) and extracellular (outside the cell) fluid. Sodium (Na+), Potassium (K+), Calcium (Ca2+) and Chloride (Cl-) are the most important of these ions.

Ach is also the neurotransmitter for all autonomic system preganglionic neurons and parasympathetic postganglionic neurons. It is also found in the central nervous system. There are two types of Ach receptors: nicotinic and muscarinic. Nicotinic receptors are found at the neuromuscular junction and the autonomic ganglia. Muscarinic receptors are found at parasympathetic postganglionic neurons.

In general, depolarising muscle relaxants (suxamethonium) are used for paralysis of rapid onset and short duration. The non-depolarising muscle relaxants are used for prolonged paralysis when rapid intubation of the trachea is not required.

Non-depolarising muscle relaxants

Non-depolarising muscle relaxant drugs compete with Ach to bind with muscle Ach receptors. They therefore block the action of Ach and prevent depolarisation of the muscle. This mechanism of action is known as competitive antagonism.

Non-depolarising muscle relaxant drugs include alcuronium, atracurium, cisatracurium, fazadinium, gallamine, mivacurium, pancuronium, pipecuronium, rocuronium, tubocurarine and vecuronium.

The selection of a non-depolarising muscle relaxant drug will depend on many factors including availability, expense, time needed to intubate the trachea, expected duration of surgery, patient’s health, drug side effects and method of metabolism.

In general all non-depolarising muscle relaxing drugs need reversal of their action by an anticholinesterase. Atropine must also be given in order to control the side effects of the anticholinesterase.

Dose recommendations

Drug Intubation dose mg/kg Supplemental dose mg/kg Infusion mg/kg/hr
Pancuronium 0.05 - 0.1 0.01 - 0.02
Tubocurarine 0.3 - 0.5 0.1
Alcuronium 0.2 - 0.3 0.05 – 0.1
Vecuronium 0.1 0.02
Atracurium 0.5 0.1 – 0.2 0.3 – 0.6
Cisatracurium 0.1 - 0.2 0.02 – 0.03 0.05 – 0.15
Rocuronium 0.6 - 1.0 0.1 0.3 – 0.6
Mivacurium 0.2 0.05 0.2 – 0.5

Depolarising muscle relaxants

Depolarising muscle relaxants (suxamethonium or succinylcholine or scoline) mimic the action of Ach. They bind to the Ach receptors, leading to depolarisation of the post-synaptic membrane and causing brief irregular muscle contractions (fasciculations) followed by a brief period of relaxation.

Depolarising muscle relaxants do not require reversal. They are rapidly metabolised. Suxamethonium is hydrolysed by plasma cholinesterase to choline and succinylmonocholine (a depolarising agent with about 1/20 the potency of suxamethonium). Succinylmonocholine is then converted to choline and succinic acid.

Reversal of action of non-depolarising muscle relaxants

All non-depolarising muscle relaxing drugs should be reversed with anticholinesterase and atropine at the end of an operation.

The anaesthetist should not attempt to reverse the non-depolarising muscle relaxants before evidence of return of muscle function (peripheral nerve stimulator or patient attempting to breathe). Most non-depolarising muscle relaxants (except mivacurium) must not be reversed for at least 20 minutes after the last dose.

The anaesthetist must never extubate a patient until they are certain that the paralysis has been reversed and that the patient has adequate muscle strength to protect their airway and breathe.

Clinical assessment of adequate reversal

Ideally the anaesthetist can monitor muscle function with a peripheral nerve stimulator. If a peripheral nerve stimulator is not available the anaesthetist must use clinical signs of adequate reversal. Rapid shallow breaths are not evidence of adequate muscle strength. Even with a tidal volume of 5ml/kg the patient may still have 80% of Ach receptors blocked. A tidal volume of 5ml/kg is a poor sign of adequate muscle strength.

Clinical signs of adequate muscle strength include a vital capacity of 20ml/kg, head lift for 5 seconds and normal handgrip. Unfortunately all require some patient cooperation which may be difficult after a general anaesthetic. The head lift should be done with the patient lying flat and must be unassisted. Handgrip needs to be tested before anaesthesia so that the anaesthetist can judge if the patient can squeeze their hand as strongly as before anaesthesia. is powered by the excellent Dokuwiki. Hosting, server, OS and design credits.
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