Depolarizing Blockade

• Examples—suxamethonium, decamethonium

Suxamethonium is the only current therapeutic example of a depolarizing blocking drug. However, any agonist of nicotinic acetylcholine receptors can also cause blockade if not rapidly cleared from the neuromuscular junction. Examples include nicotine and acetylcholine in the presence of excess anti-cholinesterase.

Mechanism of Action

A depolarizing block occurs when the agent stimulates the acetyl choline receptor and causes depolarization. Persistence of the agonist at the receptor prevents repolarization of the end plate and so it is refractory to further stimulation. As the agent diffuses away from the junctional cleft, re-polarization occurs and muscle action potentials are once more possible. The block is reversible and attachment to the receptors is competitive. The block may be enhanced by a local increase in acetylcholine as produced by anti-cholinesterases. A graphic illustration of the process by which depolarizing and non depolarizing drugs have their effects is shown in Figure NJ.3.

Clinical Features

Depolarizing blockade is characterized by rapid onset with muscle fasciculation, as groups of muscle fibres are depolarized which is subsequently followed by a prolonged refractory period, which constitutes the blockade.

Neuromuscular test stimulation results in:

• Reduced single-twitch height

• Reduced train of four, all of equal amplitude

• No post tetanic facilitation

After suxamethonium administration there may be widespread muscular pains, which are worse on movement. They are particularly common in muscular, young males after early ambulation. Muscle pains may persist for several days. Pre treatment with benzodiazepines, lidocaine or small doses of non depolarizing agents may help. Dantrolene has also been used with some success.

Figure NJ.3

Action of depolarizing and non depolarizing muscle relaxants

Figure NJ.3

Action of depolarizing and non depolarizing muscle relaxants


Suxamethonium is metabolized by plasma cholinesterase (butyryl or pseudo cholinesterase). This is a lipoprotein made in the liver. Inherited abnormalities of the enzyme prolong the blockade in a variable manner. The causes of plasma cholinesterase deficiency are listed in Figure NJ.4.


Pregnancy Collagen disorders Carcinomatosis Myocardial infarction Liver disease Hypothyroidism Blood dyscrasias Amethocaine Ketamine Pancuronium Anticholinesterases Oral contraceptives Propranolol Cytotoxic agents Ecothiopate eye drops

Figure NJ.4


Phase I blockade

Well sustained response to tetanic stimulation

No post tetanic facilitation

Train of four ratio > 0.7

Potentiated by the effect of anticholinesterases

Phase II blockade

Tetanic fade

Post tetanic facilitation

Train of four ratio < 0.3

Antagonised by the effect of anticholinesterases Tachyphylaxis

Figure NJ.5

Phase I and Phase II Blockade

Two distinct types of neuromuscular blockade (termed phase I and II blockade respectively), may result after the administration of suxamethonium. Figure NJ.5 lists the features of each type.

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