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Procedural Skills (SLO6)
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A 26 year old man is brought into ED following a road traffic collision. You are preparing to perform an RSI with suxamethonium. Suxamethonium causes prolonged paralysis by which of the following mechanisms?
Answer:
Depolarising muscle relaxants act as acetylcholine (ACh) receptor agonists, whereas non-depolarising muscle relaxants function as competitive antagonists. Depolarising muscle relaxants produce what appears to be a "persistent" depolarisation at the NMJ by binding to ACh receptors and mimicking the effect of ACh thereby generating an action potential. Unlike ACh, however, these drugs are not metabolised by acetylcholinesterase, and their concentration in the synaptic cleft does not fall as rapidly, resulting in a prolonged depolarisation of the muscle end-plate. Propagation of an action potential is prevented by the area of inexcitability that occurs around the ACh receptors. Suxamethonium is the only depolarising muscle relaxant with clinical usefulness, has the most rapid onset of action of any of the neuromuscular blocking drugs and is ideal if fast onset and brief duration of action are required. Unlike the non-depolarising neuromuscular blocking drugs, its action cannot be reversed and anticholinesterases such as neostigmine actually potentiate the neuromuscular block.Rapid Sequence Induction: Neuromuscular Blocking Drugs
Procedural Skills (SLO6)
Last Updated: 13th February 2024
Neuromuscular blocking drugs used in anaesthesia are also known as muscle relaxants. By specific blockade of the neuromuscular junction they enable light anaesthesia to be used with adequate relaxation of the muscles of the abdomen and diaphragm. They also relax the vocal cords and allow the passage of a tracheal tube. Their action differs from the muscle relaxants used in musculoskeletal disorders that act on the spinal cord or brain.
Patients who have received a neuromuscular blocking drug should always have their respiration assisted or controlled until the drug has been inactivated or antagonised. They should also receive sufficient concomitant inhalational or intravenous anaesthetic or sedative drugs to prevent awareness.
Comparison Table
| Drug | Suxamethonium | Rocuronium |
|---|---|---|
| Type | Depolarising | Non-depolarising |
| Dose | 1.5 - 2 mg/kg | 1 - 1.2 mg/kg |
| Onset |
|
1 min |
| Recovery |
|
30 - 40 min |
| Contraindications |
|
Nil |
| Side effects |
|
Anaphylaxis (rare) |
| Reversal agent | No reversal agent | Sugammadex |
Non-depolarising neuromuscular blocking drugs
Non-depolarising neuromuscular blocking drugs (also known as competitive muscle relaxants) compete with acetylcholine for receptor sites at the neuromuscular junction and their action can be reversed with anticholinesterases such as neostigmine. Non-depolarising neuromuscular blocking drugs can be divided into the aminosteroid group, comprising pancuronium bromide, rocuronium bromide, and vecuronium bromide, and the benzylisoquinolinium group, comprising atracurium besilate, cisatracurium, and mivacurium.
Non-depolarising neuromuscular blocking drugs have a slower onset of action than suxamethonium chloride. These drugs can be classified by their duration of action as short-acting (15–30 minutes), intermediate-acting (30–40 minutes), and long-acting (60–120 minutes), although duration of action is dose-dependent. Non-depolarising neuromuscular blocking drugs have no sedative or analgesic effects and are not considered to trigger malignant hyperthermia.
Rocuronium bromide exerts an effect within 2 minutes and has the most rapid onset of any of the non-depolarising neuromuscular blocking drugs. It is an aminosteroid neuromuscular blocking drug with an intermediate duration of action. It is reported to have minimal cardiovascular effects; high doses produce mild vagolytic activity. Anaphylaxis to rocuronium occurs, but is less common than anaphylaxis to suxamethonium. Some experienced practitioners favour a modified RSI using rocuronium instead of suxamethonium, and this has been further encouraged by the introduction of sugammadex as a reversal agent. Other non-depolarising muscle relaxants are unlikely to be used during RSI but may be used for maintaining muscle relaxation following recovery from suxamethonium.
Sugammadex is a cyclodextrin that encapsulates and then inactivates aminosteroid neuromuscular blocking drugs (e.g. rocuronium). It forms a complex with the muscle relaxant in the plasma, thus reducing its ability to bind with receptors at the neuromuscular junction. Because one molecule of neuromuscular blocking drug binds to one molecule of sugammadex, the dose of sugammadex required depends on the extent of neuromuscular blockade to be reversed. Most patients will have recovery of neuromuscular function by 3 minutes. However this potential benefit should be weighed up against the following consideration:
- Patient oxygenation is the absolute priority
- Sugammadex is costly and is therefore rarely drawn up before it is known that it will definitely be required thus time to injection may be delayed
- Side effects include hypersensitivity, effects on haemostasis and bradycardia
- Its use in children and adolescents has not been studied and so is not recommended
Depolarising neuromuscular blocking drugs
Suxamethonium chloride has the most rapid onset of action of any of the neuromuscular blocking drugs and is ideal if fast onset and brief duration of action are required, e.g. with tracheal intubation. Unlike the non-depolarising neuromuscular blocking drugs, its action cannot be reversed and recovery is spontaneous; anticholinesterases such as neostigmine potentiate the neuromuscular block.
Suxamethonium chloride should be given after anaesthetic induction because paralysis is usually preceded by painful muscle fasciculations. While tachycardia occurs with single use, bradycardia may occur with repeated doses in adults and with the first dose in children. Premedication with atropine reduces bradycardia as well as the excessive salivation associated with suxamethonium chloride use.
Prolonged paralysis may occur in dual block, which occurs with high or repeated doses of suxamethonium chloride and is caused by the development of a non-depolarising block following the initial depolarising block. Individuals with myasthenia gravis are resistant to suxamethonium chloride but can develop dual block resulting in delayed recovery. Prolonged paralysis may also occur in those with low or atypical plasma cholinesterase. Assisted ventilation should be continued until muscle function is restored.
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
