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Neuromuscular blocking drugs
Succinylcholine depolarises the motor end-plate and acts fast and briefly; the non-depolarising relaxants compete with acetylcholine, and each one is chosen by its speed, duration and route of elimination.
Why it matters in the exam
The exam asks about the side effects of succinylcholine (hyperkalaemia, bradycardia, myalgia, malignant hyperthermia) and what happens in pseudocholinesterase deficiency, including the dibucaine number. It also asks which relaxant suits liver or kidney failure (cisatracurium, because of Hofmann elimination), and what TOF monitoring looks like with each type of block. Neuromuscular diseases — myasthenia, Lambert-Eaton, burns — change the sensitivity and appear in almost every exam.
In a depolarising (phase I) block the four TOF responses are equally reduced, with no fade and no post-tetanic potentiation. In a non-depolarising block there is fade and post-tetanic potentiation. Large doses or a long infusion of succinylcholine produce a phase II block that looks non-depolarising. Adequate recovery is a TOF ratio of at least 0.9 measured quantitatively at the thumb.
In exam questions distinguish three things that are often asked together: the choice of relaxant (speed, duration, route of elimination), the complications of succinylcholine, and the change in sensitivity in neuromuscular disease. The physiology helps memory: when the number of receptors at the end-plate falls (myasthenia) there is resistance to the depolarising drug and sensitivity to the blockers, and when new receptors spread along the muscle (burn, immobilisation, nerve injury) there is resistance to the blockers and dangerous potassium release with succinylcholine. In questions on monitoring, picture the four TOF responses and ask whether they are equal or fading — the answer reveals at once which type of block it is and at what stage.
Key points
- Succinylcholine — fast and short; hyperkalaemia and bradycardia; forbidden in old burns and malignant hyperthermia.
- Pseudocholinesterase deficiency causes prolonged paralysis; dibucaine number about 20 in homozygotes.
- Cisatracurium undergoes Hofmann elimination — suits a diseased liver and kidney.
- Myasthenia: sensitive to non-depolarisers and resistant to succinylcholine.
- TOF of at least 0.9 before extubation.
Summary table
| Drug | Intubating dose | Elimination and duration | Exam point |
|---|---|---|---|
| Succinylcholine | 1–1.5 mg/kg | Plasma pseudocholinesterase; 5–10 minutes | Hyperkalaemia, bradycardia, triggers malignant hyperthermia |
| Rocuronium | 0.6 mg/kg (up to 1.2 mg/kg in RSI) | Mainly liver; intermediate | Fast onset; reversed by sugammadex |
| Vecuronium | 0.1 mg/kg | Liver and kidney; intermediate | Haemodynamically stable |
| Cisatracurium | 0.15–0.2 mg/kg | Hofmann elimination — independent of liver and kidney | Choice in liver or kidney failure |
| Pancuronium | 0.1 mg/kg | Mainly kidney; long | Vagolytic — tachycardia |
A free exam question
?מה מאפיין את שרירי גלגל העין (the question as examined, in Hebrew)
- א. הם שרירים חלשים במיוחד שמאפשרים תנועה עדינה ומדויקת
- ב. כל סיב שריר מעוצבב על ידי מספר תאי עצב ולא אחד
- ג. הם שרירים מהירים מאד שמאפשרים מעקב אחר עצמים נעים
- ד. Succinylcholine אינו משפיע עליהם
In the full version for subscribers
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Sources
- Miller's Anesthesia, 9th edition (2020) — Pharmacology of Neuromuscular Blocking Drugs
- ASA Practice Guidelines for Monitoring and Antagonism of Neuromuscular Blockade, 2023 — Quantitative monitoring
- Morgan & Mikhail's Clinical Anesthesiology, 7th edition (2022) — Neuromuscular Blocking Agents
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-02. The text may contain errors; when in doubt, check the source.