Pharmacology
Anaesthetics and Muscle Relaxants
General and local anaesthetics and muscle relaxants for MBBS and NEET-PG: propofol, ketamine, lignocaine, succinylcholine and malignant hyperthermia, mapped to NMC codes.
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Anaesthetics and Muscle Relaxants
General and local anaesthetics and muscle relaxants for MBBS and NEET-PG: propofol, ketamine, lignocaine, succinylcholine and malignant hyperthermia, mapped to NMC codes.
This chapter covers general anaesthetics, both inhalational and intravenous, local anaesthetics and the skeletal muscle relaxants. It explains how these drugs produce loss of sensation and paralysis, their pharmacokinetic quirks and the safety issues that dominate exam questions and clinical practice.
High-yield: Anaesthetics and Muscle Relaxants
- Minimum alveolar concentration measures inhalational anaesthetic potency; a lower value means a more potent agent.
- Halothane can cause hepatotoxicity and sensitises the myocardium to catecholamine-induced arrhythmias.
- Sevoflurane and isoflurane are the common modern inhalational agents; nitrous oxide gives good analgesia but weak anaesthesia.
- Thiopentone is an ultrashort-acting barbiturate for rapid induction; its brief action is due to redistribution, not metabolism.
- Propofol gives smooth rapid induction and recovery with antiemetic action but causes pain on injection and dose-dependent hypotension.
- Ketamine produces dissociative anaesthesia with preserved airway reflexes and bronchodilatation, but causes emergence delirium.
- Lignocaine is an amide local anaesthetic that blocks voltage-gated sodium channels and is also an antiarrhythmic.
- Adrenaline added to a local anaesthetic prolongs its action and reduces bleeding but must be avoided in end-artery sites such as fingers and toes.
- Bupivacaine is long-acting but the most cardiotoxic local anaesthetic; ester agents such as procaine can cause allergy.
- Succinylcholine is a depolarising blocker giving rapid brief paralysis for intubation, but can trigger malignant hyperthermia and hyperkalaemia.
- Non-depolarising blockers such as vecuronium and atracurium are competitive and are reversed by neostigmine with an antimuscarinic.
- Atracurium is preferred in renal and hepatic failure as it is eliminated by spontaneous Hofmann degradation.
- Malignant hyperthermia is triggered by volatile agents and succinylcholine and is treated with dantrolene.
- Local anaesthetics work poorly in infected acidic tissue because the ionised fraction cannot cross the nerve membrane.
Muscle relaxants and local anaesthetics
- **Depolarising blocker:** Succinylcholine; rapid brief paralysis; risks malignant hyperthermia and hyperkalaemia.
- **Non-depolarising blocker:** Vecuronium, atracurium; reversed by neostigmine; atracurium safe in organ failure.
- **Amide local anaesthetics:** Lignocaine, bupivacaine; bupivacaine most cardiotoxic; metabolised in the liver.
- **Malignant hyperthermia:** Triggered by volatiles and succinylcholine; treated with dantrolene.
NMC competencies in this chapter
- **PH1.15:** Skeletal muscle relaxants and their clinical uses
- **PH1.17:** General anaesthetics and pre-anaesthetic medication
- **PH1.18:** Local anaesthetics and their clinical applications
Frequently Asked Questions
What is minimum alveolar concentration?
It is the concentration of an inhalational anaesthetic that prevents movement in half of patients on surgical stimulus, and a lower value indicates a more potent agent.
Why does adrenaline prolong local anaesthesia?
Its vasoconstriction slows removal of the anaesthetic from the site, prolonging the block and reducing bleeding, but it is avoided in end-artery areas like digits.
Which muscle relaxant is safe in renal failure?
Atracurium, because it is broken down by spontaneous Hofmann degradation in the plasma and does not rely on the kidneys or liver for clearance.
Why do local anaesthetics fail in infected tissue?
The acidic environment keeps the drug ionised, so it cannot cross the nerve membrane in its uncharged form to block sodium channels.
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