# General Anaesthetics > General anaesthetics for FMGE Pharmacology: Guedel stages, propofol, ketamine, thiopentone, volatile agents, malignant hyperthermia and relaxants in notes. - Canonical URL: https://prepelephant.com/topics/fmge/pharmacology/general-anaesthetics-fmge - Exam / course: FMGE · Subject: Pharmacology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "General Anaesthetics", PrepElephant, https://prepelephant.com/topics/fmge/pharmacology/general-anaesthetics-fmge ## Direct answer Guedel described four stages of ether anaesthesia — analgesia, excitement, surgical anaesthesia (with four planes) and medullary paralysis — and although modern intravenous agents skip through them in seconds, the schema remains FMGE's favourite anaesthesia opening question, with stage II's irregular breathing and dilated pupils and stage III's loss of the corneal reflex as the examined landmarks. Agent selection then follows patient physiology: propofol for a smooth, rapid recovery; ketamine when the patient is shocked, wheezing or a child in a resource-limited setting; etomidate when the heart is failing; thiopentone never in porphyria. Malignant hyperthermia — hypercarbia, masseter spasm, then soaring temperature from suxamethonium or volatile agents — is treated by stopping the trigger, dantrolene 2.5 mg/kg, cooling and treating hyperkalaemia; and the neuromuscular blockers close the chapter, with suxamethonium's hyperkalaemia and sugammadex's clean reversal as the most quoted facts. ## What you must remember - Guedel stages (ether, unpremedicated): I analgesia and amnesia; II excitement — irregular respiration, dilated pupils, risk of laryngospasm, passed rapidly; III surgical anaesthesia — plane 1 roving eyeballs stop, plane 2 corneal reflex lost, plane 3 pupils fixed, intercostals paralysed; IV medullary paralysis — overdose. - Propofol (1.5–2.5 mg/kg induction): pain on injection (premix lignocaine), apnoea and hypotension, antiemetic at sub-hypnotic doses, green urine with prolonged infusion, and propofol infusion syndrome — rhabdomyolysis, acidosis, cardiac failure — in long intensive-care use. - Ketamine (1–2 mg/kg IV): NMDA-antagonist dissociative anaesthesia with preserved airway reflexes and analgesia; bronchodilation makes it the asthma choice; catecholamine release supports the shocked patient; it raises intracranial and intraocular pressure; emergence phenomena are blunted by midazolam premedication and a quiet recovery. - Thiopentone: ultra-short acting through redistribution; anticonvulsant; contraindicated in porphyria (induces haem synthesis); tissue necrosis on extravasation; depresses respiration and myocardium. - Etomidate: haemodynamic stability for the cardiac patient; adrenal suppression even after a single dose; myoclonus and injection pain. - Volatile agents: halothane — myocardial sensitisation to adrenaline (arrhythmias) and immune "halothane hepatitis" on re-exposure; sevoflurane — non-pungent, the paediatric mask induction agent; desflurane — fastest recovery, pungent, needs a heated vaporiser; isoflurane — airway irritant, vasodilator. - Nitrous oxide: MAC 104 per cent so never adequate alone; contributes the second gas effect and concentration effect; diffusion hypoxia at the end mandates several minutes of 100 per cent oxygen; expands closed air spaces (pneumothorax, bowel obstruction, middle ear); inactivates methionine synthase (vitamin B12) with prolonged exposure. - Malignant hyperthermia: ryanodine-receptor crisis triggered by suxamethonium and volatiles; rising end-tidal carbon dioxide and masseter spasm precede the late fever; dantrolene 2.5 mg/kg IV repeated, stop triggers, 100 per cent oxygen, cool, treat hyperkalaemia — never give calcium channel blockers with dantrolene. - Suxamethonium: depolarising, onset under a minute, duration 5–10 minutes; fasciculations then block; dangerous hyperkalaemia in burns, crush injury and denervation; trigger for malignant hyperthermia; prolonged apnoea in pseudocholinesterase deficiency (the dibucaine number). - Non-depolarising agents: rocuronium (1 mg/kg for rapid sequence intubation, an alternative to suxamethonium), vecuronium, atracurium (Hoffman elimination — laudanosine — independent of liver and kidney); reversal by neostigmine with glycopyrrolate, or selectively by sugammadex (2–4 mg/kg routine reversal, up to 16 mg/kg immediate), which encapsulates rocuronium without cholinergic stimulation. ## Worked example: anaesthesia in the shocked trauma patient A young man reaches theatre after a crush injury, hypotensive and in pain, for emergency laparotomy. Induction reasoning: propofol's vasodilation could collapse what pressure remains — ketamine 1–2 mg/kg (or etomidate where haemodynamic neutrality is preferred) is the safer induction. Suxamethonium would normally give the fastest intubating conditions, but this crush injury plus probable hyperkalaemia makes depolarisation lethal; rocuronium 1 mg/kg provides an alternative rapid-sequence paralytic, with sugammadex available for immediate reversal. Maintenance continues with ketamine or a volatile with the lowest cardiovascular penalty, guided by the blood pressure the story demands. The same reasoning in a wheezing child with a forearm fracture would choose ketamine for its bronchodilation and preserved airway, sevoflurane for a calm mask induction, and regional supplementation — three facts from one scenario. And in every patient, the theatre's malignant hyperthermia drill — dantrolene stocked, workflow rehearsed — is the safety net the exam assumes. ## Where students slip Suxamethonium is ordered for the burned or crushed patient days after injury, when the up-regulated junctional receptors release lethal potassium — the timing window (beyond 24–48 hours of injury) is the stem's buried clue. Second, halothane is paired with adrenaline-impregnated field infiltration, producing ventricular arrhythmias from sensitisation. Third, nitrous oxide continues through a bowel obstruction case and the pneumothorax expands. Fourth, thiopentone reaches the porphyric patient; any unexplained abdominal pain plus neuropsychiatric features in the family should have stopped it. Fifth, Guedel's planes are memorised as trivia but tested as ordering — which stage carries the excitement risk (II), which plane loses the corneal reflex (III, plane 2). Finally, sugammadex is presented as "another reversal"; its value is precisely that it avoids neostigmine's cholinergic bradycardia, secretions and bronchospasm. ## Frequently asked questions ### What are Guedel's four stages of ether anaesthesia? Stage I analgesia; stage II excitement with irregular breathing and dilated pupils; stage III surgical anaesthesia in four planes (corneal reflex lost in plane 2); stage IV medullary paralysis — modern agents traverse these in seconds. ### How is malignant hyperthermia treated? Stop volatile agents and suxamethonium, give 100 per cent oxygen, dantrolene 2.5 mg/kg IV repeated as needed, active cooling and treatment of hyperkalaemia; early signs are rising end-tidal carbon dioxide and masseter spasm. ### Why is suxamethonium contraindicated days after burns or crush injury? Extrajunctional acetylcholine receptor proliferation causes massive potassium release on depolarisation, producing cardiac arrest — rocuronium is the alternative for rapid-sequence intubation. ### Which induction agent suits the shocked and the asthmatic patient? Ketamine — its catecholamine release supports blood pressure (barring catecholamine depletion) and it is a bronchodilator; it must be avoided where raised intracranial pressure is unmonitored. ### What is diffusion hypoxia? At the end of nitrous oxide anaesthesia, the gas floods from blood into alveoli faster than nitrogen leaves, diluting alveolar oxygen — prevented by administering 100 per cent oxygen for several minutes. ### What advantage does sugammadex offer over neostigmine? It encapsulates rocuronium and vecuronium directly, reversing block without cholinergic stimulation — no bradycardia, secretions or bronchospasm — and can reverse profound block rapidly.