AS4.1-7 | General Anaesthesia — Practice Quiz

Propofol at 1.5–2.5 mg/kg IV is the standard induction agent for elective surgery. It produces smooth induction, has antiemetic properties, and allows rapid emergence. In stable cardiac disease without haemodynamic compromise it is appropriate; give slowly and reduce dose in elderly or ASA III patients.

Correct induction agent dose is a patient-safety fundamental: overdose causes cardiovascular collapse; underdose causes awareness. Propofol 1.5–2.5 mg/kg is the most versatile agent for elective surgery in adults.

Ketamine raises heart rate and blood pressure — undesirable here. Thiopentone's induction dose is 3–5 mg/kg (not 1–1.5 mg/kg); the low dose given would cause awareness. Etomidate's dose is 0.2–0.3 mg/kg (not 1–2 mg/kg); it causes adrenal suppression and is reserved for haemodynamic instability. Review induction-agent doses: propofol 1.5–2.5, thiopentone 3–5, ketamine 1–2, etomidate 0.2–0.3 mg/kg.

Malignant hyperthermia (MH) is a pharmacogenetic hypermetabolic crisis of skeletal muscle triggered by suxamethonium (and potent inhalational agents). Classic triad: rising ETCO₂ (earliest sign), muscle rigidity, hyperthermia. Treatment: stop the trigger, dantrolene 2.5 mg/kg IV bolus, active cooling.

Rising end-tidal CO₂ is the earliest reliable sign of MH. Suxamethonium and all potent volatile agents are triggers; immediate dantrolene 2.5 mg/kg is life-saving.

Neuroleptic malignant syndrome is triggered by antipsychotics, not opioids, and has a slower onset (days). Septic shock presents with vasodilation and hypotension, not rigidity. Thyroid storm does not cause rigidity. The intraoperative triad of rising ETCO₂ + rigidity + hyperthermia after a depolarising muscle relaxant or volatile agent = malignant hyperthermia until proven otherwise.

Neostigmine (an anticholinesterase) inhibits acetylcholinesterase, the enzyme that degrades acetylcholine in the synaptic cleft. The resulting accumulation of acetylcholine out-competes the non-depolarising NMBA for the nicotinic receptor. It must be given with glycopyrrolate or atropine to counter muscarinic side-effects (bradycardia, bronchospasm, hypersalivation).

Anticholinesterase reversal works by indirect competition: more ACh at the motor end-plate overcomes the competitive NMBA. Always co-administer an anticholinergic to prevent muscarinic overdrive.

Neostigmine does not bind to nicotinic receptors directly, nor does it stimulate nerve terminal release, nor act on ryanodine receptors (that is the MH pathway). It works entirely by enzyme inhibition. Remember: neostigmine reverses non-depolarising (competitive) NMBAs; it cannot be used to reverse suxamethonium (depolarising) because excess acetylcholine prolongs the phase I block.

Class III: only the soft palate base (and sometimes the tip of the uvula) is visible; tonsillar pillars and uvula are not seen. Class III–IV predicts increased risk of difficult laryngoscopy and intubation. This is an oropharyngeal-view grading that assesses tongue-to-pharyngeal-space ratio — a purely airway assessment distinct from ASA physical status.

Mallampati I–IV grades the oropharyngeal view, not operative risk. Class III/IV suggests tongue base encroachment on the pharyngeal space and anticipates a restricted laryngoscopic view.

Class I = soft palate, uvula, fauces, tonsillar pillars visible. Class II = soft palate, uvula, fauces visible (pillars not). Class IV = only hard palate visible. Remember: Mallampati is NOT ASA — Mallampati grades airway difficulty from mouth opening; ASA grades systemic disease severity. Confusing them is a high-yield trap.

RSI: preoxygenate (3 minutes tidal volume or 4 vital-capacity breaths) → apply cricoid pressure (Sellick's manoeuvre) → give induction agent + suxamethonium simultaneously → intubate immediately without mask ventilation (to avoid gastric insufflation). Suxamethonium 1–1.5 mg/kg achieves intubating conditions in 60 seconds.

RSI protects against pulmonary aspiration in full-stomach patients: no mask ventilation between induction and intubation; cricoid pressure throughout; suxamethonium or high-dose rocuronium provides the fastest onset.

Vecuronium has a slow onset (3–5 min) — unsuitable for RSI (though modified RSI with high-dose rocuronium is used). Waiting for spontaneous breathing to cease defeats the purpose — RSI aims for immediate controlled intubation. Mask ventilation in RSI risks gastric insufflation and aspiration. Antacid may be a pre-RSI adjunct, but the core sequence does not include a post-antacid mask-ventilation step.

During laparoscopic surgery, CO₂ used for peritoneal insufflation is absorbed across the peritoneal membrane into the bloodstream, leading to a gradual rise in ETCO₂. Management: increase minute ventilation (increase respiratory rate or tidal volume) to eliminate the extra CO₂ load. Unlike MH, the rise is gradual and there is no rigidity or temperature rise.

Capnography is essential monitoring during laparoscopy. A gradual rise in ETCO₂ during peritoneal insufflation is expected and managed by increasing minute ventilation; a sudden sharp rise raises concern for MH.

Endobronchial intubation causes hypoxia (falling SpO₂) and reduced breath sounds on one side. Circuit disconnection causes absent waveform on capnography. Venous air embolism causes a sudden fall in ETCO₂ (not a rise) due to reduced pulmonary perfusion and cardiovascular collapse. A rising ETCO₂ with normal SpO₂ during laparoscopy = peritoneal CO₂ absorption.

Propofol TIVA has intrinsic antiemetic properties. Multimodal analgesia (paracetamol + NSAID) reduces opioid requirement — opioids are a major emetogenic trigger. Ondansetron (5-HT₃ antagonist) + dexamethasone provides dual antiemetic prophylaxis. This evidence-based combination represents the fast-track / enhanced recovery approach central to safe day surgery anaesthesia.

PONV is the dominant failure mode of day surgery. Propofol TIVA + multimodal opioid-sparing analgesia + dual antiemetic prophylaxis is the evidence-based cornerstone of ambulatory anaesthesia.

Volatile agents are emetogenic — associated with a higher PONV rate than propofol TIVA. High-dose opioids increase PONV and residual sedation, both of which cause unanticipated admission. Droperidol may be used but is not the preferred combination for day surgery. Ketamine without antiemetic prophylaxis is inadequate. PONV is the leading cause of day-surgery unplanned admission — not pain, not bleeding.

The MRI suite's powerful magnetic field will accelerate any ferromagnetic object toward the magnet (projectile effect), potentially injuring patients and staff. All equipment — monitoring leads, ventilators, gas cylinders, IV stands — must be MRI-compatible (non-ferromagnetic). Standard ECG electrodes can heat and burn. Monitoring (ECG, pulse oximetry, capnography) must use dedicated MRI-safe cables and equipment.

MRI NORA hazards are unique: ferromagnetic projectile risk, MRI-compatible equipment mandatory, restricted patient access, and monitoring interference. Every object entering the MRI room must be screened.

PONV and propofol pharmacokinetics apply in any anaesthetic setting, not specifically MRI. MH risk relates to volatile agents, not location. The ferromagnetic/MRI-compatibility issue is the defining hazard that differentiates MRI NORA from all other anaesthetic environments. Additionally: the narrow tunnel, distance from the patient, and RF noise interference with monitoring are unique NORA challenges in MRI.