AS4.1-7 | General Anaesthesia — Graded Quiz

Etomidate at 0.2–0.3 mg/kg is the agent of choice in haemodynamically compromised patients because it causes the least myocardial depression of all induction agents. Propofol and thiopentone cause significant vasodilation and reduced cardiac output — catastrophic in a patient already in shock. Etomidate's drawback is transient adrenocortical suppression (single dose during crisis is acceptable).

Etomidate is the preferred induction agent in haemodynamic instability. Propofol and thiopentone are contraindicated in severe cardiovascular compromise. Know all four induction-agent doses and their primary clinical niches.

Propofol and thiopentone both reduce systemic vascular resistance and cardiac output — they would worsen the shock state. Ketamine raises sympathomimetic tone but also raises ICP (making it a poor choice in head injury, not a protective one); while ketamine could be used in shock in the absence of head injury, the question frames 'raises ICP' as the justification, which is wrong. Etomidate is the haemodynamic-stability agent for critically ill patients. Dose: 0.2–0.3 mg/kg IV.

Suxamethonium is normally metabolised rapidly (within 5–10 minutes) by plasma pseudocholinesterase (butyrylcholinesterase). Inherited deficiency (atypical pseudocholinesterase) or acquired deficiency (liver disease, burns, pregnancy, organophosphate poisoning) prolongs the depolarising block. Treatment is supportive: maintain anaesthesia and ventilation until spontaneous recovery. Do NOT give neostigmine — it worsens phase I block by increasing ACh.

Suxamethonium is metabolised by plasma pseudocholinesterase. Deficiency causes prolonged apnoea. Treatment: ventilate until spontaneous recovery; neostigmine is contraindicated.

Acetylcholinesterase is the enzyme at the NMJ that metabolises ACh — inhibiting it with neostigmine reverses non-depolarising blocks; it plays no role in suxamethonium metabolism. Monoamine oxidase and CYP3A4 are irrelevant to suxamethonium. Prolonged suxamethonium action = atypical or deficient pseudocholinesterase until proven otherwise.

Cormack-Lehane Grade III: only the arytenoids or posterior laryngeal structures are seen, with no vocal cord view. This grade indicates a difficult airway. First-line management: introduce a bougie blindly toward the arytenoids, then railroad the tracheal tube over it; or switch to a video laryngoscope which provides an improved glottic view. Grade IV (epiglottis not visible) may require an intubating LMA or surgical airway.

Cormack-Lehane grading guides the failed intubation algorithm. Grade III: attempt bougie-assisted or video laryngoscopy. Limit direct laryngoscopy to 3 attempts maximum to avoid airway trauma.

Grade I = full cord view; Grade II = partial cord view (anterior commissure not seen but most of cords visible). Grade III/IV signal a potentially cannot-intubate scenario — escalate immediately rather than making repeated blind attempts. The bougie (gum elastic bougie) is the first rescue tool for Grade III laryngoscopy.

1.8 MAC is above the standard maintenance range (0.8–1.2 MAC), indicating excessive anaesthetic depth. Volatile agents cause dose-dependent vasodilation and myocardial depression — the primary cause of hypotension here. Correct action: turn down the volatile agent, give a modest IV fluid bolus, and reassess. If hypotension persists, add a vasopressor (ephedrine or phenylephrine) and consider other causes.

Excessive volatile agent concentration is a common, correctable cause of intraoperative hypotension in the elderly. Monitoring the end-tidal agent concentration as part of depth-of-anaesthesia monitoring prevents this.

Haemorrhage is a valid differential but hip fracture repair at 15 minutes is unlikely to have caused massive blood loss yet, and the ETCO₂ and SpO₂ are maintained. Anaphylaxis presents with urticaria, bronchospasm, and cardiovascular collapse — the high MAC is a more parsimonious explanation here. PE would cause a sudden fall in ETCO₂. Always check the anaesthetic depth before attributing intraoperative hypotension to a pathological cause.

During one-lung ventilation, the collapsed (non-dependent, non-ventilated) lung continues to receive a proportion of pulmonary blood flow. This perfusion without ventilation constitutes a true intrapulmonary right-to-left shunt, directly adding deoxygenated blood to the arterial circulation. Hypoxic pulmonary vasoconstriction (HPV) partially mitigates this by redirecting blood away from the collapsed lung, but cannot fully compensate.

One-lung ventilation hypoxia = intrapulmonary shunt. HPV is a natural compensatory response. Management: optimise PEEP to the dependent lung, check tube position, apply CPAP to the collapsed lung if necessary.

Dead-space ventilation (ventilation without perfusion) increases the alveolar-arterial gradient for CO₂ but does not directly cause hypoxia. Reduced cardiac output can worsen SpO₂ when shunt is present but is not the primary mechanism here. CO₂ retention is a separate ventilation issue. The core mechanism of OLV hypoxia is shunt physiology.

The target BIS range for general anaesthesia during maintenance is 40–60. A BIS of 38 is below this range, indicating excessive depth of anaesthesia — associated with prolonged emergence, haemodynamic depression, and increased risk of post-operative cognitive dysfunction in the elderly. Appropriate action: reduce the anaesthetic agent concentration. Values of 40–60 = surgical anaesthesia; 60–80 = light sedation/anxiolysis; 80–100 = awake; <40 = deep/burst suppression.

BIS 40–60 = adequate surgical anaesthesia. Below 40 = excessive depth; above 60 = risk of awareness. BIS monitoring guides agent titration and is especially valuable in the elderly, cardiac surgery, and day-care patients.

BIS 40–60 is the target, not 38. 38 is below target = too deep. Awareness corresponds to BIS >60 (or even >80 if unresponsive). An awake individual has BIS 90–100. Do not confuse excessive depth with awareness — they are opposite problems. BIS monitoring is used to titrate depth and minimise both overdose and under-dose.

Moderate-to-severe obstructive sleep apnoea requiring nightly CPAP is a relative-to-absolute contraindication to same-day discharge after general anaesthesia, because residual opioid and anaesthetic effects markedly increase the risk of post-operative upper-airway obstruction and hypoxia during sleep. Guidelines recommend overnight monitoring and CPAP access post-operatively. Obesity (BMI 36) and well-controlled diabetes are not independent contraindications; age 58 alone is not a barrier.

Patient selection for day surgery: OSA on home CPAP is a key contraindication to same-day discharge due to post-operative respiratory risk. ASA I–II (and stable ASA III) without significant OSA are appropriate day-surgery candidates.

BMI 36 alone does not preclude day surgery if the patient is otherwise fit. Metformin-treated T2DM with good control is compatible with day surgery. Age 58 is not a barrier. OSA requiring home CPAP requires post-operative overnight monitoring — making same-day discharge unsafe.

The NORA principle is that standards of anaesthesia care must be equivalent to those in the operating theatre, regardless of location. A trained anaesthesiologist (not a radiologist) must administer and monitor sedation; full resuscitation equipment (airway trolley, defibrillator, emergency drugs, suction, oxygen) must be physically present. Regarding the shellfish allergy: there is NO evidence that shellfish allergy increases the risk of propofol reaction — the egg lecithin/soya oil in propofol emulsion is not cross-reactive with shellfish allergens.

NORA standards = operating theatre standards. Shellfish allergy is not a contraindication to propofol (the emulsion contains egg lecithin and soya, which are not shellfish cross-reactants). A trained anaesthesiologist and full resuscitation capability are mandatory at every NORA site.

The shellfish–propofol cross-reactivity myth is a well-documented clinical misconception; shellfish allergy is not a contraindication to propofol. A radiologist without anaesthesia training must never administer propofol sedation, even under remote supervision. The depth of anaesthesia required for MRI in a child is often deep enough to require airway management skills. NORA hazards are compounded by distance, unfamiliar environments, and limited access.

Laryngospasm is a reflex adduction of the vocal cords causing complete or near-complete upper airway obstruction. Paradoxical chest movements (chest sinks in on inspiration against a closed glottis = characteristic 'rocking horse' pattern) with cyanosis following extubation = laryngospasm. Management: 100% O₂ by tight mask with CPAP; gentle jaw thrust; if incomplete obstruction resolves, observe; if complete or SpO₂ worsening — low-dose suxamethonium 0.1–0.2 mg/kg IV (intubating dose not needed) to break the spasm.

Laryngospasm at emergence: paradoxical chest movement + cyanosis = immediate CPAP via tight mask; small-dose suxamethonium breaks refractory spasm. Do not give neostigmine for laryngospasm.

Neostigmine would not relax laryngeal muscles — it reverses NMBAs by increasing ACh, which would actually worsen laryngeal muscle activation. Tongue obstruction gives a more gradual snoring obstruction without paradox; responds to jaw thrust and airway adjuncts. Laryngospasm is a recognised dangerous complication of emergence and requires a definitive response, not just repositioning.

Bone cement implantation syndrome (BCIS) occurs when acrylic bone cement (polymethylmethacrylate — PMMA) is implanted under pressure, forcing fat, marrow particles, monomer, and air into the venous circulation. This embolus reaches the pulmonary vasculature causing acute pulmonary hypertension, right heart strain, and systemic cardiovascular collapse. The temporal relation (BP crash within 1–3 minutes of cementation) is the clinical key. Treatment: 100% FiO₂, vasopressors, IV fluids, and inform the surgeon.

Bone cement implantation syndrome is a sudden cardiovascular collapse within minutes of PMMA cementation in joint replacement surgery. Prevention: warn the anaesthesiologist before cementing; ensure volume loading; 100% FiO₂ before cement application.

Isoflurane-related hypotension would be gradual and present from induction, not a sudden drop at cementation. MI is plausible in this patient but the timing with cement application makes BCIS more likely — and MI would not typically show the characteristic acute pulmonary hypertension pattern. Latex anaphylaxis occurs at skin contact with latex products, not at cement application. The temporal relationship to a surgical event is the key discriminator.