Anaesthesia

Anaesthesia is one of the highest-yield-per-hour subjects in NEET PG and INI-CET. It is a compact discipline — the testable universe is small and predictable, the facts are precise (numbers, doses, MAC values, classifications), and the same themes recur year after year. A serious candidate can cover the entire exam-relevant content in 25–35 hours and walk away with 8–12 near-guaranteed marks. Treat it as a "scoring" subject, not a "background" one.

This page is the mother page for the subject. It maps how Anaesthesia is examined, then walks system-by-system through the groups that structure the question bank — General Anaesthesia, Regional, Airway, Pharmacology, Critical Care, and Pain — flagging the must-know facts, the classic associations, the exact values examiners love, and the traps that cost students marks. It closes with cross-subject overlaps, recent guideline shifts, a study roadmap, and rapid-fire one-liners.

---

How Anaesthesia Is Tested

Weightage and format

• NEET PG: Approximately 8–12 questions (out of 200), i.e. roughly 4–6%. In recent papers the count has trended upward because anaesthesia overlaps heavily with pharmacology, physiology, and critical care.
• INI-CET (AIIMS/PGI pattern): Anaesthesia is disproportionately rewarding here. INI loves precise numbers, mechanism-based reasoning, and one-liners on monitoring, local anaesthetic toxicity, MAC, and ventilator settings. Expect 6–10 questions, often with image-based or assertion-reason formats.
• FMGE: Lower yield (3–5 questions) but the same core facts.

Question styles that recur

1. Single-best-fact recall — "MAC of which agent is highest?" / "Drug of choice for malignant hyperthermia?" Pure mark-grabbers.
2. Numeric/value MCQs — MAC values, intralipid dose, max local anaesthetic dose, ETT sizes, ASA grading thresholds.
3. Clinical-vignette + management — a scenario (e.g., post-spinal hypotension, LAST, laryngospasm) asking the next best step or drug of choice.
4. Mechanism/pharmacology — receptor targets (NMDA, GABA-A), context-sensitive half-time, metabolism (Hofmann elimination, plasma cholinesterase).
5. Image-based (rising in INI-CET) — capnography traces, laryngoscope blades, airway devices, regional block landmarks, ECG/monitoring.
6. Assertion–Reason / multi-statement — typical of INI-CET; tests whether you know why, not just what.

Strategic note: Anaesthesia rewards rote precision more than any other clinical subject. Memorise the numbers exactly. "Approximately right" loses the mark.

---

Group 1: General Anaesthesia

This group covers the conduct of GA — stages, depth, inhalational and IV agents' systemic behaviour, monitoring, and crisis events like malignant hyperthermia.

Stages and depth of anaesthesia

• Guedel's stages (classically described for ether, still tested):
  1. Stage 1 – Analgesia (amnesia, analgesia)
  2. Stage 2 – Excitement/delirium (the dangerous stage: laryngospasm, vomiting, irregular breathing — get through it fast)
  3. Stage 3 – Surgical anaesthesia (4 planes; ideal operating depth)
  4. Stage 4 – Medullary paralysis (apnoea, cardiovascular collapse — overdose)
• Depth monitoring: BIS (Bispectral Index) — target 40–60 for adequate GA; <40 = too deep, >60 = risk of awareness. Entropy is the alternative.

MAC — Minimum Alveolar Concentration (the single most-tested concept)

MAC = concentration of inhalational agent (at 1 atm) that prevents movement to a standard surgical stimulus in 50% of patients. It is an index of potency (inverse: high MAC = low potency).

Agent	MAC (%)	Blood:gas coefficient	Key point
Nitrous oxide (N₂O)	104	0.47	Lowest potency; cannot give 1 MAC alone
Desflurane	6.0	0.42 (lowest)	Fastest on/off; airway irritant
Sevoflurane	2.0	0.65	Agent of choice for inhalational induction (non-irritant)
Isoflurane	1.15	1.4	Coronary steal (historical)
Halothane	0.75	2.4	Hepatotoxicity, sensitises myocardium to catecholamines

MAC traps:

• Increase MAC (need more agent): hyperthermia, chronic alcoholism, infants (highest at ~6 months), hypernatraemia, acute amphetamine/cocaine, red hair.
• Decrease MAC (need less): elderly, hypothermia, pregnancy, acute alcohol intoxication, opioids/sedatives, hyponatraemia, lithium, alpha-2 agonists, severe anaemia/hypoxia.
• MAC is unaffected by sex, duration of anaesthesia, weight, height, hypo-/hyperkalaemia, hyper-/hypocarbia within normal range, thyroid status.

Blood:gas solubility = speed. Lower coefficient → faster induction and recovery. Desflurane fastest, halothane slowest.

The second gas effect and concentration effect

• N₂O is highly diffusible. Rapid uptake of a large volume of N₂O concentrates the remaining alveolar gas (concentration effect) and speeds uptake of a co-administered second gas (second gas effect).
• Diffusion hypoxia (Fink effect): on stopping N₂O, it floods back into alveoli, diluting O₂ → give 100% O₂ for 3–5 min at the end. Classic one-liner.
• N₂O contraindicated where closed air spaces expand: pneumothorax, bowel obstruction, middle-ear/tympanoplasty, air embolism, vitreoretinal surgery with intraocular gas.

IV induction agents — systemic behaviour

Agent	Best for	Avoid in	Signature fact
Propofol	Day-care, antiemetic, smooth	Egg/soy allergy (relative), haemodynamic instability	Pain on injection; PRIS (propofol infusion syndrome); ↓BP
Thiopentone	Rapid induction, neuroprotection	Porphyria (absolute), status asthmaticus	Contraindicated in acute intermittent porphyria
Ketamine	Shock, asthma, paediatric, field	↑ICP (relative debate), ischaemic heart disease	Dissociative; NMDA antagonist; ↑BP, ↑HR, bronchodilator; emergence delirium
Etomidate	Cardiac-compromised patients	Sepsis (adrenal suppression)	Most cardiostable; adrenal suppression, myoclonus
Dexmedetomidine	Sedation, awake fibreoptic	Heart block	α₂ agonist; sedation without respiratory depression

Malignant hyperthermia (MH) — guaranteed exam favourite

• Trigger agents: all volatile anaesthetics + succinylcholine.
• Genetics: autosomal dominant; ryanodine receptor (RYR1) mutation on chromosome 19 → uncontrolled Ca²⁺ release from sarcoplasmic reticulum.
• Earliest sign: rising end-tidal CO₂ (not fever). Then masseter spasm, tachycardia, hyperthermia, rigidity, rhabdomyolysis, hyperkalaemia.
• Treatment of choice: Dantrolene (2.5 mg/kg IV, repeat to 10 mg/kg) — blocks RYR1. Plus stop triggers, 100% O₂, active cooling, treat hyperkalaemia/acidosis.
• Associations: Central core disease, King-Denborough syndrome.
• Safe agents: propofol, opioids, N₂O, non-depolarising relaxants, regional anaesthesia.

Trap: Students pick "fever" as the first sign. The earliest and most sensitive sign is a sustained rise in EtCO₂.

Preoperative assessment

• ASA Physical Status: I (normal healthy) → II (mild systemic) → III (severe systemic, not incapacitating) → IV (incapacitating, constant threat to life) → V (moribund, <24 h survival without surgery) → VI (brain-dead organ donor). Suffix "E" for emergency.
• NPO/fasting (2-4-6-8 rule): clear fluids 2 h, breast milk 4 h, light meal/formula 6 h, fatty/fried/meat 8 h.
• Mallampati for airway prediction (see Airway).

---

Group 2: Regional Anaesthesia

A reliably tested block: spinal vs epidural distinctions, local anaesthetic pharmacology, complications, and block-specific landmarks.

Spinal (subarachnoid) vs epidural — the core comparison table

Feature	Spinal	Epidural
Site	Subarachnoid (CSF), below L1 (adult cord ends L1; in children L3)	Epidural (potential) space
Needle endpoint	Free flow of CSF	Loss of resistance
Drug volume	Small (1.5–3 mL)	Large (10–20 mL)
Onset	Fast (2–5 min)	Slow (10–20 min)
Catheter	Usually single shot	Catheter for top-ups/labour
Post-dural puncture headache (PDPH)	Yes (dura punctured)	Only if accidental dural tap
Test dose	—	Lignocaine + adrenaline (detects intravascular/intrathecal)

• Level for safe spinal puncture: L3–L4 or L4–L5 (below conus). Tuffier's line (intercristal line) ≈ L4 or L4–L5.
• Saddle block: low-dose hyperbaric agent, patient sitting → perineal anaesthesia.
• PDPH: worse on sitting/standing, relieved by lying flat; due to CSF leak; risk ↑ with large-bore cutting (Quincke) needles, ↓ with pencil-point (Whitacre/Sprotte) needles. Treatment: conservative → epidural blood patch if persistent.

Spinal anaesthesia complications and physiology

• Hypotension + bradycardia — sympathetic blockade. If block above T4 → cardiac accelerator fibres blocked → bradycardia. Manage: fluids, vasopressors (phenylephrine/mephentermine/ephedrine), atropine for bradycardia.
• High/total spinal: apnoea, profound hypotension — supportive ventilation + pressors.
• Bezold–Jarisch reflex implicated in sudden bradycardia/asystole during spinal.

Local anaesthetics (LA)

Mechanism: block voltage-gated Na⁺ channels from the inner side → prevent depolarisation. Order of nerve fibre blockade: autonomic (B) → pain/temperature → touch → motor (small, myelinated, rapidly firing fibres blocked first).

LA	Class	Max dose (plain)	Notable
Lignocaine	Amide	4.5 mg/kg (with adrenaline 7 mg/kg)	Also antiarrhythmic (Class Ib)
Bupivacaine	Amide	2 mg/kg (max ~2.5 with adr.)	Most cardiotoxic; avoid IV regional
Ropivacaine	Amide	~3 mg/kg	Less cardiotoxic, more sensory-selective
Procaine	Ester	—	Short acting
Cocaine	Ester	—	Only LA that is a vasoconstrictor

• Esters metabolised by plasma pseudocholinesterase → PABA → allergy more common. Amides metabolised in liver; "amides have an i before -caine" (lidocaine, bupivacaine).
• Adrenaline added to prolong action and reduce systemic absorption; never in end-arteries (digits, penis, pinna, nose tip).

Local anaesthetic systemic toxicity (LAST) — very high yield

• Sequence: circumoral tingling/metallic taste → tinnitus → perioral numbness → tongue paraesthesia → restlessness/seizures (CNS first) → then cardiovascular collapse (bupivacaine especially).
• Treatment of choice: 20% Intralipid (lipid emulsion) — bolus 1.5 mL/kg over 1 min, then infusion 0.25 mL/kg/min; repeat bolus and double infusion if unstable; max ~12 mL/kg. Plus ABC, seizure control (benzodiazepines), avoid vasopressin/large epinephrine doses.

Trap: CNS signs precede cardiovascular collapse for most LAs — but bupivacaine can cause cardiac collapse early ("fast in, slow out" of Na channels), which is why it is the most feared.

Peripheral nerve blocks (USG-guided is now standard)

• Brachial plexus: interscalene (shoulder; risk phrenic palsy), supraclavicular ("spinal of the arm"; risk pneumothorax), infraclavicular, axillary.
• Bier's block (IVRA): double tourniquet + lignocaine (NOT bupivacaine — cardiotoxic).
• TAP block, fascia iliaca, adductor canal — increasingly tested with multimodal analgesia.

---

Group 3: Airway Management

The airway group is image-heavy and algorithm-heavy. Examiners test prediction of difficult airway, devices, and the difficult-airway/failed-intubation drill.

Predicting the difficult airway

• Mallampati classification (mouth open, tongue out, sitting):
  • Class I — soft palate, uvula, fauces, pillars
  • Class II — soft palate, uvula, fauces
  • Class III — soft palate + base of uvula
  • Class IV — only hard palate
  • III & IV predict difficult intubation.
• LEMON (Look, Evaluate 3-3-2, Mallampati, Obstruction, Neck mobility).
• 3-3-2 rule: 3 fingers mouth opening, 3 fingers chin–hyoid, 2 fingers hyoid–thyroid notch.
• Thyromental distance < 6 cm (or < 3 finger-breadths) predicts difficulty.
• Cormack–Lehane grading (laryngoscopic view): I (full glottis) → IV (no glottis/epiglottis); grades III–IV are difficult.

Devices and tubes

• ETT internal diameter (uncuffed, paediatric): (Age/4) + 4 mm; length (oral) = (Age/2) + 12 cm. Cuffed: (Age/4) + 3.5.
• Adult ETT: male ~8.0–9.0 mm, female ~7.0–8.0 mm.
• Laryngoscope blades: Macintosh (curved) sits in vallecula, lifts epiglottis indirectly; Miller (straight) lifts epiglottis directly — preferred in infants (large floppy epiglottis).
• Supraglottic airway: LMA — used when intubation not needed; does NOT protect against aspiration (avoid in full stomach). Proseal/i-gel allow gastric drainage.
• Rapid Sequence Induction (RSI): for full stomach/aspiration risk — preoxygenation, cricoid pressure (Sellick's manoeuvre), fast-acting induction + succinylcholine (or rocuronium), no bag-mask ventilation. Sugammadex now allows rocuronium-based RSI reversal.

Airway emergencies

• Laryngospasm: commonest in stage 2/light anaesthesia, in children, after extubation. Treat: remove stimulus, 100% O₂ + positive pressure, deepen anaesthesia/propofol, succinylcholine if refractory. Larson's point pressure can help.
• Can't intubate, can't oxygenate (CICO): the end of the difficult-airway algorithm → emergency front-of-neck access (cricothyroidotomy).
• Capnography (EtCO₂): confirms tube in trachea (gold standard for placement) and is the earliest monitor of MH (rising EtCO₂), malposition, disconnection, embolism (sudden drop).

Capnography pattern	Meaning
Absent trace after intubation	Oesophageal intubation
Sudden drop to zero	Disconnection, obstruction, cardiac arrest
Gradual fall	Hyperventilation, ↓CO, hypothermia, embolism
Rising baseline	Rebreathing (exhausted soda lime / faulty valve)
"Shark fin" (sloped)	Bronchospasm/obstructive (COPD/asthma)

---

Group 4: Pharmacology

The pharmacology group is where Anaesthesia overlaps most with the Pharmacology subject — muscle relaxants, reversal agents, and agent kinetics.

Neuromuscular blocking agents

Depolarising — Succinylcholine (suxamethonium):

• Mechanism: ACh-receptor agonist → persistent depolarisation → flaccid paralysis after initial fasciculations.
• Fastest onset, shortest duration (~5 min); metabolised by plasma (pseudo)cholinesterase.
• Prolonged apnoea with atypical/deficient pseudocholinesterase — assessed by dibucaine number (normal ~80; low ~20 in homozygous atypical).
• Adverse effects: hyperkalaemia (dangerous in burns, crush injury, spinal cord injury, neuromuscular disease — avoid), myalgia, raised ICP/IOP/intragastric pressure, bradycardia (esp. repeat doses in children), trigger for MH, masseter spasm.

Non-depolarising (competitive antagonists):

Drug	Duration	Elimination	Key fact
Atracurium / Cisatracurium	Intermediate	Hofmann elimination (organ-independent)	Best in hepatic/renal failure; laudanosine metabolite
Rocuronium	Intermediate	Hepatic	Fast onset (RSI alternative); reversed by sugammadex
Vecuronium	Intermediate	Hepatic/renal	Cardiostable
Pancuronium	Long	Renal	Vagolytic → tachycardia
Mivacurium	Short	Plasma cholinesterase	—

• Reversal: Neostigmine (anticholinesterase) + glycopyrrolate/atropine (to block muscarinic effects). Sugammadex selectively encapsulates rocuronium/vecuronium — reverses even deep block, no anticholinergic needed.
• Monitoring: Train-of-four (TOF) — ratio >0.9 indicates adequate recovery before extubation.

Opioids in anaesthesia

• Remifentanil: ultra-short, metabolised by plasma/tissue esterases, context-sensitive half-time stays constant regardless of infusion duration — ideal for titratable analgesia.
• Fentanyl: 100× morphine potency; rapid; histamine-sparing.
• Morphine: histamine release, active metabolite (M6G) accumulates in renal failure.
• Reversal: Naloxone (pure antagonist). Watch for renarcotisation (short t½).

Antiemetics / adjuncts

• PONV prophylaxis: ondansetron (5-HT₃), dexamethasone, droperidol; propofol is antiemetic. Risk factors (Apfel score): female, non-smoker, history of PONV/motion sickness, postoperative opioids.

---

Group 5: Critical Care

This group bridges into Medicine and Pulmonology. Examiners focus on shock, ventilation, ARDS, sepsis bundles, and CPR/ACLS.

Mechanical ventilation & ARDS

• ARDS — Berlin definition: acute onset (≤1 week), bilateral infiltrates, not fully explained by cardiac failure/overload, and PaO₂/FiO₂ ratio:
  • Mild 200–300, Moderate 100–200, Severe <100 (on PEEP ≥5).
• Lung-protective ventilation (ARDSNet): tidal volume 6 mL/kg predicted body weight, plateau pressure < 30 cmH₂O, permissive hypercapnia, adequate PEEP. Prone positioning improves survival in severe ARDS.
• PEEP recruits alveoli, improves oxygenation; excessive PEEP → barotrauma, ↓venous return.

Shock and haemodynamics

Shock type	CVP/PCWP	Cardiac output	SVR	Example
Hypovolaemic	↓	↓	↑	Haemorrhage
Cardiogenic	↑	↓	↑	MI
Distributive (septic)	↓/N	↑ (early)	↓	Sepsis, anaphylaxis
Obstructive	↑	↓	↑	Tamponade, PE, tension pneumothorax

• Septic shock (Surviving Sepsis): early broad-spectrum antibiotics within 1 hour, balanced crystalloids 30 mL/kg, noradrenaline = first-line vasopressor, target MAP ≥ 65 mmHg, lactate clearance.
• Anaphylaxis (under anaesthesia, often muscle relaxants/latex/antibiotics): adrenaline IM 0.5 mg (1:1000) first-line; IV titrated in arrest.

CPR / ACLS (current guideline emphasis)

• High-quality CPR: rate 100–120/min, depth 5–6 cm, full recoil, minimise interruptions, compression:ventilation 30:2 (single rescuer adult).
• Shockable rhythms: VF / pulseless VT → defibrillate → adrenaline 1 mg every 3–5 min → amiodarone 300 mg after 3rd shock.
• Non-shockable: PEA / asystole → CPR + adrenaline, no shock; treat reversible causes (5 Hs & 5 Ts: Hypoxia, Hypovolaemia, Hydrogen ion/acidosis, Hypo/hyperkalaemia, Hypothermia; Tension pneumothorax, Tamponade, Toxins, Thrombosis-coronary, Thrombosis-pulmonary).

Monitoring & fluids

• Standard ASA monitoring: oxygenation (SpO₂), ventilation (capnography), circulation (ECG, NIBP), temperature.
• Maintenance fluids (4-2-1 rule): 4 mL/kg first 10 kg + 2 mL/kg next 10 kg + 1 mL/kg thereafter, per hour.

---

Group 6: Pain Medicine

The smallest group but reliably yields 1–2 questions, often on the WHO ladder, multimodal analgesia, and chronic-pain pharmacology.

Acute and post-operative pain

• WHO analgesic ladder (originally cancer pain):
  1. Non-opioid (paracetamol/NSAID) ± adjuvant
  2. Weak opioid (tramadol/codeine) + non-opioid ± adjuvant
  3. Strong opioid (morphine) + non-opioid ± adjuvant
• Multimodal analgesia: combine paracetamol + NSAID + regional/local + opioid-sparing adjuncts (dexmedetomidine, ketamine, gabapentinoids) to minimise opioid load — current best practice and ERAS cornerstone.
• PCA (patient-controlled analgesia): IV opioid with lockout interval; safe, improves satisfaction.

Chronic and neuropathic pain

• Neuropathic pain first-line: gabapentin/pregabalin, amitriptyline (TCA), duloxetine/SNRI. NSAIDs and pure opioids are relatively ineffective.
• Trigeminal neuralgia: carbamazepine is drug of choice.
• Complex regional pain syndrome (CRPS): physiotherapy + multimodal; sympathetic blocks.
• Cancer pain breakthrough: immediate-release opioid; consider coeliac plexus block for pancreatic/upper-abdominal cancer pain.

---

Cross-Subject Integration Points

Anaesthesia is a connector subject. Many of its highest-yield facts are equally testable from other subjects:

Overlap	Concept
Pharmacology	Muscle relaxants, LA Na-channel block, opioid pharmacokinetics, context-sensitive half-time
Physiology	Oxygen dissociation curve, CO₂ transport, autonomic control of BP/HR during spinal
Medicine / Pulmonology	ARDS, mechanical ventilation, sepsis bundles, ABG interpretation
Biochemistry	Pseudocholinesterase deficiency, porphyria (thiopentone), RYR1/calcium handling in MH
Surgery / ERAS	Pre-op fasting, multimodal analgesia, fluid management, prehabilitation
Paediatrics	Straight blade, cord ends at L3, ETT size formula, atropine before succinylcholine
Obstetrics	Labour epidural, aortocaval compression (left lateral tilt), failed obstetric intubation, MAC ↓ in pregnancy
Forensic / Toxicology	LA toxicity, opioid overdose & naloxone, CO poisoning and oximetry pitfalls

Pulse oximetry pitfalls (loved by INI-CET): carboxyhaemoglobin falsely normal/high SpO₂; methaemoglobinaemia reads ~85% regardless of true saturation; nail polish, motion, and poor perfusion give errors; it does not detect hypoventilation if FiO₂ is high.

---

Recent Update Themes & Guideline Shifts

Examiners increasingly draw from updated guidelines. Be current on:

• Sugammadex as a reversal agent — now standard for rocuronium/vecuronium; reverses deep block, enables rocuronium RSI. Increasingly the "best reversal" answer.
• Surviving Sepsis Campaign: antibiotics within 1 hour, noradrenaline first-line, balanced crystalloids preferred over normal saline, vasopressin/adrenaline as add-ons.
• Difficult Airway Society (DAS) algorithms and emphasis on videolaryngoscopy as first-line in many settings; front-of-neck access (scalpel-bougie cricothyroidotomy) for CICO.
• ERAS protocols: shortened fasting with carbohydrate loading, opioid-sparing multimodal analgesia, goal-directed fluid therapy, early mobilisation.
• Lipid emulsion (Intralipid) for LAST — now a fixed algorithmic answer; know the exact dosing.
• Updated CPR (AHA): continued emphasis on high-quality compressions, capnography to guide CPR quality and confirm ROSC, de-emphasis of routine atropine in PEA/asystole.
• Lung-protective ventilation universal (not just ARDS): low tidal volumes intra-operatively.
• Balanced salt solutions over 0.9% saline to avoid hyperchloraemic acidosis (SMART/PLUS trials).

---

Study Roadmap

Phase 1 — Build the skeleton (Week 1–2)

• Read a concise source (Ajay Yadav / Marino-lite high-yield notes). Cover one group at a time in the order: Pharmacology → General → Airway → Regional → Critical Care → Pain.
• Make a one-page numbers sheet: MAC values, blood:gas coefficients, LA max doses, Intralipid dosing, ETT formulae, ASA grades, NPO rules, TOF target.

Phase 2 — Drill MCQs (Week 3–4)

• Do topic-wise MCQs immediately after each group. Anaesthesia questions are repetitive — pattern recognition is everything.
• Maintain an error log: every wrong MCQ → write the corrected one-liner.

Phase 3 — Integration (ongoing)

• Co-revise with Pharmacology (relaxants, LAs) and Medicine (ventilation, sepsis, ACLS). Don't silo.

Last-week revision strategy

1. Read only the numbers sheet + error log — no new material.
2. Re-look at MAC table, LA toxicity algorithm, MH management, capnography traces, NMB drugs, ASA & NPO. These six clusters cover the majority of marks.
3. Revise image stems: laryngoscope blades, capnograph patterns, airway devices.
4. Do one timed mixed test to keep retrieval sharp.
5. Sleep on the high-yield one-liners below the night before.

---

High-Yield Mnemonics

• MAC increases: "HER CHIA" — Hyperthermia, Ethanol chronic, Red hair, Cocaine/amphetamine acute, Hypernatraemia, Infants, Age young.
• Amide LAs have an "i" before -caine: lidocaine, bupivacaine, ropivacaine (esters do not: procaine, cocaine, tetracaine).
• Succinylcholine cautions — "BUMS": Burns, Uraemia/renal, Muscular dystrophy/neuromuscular, Spinal cord injury (hyperkalaemia risk).
• MH triggers: all volatiles + sux; dantrolene to the rescue.
• 5 Hs & 5 Ts for reversible arrest causes (see Critical Care).
• Hofmann elimination = atracurium → organ-independent → use in liver/kidney failure.

---

Rapid-Fire One-Liners

1. Earliest sign of malignant hyperthermia → rising end-tidal CO₂; treatment → dantrolene.
2. Drug of choice for inhalational induction → sevoflurane (non-irritant).
3. Fastest-acting inhalational agent → desflurane (lowest blood:gas coefficient 0.42).
4. Highest MAC / lowest potency agent → nitrous oxide (104).
5. Treatment of local anaesthetic systemic toxicity (LAST) → 20% Intralipid 1.5 mL/kg bolus, then 0.25 mL/kg/min.
6. Most cardiotoxic local anaesthetic → bupivacaine; only vasoconstrictor LA → cocaine.
7. Muscle relaxant of choice in hepatic + renal failure → cis/atracurium (Hofmann elimination).
8. Induction agent of choice in shock / asthma → ketamine; most cardiostable → etomidate (but causes adrenal suppression).
9. Adult spinal cord ends at L1 (children L3); safe spinal puncture at L3–L4 / L4–L5.
10. First-line vasopressor in septic shock → noradrenaline; target MAP ≥ 65 mmHg.
11. ARDS PaO₂/FiO₂: mild 200–300, moderate 100–200, severe <100; ventilate at 6 mL/kg Vt, Pplat <30.
12. Adequate neuromuscular recovery → train-of-four ratio > 0.9; reversal of rocuronium → sugammadex.
13. Methaemoglobinaemia → pulse oximeter stuck at ~85%; carboxyhaemoglobin falsely normal/high.
14. Avoid thiopentone in → acute intermittent porphyria; avoid succinylcholine in → burns/spinal injury (hyperkalaemia).

---

This mother page is the anchor for the Anaesthesia module set. Pair it with the topic-wise MCQ banks and your personal numbers sheet for maximum retention.