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Pulmonary Hypertension — Classification, Pathophysiology & Perioperative Management Define pulmonary hypertension and describe its WHO classification [2]. Explain the pathophysiology of right ventricular failure in pulmonary hypertension [4]. Outline the specific anaesthetic goals and management for a patient with severe pulmonary hypertension presenting for non-cardiac surgery [4]."

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" Q76 - Pulmonary Hypertension — Classification, Pathophysiology & Perioperative Management

Q76 · Paper II · 10 MARKS · Long Answer

Pulmonary Hypertension — Classification, Pathophysiology & Perioperative Management

Question: Define pulmonary hypertension and describe its WHO classification [2]. Explain the pathophysiology of right ventricular failure in pulmonary hypertension [4]. Outline the specific anaesthetic goals and management for a patient with severe pulmonary hypertension presenting for non-cardiac surgery [4].

Core ConceptPulmonary hypertension (PH) — mPAP ≥20 mmHg at rest — carries perioperative mortality of 7–24% for major non-cardiac surgery. The right ventricle is catastrophically vulnerable to acute afterload increases. Understanding RV physiology and the triggers of RV failure is key to safe anaesthetic management.

A. Definition & WHO Classification2 marks

Definition (ESC/ERS 2022): mPAP ≥20 mmHg at right heart catheterisation; PAH (Group 1) additionally requires PVR >2 Wood units AND PAWP ≤15 mmHg (pre-capillary).

WHO Group	Mechanism	Examples
Group 1 – PAH	Smooth muscle hypertrophy + intimal proliferation + in-situ thrombosis → ↑PVR (pre-capillary)	Idiopathic PAH; scleroderma (highest risk); Eisenmenger; drug-induced
Group 2 – Left heart disease	↑LA pressure → pulmonary venous hypertension (post-capillary)	LV failure; mitral stenosis; constrictive pericarditis
Group 3 – Lung disease/hypoxia	Hypoxic pulmonary vasoconstriction → chronic ↑PVR	COPD; ILD; OSA; high-altitude PH
Group 4 – CTEPH	Unresolved PE → organised thrombus → mechanical obstruction	Complicates 2–4% of acute PE; surgically curable
Group 5 – Multifactorial	Heterogeneous	Haemolytic anaemia, sarcoidosis, fibrosing mediastinitis

B. Pathophysiology of RV Failure4 marks

Normal RV: thin-walled, low pressure (~25 mmHg), high compliance chamber; tolerates volume but not sudden afterload.
Chronic adaptation: ↑PVR → concentric RVH → ↓compliance → ↑RVEDP → systemic venous hypertension.
RV–PA uncoupling: RV Emax cannot match rising Ea → RV dilates → ↑wall stress → ↑O₂ demand → subendocardial ischaemia.
Coronary perfusion – the critical vulnerability: once RV systolic pressure ≥ aortic diastolic pressure, RV is perfused only in diastole (like the LV) → dependent on DBP.
Ventricular interdependence (death spiral): ↑PVR → RV dilates → D-shaped septum → ↓LV filling → ↓CO → ↓DBP → ↓RV perfusion → RV ischaemia → further ↓CO.

Key Anaesthetic Goals – ""Prevent the RV Failure Death Spiral""Avoid: ↑PVR (hypoxia, hypercapnia, acidosis, hypothermia, pain) · Avoid ↓systemic BP (maintain RV coronary perfusion) · Avoid ↓HR · Maintain RV preload without overload · Optimise RV contractility.

C. Anaesthetic Goals & Management4 marks

Goal	Intervention
↓PVR	FiO₂ ≥0.6, normoventilation (PaCO₂ 35–40), warming, analgesia, PEEP ≤5, avoid N₂O, continue PH therapy
Pulmonary vasodilators	Inhaled NO 10–40 ppm; inhaled iloprost/epoprostenol; IV sildenafil; milrinone (inodilator)
Maintain systemic BP	Vasopressin or phenylephrine preferred (↑SVR w/o ↑PVR); avoid vasodilators/high spinal
RV contractility	Dobutamine, milrinone, adrenaline, levosimendan; avoid myocardial depressants (propofol bolus, ≥1 MAC volatile)
Induction	Slow titrated GA (etomidate + ketamine + opioid); avoid high spinal/epidural; arterial line + CVC pre-induction; TOE intraoperatively

Examiner's PearlPH definition: mPAP ≥20 mmHg. PAH (Group 1): pre-capillary, PVR >2 WU, PAWP ≤15. RV death spiral: ↑PVR → RV dilates → D-septum → ↓LV filling → ↓CO → ↓DBP → RV ischaemia → death. Avoid hypoxia/hypercapnia/N₂O/↑PEEP/vasodilation. Vasopressor of choice: vasopressin. Pulmonary vasodilator: inhaled NO.

References: Simonneau G et al. Eur Respir J 2019;53:1801913. Price LC et al. Eur Respir Rev 2010;19:35-42. ESC/ERS PH Guidelines 2022. Miller's Anaesthesia, 9th Ed.

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Cardiac Implantable Electronic Devices — Pacemakers, ICDs & EMI Write short notes on: (a) Classification of pacemakers (NBG code) and indications for perioperative pacing [3] (b) Electromagnetic interference (EMI) from diathermy – mechanisms and prevention [4] (c) Perioperative management of implantable cardioverter-defibrillators (ICDs) [3].

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" Q77 - Cardiac Implantable Electronic Devices — Pacemakers, ICDs & EMI

Q77 · Paper II · 10 MARKS · Short Notes

Cardiac Implantable Electronic Devices — Pacemakers, ICDs & EMI

Question: Write short notes on: (a) Classification of pacemakers (NBG code) and indications for perioperative pacing [3] (b) Electromagnetic interference (EMI) from diathermy – mechanisms and prevention [4] (c) Perioperative management of implantable cardioverter-defibrillators (ICDs) [3].

Core ConceptOver 750,000 pacemakers and 250,000 ICDs are implanted annually. These devices can be profoundly affected by surgical diathermy. A structured approach involving the implanting cardiologist, device interrogation, and reprogramming is mandatory for safe surgery.

A. NBG Code & Perioperative Pacing3 marks

NBG 5-letter code: I=Chamber paced, II=Chamber sensed, III=Response to sensing, IV=Rate modulation, V=Multisite.

Mode	Meaning	Use
VVI	Paces/senses ventricle, inhibited by native beat	Chronic AF with bradycardia
DDD	Paces & senses both chambers (most physiological)	SND + AV block; commonest modern PM
DOO/VOO	Fixed-rate, no sensing (asynchronous)	Used intraoperatively when EMI risk high; R-on-T risk
DDI	Paces/senses both, inhibited only	Prevents rate-adaptive tracking in AF

Temporary pacing indications: complete heart block, symptomatic bradycardia refractory to atropine, new bifascicular block + prolonged PR, post-cardiac surgery bradyarrhythmia.

B. EMI from Diathermy4 marks

Mechanism: diathermy generates high-frequency current (0.3–3 MHz) → CIED leads act as antennae → device misreads EMI as intrinsic activity → inhibition (asystole if PM-dependent) or ICD misreads as VF → inappropriate shock.
Risk factors: monopolar diathermy (highest risk), proximity <15 cm, pacemaker dependence.
Prevention: use bipolar diathermy where possible; short bursts <1 s at lowest power; reprogram to DOO/VOO if monopolar within 15 cm or PM-dependent; alternatives – ultrasonic scalpel/LigaSure; external pacing/defib pads available; re-interrogate post-op.

C. Perioperative ICD Management3 marks

ICDs risk inappropriate shocks (up to 40 J) if EMI misread as VF → pain, myocardial damage, R-on-T VF.
Pre-op: cardiology consult + device interrogation; suspend shock therapies before monopolar diathermy (reprogramming preferred; magnet effect is manufacturer-dependent – do not assume universal).
Continue pacing function if PM-dependent; attach external defibrillator pads (AP position) throughout.
Post-op: re-enable ICD therapies before leaving monitored area.
Emergency (repeated shocks): stop diathermy, apply magnet, confirm rhythm, external defibrillation if true VF.

Examiner's PearlNBG: Chamber Paced–Sensed–Response–Rate–Multisite. DOO/VOO = asynchronous, EMI-safe but R-on-T risk. Monopolar diathermy → PM inhibition (asystole) or ICD inappropriate shock. Reprogram to DOO/VOO + suspend ICD therapies if monopolar within 15 cm. Magnet suspends ICD therapy – manufacturer dependent. Always have external pacing/defib ready.

References: Crossley GH et al. Heart Rhythm 2011;8:1114-1154. BHRS/BSIR/BCS Advisory Statement 2015. Miller's Anaesthesia, 9th Ed, Ch 35.

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Surgical Positioning — Physiological Effects, Nerve Injuries & Complications Write short notes on: (a) Physiological effects of the supine, prone, and lateral decubitus positions on cardiovascular and respiratory function [4] (b) Nerve injuries associated with surgical positioning – mechanisms, at-risk nerves and prevention [4] (c) Specific complications of the prone and lithotomy positions [2].

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" Q78 - Surgical Positioning — Physiological Effects, Nerve Injuries & Complications

Q78 · Paper II · 10 MARKS · Short Notes

Surgical Positioning — Physiological Effects, Nerve Injuries & Complications

Question: Write short notes on: (a) Physiological effects of the supine, prone, and lateral decubitus positions on cardiovascular and respiratory function [4] (b) Nerve injuries associated with surgical positioning – mechanisms, at-risk nerves and prevention [4] (c) Specific complications of the prone and lithotomy positions [2].

Core ConceptPositioning is a shared responsibility between anaesthetist, surgeon and scrub team. Position-related injuries are the second most common cause of claims against anaesthetists (after awareness). Nerve injuries may not manifest until the patient regains consciousness.

A. Physiological Effects of Positions4 marks

Position	CVS Effects	Respiratory Effects
Supine	↑venous return vs upright; aortocaval compression in pregnancy >20 wk → supine hypotension syndrome	FRC ↓25%
Prone	↓venous return if abdomen unsupported; use prone frame to free abdomen; cardiac arrest – CPR near-impossible	FRC ↑; V/Q matching improves (ARDS proning); airway oedema in prolonged cases
Lateral decubitus	Dependent lung ↑perfusion; non-dependent ↑ventilation → V/Q mismatch (worse with OLV)	Compounded by thoracotomy mediastinal shift
Trendelenburg	↑venous return/CO; ↑ICP transiently; ↑intragastric pressure	FRC ↓; steep version → ocular hypertension/AION risk

B. Position-Related Nerve Injuries4 marks

Nerve	At-risk Position	Presentation/Prevention
Ulnar (commonest, 28%)	Elbow flexed on table edge	Ring/little finger paraesthesia; pad elbow, avoid flexion >90°
Brachial plexus	Arm abducted >90° + head turned; sternal retraction	Whole-arm weakness; axillary roll CAUDAL to axilla, limit abduction ≤90°
Common peroneal	Lithotomy stirrups at fibular head	Foot drop; pad fibular head
Radial	Arm hanging over table edge	Wrist drop (""Saturday night palsy""); support arm
Femoral	Lithotomy with excessive hip flexion; retractors	↓knee extension; limit hip flexion <90°

C. Prone & Lithotomy Complications2 marks

Prone: PION/CRAO (visual loss – risk >4h, hypotension, blood loss); facial/airway oedema – cuff-leak test before extubation; pressure areas (breasts, genitalia, knees).
Lithotomy: lower-limb compartment syndrome (>4h elevation); peroneal nerve injury; rapid leg-lowering → sudden ↑preload → pulmonary oedema risk in poor LV function.

Examiner's PearlUlnar nerve = commonest claim (28%) – pad elbow, avoid flexion >90°. Brachial plexus: axillary roll CAUDAL to axilla. Prone: PION/CRAO – padded eyes, cuff-leak before extubation. Lithotomy >4h → compartment syndrome risk → fasciotomy.

References: Welch MB et al. Anesthesiology 2009;111:490-497. Warner MA et al. Anesthesiology 1994;81:1332-1340. Miller's Anaesthesia, 9th Ed, Ch 41.

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Vascular Surgery — Open AAA vs EVAR, Cross-Clamping & Spinal Cord Protection Compare open AAA repair with EVAR – patient selection, physiological insults and anaesthetic implications [4]. Describe the haemodynamic consequences of aortic cross-clamping and unclamping [3]. Outline strategies for spinal cord protection during thoracoabdominal aortic surgery [3].

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" Q79 - Vascular Surgery — Open AAA vs EVAR, Cross-Clamping & Spinal Cord Protection

Q79 · Paper II · 10 MARKS · Long Answer

Vascular Surgery — Open AAA vs EVAR, Cross-Clamping & Spinal Cord Protection

Question: Compare open AAA repair with EVAR – patient selection, physiological insults and anaesthetic implications [4]. Describe the haemodynamic consequences of aortic cross-clamping and unclamping [3]. Outline strategies for spinal cord protection during thoracoabdominal aortic surgery [3].

Core ConceptAortic aneurysm repair is the highest-risk elective surgery in anaesthesia – open repair carries 3–5% 30-day mortality (40–50% for rupture). EVAR offers lower 30-day mortality but requires lifelong surveillance.

A. Open AAA vs EVAR4 marks

Feature	Open Repair	EVAR
Technique	GA + thoracic epidural, laparotomy, aortic cross-clamp	GA/regional/local; fluoroscopy; usually no cross-clamp
Insult	Major – clamp instability, blood loss, 3–6h duration	Minimal – contrast nephropathy, endoleak risk, radiation
30-day mortality	3–5% elective; 40–50% rupture	1–2% elective; no long-term survival benefit (EVAR trial 1)
Limitations	High-risk cardiorespiratory disease	Requires suitable anatomy (60–70% eligible)

B. Cross-Clamping & Unclamping3 marks

Clamping (""afterload crisis""): sudden ↑↑SVR/MAP above clamp; ↑LV afterload → risk of pulmonary oedema; ↓flow below clamp (kidney, cord, gut ischaemia). Manage: vasodilators (GTN/SNP) + TOE guidance; mannitol before clamping.
Unclamping: dramatic ↓↓SVR/MAP from ischaemic vasodilated bed + metabolite washout (lactate, K⁺, CO₂) → ""declamping hypotension"". Manage: slow release over 3–5 min, volume load pre-unclamp, vasopressors ready, treat hyperkalaemia/acidosis.

C. Spinal Cord Protection (TAAA)3 marks

Artery of Adamkiewicz (T9–T12) is dominant anterior spinal artery feeder – ligated segmental arteries risk anterior cord syndrome; incidence 2–17% (Crawford II highest, 15–40%).
CSF drainage: lumbar drain, target SCPP ≥70 mmHg (SCPP = MAP − CSF pressure).
Mild hypothermia: systemic or epidural cord cooling ↓metabolic rate.
MAP ≥80–90 mmHg throughout and 48h post-op.
Segmental artery reimplantation where feasible.
Neuromonitoring: MEPs (most sensitive for anterior cord) – requires TIVA, no paralysis.

Examiner's PearlEVAR: ↓30-day mortality but no long-term survival benefit (EVAR trial 1); lifelong surveillance needed. Cross-clamp = afterload crisis (vasodilators + TOE); unclamp = declamping hypotension (slow release + volume + vasopressors). Spinal cord: CSF drain (SCPP ≥70) + MAP ≥80–90 + hypothermia + MEP monitoring + TIVA. Artery of Adamkiewicz T9–T12.

References: EVAR trial participants. Lancet 2005;365:2179-2186. Acher CW. Semin Vasc Surg 2000;13:265-272. Miller's Anaesthesia, 9th Ed, Ch 72.

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Anaesthesia for Neurosurgery — Craniotomy, Awake Craniotomy & IONM Describe the anaesthetic management of craniotomy for supratentorial tumour resection [4]. Explain the conduct of awake craniotomy including asleep-awake-asleep technique [3]. Outline the principles of intraoperative neurophysiological monitoring (IONM) [3].

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" Q80 - Anaesthesia for Neurosurgery — Craniotomy, Awake Craniotomy & IONM

Q80 · Paper II · 10 MARKS · Long Answer

Anaesthesia for Neurosurgery — Craniotomy, Awake Craniotomy & IONM

Question: Describe the anaesthetic management of craniotomy for supratentorial tumour resection [4]. Explain the conduct of awake craniotomy including asleep-awake-asleep technique [3]. Outline the principles of intraoperative neurophysiological monitoring (IONM) [3].

Core ConceptCraniotomy for brain tumour requires simultaneous management of raised ICP, haemodynamic stability, brain relaxation, and rapid emergence for neurological assessment. Awake craniotomy enables resection near eloquent cortex with real-time mapping.

A. Craniotomy — Anaesthetic Management4 marks

Pre-op: assess ICP signs, continue anticonvulsants, dexamethasone 8–16 mg/day, review imaging (eloquence, midline shift).
Monitoring: invasive arterial line, CVC, urinary catheter, BIS/entropy, NMB monitoring.
Induction: smooth – propofol + remifentanil TCI; avoid coughing/straining; scalp block/local before pin insertion.
Maintenance: TIVA preferred (preserves autoregulation, ↓ICP, ↓PONV, preserves MEPs); mannitol 0.5–1 g/kg for brain relaxation; mild hyperventilation (PaCO₂ 32–35, short term only); head-up 15–30°.
Emergence: smooth – avoid coughing/bucking (↑ICP/haemorrhage risk); lidocaine 1.5 mg/kg before extubation; immediate neuro assessment.

B. Awake Craniotomy — Asleep-Awake-Asleep3 marks

Indication: tumour in/near eloquent cortex (motor, speech, sensory areas) – enables real-time cortical mapping.
Phase 1 (Asleep): TIVA + LMA/nasal airway; scalp block (6 nerves) + pin-site infiltration.
Phase 2 (Awake): wean TIVA; nasal airway + O₂ ± dexmedetomidine (sedation without respiratory depression); cortical mapping + resection with patient testing.
Phase 3 (Asleep): restart TIVA for closure.
Complications: airway loss (seizure), intraoperative seizure (cold saline terminates), patient distress, PONV.

C. Intraoperative Neurophysiological Monitoring3 marks

Modality	Monitors	Anaesthetic Implication
MEPs	Anterior/motor corticospinal tracts	TIVA mandatory – volatile >0.5 MAC suppresses; NMB must be 0
SSEPs	Posterior/sensory cord	More volatile-tolerant (≤0.5 MAC possible)
EEG	Cortical activity/ischaemia	Used in carotid endarterectomy for shunt decision
EMG	Cranial nerve/nerve root	NMB abolishes signal – avoid or monitor TOF carefully

Examiner's PearlBrain relaxation: mannitol 0.5–1 g/kg + short hyperventilation (PaCO₂ 32–35) + head-up + TIVA. Awake craniotomy: scalp block (6 nerves) + dexmedetomidine. IONM: TIVA mandatory for MEPs (volatile >0.5 MAC suppresses); NMBs abolish EMG/MEPs. MEP alert: ≥50% amplitude ↓ or ≥10% latency ↑.

References: Berger MS et al. Neurosurgery 2005;56:232-240. Szelenyi A et al. Br J Anaesth 2016;116:i25-38. Miller's Anaesthesia, 9th Ed, Ch 57.

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Obstetric Emergencies — Category 1 CS, Failed Intubation & Cord Prolapse Outline the decision-to-delivery interval (DDI) targets for caesarean section categories and the anaesthetic strategy for Cat 1 CS [3]. Describe the management of failed intubation in the pregnant patient [4]. Discuss the management of cord prolapse as an obstetric emergency [3].

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" Q81 - Obstetric Emergencies — Category 1 CS, Failed Intubation & Cord Prolapse

Q81 · Paper II · 10 MARKS · Long Answer

Obstetric Emergencies — Category 1 CS, Failed Intubation & Cord Prolapse

Question: Outline the decision-to-delivery interval (DDI) targets for caesarean section categories and the anaesthetic strategy for Cat 1 CS [3]. Describe the management of failed intubation in the pregnant patient [4]. Discuss the management of cord prolapse as an obstetric emergency [3].

Core ConceptObstetric anaesthesia manages two patients simultaneously. Maternal airway risk is 8× higher than non-pregnant (1:390 vs 1:2,230). Failed obstetric intubation remains a recurring cause of maternal death (NAP4, MBRRACE).

A. CS Categories & Cat 1 Anaesthesia3 marks

Category	Target DDI	Preferred Anaesthesia
1 – Immediate threat	30 min (<15 min if acute compromise)	GA (fastest) or rapid spinal (<5 min) or epidural top-up
2 – Compromise, not life-threatening	75 min	Spinal preferred
3 – No compromise, early delivery	Agreed time	Spinal preferred
4 – Elective	Scheduled	Spinal (overwhelmingly preferred)

Cat 1 GA (RSI): pre-oxygenation, left lateral tilt 15°, thiopentone/propofol + suxamethonium, cricoid pressure until tube confirmed, FiO₂ 0.5 + volatile 1 MAC, oxytocin infusion (no bolus). Awake extubation only.

B. Failed Intubation (DAS Obstetric 2015)4 marks

Call for help immediately; after one failed optimised attempt → declare ""failed intubation"".
Maintain oxygenation: facemask/CPAP, 2-person BMV, 2nd-generation LMA (ProSeal/Supreme) if BMV fails.
Critical decision: wake the patient up (if foetal condition allows) OR proceed with LMA anaesthesia (if immediate risk unacceptable – cord prolapse, severe bradycardia).
If LMA used: maintain cricoid pressure, limit tidal volume, surgeon ready for rapid delivery.
CICO: scalpel-bougie cricothyrotomy immediately – leading cause of anaesthesia-related maternal death (NAP4).
Extubation is also high-risk – extubate only when fully awake.

C. Cord Prolapse Management3 marks

Umbilical cord descends alongside/ahead of presenting part after membrane rupture → compression → foetal bradycardia/asphyxia.
Immediate: manual elevation of presenting part (maintained until delivery); bladder filling 500–750 mL saline; knee-chest/Trendelenburg position; do NOT apply traction to exposed cord.
Definitive: emergency Cat 1 CS – DDI <30 min (<15 min if severe bradycardia); epidural top-up fastest if in situ; rapid spinal if <5 min setup; GA if spinal too slow or foetal condition critical.

Examiner's PearlCat 1 DDI: 30 min (<15 min if cord prolapse/acute bradycardia). Failed intubation: DECLARE → maintain oxygenation (2nd-gen LMA) → wake vs proceed decision → CICO = scalpel-bougie immediately. Cord prolapse: manual elevation + bladder filling + Trendelenburg → Cat 1 CS; epidural top-up = fastest.

References: Mushambi MC et al. Anaesthesia 2015;70:1286-1306. MBRRACE-UK 2023. NICE NG192 (2021).

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Paediatric Pain and Regional Anaesthesia — Caudal Block, Pain Scales & Opioid-Free Strategy Describe the anatomy and technique of the caudal block including drugs and dosing [4]. Outline validated pain assessment tools for preverbal children [3]. Describe multimodal opioid-free analgesia strategies for paediatric day surgery [3].

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" Q82 - Paediatric Pain and Regional Anaesthesia — Caudal Block, Pain Scales & Opioid-Free Strategy

Q82 · Paper II · 10 MARKS · Long Answer

Paediatric Pain and Regional Anaesthesia — Caudal Block, Pain Scales & Opioid-Free Strategy

Question: Describe the anatomy and technique of the caudal block including drugs and dosing [4]. Outline validated pain assessment tools for preverbal children [3]. Describe multimodal opioid-free analgesia strategies for paediatric day surgery [3].

Core ConceptNeonates and infants have fully developed nociceptive pathways from 28 weeks gestation and may be MORE sensitive to pain than adults. The caudal block is the commonest paediatric regional technique, providing excellent infraumbilical analgesia.

A. Caudal Block — Anatomy, Technique, Dosing4 marks

Anatomy: sacral hiatus (failure of S4–S5 laminae fusion), bounded by sacral cornua, covered by sacrococcygeal membrane. Dural sac extends to S3–S4 in infants (vs S2 adults) – ↑ dural puncture risk.
Technique: under GA, 21G needle at 45° through membrane (""give"" felt), angle to 20–30°, advance 2–3 mm; aspirate; test dose with adrenaline 1:200,000; inject slowly; USG guidance where available.

Volume (mL/kg)	Level	Surgery
0.5	Sacral (S1–S5)	Perineal, scrotal, anal, distal hypospadias
1.0	Lower thoracic (T10)	Inguinal hernia, orchidopexy, circumcision
1.25	Mid-thoracic (T4–T6)	Upper abdominal (rarely used)

Additives: clonidine 1–2 mcg/kg (3–4× duration); dexmedetomidine 1 mcg/kg; S(+) ketamine 0.5 mg/kg; morphine 30 mcg/kg (needs monitored overnight setting).

B. Pain Assessment Tools (Preverbal)3 marks

Tool	Age	Notes
FLACC	2 mo–7 yr	5 domains, 0–10; ≥4 = treat
NIPS	Preterm–6 mo	6 indicators, most validated neonatal scale
Wong-Baker FACES	3–18 yr (self-report)	6 faces, may be confounded by emotion
CRIES	32–60 wk postconceptual	Standard post-op neonatal assessment

C. Opioid-Free Analgesia (Day Surgery)3 marks

Rationale: opioids → PONV, respiratory depression (esp. ex-premature, OSA), parental opioid phobia.
Multimodal (ERAS Paediatric): regional block (caudal + clonidine) + paracetamol 15–20 mg/kg + NSAID (avoid ketorolac in tonsillectomy) + dexmedetomidine (↓emergence delirium) + sub-anaesthetic ketamine 0.25–0.5 mg/kg.

Examiner's PearlArmitage dosing: 0.5 mL/kg sacral, 1.0 mL/kg T10, 1.25 mL/kg T4–T6. Clonidine 1–2 mcg/kg additive prolongs 3–4×. Infant dural sac to S3–S4 – ↑puncture risk. FLACC 2mo–7yr, ≥4=treat. Opioid-free day surgery = caudal + paracetamol + NSAID + dexmedetomidine + ketamine.

References: Armitage EN. Anaesthesia 1979;34:396-398. Lönnqvist PA, Morton NS. Br J Anaesth 2005;95:59-68. Merkel SI et al. Pediatr Nurs 1997;23:293-297. APAGBI 2012.

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Point-of-Care Ultrasound (POCUS) in Anaesthesia — Lung, FATE & Gastric Describe the technique and findings of lung ultrasound in the perioperative period [3]. Explain the basic cardiac POCUS assessment – FATE protocol – and its perioperative utility [4]. Outline gastric ultrasound for aspiration risk assessment [3].

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" Q83 - Point-of-Care Ultrasound (POCUS) in Anaesthesia — Lung, FATE & Gastric

Q83 · Paper II · 10 MARKS · Short Notes

Point-of-Care Ultrasound (POCUS) in Anaesthesia — Lung, FATE & Gastric

Question: Describe the technique and findings of lung ultrasound in the perioperative period [3]. Explain the basic cardiac POCUS assessment – FATE protocol – and its perioperative utility [4]. Outline gastric ultrasound for aspiration risk assessment [3].

Core ConceptPOCUS changes clinical management in 20–30% of cases and is now expected competency in anaesthesia – the stethoscope of the 21st century.

A. Lung Ultrasound3 marks

A-lines: normal aeration or pneumothorax (with absent lung sliding).
Lung sliding: rules OUT pneumothorax; M-mode ""seashore"" (present) vs ""barcode"" (absent = pneumothorax).
B-lines: ≥3/interspace = interstitial syndrome (pulmonary oedema, ARDS, pneumonia).
Consolidation: liver-like tissue + dynamic air bronchograms = pneumonia.
Pleural effusion: anechoic collection + ""spine sign"".
BLUE protocol: diagnoses cause of acute dyspnoea at bedside within 3 minutes.

B. Cardiac POCUS — FATE Protocol4 marks

View	Assesses	Key Question
Subcostal 4-chamber	Effusion/tamponade, RV:LV ratio, IVC	Tamponade? Volume responsive?
Parasternal long axis	LV, LVOT, valves	LV function good/poor? Valve pathology?
Parasternal short axis	LV cross-section, D-sign	RV overload/PE? Regional wall abnormality?
Apical 4-chamber	RV:LV ratio, TR	RV dilated? LV function?

Utility: unexplained hypotension diagnosis in minutes; detects tamponade pre-induction; guides fluid resuscitation (IVC); classifies PEA arrest.

C. Gastric Ultrasound3 marks

Technique: right lateral decubitus, curvilinear probe, antrum between liver and aorta.
Grade 0: empty in both positions – low risk.
Grade 1: fluid in right lateral only – low risk if no other factors.
Grade 2: content in both positions – HIGH risk → RSI indicated.
CSA formula: gastric volume = 27 + 14.6×right-lateral CSA − 1.28×age.

Examiner's PearlLung: A-lines normal/PTX; B-lines (≥3) = interstitial fluid; absent sliding = pneumothorax. FATE: SC4C (tamponade/IVC), PLAX (LV function), PSAX (D-sign=RV overload), A4C (RV:LV). Gastric: Grade 0/1 low risk, Grade 2 high risk → RSI. IVC <2cm + >50% collapse = fluid responsive.

References: Lichtenstein DA. Chest 2008;134:117-125. Jensen MB et al. Eur J Emerg Med 2004;11:15-23. Van de Putte P, Perlas A. Br J Anaesth 2014;113:12-22.

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Pharmacology of Local Anaesthetics — Structure, Mechanism, Differential Block & Toxicity Describe the structure-activity relationship and mechanism of action of local anaesthetics [3]. Explain differential nerve block and its basis [3]. Describe the pharmacokinetic determinants of systemic toxicity and compare bupivacaine, ropivacaine and lidocaine [4].

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" Q84 - Pharmacology of Local Anaesthetics — Structure, Mechanism, Differential Block & Toxicity

Q84 · Paper II · 10 MARKS · Long Answer

Pharmacology of Local Anaesthetics — Structure, Mechanism, Differential Block & Toxicity

Question: Describe the structure-activity relationship and mechanism of action of local anaesthetics [3]. Explain differential nerve block and its basis [3]. Describe the pharmacokinetic determinants of systemic toxicity and compare bupivacaine, ropivacaine and lidocaine [4].

Core ConceptLocal anaesthetics are the cornerstone of regional anaesthesia. Their mechanism (voltage-gated Na⁺ channel block) is simple, but pharmacokinetics are complex. Systemic toxicity (LAST) is potentially fatal yet preventable.

A. Structure-Activity Relationship & Mechanism3 marks

Structure: aromatic ring (lipophilic) – intermediate chain (ester or amide) – tertiary amine (hydrophilic, determines pKa).
Esters (procaine, chloroprocaine): plasma cholinesterase hydrolysis, PABA metabolite → allergy. Amides (lidocaine, bupivacaine, ropivacaine): hepatic CYP450 metabolism, true allergy rare.
Mechanism: unionised form penetrates membrane → ionised cation binds Na⁺ channel intracellularly (use-dependent block) → prevents depolarisation. Lower pKa → faster onset.

B. Differential Nerve Block3 marks

Block sequence: autonomic (B-fibres) → pain/temperature (C, Aδ) → motor (Aα).
Determinants: fibre diameter, myelination (saltatory conduction needs fewer nodes blocked), firing frequency (use-dependent block favours high-frequency C-fibres).
Clinical application: dilute LA (0.1% bupivacaine) → sensory block with motor sparing (""walking epidural""); higher concentration (0.5%) → complete motor block.

C. LAST Pharmacokinetics & Drug Comparison4 marks

Risk factors: injection site vascularity (intercostal>caudal>epidural>brachial plexus>SC), total dose, adrenaline reduces peak level 30–50%.

Toxicity sequence: CNS more sensitive than CVS – excitatory (perioral tingling, tinnitus, agitation) → inhibitory (seizures, coma); bupivacaine can cause CVS collapse WITHOUT CNS warning.

Feature	Lidocaine	Bupivacaine	Ropivacaine
Cardiotoxicity	Low, easily reversed	HIGH – refractory VF (""fast in, slow out"")	Lower than bupivacaine (S-enantiomer)
Max dose (plain/+adr)	3/7 mg/kg	2/2.5 mg/kg	3/4 mg/kg
Duration	1–2h	4–8h	3–6h
Preferred use	IVRA, top-up	Spinal (hyperbaric)	Epidural, large-volume PNB

Examiner's PearlAmides: hepatic CYP450. Esters: plasma cholinesterase (PABA allergy). Mechanism: ionised cation blocks Na⁺ channel intracellularly. Differential block: Aδ/C before Aα – use dilute LA. Bupivacaine ""fast in, slow out"" → refractory VF; ropivacaine safer (S-enantiomer).

References: Covino BG, Vassallo HG. Local Anaesthetics 1976. AAGBI LAST Guidelines 2010 (updated 2023). Miller's Anaesthesia, 9th Ed, Ch 36.

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Anaesthesia for Renal Transplantation — ESRD, Fluid Strategy & Immunosuppressants Describe the perioperative physiological challenges in a patient with end-stage renal disease presenting for renal transplantation [4]. Outline the fluid and haemodynamic management strategy to optimise early graft function [3]. Discuss the anaesthetic implications of immunosuppressant drugs [3].

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" Q85 - Anaesthesia for Renal Transplantation — ESRD, Fluid Strategy & Immunosuppressants

Q85 · Paper II · 10 MARKS · Long Answer

Anaesthesia for Renal Transplantation — ESRD, Fluid Strategy & Immunosuppressants

Question: Describe the perioperative physiological challenges in a patient with end-stage renal disease presenting for renal transplantation [4]. Outline the fluid and haemodynamic management strategy to optimise early graft function [3]. Discuss the anaesthetic implications of immunosuppressant drugs [3].

Core ConceptRenal transplantation is the definitive treatment for ESRD. Anaesthesia must address ESRD physiology, optimise graft perfusion at reperfusion, and manage immunosuppressant effects. Primary non-function and delayed graft function are largely preventable.

A. ESRD Physiological Challenges4 marks

System	Changes	Implication
Cardiovascular	Hypertension, LVH, CAD (40–50%), pericardial effusion, arrhythmias	Pre-op cardiac assessment vital; K⁺ <5.5 before surgery; protect AV fistula
Haematological	Normochromic anaemia, platelet dysfunction	Hb target 100–120 g/L; DDAVP if bleeding risk
Electrolytes/Acid-base	Hyperkalaemia, metabolic acidosis, hypocalcaemia	Avoid suxamethonium if K⁺ >5.0; avoid normal saline
Drug handling	↓Renal clearance, ↑free drug fraction	Avoid morphine, vecuronium; use atracurium/cisatracurium, fentanyl
GI	Gastroparesis → ↑aspiration risk	RSI precautions, PPI premedication

B. Fluid & Haemodynamic Strategy3 marks

Goal: optimise graft perfusion at reperfusion – ↓delayed graft function; target CVP 10–15 mmHg (higher than usual).
Fluid: Hartmann's/PlasmaLyte preferred over normal saline (avoids hyperchloraemic acidosis/hyperkalaemia).
MAP ≥70–80 mmHg at reperfusion (new graft has no autoregulation); noradrenaline or cautious dopamine if needed.
Mannitol 0.25–0.5 g/kg before reperfusion – osmotic diuresis + ROS scavenging; methylprednisolone 250–500 mg IV before reperfusion.

C. Immunosuppressant Implications3 marks

Drug	Implication
Ciclosporin/Tacrolimus	Nephrotoxic, hepatotoxic, hypertension, ↑infection risk; continue perioperatively
Corticosteroids	HPA suppression – steroid cover (hydrocortisone 100 mg 6-hrly); hyperglycaemia
Azathioprine/Mycophenolate	Bone marrow suppression; azathioprine + allopurinol = FATAL interaction
Basiliximab (anti-IL-2R)	Induction only; rare anaphylaxis

Examiner's PearlESRD drugs: atracurium/cisatracurium (Hofmann), fentanyl (no active metabolite); avoid morphine, vecuronium, suxamethonium if K⁺>5.0, normal saline. Fluid: Hartmann's, CVP 10–15, MAP ≥70–80 at reperfusion. Mannitol pre-reperfusion. Azathioprine+allopurinol = fatal marrow suppression. Steroid cover mandatory.

References: Sprung J et al. Anesthesiology 2006;105:405-424. Pöge U et al. Br J Anaesth Educ 2013;13:70-74. Miller's Anaesthesia, 9th Ed.

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Pulmonary Hypertension — Classification, Pathophysiology & Perioperative Management

A. Definition & WHO Classification2 marks

B. Pathophysiology of RV Failure4 marks

C. Anaesthetic Goals & Management4 marks

Cardiac Implantable Electronic Devices — Pacemakers, ICDs & EMI

A. NBG Code & Perioperative Pacing3 marks

B. EMI from Diathermy4 marks

C. Perioperative ICD Management3 marks

Surgical Positioning — Physiological Effects, Nerve Injuries & Complications

A. Physiological Effects of Positions4 marks

B. Position-Related Nerve Injuries4 marks

C. Prone & Lithotomy Complications2 marks

Vascular Surgery — Open AAA vs EVAR, Cross-Clamping & Spinal Cord Protection

A. Open AAA vs EVAR4 marks

B. Cross-Clamping & Unclamping3 marks

C. Spinal Cord Protection (TAAA)3 marks

Anaesthesia for Neurosurgery — Craniotomy, Awake Craniotomy & IONM

A. Craniotomy — Anaesthetic Management4 marks

B. Awake Craniotomy — Asleep-Awake-Asleep3 marks

C. Intraoperative Neurophysiological Monitoring3 marks

Obstetric Emergencies — Category 1 CS, Failed Intubation & Cord Prolapse

A. CS Categories & Cat 1 Anaesthesia3 marks

B. Failed Intubation (DAS Obstetric 2015)4 marks

C. Cord Prolapse Management3 marks

Paediatric Pain and Regional Anaesthesia — Caudal Block, Pain Scales & Opioid-Free Strategy

A. Caudal Block — Anatomy, Technique, Dosing4 marks

B. Pain Assessment Tools (Preverbal)3 marks

C. Opioid-Free Analgesia (Day Surgery)3 marks

Point-of-Care Ultrasound (POCUS) in Anaesthesia — Lung, FATE & Gastric

A. Lung Ultrasound3 marks

B. Cardiac POCUS — FATE Protocol4 marks

C. Gastric Ultrasound3 marks

Pharmacology of Local Anaesthetics — Structure, Mechanism, Differential Block & Toxicity

A. Structure-Activity Relationship & Mechanism3 marks

B. Differential Nerve Block3 marks

C. LAST Pharmacokinetics & Drug Comparison4 marks

Anaesthesia for Renal Transplantation — ESRD, Fluid Strategy & Immunosuppressants

A. ESRD Physiological Challenges4 marks

B. Fluid & Haemodynamic Strategy3 marks

C. Immunosuppressant Implications3 marks

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