DNB Anesthesia Question Bank 2020–2024: CVS — Complete Answers

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Q1. Off-Pump CABG (OPCAB)

a) Indications of Off-Pump CABG

1. Severe aortic atherosclerosis (calcified/porcelain aorta) — avoids aortic cannulation and clamping, reducing embolic stroke risk
2. Severe renal dysfunction (creatinine >1.5 mg/dL) — CPB worsens renal perfusion
3. Severe pulmonary dysfunction — avoids CPB-induced inflammatory lung injury
4. Previous cerebrovascular accidents / carotid artery disease — reduces risk of neurological injury
5. Severe coagulopathy / bleeding diathesis — avoids heparin doses required for CPB
6. Jehovah's Witnesses — minimizes haemodilution and blood use
7. Elderly patients (>75 years) with multiple comorbidities

• Previous cardiac surgery (redo surgery)
• Hepatic failure
• Haematological malignancies
• Patients with HIT (heparin-induced thrombocytopenia) where full heparinization is unsafe

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b) Technique, Advantages and Disadvantages

1. Median sternotomy performed; CPB circuit is set up on standby but not initiated
2. Stabilizers (mechanical or suction-based, e.g., Octopus tissue stabilizer) are applied to the target coronary vessel territory to create a relatively motionless field
3. Intracoronary shunts are placed to maintain distal coronary perfusion during anastomosis
4. Heart positioning devices (e.g., pericardial sutures, deep pericardial sutures) are used to expose lateral and posterior vessels; the Trendelenburg and right-lateral tilt position helps
5. Blower-mister device clears the anastomotic field
6. Target ACT maintained at 300–350 seconds (vs. ≥480 seconds for CPB)
7. Anastomosis is performed on a beating, contracting heart

• Aggressive haemodynamic monitoring (TEE mandatory)
• Vasopressors (phenylephrine, norepinephrine) and inotropes (dobutamine) on standby
• Heart rate control (beta-blockade) for RCx/PDA territory anastomoses
• Maintain normothermia; cell salvage used

1. Technically demanding — anastomosis quality may be inferior (especially for posterior/lateral vessels)
2. Haemodynamic instability during cardiac manipulation (bradycardia, hypotension)
3. Incomplete revascularization in complex multi-vessel disease
4. Conversion to on-pump required in 2–5% of cases (emergent, high mortality)
5. Long-term graft patency may be slightly inferior (ongoing debate — ROOBY and CORONARY trials showed non-inferiority only for selected patients)
6. Requires specialized equipment and training

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Q2. Preload, Afterload, and Determinants of LV Diastolic Function

a) Preload and Afterload

• The ventricular wall tension at end-diastole, determined by the volume of blood in the ventricle just before contraction (end-diastolic volume, EDV)
• Clinically represented by LVEDP or PCWP (pulmonary capillary wedge pressure)
• Determined by venous return, blood volume, venous compliance, atrial kick, and heart rate
• Governed by Frank-Starling law: as preload increases, stroke volume increases (up to a point)
• Formula: Preload ∝ End-diastolic fibre length (Sarcomere length)

• The ventricular wall tension during systolic ejection — the resistance against which the ventricle contracts
• For LV: represented by Systemic Vascular Resistance (SVR) = (MAP – CVP) × 80 / CO
• For RV: represented by Pulmonary Vascular Resistance (PVR)
• Clinically: blood pressure, aortic impedance, arterial compliance
• Increased afterload → reduces stroke volume → increases myocardial oxygen demand
• Formula (Laplace's law): Wall stress = (Pressure × Radius) / (2 × Wall thickness)

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b) Determinants of Left Ventricular Diastolic Function

• Energy-dependent process (requires ATP)
• Determined by: cytosolic Ca²⁺ reuptake into SR (SERCA2a activity), myosin-actin cross-bridge dissociation
• Impaired by ischaemia, hypertrophy, tachycardia

• Determined by chamber stiffness (myocardial fibrosis, concentric hypertrophy, pericardial constraint)
• Titin protein's extensibility
• Collagen cross-linking in the extracellular matrix

• Grade I: Impaired relaxation (E/A < 0.8, E/e' < 8)
• Grade II: Pseudonormal (E/A 0.8–2, E/e' 9–14)
• Grade III: Restrictive (E/A > 2, E/e' > 14, irreversible)

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Q3. Extracorporeal Membrane Oxygenation (ECMO)

Types:

Indications:

• Severe ARDS (P/F ratio < 80 despite optimal ventilation)
• Status asthmaticus refractory to therapy
• Pulmonary haemorrhage, bridge to lung transplant

• Cardiogenic shock refractory to inotropes/IABP
• Massive pulmonary embolism with haemodynamic compromise
• Refractory ventricular fibrillation/pulseless VT (ECPR — extracorporeal CPR)
• Fulminant myocarditis
• Post-cardiotomy shock
• Bridge to ventricular assist device (VAD) or transplant
• Drug overdose with refractory cardiac arrest

Circuit Components:

1. Cannulas (drainage + return)
2. Centrifugal pump (roller pump in older systems)
3. Membrane oxygenator (hollow fibre — polymethylpentene)
4. Heat exchanger
5. Monitor console (flow, pressure, FiO₂)

ECMO Flow:

• Typical flow: 3–5 L/min (60–80 mL/kg/min)
• Anticoagulation: UFH to maintain ACT 160–200 seconds (anti-Xa 0.3–0.5 IU/mL)

Complications:

• Mechanical: circuit thrombosis, oxygenator failure, cannula malposition, air embolism
• Patient-related: bleeding (HIT, thrombocytopenia, surgical site), stroke, limb ischaemia (peripheral VA-ECMO), NORTH SOUTH syndrome (differential hypoxia in VA-ECMO), renal failure, infection

ECMO Management Principles:

• Lung-protective ventilation during ECMO (low tidal volume, low rate — "lung rest")
• Sweep gas (FiO₂ + flow rate) controls CO₂ clearance
• ECMO FiO₂ controls oxygenation
• Daily echocardiography, LV unloading assessment
• Daily neurological checks
• Weaning: trial of reduced flows; VV — FiO₂ reduction trial; VA — gradual flow reduction with echocardiographic assessment

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Q4. Post-Cardiac Arrest Care

Goals of Post-Cardiac Arrest Care (AHA 2020 Guidelines):

• Secure airway (endotracheal intubation if not already done)
• Target SpO₂ 94–98% — avoid hyperoxia (worsens neurological outcomes)
• Target PaCO₂ 35–45 mmHg — avoid hypocapnia (causes cerebral vasoconstriction)

• Target MAP ≥ 65–70 mmHg (some guidelines suggest MAP 80–100 mmHg)
• Avoid hypotension (SBP < 90 mmHg)
• IV fluids + vasopressors (norepinephrine preferred; dopamine as alternative)
• Obtain 12-lead ECG immediately — emergent coronary angiography if STEMI or high suspicion of cardiac cause

• 2021 TTM-2 trial shifted guidance: maintain normothermia (36°C) and aggressively prevent fever (>37.7°C) for at least 72 hours
• Previous recommendation of therapeutic hypothermia (32–36°C) for 24 hours still acceptable
• TTM applies to comatose survivors after both shockable and non-shockable rhythms

• Avoid hypoglycaemia and hyperglycaemia (target glucose 140–180 mg/dL)
• No routine seizure prophylaxis; treat clinical/EEG-confirmed seizures aggressively
• Neurological prognostication: not before 72 hours (to allow TTM washout):
  • Clinical exam (pupillary light reflex, corneal reflex, motor response)
  • EEG (burst suppression, seizures)
  • SSEP (bilateral absence of N20 = poor prognosis)
  • Serum NSE (neuron-specific enolase)
  • CT/MRI brain (grey-white ratio)

• Hypoxia, Hypovolaemia, Hypo/Hyperkalaemia, Hypothermia
• Tension pneumothorax, Tamponade, Toxins, Thromboembolism

• Urgent PCI if STEMI on post-ROSC ECG
• Consider coronary angiography even without ST elevation if cardiac cause suspected

• Avoid secondary brain injury: maintain normoglycaemia, normocapnia, normoxia
• Bedside echo: assess LV/RV function, pericardial effusion
• Consider IABP/VA-ECMO if haemodynamic instability persists (cardiogenic shock post-arrest)
• Rehabilitation planning on recovery of consciousness

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Q5. Anaesthetic Considerations: 75-Year-Old Chronic Smoker with Permanent Pacemaker for TURP

Pre-operative Assessment:

• History: pack-years, current or ex-smoker; if current, advise cessation ≥8 weeks pre-op (ideal for pulmonary benefit)
• Spirometry, chest X-ray
• Risk of COPD, reactive airways, increased secretions, impaired mucociliary clearance

• Full cardiac history: symptoms of heart failure, angina, syncope
• 12-lead ECG — assess baseline rhythm, pacing spikes, intrinsic rate
• Identify pacemaker type (single vs. dual chamber), indication (complete heart block, sick sinus), and pacing dependency
• Recent pacemaker check/interrogation report — demand rate, sensing threshold, battery life
• Echo if LV function unknown

• Monopolar diathermy (electrocautery) in TURP can cause:
  • Pacemaker inhibition (sensing current as cardiac activity → no pacing in dependent patient)
  • Rarely: pacemaker reprogramming, ventricular fibrillation (if falls on T-wave)
• Strategies:
  • Use bipolar diathermy whenever possible (safe; localized current)
  • If monopolar unavoidable: place return electrode away from pacemaker; use short, intermittent bursts at lowest effective power
  • Magnet application: converts most pacemakers to asynchronous mode (DOO/VOO/AOO) — paces at fixed rate regardless of intrinsic rhythm; eliminates inhibition risk. Place magnet over pacemaker during monopolar diathermy periods
  • Cardiology review pre-op; consider temporary reprogramming to asynchronous mode
  • External defibrillator/pacemaker pads applied before induction
  • Post-op pacemaker interrogation mandatory

• TURP syndrome risk: hyponatraemia, fluid overload from glycine/saline irrigation absorption; especially with resection >1 hour or prostatic capsule perforation
• Symptoms: confusion, seizures, bradycardia, visual disturbances (glycine), haemoglobin dilution
• Treatment: stop procedure, furosemide, hypertonic saline (3%) if Na⁺ <120 mEq/L, seizure management

Anaesthetic Technique:

• Regional (spinal) anaesthesia preferred for TURP:
  • Allows conscious assessment for TURP syndrome symptoms
  • Avoids airway manipulation
  • Level T10 required (bladder distension sensation)
• If spinal preferred: hyperbaric bupivacaine 0.5% 2–2.5 mL
• If GA required (patient refusal, bleeding, conversion): LMA or ETT; TIVA preferred (avoids volatile agents that may worsen haemodynamics)

Intraoperative Monitoring:

• Standard AAGBI monitoring + SpO₂, capnography
• ECG continuous monitoring — observe for pacing spikes and any induced arrhythmias
• Defibrillator pads in place before induction
• Urine output monitoring; serum electrolytes (Na⁺) checked during long procedures

Postoperative:

• PACU ECG monitoring; pacemaker interrogation within 24 hours
• Chest physiotherapy (chronic smoker), bronchodilators if needed
• Fluid balance monitoring (risk of TURP syndrome, LVF in elderly)

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Q6. Non-Invasive Cardiac Output Monitoring

Methods:

• Gold standard non-invasive method
• CO = LVOT VTI × LVOT area × HR
• Advantage: structural + functional assessment
• Limitation: operator-dependent, intermittent

• Probe in oesophagus; Doppler measures aortic blood flow
• Derives: SV, CO, FTc (corrected flow time — preload marker), peak velocity (contractility)
• Minimally invasive (classified as such — requires probe insertion)
• Advantage: real-time, continuous, guides fluid therapy
• Limitation: requires sedation/anaesthesia; 10% measurement error vs. PAC

• Electrodes measure thoracic impedance changes during cardiac cycle
• CO derived from impedance signal
• Non-invasive, easy to apply
• Limitation: inaccurate with arrhythmias, obesity, lung pathology

• Variation of ICG; measures phase shift in transthoracic electrical current
• More robust than ICG; less affected by artefact
• Good tracking of CO changes; useful in goal-directed fluid therapy

• Finger cuff arterial waveform analysis
• Derives CO via pulse contour algorithm
• Continuous, non-invasive; useful in theatre/ICU
• Limitation: accuracy compromised in vasoconstricted states

• Masimo Radical-7 with hemodynamic parameter estimation
• Less validated for absolute CO values

• Based on Fick principle with CO₂
• Requires intubated patient; non-invasive in terms of vascular access
• Intermittent readings; less accurate in shunts/ARDS

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Q7. Use of Heparin During Cardiopulmonary Bypass

Rationale:

Mechanism of Action:

• UFH binds antithrombin III (AT-III), accelerating its inhibitory action on thrombin (IIa) and factor Xa by 1000-fold
• Also inhibits factors IXa, XIa, XIIa
• Reversal: protamine sulphate (1 mg per 100 units heparin given; maximum 2.6 mg per 100 units to avoid platelet dysfunction)

Dosing Protocol:

• Initial dose: 300–400 units/kg IV bolus before cannulation
• Target ACT: ≥ 480 seconds before initiating CPB (some centres use ≥400 seconds)
• During CPB: check ACT every 30–60 minutes; supplement heparin if ACT falls below target
• Additional heparin 100 units/kg if ACT < 400 seconds

Monitoring:

• Activated Clotting Time (ACT): Point-of-care test; normal 90–120 seconds; target >480 seconds on CPB
• Anti-Xa assay: Used when ACT unreliable (haemodilution, hypothermia affect ACT)
• Heparin concentration assay (HMS — Heparin Management System)

Heparin Resistance:

• ACT fails to reach target despite 600–800 units/kg
• Causes: AT-III deficiency (congenital or acquired), elevated heparin-binding proteins, preoperative heparin use, high platelet count
• Management:
  • Fresh frozen plasma (source of AT-III)
  • AT-III concentrate preferred
  • Larger heparin doses

Protamine Reversal:

• After CPB separation and decannulation: protamine 1–1.3 mg per 100 units of total heparin administered
• Protamine reactions: anaphylaxis, pulmonary hypertension, systemic hypotension, RV failure
  • Risk factors: NPH insulin use, fish allergy, prior protamine exposure
  • Treatment: slow administration (>5 minutes), epinephrine, inhaled prostacyclin for pulmonary hypertension, return to CPB if severe

Alternatives (for Heparin-Induced Thrombocytopenia — HIT):

• Bivalirudin (direct thrombin inhibitor) — most commonly used; no reversal agent available
• Argatroban
• Fondaparinux (limited evidence for CPB)

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Q8. Management of Ventricular Tachycardia in an Adult Patient

Classification:

• Haemodynamically stable (pulse present, BP maintained) vs. Unstable (hypotension, altered consciousness, ischaemia, pulmonary oedema)
• Monomorphic VT vs. Polymorphic VT (Torsades de Pointes)
• Sustained (>30 sec) vs. Non-sustained (<30 sec)

Algorithm:

• Immediate defibrillation: 200 J biphasic (360 J monophasic)
• CPR 2 minutes between shocks
• IV adrenaline (epinephrine) 1 mg every 3–5 minutes
• After 3rd shock: amiodarone 300 mg IV bolus; repeat 150 mg once
• Lidocaine if amiodarone unavailable: 1–1.5 mg/kg IV

• Immediate synchronized DC cardioversion: 100 J biphasic (monomorphic VT)
• Sedate before cardioversion if time permits (midazolam + fentanyl)
• If refractory: escalate energy (150 → 200 J), change paddle position
• Amiodarone 150 mg IV over 10 min, then infusion 1 mg/min (maintenance)

• IV antiarrhythmic therapy:
  • Amiodarone: 150 mg IV over 10 min (first-line in structural heart disease)
  • Lidocaine: 1–1.5 mg/kg IV (especially ischaemia-related VT)
  • Procainamide: 15–17 mg/kg IV over 20–60 min (avoid in reduced EF)
  • Flecainide/Sotalol for idiopathic VT (no structural disease)
• If drug-refractory: synchronized cardioversion

• Stop QT-prolonging drugs
• IV magnesium sulphate 2 g over 2–3 min (first-line)
• Correct hypokalaemia (target K⁺ > 4.5 mEq/L)
• Overdrive pacing (100–110/min) to suppress Torsades
• If baseline QT normal (ischaemia-related): treat underlying ischaemia

Identify and Correct Reversible Causes:

• Ischaemia/infarction (STEMI — emergent revascularization)
• Electrolyte imbalance (K⁺, Mg²⁺, Ca²⁺)
• Drug toxicity (digoxin, tricyclics, proarrhythmic drugs)
• Hypoxia, acidosis

Long-Term Management:

• ICD implantation if sustained VT/VF with structural heart disease or genetic channelopathy
• Antiarrhythmic therapy (amiodarone, sotalol, mexiletine)
• Beta-blockers (reduce sudden cardiac death in post-MI patients)
• Catheter ablation for recurrent monomorphic VT (especially idiopathic RVOT VT)
• Treat underlying structural disease (revascularization, ACE inhibitors, CRT)

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Q9. Diagnosis and Management of Myocardial Ischaemia Under General Anaesthesia

Risk Factors / Predisposing Conditions:

• Known CAD, previous MI, diabetes, hypertension, peripheral vascular disease
• High-risk surgeries: cardiac, major vascular, thoracic

Diagnosis Under GA:

• Standard: 5-lead ECG with continuous monitoring of II + V5 (detects 80% of ischaemic events); adding V4 increases sensitivity to 96%
• ST-segment changes:
  • ST depression ≥1 mm (horizontal or downsloping) = subendocardial ischaemia
  • ST elevation ≥2 mm = transmural ischaemia/STEMI equivalent
  • T-wave inversion, new LBBB
• New regional wall motion abnormalities (RWMA) on TEE are the earliest and most sensitive sign of ischaemia

• New or worsening RWMA in a coronary distribution precedes ECG changes by 30–60 seconds
• Assess: global LV function (EF), segmental wall motion, wall thickening, valvular complications
• Essential in cardiac surgery; extremely valuable in major non-cardiac surgery

• Sudden hypotension, tachycardia, new wall motion abnormality on TEE
• New ST changes with pulmonary artery catheter: ↑ PCWP, ↑ PAP (diastolic dysfunction)
• V-waves on PCWP trace (papillary muscle ischaemia → mitral regurgitation)

• Troponin I/T (perioperative MI diagnosis)
• CKMB (less specific)

Management Under GA:

• Hypotension → increase preload (fluids, Trendelenburg), vasopressors (phenylephrine, norepinephrine)
• Tachycardia → beta-blocker (metoprolol IV), correct pain/hypovolaemia
• Anaemia → transfuse (target Hb 8–10 g/dL in CAD patients)
• Hypoxia → increase FiO₂, PEEP

• Nitroglycerin (IV infusion 0.5–1 mcg/kg/min): relieves coronary spasm, reduces preload
• Beta-blockers (IV esmolol): reduce heart rate and O₂ demand
• Calcium channel blockers (diltiazem IV) if coronary spasm suspected
• Maintain mean arterial pressure adequately (avoid hypotension — worsens ischaemia)
• Correct electrolytes (K⁺, Mg²⁺)

• Discuss with surgeon — expedite surgery or pause if prolonged ischaemia
• Consider regional anaesthesia supplements to reduce sympathetic stress
• Intra-aortic balloon pump (IABP) if cardiogenic compromise

• ECG, troponin T/I at 6 and 24 hours post-op
• If perioperative STEMI confirmed: emergent cardiology consultation, revascularization decision

• Demand = Heart Rate × Contractility × Wall Tension (preload + afterload)
• Supply = Coronary perfusion pressure (DBP – LVEDP) × coronary vasomotor tone × Hb × O₂ content

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Q10. Anaesthetic Management: 53-Year-Old Hypertensive Patient for Laparoscopic Cholecystectomy

Pre-operative Management (2 marks):

• Stage (JNC): Stage 1 (130–139/80–89), Stage 2 (≥140/90), Hypertensive urgency/emergency
• Key principle: Elective surgery should be postponed if SBP >180 mmHg or DBP >110 mmHg (Stage 3)
• ECG: LVH (high R in V5, S in V1, strain pattern), LBBB, AF
• Echocardiography if LVH, poor exercise tolerance
• Renal function (urine protein, creatinine, eGFR), serum electrolytes (hypokalaemia from diuretics)
• Fundoscopy: grade of hypertensive retinopathy (Keith-Wagener-Barker classification)
• Blood glucose, lipid profile
• Continue antihypertensive medications up to day of surgery except ACE-I/ARBs (hold on morning of surgery to reduce risk of intraoperative hypotension — refractory vasodilation)
• Optimize BP pre-operatively: target <160/100 mmHg at minimum

Intraoperative Management (6 marks):

• Laryngoscopy and intubation is a period of significant haemodynamic stress
• Premed: oral clonidine or oral labetalol to blunt response
• Blunt laryngoscopic response: IV lignocaine 1.5 mg/kg or IV esmolol 1 mg/kg + IV fentanyl 2–3 mcg/kg before laryngoscopy
• Induction agents: propofol (reduces BP), thiopentone; avoid ketamine (hypertensive)
• Succinylcholine or rocuronium for intubation

• Invasive arterial BP (arterial line) if Stage 2/3 hypertension
• Standard AAGBI + ECG (II + V5), SpO₂, ETCO₂
• Temperature (laparoscopy + gas causes hypothermia)

• Pneumoperitoneum (CO₂, 12–15 mmHg pressure) causes:
  • Initial: vagal bradycardia from peritoneal stretch
  • Sustained: ↑ SVR (absorbed CO₂ + catecholamine release) → hypertension
  • Trendelenburg position → ↑ venous return → ↑ preload
  • CO₂ absorption → hypercarbia → ↑ HR, ↑ BP
• Management: maintain normocarbia (adjust ventilation), vasodilators (hydralazine IV, GTN infusion) for hypertension
• Arrhythmias: usually managed by desufflating and waiting; correct hypercarbia

• GTN (nitroglycerin) infusion — primarily venodilator
• Sodium nitroprusside — balanced; rapid action
• Labetalol IV — alpha + beta blockade
• Esmolol — rapid-acting beta-blocker for tachycardia/hypertension
• Hydralazine — arteriolar dilator (slower onset, unpredictable)
• Urapidil — alpha-blocker (Europe)

• Volatile anaesthetic (isoflurane, sevoflurane) + O₂/air + opioid infusion
• Maintain ETCO₂ 35–40 mmHg; watch for CO₂ accumulation especially in long procedures
• Adequate analgesia (reduces sympathetic hypertensive surges)

Post-operative Management (2 marks):

• PACU: BP monitoring, adequate analgesia (multimodal — paracetamol + NSAID + opioid if needed)
• Resume antihypertensive medications at earliest (IV labetalol/hydralazine if cannot take oral)
• Watch for post-extubation hypertension (pain, anxiety, hypercapnia, urinary retention)
• Nausea/vomiting management (dexamethasone + ondansetron) — vomiting causes Valsalva-induced hypertension
• Discharge criteria: SBP <180 mmHg consistently

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Q11. Preoperative Preparation: 65-Year-Old Female, CAD with Drug-Eluting Stent (1 year), for Total Knee Replacement

Stent Timeline:

• Drug-eluting stents (DES): require dual antiplatelet therapy (DAPT) — aspirin + P2Y12 inhibitor (clopidogrel/ticagrelor/prasugrel) — for at least 12 months due to risk of late stent thrombosis
• At 1 year: DES is no longer "new" — transition period; patient may be on single antiplatelet (aspirin alone) if 12 months completed
• Bare metal stents: DAPT minimum 4–6 weeks

1. Confirm stent type and exact implant date
2. Current antiplatelet medications — aspirin only, or still on DAPT?
3. Cardiologist review mandatory — cardiology clearance letter
4. Active cardiac symptoms: angina, dyspnoea, palpitations (if present → workup needed)
5. Assess LV function: recent echo or stress test
6. Lee Revised Cardiac Risk Index (RCRI): ≥3 factors = high risk for perioperative MACE
   • Ischaemic heart disease, CCF, cerebrovascular disease, diabetes on insulin, CKD, high-risk surgery
7. Functional capacity: if >4 METs (climb stairs, brisk walking) — proceed without further testing
8. If <4 METs with 3+ RCRI factors — consider stress testing (dobutamine stress echo)

• If still on DAPT (clopidogrel + aspirin) and surgery at 1 year:
  • Do not stop aspirin — continue perioperatively
  • Clopidogrel: hold for 5–7 days pre-op; if high thrombotic risk → discuss with cardiologist about bridging or proceeding with increased bleeding precautions
  • Ticagrelor: hold 5 days pre-op; Prasugrel: hold 7 days pre-op
• Never stop both antiplatelet agents without cardiology input — catastrophic stent thrombosis risk
• If surgery is elective and stent is within 12 months: postpone surgery if possible until 12 months of DAPT complete

• Statin therapy: continue; perioperative statins reduce cardiac complications
• Beta-blockers: if on beta-blocker for angina, continue; do not initiate new beta-blocker abruptly
• ACE inhibitors: hold morning of surgery
• Optimize comorbidities: anaemia (TKR blood loss ≥500 mL; iron therapy, EPO), HbA1c if diabetic
• Blood conservation: Cell Saver, pre-donate autologous blood if Hb borderline

• Regional anaesthesia (spinal or combined spinal-epidural, peripheral nerve blocks) preferred for TKR
• Reduces DVT, blood transfusion, stress response, improves post-op analgesia
• Aspirin does not contraindicate neuraxial anaesthesia
• If clopidogrel held ≥5 days: safe to proceed with spinal
• If clopidogrel NOT held: avoid epidural/spinal catheter placement (risk of spinal haematoma)

• LMWH or factor Xa inhibitor post-op (after haemostasis confirmed); assess timing carefully if antiplatelet agents used concurrently

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Q12. Cardioplegia

Purpose:

1. Create a motionless, bloodless operative field
2. Reduce myocardial oxygen consumption (from 8–10 mL/100g/min to near zero)
3. Prevent ischaemic injury during cross-clamping

Mechanism of Arrest:

• Potassium (K⁺) is the universal arresting agent: K⁺ 15–30 mEq/L
• Depolarizes the resting membrane potential → inactivates fast Na⁺ channels → arrested in diastole
• Some solutions add Mg²⁺ (membrane stabilizer), procaine/lidocaine (additional Na⁺ channel blockade)

Types of Cardioplegia:

• Cold (4–10°C): reduces metabolic rate by 50% per 10°C drop; most widely used; risk of inhomogeneous cooling
• Warm (blood cardioplegia): near 37°C; continuous warm antegrade; provides oxygenated blood; may reduce ischaemia more effectively; used in Calafiore technique

• Antegrade (via aortic root or coronary ostia): physiological, rapid arrest; distribution poor if coronary stenosis
• Retrograde (via coronary sinus): uniform distribution even in obstructed coronaries; preferred as supplement
• Combined antegrade + retrograde: most complete protection

Cardioplegia Solutions:

• St. Thomas' Hospital solution (Plegisol): K⁺ 16 mEq/L, Mg²⁺, procaine, cold crystalloid
• HTK (Histidine-Tryptophan-Ketoglutarate — Custodiol): single large-volume dose (20 mL/kg); good for >2 hours cross-clamp; buffers intracellular acidosis
• Del Nido: paediatric cardioplegia; single dose, long protection (60–90 min)

Re-dosing:

• Intermittent cardioplegia: every 15–20 minutes (or if ECG activity resumes)
• Continuous warm blood cardioplegia: no re-dosing needed; continuous delivery

Additives:

• Mannitol: osmotic; reduces cell swelling
• Bicarbonate: buffers acidosis
• Amino acids (glutamate, aspartate): substrate for aerobic metabolism recovery
• Adenosine: initiates arrest; preconditions myocardium

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Q13a. Cardioversion

DC Cardioversion (Synchronized):

• Principle: Shock delivered synchronously with the R wave (sync mode) to avoid the T-wave (vulnerable period) that could trigger VF
• Difference from defibrillation: Defibrillation is unsynchronized, used for pulseless VF/VT

1. Atrial fibrillation (AF) — haemodynamically unstable or elective
2. Atrial flutter
3. Paroxysmal SVT (failed vagal manoeuvres + adenosine)
4. Stable VT not responding to drugs

1. Confirm no contraindications: digitalis toxicity (relative CI), electrolyte imbalance (correct K⁺ first), no anticoagulation for >48 hours AF without TOE exclusion of thrombus
2. Sedation: propofol or midazolam + fentanyl
3. Pre-oxygenate and have airway equipment ready
4. Apply pads (anteroposterior or anterolateral)
5. Engage sync mode — confirm R-wave synchronization markers
6. Charge to selected energy
7. Deliver shock — press and hold until delivered (R-wave triggered)
8. Reassess rhythm immediately

• AF >48 hours or unknown duration: anticoagulate for 3 weeks pre-cardioversion OR perform TOE to exclude LAA thrombus
• Post-cardioversion: anticoagulate for minimum 4 weeks (stunning of LAA)
• If haemodynamically unstable: immediate cardioversion regardless of anticoagulation status

• AF < 48 hours: flecainide (no structural disease), amiodarone (structural disease)
• Ibutilide: IV; effective for flutter and AF
• Vernakalant: atrial-selective; faster cardioversion

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Q13b. Aortocaval Compression

• The uterus (from 20 weeks gestation onward) compresses the IVC against the lumbar vertebrae in supine position
• IVC compression → ↓ venous return → ↓ preload → ↓ cardiac output (up to 30%)
• Aortic compression → ↓ uteroplacental perfusion → foetal distress
• Maternal: hypotension, dizziness, nausea ("supine hypotensive syndrome" in 10–15%)
• Compensatory mechanisms (venoconstriction, tachycardia) maintain BP in most, but under GA/spinal these compensatory mechanisms fail

• Regional (spinal/epidural) anaesthesia causes sympathectomy → vasodilation + blocked compensatory vasoconstriction → severe hypotension
• Enhanced by vasodilatory effects of volatile agents under GA

• Left lateral uterine displacement (LUD): 15–30° left tilt (wedge under right hip) — standard practice from 20 weeks until delivery
• Manual uterine displacement to the left
• Rapid IV fluid preloading (crystalloid or colloid)

1. Immediate left lateral tilt
2. IV fluid bolus (500–1000 mL)
3. Vasopressors: phenylephrine (first-line for spinal hypotension in Caesarean; maintains uterine blood flow better than ephedrine); ephedrine (mixed α/β agonist; used if bradycardia present)
4. 2021 guidelines: phenylephrine infusion prophylactically post-spinal preferred to reactive dosing

• CPR with manual LUD or 15° left tilt
• If >20 weeks gestation and no ROSC within 4 minutes of arrest: perimortem Caesarean section (resuscitative hysterostomy) within 5 minutes to relieve aortocaval compression and improve CPR efficacy

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Q14. Prerequisites Before Weaning from Cardiopulmonary Bypass

CHECKLIST Before Attempting Weaning:

• All cardiac repair/anastomoses completed
• Haemostasis achieved (no active bleeding from suture lines)
• Cardiac chambers de-aired (confirmed by TOE — no residual air in LV, aorta)
• Aortic cross-clamp released; heart reperfused for adequate time (minimum 30 min for complex surgery)

• Core temperature ≥ 36.0°C (nasopharyngeal or bladder temperature)
• Rewarming completed on CPB before weaning attempt

• Sinus rhythm or acceptable paced rhythm established
• Rate 70–100 bpm optimal
• Defibrillation if VF present (10–20 J internal paddles or 200 J external)
• Pacing wires placed and functioning; pacemaker threshold confirmed
• Correct electrolytes: K⁺ 4.0–4.5 mEq/L (hypokalaemia → arrhythmias); Mg²⁺ supplemented

• Haematocrit ≥ 21–24% (or Hb ≥ 7–8 g/dL) — allows adequate oxygen delivery
• ACT ≥ 480 seconds (still anticoagulated — protamine given only after CPB discontinued)
• Platelets and coagulation reasonable

• Correct severe acidosis (pH ≥ 7.30)
• Correct hypocalcaemia (ionized Ca²⁺ ≥ 1.1 mmol/L) — ionized calcium critical for myocardial contractility
• Blood glucose in acceptable range
• Serum K⁺, Mg²⁺, Na⁺ reviewed

• Lungs reinflated and ventilated (atelectasis cleared)
• ETCO₂ confirmed; FiO₂ 1.0 during weaning attempt
• Bilateral chest auscultation

• Baseline contractility assessed via TOE: new RWMA, LV/RV function
• Plan inotropes if pre-existing LV dysfunction: dopamine, dobutamine, milrinone, adrenaline
• Vasopressors if low SVR expected: norepinephrine, vasopressin

• Arterial line functioning (continuous BP)
• Central venous or PA catheter zeroed
• TOE probe in position for assessment during/after weaning

Weaning Process:

1. Gradually reduce CPB flow (venous clamp gradually closed)
2. LV filling observed via TOE/PAP/CVP
3. Blood transfused from CPB reservoir into patient (volume loading)
4. If haemodynamically stable with adequate filling → clamp venous line, stop pump
5. Assess: HR, BP, cardiac filling, regional wall motion, valve competence on TOE
6. If failure to separate: return to full CPB flow, reassess cause, add inotropes/IABP

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Q15. Atrial Fibrillation Under Anaesthesia: Causes, Diagnosis and Treatment

Causes of New-Onset AF Under Anaesthesia:

• Myocardial ischaemia/infarction
• Cardiac surgery (most common; post-cardiac surgery AF in 20–40% patients)
• Cardiomyopathy, valvular disease (mitral stenosis classically)
• Pre-existing undetected paroxysmal AF

• Hypoxia, hypercarbia
• Hypothermia (<35°C)
• Electrolyte abnormalities: hypokalaemia, hypomagnesaemia, hypercalcaemia
• Thyrotoxicosis
• Sepsis

• Central venous catheter in right atrium → mechanical irritation
• Pericardial effusion
• Vagal or sympathetic stimulation (light anaesthesia, surgical manipulation)
• Pulmonary embolism

• Excessive sympathomimetics (epinephrine, high-dose dobutamine)
• Succinylcholine (causes fasciculation → sympathetic surge)
• Atropine-induced tachycardia allowing flutter breakthrough

Diagnosis:

• ECG: Irregularly irregular rhythm, absent P waves, fibrillatory baseline, variable RR intervals
• Note: under GA, differentiate from:
  • Multifocal atrial tachycardia (P waves present, different morphologies)
  • Atrial flutter (regular sawtooth flutter waves, 2:1–4:1 block)
• Assess haemodynamic impact: BP, SpO₂, ETCO₂

Treatment:

• Immediate synchronized DC cardioversion: 200 J biphasic (AF)
• Sedate if conscious; if under GA, no additional sedation needed

• Beta-blockers: IV metoprolol 2.5–5 mg (max 15 mg); IV esmolol infusion 50–200 mcg/kg/min
• Calcium channel blockers: IV diltiazem 0.25 mg/kg over 2 min; IV verapamil (avoid if WPW or LV dysfunction)
• Digoxin: IV 0.5 mg loading (slow onset; preferred if heart failure present)
• Amiodarone: IV 150–300 mg over 30 min; useful for rate control AND chemical cardioversion

• IV amiodarone 150 mg over 10 min then infusion — preferred if structural heart disease, post-cardiac surgery
• Elective cardioversion after rate control

• Increase FiO₂ if hypoxic
• Rewarm if hypothermic
• IV Mg²⁺ 2 g if hypomagnesaemia or refractory
• Reposition CVP catheter tip from RA into SVC
• Treat ischaemia
• Correct K⁺ (target 4.5–5 mEq/L)

• Under GA, acute new-onset AF <48 hours: thromboembolism risk lower but present
• Post-cardiac surgery AF: anticoagulation protocol per institution
• Haemodynamically stable, duration <48 hours: proceed to cardioversion (electrical or pharmacological)

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Q16. Blood Pressure: Definition, Accurate Measurement, Types of Hypertension

What is Blood Pressure?

• Systolic BP (SBP): Peak pressure during ventricular systole
• Diastolic BP (DBP): Minimum pressure during ventricular diastole
• Pulse pressure (PP): SBP − DBP (normal 40 mmHg); elevated PP in aortic regurgitation, atherosclerosis
• Mean Arterial Pressure (MAP): DBP + ⅓ PP (or [SBP + 2×DBP] / 3); represents average perfusion pressure; normal 70–100 mmHg

Accurate Measurement of Blood Pressure:

• Seated at rest for 5 minutes (avoid exercise, caffeine, smoking 30 min prior)
• Feet flat on floor; back supported; arm at heart level
• Bladder emptied

1. Use appropriate cuff size: cuff bladder should encircle 80% of arm circumference; 40% of arm length
   • Too small cuff → falsely high reading
   • Too large cuff → falsely low reading
2. Apply cuff 2–3 cm above antecubital fossa
3. Palpate brachial artery; inflate cuff to obliterate radial pulse (estimate systolic + 30 mmHg)
4. Place stethoscope over brachial artery
5. Deflate at 2–3 mmHg/second
6. Korotkoff sounds:
   • Phase I: First appearance of sounds = SBP
   • Phase II: Soft murmur
   • Phase III: Louder tapping
   • Phase IV: Muffling
   • Phase V: Disappearance = DBP (use Phase IV in pregnancy/aortic regurgitation where sounds persist to zero)
7. Take mean of 2 readings 1–2 minutes apart

• White coat hypertension (clinic BP > home BP)
• Auscultatory gap (Phase II sounds disappear momentarily in hypertensive patients)
• Always measure in both arms (first visit); right-left difference >10–15 mmHg → investigate subclavian stenosis

Types of Hypertension:

• Normal: <120/<80
• Elevated: 120–129/<80
• Stage 1: 130–139/80–89
• Stage 2: ≥140/≥90
• Hypertensive Crisis: >180/>120
  • Urgency (no end-organ damage)
  • Emergency (end-organ damage: encephalopathy, aortic dissection, STEMI, eclampsia, APO)

• Isolated Systolic Hypertension: SBP ≥140, DBP <90 (elderly; due to arteriosclerosis)
• White Coat Hypertension: Clinic BP elevated, ABPM normal
• Masked Hypertension: Clinic BP normal, ABPM elevated
• Resistant Hypertension: BP uncontrolled despite 3 drugs including diuretic at maximum doses
• Pulmonary Hypertension: mPAP >20 mmHg (WHO classification: Groups I–V)
• Portal Hypertension: Portal venous pressure >10 mmHg (cirrhosis, Budd-Chiari)
• Pregnancy-Induced Hypertension: Gestational HTN, pre-eclampsia, eclampsia, HELLP

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Q17. Coronary Circulation and Monitoring of Ischaemia

Coronary Circulation (Labelled Description):

• Left Coronary Artery (LCA): Arises from left aortic sinus → Left Main Coronary Artery (LMCA, 0.5–2 cm) → bifurcates into:
  1. Left Anterior Descending (LAD): Descends in anterior interventricular sulcus; supplies anterior LV, anterior IVS, apex, anterior papillary muscle; gives off septal perforators and diagonal branches
  2. Left Circumflex (LCX): Runs in left atrioventricular groove; supplies lateral and posterior LV; gives off obtuse marginal (OM) branches; gives rise to SA node artery in 40%
• Right Coronary Artery (RCA): Arises from right aortic sinus → runs in right AV groove → gives right marginal branch → turns to posterior interventricular groove as Posterior Descending Artery (PDA); supplies RV, inferior LV, inferior IVS, SA node (60%), AV node (85%), posterior papillary muscle

• Right dominant (85%): PDA from RCA
• Left dominant (8%): PDA from LCX
• Codominant (7%)

• Total: ~250 mL/min at rest (5% of CO); increases to 1200 mL/min with exercise (4-fold)
• Diastolic flow dominant (especially LCA — LCA flow is reversed/reduced in systole due to intramyocardial compression)
• Coronary perfusion pressure (CPP) = Diastolic BP − LVEDP
• Autoregulation: 60–130 mmHg (loses autoregulation below 60 mmHg)
• O₂ extraction: 70–80% at rest (cannot increase much; depends on ↑ flow for more O₂)

• Coronary sinus (drains 85% of LV venous blood) → right atrium
• Anterior cardiac veins → directly to RA
• Thebesian veins → direct drainage into cardiac chambers

Monitoring Ischaemia During Anaesthesia:

• II + V5: detects 80% of ischaemic episodes
• Adding V4 increases to 96%
• ST depression >1 mm (horizontal/downsloping) = subendocardial ischaemia
• ST elevation >2 mm = transmural ischaemia

• New Regional Wall Motion Abnormality (RWMA) = earliest sign; precedes ECG changes by 30–60 seconds
• 16-segment model; each segment correlates with a coronary distribution
• Also detects: LV/RV dysfunction, valve complications, pericardial effusion

• New PCWP elevation + V-waves = papillary muscle ischaemia → acute MR
• PA diastolic pressure rises with LV diastolic dysfunction

• Troponin I/T post-op: gold standard for perioperative MI diagnosis
• CKMB (less specific)

• Cerebral oximetry (rSO₂) — indirect ischaemia detection

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Factors Affecting Myocardial Oxygen Consumption (MVO₂):

1. Heart Rate — most important single determinant (rate × work = rate-pressure product); tachycardia doubles MVO₂
2. Contractility (inotropy) — increased sympathetic tone, catecholamines
3. Wall Tension (systolic) = Preload (EDV) + Afterload (SVR) — via Laplace's law

• Basal metabolic rate of myocardium
• Depolarization energy (small)
• External work (pressure–volume work)

• Tachycardia is most detrimental: ↑ MVO₂ + ↓ coronary perfusion time (shorter diastole) → double jeopardy
• Hypertension → ↑ afterload → ↑ wall tension → ↑ MVO₂
• Anaemia → ↓ O₂ supply; must maintain Hb ≥8–10 g/dL in CAD
• LVH → ↑ wall tension; subendocardial ischaemia even without stenosis
• Vasospasm → ↓ supply (Prinzmetal angina)
• Targets: HR 50–70/min, DBP maintained (CPP), normoxia, normocarbia, normothermia

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Q18. Rheumatic Heart Disease, Severe Mitral Stenosis, 36-Week Pregnant for LSCS

a) Pathophysiology of Mitral Stenosis (5 marks)

• Mild MS: MVA 1.5–2.5 cm² (symptoms with exertion)
• Moderate MS: MVA 1.0–1.5 cm²
• Severe MS: MVA < 1.0 cm² (symptoms at rest)

1. Mitral valve obstruction → restricted LV filling
2. ↑ Left atrial pressure (LAP) → LA dilatation → AF risk
3. ↑ Pulmonary venous pressure → pulmonary oedema (once LAP >25 mmHg)
4. Reactive pulmonary hypertension: initially reversible (vasoconstriction), then irreversible (medial hypertrophy)
5. ↑ RV afterload → RV hypertrophy → eventual RV failure → TR
6. Fixed cardiac output: LV is protected (often normal LV function) but output cannot increase; exertion, tachycardia, pregnancy → acute decompensation

• Slow heart rate (60–80/min): Tachycardia reduces diastolic filling time → dramatic rise in LAP → flash pulmonary oedema
• Maintain sinus rhythm (atrial kick contributes significantly due to stiff mitral valve gradient)
• Avoid sudden ↑ preload (worsens pulmonary oedema)
• Avoid ↓ SVR (hypotension → reflex tachycardia → decompensation)
• Avoid pulmonary vasodilators if severe PHT with fixed PVR (can ↓ RV afterload abruptly)

• Plasma volume ↑ 40–50% (↑ preload → ↑ LAP)
• HR physiologically ↑ 15–20 bpm (↓ diastolic filling time)
• Second stage labour: Valsalva → sudden preload changes
• Uterine contractions → autotransfusion of 300–500 mL with each contraction
• Peak risk: 28–32 weeks and post-partum (autotransfusion after delivery)

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b) Anaesthetic Plan for LSCS in Severe MS (5 marks)

• Cardiology review; echocardiogram (confirm MVA, gradient, PAP, LV function, LA thrombus)
• Diuretics: careful diuresis if pulmonary congestion (avoid over-diuresis → ↓ preload → ↓ CO)
• Rate control: Beta-blockers (metoprolol, atenolol — safe in pregnancy); digoxin if AF with rapid ventricular response
• Anticoagulation (warfarin in metallic valves — switch to LMWH near term)
• Antibiotic prophylaxis: no longer routine for dental/obstetric procedures per NICE 2008 guidelines, but many centres continue for high-risk RHD
• If LA thrombus + severe MS + no prior intervention: consider balloon mitral valvuloplasty before delivery if MVA <1.0 cm² and symptoms uncontrolled

• Epidural (CSE) is preferred over single-shot spinal:
  • Slow, controlled onset of sympathectomy → avoids sudden SVR drop → avoids reflex tachycardia
  • Allows titration to haemodynamics
  • Provides post-op analgesia (pain → tachycardia)
  • Single-shot spinal risk: sudden profound hypotension → reflex tachycardia → decompensation
• Low-dose combined spinal-epidural (CSE) with intrathecal bupivacaine (7.5 mg) + fentanyl (15 mcg) + epidural top-up prn: acceptable with invasive monitoring

• Invasive arterial line (pre-induction, for beat-to-beat BP)
• CVP / PA catheter consideration (severe PHT or RV dysfunction)
• SpO₂, ETCO₂
• Continuous ECG (detect AF)
• Foetal heart rate monitoring until incision

• Avoid tachycardia at all costs:
  • IV esmolol/metoprolol for HR >90/min
  • If new AF with rapid ventricular rate: rate control immediately (digoxin, metoprolol)
  • If AF with haemodynamic compromise: synchronized DC cardioversion
• Vasopressors: Use phenylephrine (pure alpha-agonist) — maintains SVR without tachycardia (preferred over ephedrine which causes reflex tachycardia)
• Maintain preload carefully — not excessive: modest IV crystalloid
• Oxytocin: Give as slow infusion (2–5 units over 20 min), not as bolus (causes tachycardia, vasodilation → catastrophic in MS)
• Ergometrine: Contraindicated (causes pulmonary vasoconstriction → ↑ PHT)
• Carboprost (15-methyl PGF2α): Contraindicated (pulmonary bronchoconstriction and vasoconstriction)
• Dinoprostone (PGE2) acceptable if needed

• HDU/ICU admission
• Highest risk: first 24–48 hours post-partum (autotransfusion → volume overload)
• Continue heart rate control and diuretics
• Thromboprophylaxis (LMWH when haemostasis confirmed)
• Restart anticoagulation in 12–24 hours post-surgery

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Q19. Pre-Anaesthetic Evaluation: 70-Year-Old Chronic Smoker, 10 Years Systemic Hypertension on Medications, for Total Hip Replacement (THR)

Systematic Pre-Anaesthetic Evaluation:

• Functional capacity (METs): Can patient climb one flight of stairs? Walk on level ground? (>4 METs = adequate; <4 METs = investigate)
• Smoking history: pack-years; current or ex-smoker; cough, sputum, wheeze (COPD severity)
• Hypertension: duration (10 years), compliance with medications, end-organ damage (headache, visual disturbance, chest pain, shortness of breath, oliguria)
• Cardiovascular: angina (exertional/rest), dyspnoea (NYHA class), palpitations, orthopnoea, oedema, previous MI, previous cardiac procedures
• Cerebrovascular: history of stroke, TIA
• Renal: polyuria, nocturia, peripheral oedema
• Previous anaesthesia and any complications
• Drug history: antihypertensives (beta-blockers, CCBs, ACE-I, ARBs, diuretics), antiplatelet agents, anticoagulants, OTC drugs
• Allergies
• Last meal time (fasting status)

• General: BMI, body habitus, obesity
• Airway assessment: Mallampati grade, mouth opening, neck mobility, thyromental distance, prognathia — predict difficult airway
• Cardiovascular: HR (resting), rhythm, BP in both arms; carotid bruits; JVP elevation; apex beat (laterally displaced in LVH/CCF); added heart sounds (S3 = CCF, S4 = diastolic dysfunction); murmurs (new MR, AS); peripheral oedema
• Respiratory: Trachea, chest expansion, percussion, auscultation; wheeze (COPD/asthma), crepitations (CCF/pneumonia), reduced air entry
• Neurological: Any focal deficits suggesting prior stroke
• Musculoskeletal: Spine (for neuraxial anaesthesia feasibility — degenerative changes, scoliosis common in elderly)

• Revised Cardiac Risk Index (RCRI): score ≥3 = high perioperative cardiac risk
  • High-risk surgery ✓, ischaemic heart disease, CCF, cerebrovascular disease, DM on insulin, Cr >2 mg/dL
• AHA/ACC Guidelines: Calculate risk of MACE (Major Adverse Cardiac Events); if >1% → consider further workup
• RCRI for this patient: High-risk surgery (orthopedic; total hip) + smoking/hypertension = intermediate-high risk

• Ensure BP controlled: target <160/100 mmHg; ideally <140/90 mmHg
• Continue antihypertensives (hold ACE-I/ARBs morning of surgery)
• Beta-blockers: continue if on them; do NOT start de novo for non-cardiac surgery ≤1 day pre-op (harm)
• Statin therapy: optimise/start (pleiotropic vascular benefit)
• Treat any active cardiac issues (decompensated CCF, unstable angina)

• Smoking cessation: minimum 8 weeks for pulmonary benefit; shorter cessation still helps (CO levels drop within 12–24 hours — improves O₂ delivery)
• Chest physiotherapy pre-op; nebulisers (salbutamol + ipratropium if COPD)
• Steroid inhalers if significant COPD/asthma
• Optimise COPD: FEV₁ > 50% acceptable for elective surgery

• Correct hypokalaemia if on diuretics (target K⁺ >3.5 mEq/L)
• Optimize glycaemic control if diabetic (HbA1c <8%)
• Address anaemia: pre-operative iron therapy, EPO if time permits (planned THR — 4–6 weeks pre-op optimization)

• Spinal / Regional anaesthesia preferred for THR:
  • Reduces DVT, pulmonary embolism, blood loss, post-op confusion (reduced cognitive dysfunction in elderly)
  • Avoids need for ETT (better for COPD)
  • Check spine: degenerative changes may complicate needle placement
  • Hyperbaric bupivacaine 0.5% 3 mL ± intrathecal opioid (fentanyl 15–25 mcg)
• Peripheral nerve blocks (femoral nerve + sciatic, or PENG block, L-FICB): excellent post-op analgesia, reduce opioid requirements in elderly
• General anaesthesia if regional contraindicated (anticoagulation, spine pathology, patient refusal):
  • Risk of aspiration, post-op confusion, respiratory complications (COPD)
  • LMA vs ETT based on airway assessment

• Mandatory in THR: mechanical (TED stockings + IPD) + pharmacological (LMWH or rivaroxaban 10 mg OD for 35 days post-THR)

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