Anesthesia

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"epidural analgesia (TEA) with paravertebral block (PVB) for thoracotomy analgesia including evidence [4]. List the complications specific to each technique [3]. ⚙ Core Concept Thoracic epidural analgesia has been the gold standard for post-thoracotomy and post-thoracoscopy pain management for decades. The paravertebral block has emerged as a compelling alternative — equivalent analgesia with a more favourable side-effect profile (less hypotension, urinary retention, motor block). The choice between them depends on surgical approach, patient factors, and institutional expertise. (Richardson J — PVB; Joshi GP — TEA vs PVB meta-analysis; Miller's Anaesthesia 9th Ed) A. Paravertebral Space Anatomy and Block Mechanism 3 marks Paravertebral space (PVS) anatomy: the PVS is a wedge-shaped space lying alongside the vertebral column; boundaries: anterior — parietal pleura (and endothoracic fascia separating PVS from pleura); posterior — superior costotransverse ligament (running from the transverse process above to the rib below); medial — vertebral body, intervertebral disc, and intervertebral foramen; lateral — the space is open laterally and communicates freely with the intercostal space; the PVS contains: the spinal nerve (dorsal and ventral rami), the rami communicantes, the sympathetic chain (lies in the anterior PVS), intercostal vessels, and fatty areolar tissue Communication between levels: the PVS is not a discrete compartment — it communicates freely with adjacent levels via the endothoracic fascia (which is loosely attached medially) → a single injection of 15–20 mL LA typically spreads 4–5 dermatomal levels; bilateral PVBs can be performed for bilateral thoracic analgesia Mechanism of block: LA injected into the PVS directly contacts the spinal nerve before it divides into dorsal and ventral rami → blocks the spinal nerve root → ipsilateral somatic block of the dermatomal level; LA also contacts the sympathetic chain (anterior PVS) → ipsilateral sympathetic block; because the sympathetic block is ipsilateral only (not bilateral as in epidural), haemodynamic stability is significantly better than thoracic epidural Technique: landmark: 2.5 cm lateral to the midline at the spinous process of the target vertebra; needle inserted perpendicular until it contacts the transverse process (typically at 2–4 cm depth) → walk the needle caudally or cranially off the transverse process → advance 1 cm further → loss of resistance as needle passes through the superior costotransverse ligament into the PVS; inject 5 mL per level (or 20–25 mL for 4–5 level spread at one injection); ultrasound- guided: high-frequency probe parasagittal at 2.5 cm lateral → identify transverse processes, pleura, and the hyperechoic costotransverse ligament → inject under real-time visualisation with pleural depression as the endpoint (pleura pushed anteriorly as LA fills the PVS) B. TEA vs PVB — Comparison and Evidence 4 marks Parameter Thoracic Epidural (TEA) Paravertebral Block (PVB) Analgesia quality Excellent bilateral analgesia; gold standard; superior for bilateral thoracic pain or median sternotomy Equivalent to TEA for unilateral thoracotomy (multiple RCTs and meta-analyses confirm non-inferiority); slightly inferior for bilateral procedures Hypotension Common (15–30%) — bilateral sympathetic block → bilateral vasodilation; requires vasopressor support Significantly less (5–10%) — unilateral sympathetic block only; haemodynamic stability superior to TEA Urinary retention Very common (20–40%) — sacral parasympathetic block; almost universal need for urinary catheter Rare — no sacral nerve involvement; catheter often not needed Motor block (legs) Common — LA spreads to lumbar segments → leg weakness; limits mobilisation Rare — LA stays in thoracic PVS; legs unaffected; early mobilisation possible Nausea/vomiting More common (motor block + hypotension + opioid + N₂O interactions) Less common Technical difficulty High in thoracic region — T4–T6 (narrow interspinous spaces, steep spinous processes require paramedian approach) Relatively easier — posterior landmark technique or USG; lower failure rate in experienced hands Failure rate 20–30% for incomplete or inadequate epidural block ~10% with landmark technique; <5% with USG-guidance Contraindications Coagulopathy, anticoagulation, raised ICP, infection at site, patient refusal Fewer absolute contraindications; coagulopathy remains a relative contraindication (but the risk of haematoma is lower than epidural — PVS is not enclosed within the spinal canal) Serious complications Epidural haematoma (1:150,000 — NAP3), epidural abscess, total spinal, spinal cord ischaemia Pneumothorax (0.5–1%), pleural puncture, intravascular injection (intercostal vessels), haematoma (lower risk than epidural), Horner's syndrome (stellate ganglion block) ⭐ Key Evidence Richardson J et al. (Anaesthesia 1999): first major RCT — PVB = TEA for post-thoracotomy analgesia with fewer side effects. Joshi GP et al. (Chest 2008): meta-analysis — PVB provides equivalent analgesia to TEA but with significantly lower rates of hypotension, urinary retention, nausea/vomiting, and pulmonary complications after thoracotomy. PROSPECT (Procedure-Specific Postoperative Pain Management) guidelines: either TEA or PVB is recommended for thoracotomy — the choice depends on surgeon/anaesthetist preference and patient factors. C. Complications Specific to Each Technique 3 marks TEA-Specific Complications PVB-Specific Complications Epidural haematoma — life-threatening; must follow ASRA anticoagulation timing guidelines Pneumothorax — most feared complication; incidence 0.5–1%; may be small and self- limiting or require intercostal drain; minimised by USG guidance (direct pleura visualisation) Epidural abscess — delayed (days) back pain + fever + neurological deficit → emergency MRI + surgical drainage Horner's syndrome — LA spreads to stellate ganglion (ptosis, miosis, anhidrosis) — alarming for patient but harmless and self-limiting; occurs in 1–5% Dural puncture → PDPH — risk with thoracic epidural is lower than lumbar (steep angle, experienced hands) but catastrophic if unrecognised → high spinal Vascular injection — intercostal vessels in PVS → LA systemic absorption → LAST; incremental injection with aspiration before each aliquot Total spinal — inadvertent intrathecal injection of epidural dose Bilateral spread — if LA passes medially through the intervertebral foramen → epidural spread → may produce bilateral block (5–10%); rarely problematic Spinal cord ischaemia — rare but devastating; risk with inadvertent intra- arterial injection (artery of Adamkiewicz) Failure to enter PVS — needle enters muscle or pleural space without entering PVS; USG reduces failure rate ★ Examiner's Pearl PVS boundaries: anterior = parietal pleura; posterior = superior costotransverse ligament; medial = vertebral body/IVF; lateral = open to intercostal space. PVB advantage over TEA: unilateral sympathetic block → haemodynamic stability (↓ hypotension, ↓ urinary retention, ↓ motor block). Evidence: PVB = TEA for post- thoracotomy analgesia (Richardson 1999; Joshi 2008 meta-analysis). PVB-specific complication: pneumothorax (0.5–1%). TEA-specific: epidural haematoma (1:150,000). Horner's syndrome from PVB = benign (stellate ganglion block). References: Richardson J et al. Thoracic paravertebral block vs thoracic epidural (Anaesthesia 1999;54:1023-1030). Joshi GP et al. Systematic review of TEA vs PVB (Chest 2008;134:1271- 1279). Davies RG et al. A comparison of the analgesic efficacy of TEA and PVB for thoracotomy (Br J Anaesth 2006;96:418-426). Miller RD et al. Miller's Anaesthesia, 9th Ed."

"and outline the principles of ICP management in traumatic brain injury [4]. Compare the effects of volatile anaesthetic agents and propofol-based TIVA on ICP and cerebrovascular autoregulation [3]. ⚙ Core Concept The skull is a rigid box — any increase in intracranial volume must be compensated by reduction in another compartment or ICP will rise. Understanding this pressure-volume relationship, and the physiological mechanisms that regulate it, is the foundation of all neuroanaesthetic management — from the positioning of a craniotomy patient to the management of a comatose TBI patient in the ICU. (Monroe A 1783; Kellie G 1824; Rosner MJ — CPP optimisation; Miller's Anaesthesia 9th Ed) A. Monroe-Kellie Doctrine and ICP-Volume Relationship 3 marks Monroe-Kellie doctrine: the cranial vault is a rigid, fixed-volume container; total intracranial volume = brain parenchyma (80–85%) + CSF (10%) + blood (cerebral blood volume — CBV, 5–10%); because the skull is rigid, the total volume is constant: V brain + V CSF + V blood + V lesion = constant; any increase in any one component must be compensated by a decrease in another — or ICP will rise Compensatory mechanisms: initial compensatory mechanisms are highly effective — displacement of CSF from the cranial to the spinal subarachnoid space (300–400 mL capacity); compression of cerebral venous blood out of the cranium via the jugular veins; these mechanisms allow significant increases in intracranial volume with minimal rise in ICP (the ""compensated"" or flat part of the pressure-volume curve) ICP-volume (compliance) curve — exponential relationship: the relationship between intracranial volume and ICP is NOT linear but exponential; as the compensatory reserve is exhausted, the curve becomes steep — small additional increases in volume → dramatic rises in ICP (""decompensated"" phase); the point of inflection is where compensatory mechanisms fail; normal ICP: 5–15 mmHg supine (adult); ICP >20 mmHg sustained = raised ICP requiring treatment; ICP >40 mmHg = severe, life-threatening; pressure-volume index (PVI): the volume required to raise ICP 10-fold — normal PVI ≈ 26 mL; reduced PVI = reduced compliance = patient on the steep part of the curve ICP waveforms (Lundberg classification): A-waves (plateau waves) — sustained ↑ ICP to 50–100 mmHg for 5–20 minutes → pathological, indicates critically reduced compliance → medical emergency; B-waves — rhythmic ↑ ICP at 0.5–2/min, amplitude 20–50 mmHg → associated with Cheyne-Stokes breathing, less urgent; C-waves — small rhythmic variations at 4–8/min, may be normal B. Cerebral Perfusion Pressure and ICP Management in TBI 4 marks Definitions: CPP = MAP − ICP (or MAP − CVP if CVP > ICP — rarely clinically relevant); target CPP in TBI: 60–70 mmHg (Brain Trauma Foundation guidelines); below 50 mmHg → cerebral ischaemia; above 70 mmHg → risk of adult respiratory distress syndrome (ARDS) from aggressive vasopressor use; CBF autoregulation: normally maintains constant CBF over MAP 50–150 mmHg via myogenic and metabolic mechanisms; in TBI: autoregulation may be impaired → ""pressure-passive"" flow — CBF directly proportional to CPP (loss of autoregulation increases vulnerability to both hypotension and hypertension) Intervention Mechanism Target / Detail Head position Head-of-bed elevation 30° → facilitates jugular venous drainage → ↓ CBV → ↓ ICP; avoid neck flexion or rotation (impairs jugular drainage) 30° head-up — not flat (increases CBV) and not excessively elevated (reduces CPP) Normoventilation PaCO₂ 35–40 mmHg; CO₂ is the most potent regulator of CBF: ↑ PaCO₂ → vasodilation → ↑ CBV → ↑ ICP; hyperventilation (↓ PaCO₂) → vasoconstriction → ↓ CBV → ↓ ICP; but: prolonged hyperventilation → ischaemia (vasoconstriction reduces O₂ delivery); use only as a short-term measure (crisis) Target PaCO₂ 35–40 mmHg; hyperventilation to PaCO₂ 30– 35 mmHg only as bridge to definitive treatment (max 30 min) Hyperosmolar therapy Mannitol 20% (0.25–1 g/kg) — osmotic diuretic; creates osmotic gradient across intact BBB → draws water from oedematous brain tissue into intravascular compartment → ↓ brain water → ↓ ICP; onset 15–30 min; also: ↑ blood rheology (↓ viscosity → ↑ CBF at same CPP); monitor serum osmolality (target <320 mOsm/kg — above this, risk of AKI); hypertonic saline (3% or 23.4%) — equivalent or superior to mannitol; no diuresis (useful in haemodynamically unstable patients) Mannitol 0.25–1 g/kg IV over 20 min; repeat 6-hourly; stop if serum osmolality >320 CSF drainage External ventricular drain (EVD) — catheter placed in lateral ventricle; allows direct ICP measurement AND therapeutic CSF drainage (removing CSF directly reduces intracranial volume → ↓ ICP immediately); most effective for ICP control Drain 1–5 mL CSF → ↓ ICP rapidly; gold standard for ICP monitoring and management in severe TBI Sedation and analgesia Propofol infusion → ↓ CMRO₂ → ↓ CBF → ↓ CBV → ↓ ICP; also ↓ sympathetic surges that raise ICP (coughing, suctioning); opioids (fentanyl/remifentanil) → blunt noxious stimuli → prevent ICP spikes; avoid ketamine (historically; recent evidence is less clear — may be used with concurrent sedation) Target RASS −2 to −3; midazolam + fentanyl or propofol + remifentanil Neuromuscular blockade Prevents coughing, straining, Valsalva → prevents ICP spikes; use when other measures fail to control ICP Cisatracurium or vecuronium infusion; monitor with TOF Decompressive craniectomy Surgical removal of a bone flap → ↑ effective cranial compliance → allows brain swelling without ICP rise; last- resort for refractory raised ICP DECRA trial: craniectomy ↓ ICP but worse neurological outcomes; RESCUEicp trial: ↓ mortality but ↑ vegetative survivors — controversial C. Volatile Agents vs Propofol TIVA — ICP and Autoregulation 3 marks Property Volatile Agents (Isoflurane, Sevoflurane, Desflurane) Propofol TIVA (+ Remifentanil) CBF effect Direct cerebrovascular vasodilation (dose-dependent) → ↑ CBF despite ↓ CMRO₂ — ""luxury perfusion""; uncouples CMRO₂-CBF relationship at >1 MAC; desflurane > isoflurane > sevoflurane in vasodilating effect ↓ CBF proportional to ↓ CMRO₂ — COUPLING PRESERVED; no direct vasodilatory effect; propofol reduces both CMRO₂ and CBF proportionally → maintains cerebrovascular coupling ICP effect ↑ ICP (at >0.5–1 MAC) — vasodilation → ↑ CBV → ↑ ICP; this effect is attenuated by concurrent hyperventilation (↓ PaCO₂ → vasoconstriction counteracts volatile vasodilation); sevoflurane has the least vasodilatory effect of the halogenated agents — preferred if volatile is used for neuroanaesthesia ↓ ICP — ↓ CBV via ↓ CMRO₂-coupled CBF reduction; preferred for patients with raised ICP or reduced intracranial compliance Autoregulation Impairs cerebrovascular autoregulation in a dose-dependent manner (≥1 MAC significantly impairs autoregulation) → CBF becomes pressure-passive; sevoflurane preserves autoregulation better than isoflurane or desflurane at 1 MAC Preserves cerebrovascular autoregulation at clinical doses — an important advantage in TBI where autoregulation may already be impaired and any further loss increases vulnerability Intraoperative neurophysiological monitoring (IONM) Significantly suppress MEPs (motor evoked potentials) in a dose-dependent manner; >0.5 MAC severely impairs MEP amplitude → unreliable for spinal cord monitoring during spine surgery TIVA with propofol + remifentanil: MEPs well-preserved at clinical doses → the preferred technique for all surgeries requiring IONM (scoliosis correction, intradural spinal tumours, skull base surgery) Neuroanaesthesia recommendation If used: ≤1 MAC with hyperventilation to normal PaCO₂; sevoflurane preferred; avoid desflurane in patients with raised ICP; not recommended for patients with severe TBI or reduced compliance Preferred for: patients with raised ICP; craniotomy for tumour/aneurysm; TBI anaesthesia; any procedure requiring IONM; essentially the modern standard for neuroanaesthesia ★ Examiner's Pearl Monroe-Kellie: V brain + V CSF + V blood = constant (rigid skull); ICP-volume curve is exponential — flat compensated phase then steep decompensated phase. CPP = MAP − ICP; target 60–70 mmHg in TBI. ICP management hierarchy: head 30° → normoventilation → mannitol/HTS → CSF drainage → sedation → decompressive craniectomy. Volatile agents: ↑ ICP (vasodilation → ↑ CBV) + impair autoregulation (dose-dependent). Propofol TIVA: ↓ ICP + preserves autoregulation + preserves MEPs → preferred for neuroanaesthesia and IONM. References: Brain Trauma Foundation. Guidelines for the Management of Severe TBI, 4th Ed (2016). Rosner MJ. CPP management in TBI (J Neurosurg 1995;83:949-962). Lam AM. Cerebral blood flow monitoring (Anesthesiology 1994;81:1256-1263). Miller RD et al. Miller's Anaesthesia, 9th Ed, Chapter 57."

"including specific mechanisms relevant to cardiac surgery [4]. Outline evidence-based strategies for perioperative renal protection [4]. ⚙ Core Concept Perioperative AKI is one of the most common and consequential complications of major surgery — occurring in 5–30% of cardiac surgical patients and associated with 5-fold increase in 30-day mortality. Despite decades of research, no pharmacological renal protection strategy has proven effective in RCTs — ""do no harm"" and optimising haemodynamics remain the most evidence-based approach. (KDIGO AKI Work Group 2012; Kellum JA; Meersch M — RESPONSE trial; Miller's Anaesthesia 9th Ed) A. KDIGO Classification 2 marks KDIGO Stage Serum Creatinine Criterion Urine Output Criterion Clinical Significance Stage 1 1.5–1.9× baseline within 7 days, OR ↑ ≥26.5 μmol/L (≥0.3 mg/dL) within 48h <0.5 mL/kg/h for 6–12h Early AKI — often reversible; ICU monitoring, avoid nephrotoxins, optimise fluid balance Stage 2 2.0–2.9× baseline <0.5 mL/kg/h for ≥12h Established AKI — significant risk of progression; consider renal replacement therapy if not improving Stage 3 ≥3× baseline, OR ≥353.6 μmol/L (≥4.0 mg/dL) with acute rise ≥44.2 μmol/L, OR initiation of renal replacement therapy, OR (in patients <18 years) eGFR <35 mL/min/1.73m² <0.3 mL/kg/h for ≥24h, OR anuria for ≥12h Severe AKI — RRT usually required; mortality greatly elevated; long-term CKD risk in survivors B. Pathophysiology of Perioperative AKI 4 marks Normal renal physiology relevant to AKI: the kidney receives 20–25% of cardiac output (1.0–1.2 L/min) — disproportionate to its mass; the outer medulla (thick ascending limb of loop of Henle) is the most vulnerable region — it has the highest O₂ consumption of any tubular segment (active Na ⁺ -K ⁺ -ATPase driven co-transport) but the lowest PO₂ in the body (10–20 mmHg in the medulla vs 50–60 mmHg in the cortex) — already on the verge of ischaemia at baseline; renal autoregulation maintains GFR over MAP 70–160 mmHg via afferent arteriolar myogenic response and tubuloglomerular feedback; below MAP 70 mmHg → autoregulation fails → pressure-passive GFR General mechanisms of perioperative AKI: Ischaemia-reperfusion injury: hypotension + ↓ renal perfusion → renal tubular cell ischaemia → necrosis (acute tubular necrosis — ATN — the most common form of perioperative AKI); reperfusion → reactive oxygen species (ROS) → further oxidative injury → apoptosis; the medullary thick ascending limb is the first and most severely affected Haemodynamic compromise: reduced MAP → ↓ renal perfusion pressure; reduced CO → ↓ renal blood flow; renovascular disease (atherosclerotic renal artery stenosis → autoregulation curve shifted right → autoregulation fails at MAP 80–90 mmHg → higher MAP target required) Inflammatory cascade: surgical stress → systemic inflammatory response → cytokine release (TNF-α, IL-6, IL-18) → direct tubular cell injury independent of ischaemia; neutrophil activation → microthrombi in peritubular capillaries Nephrotoxins: contrast media (direct tubular toxicity + vasoconstriction); aminoglycosides (proximal tubule accumulation); NSAIDs (↓ prostaglandin- mediated afferent arteriolar dilation → ↓ GFR particularly in low-flow states); ACE inhibitors/ARBs (blunt the angiotensin II-mediated efferent arteriolar constriction that maintains GFR during low-flow → GFR falls further) Cardiac surgery-specific mechanisms (additional): Cardiopulmonary bypass (CPB) — non-pulsatile flow: CPB replaces normal pulsatile cardiac output with non-pulsatile (laminar) flow → loss of pulsatility activates renin-angiotensin-aldosterone system (RAAS) → ↑ angiotensin II → renal vasoconstriction → ↓ renal blood flow despite adequate mean perfusion pressure Haemolysis on CPB: shear forces in the pump → RBC haemolysis → free haemoglobin in plasma → exceeds haptoglobin binding capacity → free Hb reaches renal tubules → oxidative injury + tubular obstruction → pigment nephropathy Microemboli: air, particulate, and fat microemboli from CPB circuit → lodge in renal microvasculature → focal ischaemia Hypothermia: deliberate hypothermia on CPB → ↓ metabolic rate (protective) but also ↓ renal blood flow; on rewarming → reperfusion injury Inflammatory activation: blood-foreign surface contact in CPB circuit → complement activation → massive SIRS → cytokine-mediated AKI C. Perioperative Renal Protection Strategies 4 marks Strategy Evidence / Rationale Recommendation Haemodynamic optimisation — MOST IMPORTANT Maintaining MAP ≥65–70 mmHg (higher in chronic hypertensives — MAP ≥80 mmHg); preventing prolonged hypotension (>5–10 min below MAP 65 mmHg → AKI risk increases linearly with hypotension duration and depth — Bijker et al. 2009); goal-directed therapy (GDT) using cardiac output monitoring to optimise DO₂ → reduced AKI in high-risk surgical patients Grade 1A recommendation: prevent and promptly treat intraoperative hypotension; MAP ≥65 mmHg (or ≥80 mmHg in chronic hypertensives); avoid sustained MAP <55 mmHg Balanced crystalloid resuscitation SMART trial (Semler et al. NEJM 2018): balanced crystalloids (Lactated Ringer's/PlasmaLyte) vs 0.9% normal saline — balanced crystalloids ↓ major adverse kidney events (MAKE30) by 1.1% (NNT 94); normal saline → hyperchloraemic metabolic acidosis → renal vasoconstriction; avoid large volumes of normal saline perioperatively Use balanced crystalloids (Hartmann's, PlasmaLyte) rather than 0.9% NaCl for IV fluid resuscitation — GRADE 2B recommendation Avoiding nephrotoxins Hold NSAIDs in high-risk patients; hold ACE-I/ARB on day of major surgery (especially vascular, cardiac); avoid aminoglycosides if alternatives exist; contrast nephropathy: pre-hydration with isotonic crystalloid (1 mL/kg/h for 12h before and after contrast) ± N-acetylcysteine (evidence limited but cheap and safe) Pre-operatively identify and hold nephrotoxins; review drug chart; avoid contrast within 48h of surgery where possible Remote ischaemic preconditioning (RIPC) Brief cycles of upper limb ischaemia-reperfusion (3 × 5 min ischaemia/5 min reperfusion with blood pressure cuff) before cardiac surgery → activates endogenous cytoprotective pathways (adenosine, NO, δ-opioid receptor signalling) → reduces renal tubular injury; ERICCA and RIPHeart trials: no reduction in AKI in propofol-based TIVA but positive results in volatile anaesthesia — propofol may blunt the protective signalling pathway RIPC is simple, safe, and low-cost; consider in cardiac surgery patients receiving volatile anaesthesia (NOT with propofol TIVA) Pharmacological ""renoprotection"" — largely INEFFECTIVE Low-dose dopamine (""renal dose""): CONCLUSIVELY PROVEN INEFFECTIVE (ANZICS trial 2000) — no reduction in AKI, RRT, or mortality; AVOID; Fenoldopam (selective DA1 agonist → renal vasodilation): some early positive data; meta-analyses inconclusive; expensive; not standard of care; NAC: cheap, safe, insufficient evidence; Diuretics (fentyl/mannitol): do NOT prevent AKI; may be useful to manage fluid overload once AKI established but do NOT prevent it; Erythropoietin, ANP: no clinical benefit in RCTs NO pharmacological agent has proven renal protective effect in adequately powered RCTs — haemodynamic optimisation remains the cornerstone Early biomarker- guided intervention (emerging) Novel AKI biomarkers: TIMP-2 × IGFBP-7 (NephroCheck™) — predicts AKI before creatinine rises; RESPONSE pilot trial (Meersch 2017): biomarker-guided care bundle (avoid nephrotoxins, fluid optimisation, haemodynamic monitoring) → ↓ severe AKI incidence; currently research setting Emerging — not yet standard of care; NephroCheck may identify high-risk patients 12–24h before creatinine rises, allowing proactive management ★ Examiner's Pearl KDIGO Stage 1: Cr ×1.5–1.9 or ↑ ≥26.5 μmol/L in 48h or UO <0.5 mL/kg/h ×6h. Most vulnerable renal region: outer medulla (thick ascending limb) — highest O₂ consumption + lowest PO₂. Cardiac surgery AKI extras: non-pulsatile CPB → RAAS activation; haemolysis → free Hb pigment nephropathy; microemboli. Low-dose dopamine: PROVEN INEFFECTIVE (ANZICS 2000) — do NOT use. Balanced crystalloids > normal saline (SMART trial). Haemodynamic optimisation (MAP ≥65, GDT): the only proven strategy. References: KDIGO AKI Work Group. KDIGO Clinical Practice Guideline for AKI (Kidney Int Suppl 2012;2:1-138). Semler MW et al. SMART trial (NEJM 2018;378:819-828). Bellomo R et al. Low-dose dopamine in ICU (Lancet 2000;356:2139-2143). Miller RD et al. Miller's Anaesthesia, 9th Ed, Chapter 66."

"thromboelastography (TEG) and rotational thromboelastometry (ROTEM) and their clinical parameters [4]. Outline a goal-directed massive transfusion protocol using viscoelastic testing [3]. ⚙ Core Concept The classic coagulation cascade (intrinsic/extrinsic pathways) is a useful laboratory model but fails to explain real haemostasis in vivo. The cell-based model (Hoffman & Monroe 2001) better explains clinical coagulopathies and the role of platelets. TEG/ROTEM provide a global, real-time picture of haemostasis — from clot initiation through formation to lysis — and guide goal-directed transfusion therapy that has been shown to reduce blood product use and mortality. (Hoffman M — cell-based model; Sørensen B — ROTEM-guided MTP; CRASH-2; Miller's Anaesthesia 9th Ed) A. Cell-Based Model vs Classical Cascade 3 marks Classical cascade (Macfarlane 1964; Davie & Ratnoff 1964): described TWO pathways — extrinsic (tissue factor/VIIa) and intrinsic (contact activation XII→XI→IX→VIII) — converging at a common pathway (X→Xa → prothrombin → thrombin → fibrin); measured by PT (extrinsic — seconds) and APTT (intrinsic — seconds); limitation: the intrinsic pathway (Factor XII deficiency) does NOT cause clinical bleeding — yet APTT is prolonged; and the small amount of thrombin generated by the extrinsic pathway should be rapidly neutralised by antithrombin without intact intrinsic pathway amplification — but patients with Factor XII deficiency do NOT bleed; the cascade is a laboratory model, NOT a physiological one Cell-based model of coagulation (Hoffman & Monroe 2001) — three overlapping phases: Phase 1 — Initiation (on tissue factor-bearing cells): vascular injury exposes subendothelial tissue factor (TF) → TF binds circulating Factor VIIa → TF-VIIa complex → activates small amounts of Xa and IXa → small amount of thrombin generated (NOT enough to clot fibrinogen — ""trigger thrombin""); this initial thrombin is critical — it activates platelets and amplifies coagulation Phase 2 — Amplification (on platelet surface): the small amount of trigger thrombin → activates platelets at the injury site (thrombin is the most potent platelet activator) → activated platelets express phosphatidylserine on their surface (provides the negatively charged lipid surface for tenase and prothrombinase complexes) → also releases platelet granule contents (ADP, thromboxane A₂ → recruit more platelets → platelet plug formation); thrombin also activates cofactors V and VIII (on platelet surface) → massive amplification Phase 3 — Propagation (on activated platelet surface): activated platelet surface → assembles intrinsic Xase complex (IXa-VIIIa) + prothrombinase complex (Xa-Va) → generates THROMBIN BURST (1,000× more thrombin than Phase 1) → cleaves fibrinogen → fibrin monomers → cross-linked fibrin polymer (Factor XIIIa — also activated by thrombin — cross-links fibrin) → stable clot Clinical implications of cell-based model: explains why: (1) Factor VII deficiency → severe bleeding (TF-VIIa is the initiator); (2) Factor VIII/IX deficiency (haemophilia A/B) → severe bleeding (amplification and propagation fail); (3) Factor XII deficiency → NO clinical bleeding (APTT prolonged but XII is not in the cell-based pathway); (4) thrombocytopenia → severe bleeding (platelets are the surface for propagation) B. TEG and ROTEM — Principles and Parameters 4 marks Principle: viscoelastic haemostasis tests measure the physical properties (viscoelasticity) of a developing clot in whole blood in real-time; a pin suspended in a rotating (ROTEM) or oscillating (TEG) cup of blood — as the clot forms, the clot's viscoelastic strength transmits torque from the rotating cup to the pin (or vice versa) — the changing amplitude of pin movement is plotted against time → a characteristic waveform that reflects the entire haemostatic process from initiation to lysis Parameter TEG Name ROTEM Name What It Measures Normal Range Abnormal = Treatment Time to first clot detection R time (reaction time) CT (clotting time) Time from start to first 2mm amplitude — reflects clotting factor activity (intrinsic pathway); equivalent to APTT TEG: 5–10 min; ROTEM INTEM CT: 100–240 s Prolonged R/CT → factor deficiency → FFP; or heparin effect (HEPARINASE ROTEM shows normalization) Clot kinetics / rate of clot formation K time / α- angle CFT / α- angle Speed of clot strengthening from 2mm to 20mm amplitude (K time); angle of tangent at 2mm (α- angle); reflects fibrinogen and platelet contribution to clot strength TEG K: 1–3 min; α: 53–72° ↑ K / ↓ α-angle → fibrinogen deficiency → cryoprecipitate or fibrinogen concentrate Maximum clot strength MA (maximum amplitude) MCF (maximum clot firmness) Maximum clot strength — reflects platelet function (80%) and fibrinogen (20%); the most clinically important parameter TEG MA: 55– 73 mm; ROTEM EXTEM MCF: 50–72 mm ↓ MA/MCF with normal fibrinogen → platelet deficiency → platelet transfusion; ↓ MA/MCF with ↓ fibrinogen amplitude (FIBTEM) → fibrinogen depleted first → cryoprecipitate Clot lysis LY30 (% lysis at 30 min) LI30 / ML (maximum lysis) Percentage reduction in clot amplitude 30 min after MA — detects hyperfibrinolysis (clot dissolving too fast) or hypofibrinolysis TEG LY30: <8%; ROTEM LI30: >85% ↑ LY30 (>3% in trauma) / ↓ LI30 → fibrinolysis → tranexamic acid (TXA); complete lysis → systemic fibrinolysis emergency ROTEM Specific Assays EXTEM: tissue factor-activated (extrinsic pathway — global screen); INTEM: contact-activated (intrinsic pathway — heparin-sensitive); FIBTEM: EXTEM + cytochalasin D (platelet inhibitor) → measures FIBRINOGEN contribution alone (MCF in FIBTEM = pure fibrinogen clot strength — normal 9–25 mm); HEPTEM: INTEM + heparinase → if HEPTEM normalises a prolonged INTEM CT → heparin effect confirmed (not factor deficiency) C. Goal-Directed MTP Using Viscoelastic Testing 3 marks Traditional MTP (empirical 1:1:1): RBC:FFP:Platelets in 1:1:1 ratio — reduces mortality vs RBC-only resuscitation (PROPPR trial: 1:1:1 → ↑ 24h haemostasis, ↑ survival at 24h); but it is EMPIRICAL — not all patients need FFP or platelets in equal proportions; over-transfusion of any blood component → TACO (transfusion-associated circulatory overload), TRALI, immunosuppression TEG/ROTEM-guided goal-directed MTP (superior to empirical): Prolonged CT/R time → FFP (factor deficiency); if HEPTEM normal → heparin → give protamine NOT FFP ↓ FIBTEM MCF (<9 mm) → fibrinogen concentrated (cryoprecipitate or Fibrinogen concentrate 2–4g IV) — treat fibrinogen FIRST as it is always depleted first in massive haemorrhage ↓ EXTEM MCF with normal FIBTEM → platelet transfusion (isolated platelet deficiency or dysfunction) ↑ LY30 / fibrinolysis → tranexamic acid (TXA) 1g IV (+ 1g over 8h); administer EARLY (CRASH-2 trial: TXA within 3h ↓ mortality; >3h → ↑ mortality from fibrinolysis inhibition; so give TXA EARLY before TEG result if clinically bleeding) Evidence: Gonzalez et al. (J Trauma 2016) and multiple RCTs: TEG-guided transfusion → 40–50% reduction in FFP and platelet use; ↓ transfusion-related complications; no increase in mortality; cost-effective despite device costs; now recommended by ESAIC and AABB for MTP guidance in trauma and cardiac surgery ★ Examiner's Pearl Cell-based model 3 phases: Initiation (TF-VIIa → trigger thrombin on TF-bearing cells); Amplification (trigger thrombin activates platelets + cofactors V, VIII); Propagation (platelet surface → thrombin burst → fibrin clot). TEG/ROTEM key parameters: R/CT = factor activity; α-angle/K/CFT = fibrinogen + kinetics; MA/MCF = clot strength (platelet 80% + fibrinogen 20%); LY30/ML = fibrinolysis. FIBTEM MCF <9 mm → cryoprecipitate (treat fibrinogen first — depleted first in MH). TXA: give within 3 hours of haemorrhage (CRASH-2) — after 3 hours → HARMFUL. References: Hoffman M, Monroe DM. A cell-based model of hemostasis (Thromb Haemost 2001;85:958-965). Holcomb JB et al. PROPPR trial (JAMA 2015;313:471-482). Shakur H et al. CRASH-2 trial (Lancet 2010;376:23-32). Miller RD et al. Miller's Anaesthesia, 9th Ed, Chapter 61."

"and management strategies [3]. Discuss ERAS (Enhanced Recovery After Surgery) principles applied to bariatric surgery [3]. ⚙ Core Concept Morbid obesity (BMI ≥40 kg/m²) is a multisystem disease with profound anaesthetic implications — it is simultaneously the commonest cause of difficult airway, the commonest reason for obstructive sleep apnoea, the commonest cause of physiological reserve reduction, and associated with the highest PONV risk. Bariatric surgery produces the greatest long-term metabolic benefit of any obesity intervention, but carries significant perioperative risk. (Brodsky JB; Dixon BJ — obese airway; Mechanick JI — ASMBS ERAS guidelines; Miller's Anaesthesia 9th Ed) A. Physiological Changes in Morbid Obesity 4 marks System Changes Anaesthetic Implication Respiratory ↓ FRC (excess thoracoabdominal fat compresses diaphragm; ↓ FRC 50% in supine morbidly obese vs 25% in normal weight); FRC may fall below closing capacity → airway closure during normal tidal breathing → V/Q mismatch → hypoxaemia; ↑ O₂ consumption (↑ metabolic mass); ↑ CO₂ production; ↑ work of breathing; obstructive sleep apnoea (OSA) in 40–70%; OHS (obesity hypoventilation syndrome) in 5–10% — chronic hypercapnia (PaCO₂ >45 mmHg) from impaired central chemoreceptor response Safe apnoea time drastically reduced (normal adult: 8–10 min; morbidly obese: 2–3 min); position matters: upright/ramped position → ↑ FRC by 25%; CPAP/PEEP essential; avoid supine flat position; OSA → ↑ sensitivity to opioids + sedatives; post-op CPAP required Cardiovascular ↑ Circulating blood volume (↑ 30–50 mL per kg of adipose tissue); ↑ CO (↑ SV + ↑ HR from ↑ metabolic demand); LVH (LV eccentric hypertrophy from ↑ preload + volume overload); RVH (from OSA-related pulmonary hypertension → cor pulmonale in advanced OHS); metabolic syndrome: hypertension, dyslipidaemia, T2DM, coronary artery disease; ↑ risk of sudden cardiac death (fatty infiltration of conduction system → arrhythmias) Potential difficult IV access (subcutaneous fat); ECG abnormalities (arrhythmias, LVH changes, ST changes); higher induction dose requirements (↑ Vd); hypotension risk from epidural; ↑ perioperative MI risk if undiagnosed CAD Gastrointestinal ↑ Intra-abdominal pressure → ↓ lower oesophageal sphincter competence → GORD (gastro- oesophageal reflux); ↑ gastric volume and ↑ gastric acidity; ↑ risk of aspiration; note: post- bariatric patients (especially Roux-en-Y gastric bypass) → dramatically altered gastric anatomy — very small gastric pouch → low gastric volume but rapid gastric emptying; NSAID/opioid analgesics → ↑ GORD risk RSI standard for induction in morbidly obese (aspiration risk); antacid premedication (omeprazole/ranitidine + sodium citrate); post- bariatric patients: drug absorption altered (↓ oral bioavailability of many drugs) Pharmacological ↑ Vd for lipophilic drugs (↑ fat compartment → ↑ Vd → ↑ loading dose but ↑ duration); for hydrophilic drugs: Vd not greatly changed → dose on LEAN body weight (LBW) or ideal body weight (IBW); ↑ hepatic blood flow → ↑ metabolic clearance; adipose cytokines alter drug protein binding Dosing conventions: propofol — LBW (lean body weight); thiopentone — LBW; NMBDs — IBW (ideal body weight); succinylcholine — TBW (total body weight — 2 mg/kg); opioids — LBW; volatile agents — titrate to clinical effect; LBW = IBW + 0.3 × (TBW − IBW) Haematological ↑ Risk of DVT/PE (Virchow's triad: stasis from immobility + hypercoagulable state from ↑ fibrinogen, PAI-1 + endothelial dysfunction from adipokines); ↑ risk of perioperative PE Thromboprophylaxis: LMWH dose adjustment (enoxaparin 40 mg BD or 60 mg OD based on anti-Xa levels); TED stockings (compression devices throughout surgery); early mobilisation B. Airway Management in Morbid Obesity 3 marks Why obesity increases airway difficulty: excess submandibular, pharyngeal, and parapharyngeal fat deposits → ↓ pharyngeal lumen → Mallampati class often III–IV; short fat neck → ↓ neck extension; OSA → pharyngeal collapse tendency; large tongue (macroglossia relative to airway); breast hypertrophy → laryngoscope handle may not fit between sternum and chin; ↑ gastric aspiration risk (see above) Positioning — THE RAMPED POSITION: most impactful airway intervention; raise head, shoulders, and upper body on pillows/ramp until the external auditory meatus is at the same horizontal level as the sternal notch (EAM–sternal notch horizontal alignment); this brings the laryngeal axis more in line with the oral axis → dramatically improves laryngoscopic view; ↑ FRC by 25% compared to supine; Dixon et al. (Anesth Analg 2005): ramped position → significantly improved Cormack-Lehane grade in morbidly obese patients vs ""sniffing"" position Pre-oxygenation: standard 3-minute tidal volume breathing or 8 vital capacity breaths at FiO₂ 1.0 → achieved EtO₂ of 87% in non-obese patients but only 75% in morbidly obese; therefore: pre-oxygenation with NIV (BiPAP or CPAP at 10 cmH₂O) → ↑ EtO₂ to 90–95% + ↑ FRC → longer safe apnoea time; apnoeic oxygenation at 15 L/min via nasal cannulae during laryngoscopy → extends safe apnoea time RSI technique in obesity: standard for morbidly obese — aspiration risk + rapid desaturation; modified RSI: after adequate pre-oxygenation (NIV), apply GENTLE positive pressure ventilation (8–10 cmH₂O) with cricoid pressure until intubation — prevents passive atelectasis and hypoxaemia during apnoea (traditionally RSI avoided any ventilation, but the risk of desaturation in morbid obesity justifies gentle BMV with cricoid pressure); videolaryngoscopy as primary or rescue device (↑ view, ↓ failed intubation rate in obese) Extubation: extubate in reverse Trendelenburg (semi-upright); ensure full reversal of NMB (TOF ratio ≥0.9 by quantitative monitoring — obese patients are at highest RNMB risk from atelectasis + hypoventilation); suggest CPAP post-operatively for OSA patients; keep awake until fully conscious C. ERAS Principles in Bariatric Surgery 3 marks ERAS Element Bariatric-Specific Application Pre-operative carbohydrate loading Oral carbohydrate drink (12.5% CHO — 400 mL the night before, 200 mL 2h pre-op) → ↓ insulin resistance, ↓ protein catabolism; in bariatric patients: clear liquid diet day before surgery; 2h fasting for clear liquids (standard AAGBI guidelines — modified for bariatric: due to GORD risk, some centres prefer 4h for clear liquids + PPI pre-medication) Multimodal analgesia Avoid or minimise opioids (↑ OSA risk, ↑ PONV, ↑ sedation risk); mainstays: paracetamol 1g QDS (if tolerated post-op — route issue after Roux-en-Y); IV ketorolac/ibuprofen (avoid if GI anastomosis — risk of anastomotic leak); gabapentin 300 mg pre-op (anxiety + pain reduction); LA infiltration of port sites (laparoscopic bariatric surgery); TAP block or rectus sheath block for laparotomy PONV prophylaxis Obesity + laparoscopy + opioids + female = Apfel score 3–4 → triple therapy: ondansetron 4 mg IV + dexamethasone 8 mg IV + TIVA with propofol (propofol reduces PONV vs volatile) + scopolamine patch; dexamethasone 8 mg at induction (reduces opioid requirements + PONV — note: blood glucose monitoring in T2DM patients as dexamethasone raises BGL) VTE prophylaxis Anti-embolism stockings pre-operatively; LMWH 12h before surgery; mechanical pneumatic compression devices throughout surgery and postoperatively; early ambulation within 6h of surgery; extended LMWH for 10–28 days post-discharge (bariatric VTE risk elevated for weeks) Lung recruitment + ventilation strategy Intraoperative: PEEP 10–15 cmH₂O throughout; pressure-controlled ventilation; periodic recruitment manoeuvres (30 cmH₂O sustained inflation every 30 min); reduces intraoperative and post-operative atelectasis; lower tidal volumes (5–7 mL/kg IBW — lung protective); FiO₂ 0.4–0.6 (avoid 1.0 → promotes resorption atelectasis) Early oral nutrition Clear liquids 6h post-operatively; post-bariatric structured diet progression (liquid → purée → soft → normal over 6–8 weeks); ensure protein supplement (protein intake critical post-bariatric to prevent muscle wasting and surgical site healing) ★ Examiner's Pearl Morbid obesity: ↓ FRC (50% in supine), safe apnoea time 2–3 min (vs 8 min normal). Ramped position: EAM–sternal notch horizontal alignment → best laryngoscopic view + ↑ FRC 25% (Dixon 2005). RSI + GENTLE BMV (8–10 cmH₂O) + cricoid pressure = modified RSI for obese. Drug dosing: succinylcholine = TBW (2 mg/kg); NMBDs = IBW; propofol = LBW; opioids = LBW. ERAS bariatric: TIVA (↓ PONV), multimodal analgesia (minimise opioids), PEEP 10–15 cmH₂O, VTE extended prophylaxis, early ambulation. References: Dixon BJ et al. The effect of obesity on the Cormack-Lehane grade and intubation conditions (Anesth Analg 2005;100:1519-1525). Nightingale CE et al. Peri-operative management of the obese surgical patient (Anaesthesia 2015;70:859-876). Thorell A et al. ERAS guidelines for bariatric surgery (Obes Surg 2016;26:2065-2083). Miller RD et al. Miller's Anaesthesia, 9th Ed."

"exercise testing (CPET) — principles and parameters used for surgical risk stratification [4] (c) Perioperative beta- blockade — evidence and current recommendations [3]. A. Revised Cardiac Risk Index (Lee RCRI) 3 marks ⚙ Core Concept Perioperative cardiac complications (MACE — Major Adverse Cardiac Events) are the leading cause of perioperative death. Risk stratification allows appropriate investigation, optimisation, and monitoring resources to be directed to high-risk patients. (Lee TH — RCRI; Older P — CPET; POISE-2 trial — periop beta-blockade; ESC/ESA 2022 guidelines) Lee RCRI (1999) — 6 independent predictors of major cardiac complications: 1. High-risk surgery (intraperitoneal, intrathoracic, suprainguinal vascular surgery) 2. Ischaemic heart disease (history of MI, positive stress test, current angina, nitrate use, Q waves on ECG) 3. Congestive heart failure (history of, pulmonary oedema, paroxysmal nocturnal dyspnoea, bilateral basal crepitations, S3 gallop, CXR showing pulmonary vascular redistribution) 4. Cerebrovascular disease (history of TIA or stroke) 5. Diabetes mellitus requiring insulin 6. Pre-operative serum creatinine >177 μmol/L (2.0 mg/dL) Risk stratification: RCRI Score Risk Class Major Cardiac Event Rate (MACE) Action 0 Very low 0.4% Proceed — no additional cardiac investigation required 1 Low 0.9% Proceed with standard monitoring 2 Moderate 6.6% Consider additional investigation (stress echo, CPET); optimise risk factors ≥3 High 11% Formal cardiological assessment; CPET; consider if surgery can be deferred/modified; HDU/ICU post-op monitoring Limitations of RCRI: does not account for emergency surgery; underestimates risk in vascular surgery; does not incorporate functional capacity; most predictive for non-fatal MI and cardiac arrest — less sensitive for all-cause mortality; ESC/ESA guidelines (2022) now recommend RCRI as first-line screening tool for all patients undergoing intermediate to high-risk surgery B. Cardiopulmonary Exercise Testing (CPET) 4 marks Principle: CPET provides an objective, integrative assessment of cardiopulmonary, haematological, and musculoskeletal response to maximal exercise; the patient exercises on a cycle ergometer with progressively increasing workload (ramp protocol) while: expired gases (O₂ and CO₂) are continuously analysed; ECG and SpO₂ are monitored; the test reveals the limiting organ system (cardiac vs respiratory vs deconditioning) and quantifies functional reserve Key parameters used in surgical risk stratification: Parameter Definition Risk Threshold Significance VO₂max (peak) Maximal O₂ consumption achieved during exercise (mL/min/kg) <15 mL/min/kg = ↑ risk; <10 = very high risk Overall cardiopulmonary fitness; the most comprehensive measure of functional reserve; patients with VO₂max <10 have very high perioperative mortality Anaerobic threshold (AT) The VO₂ at which anaerobic metabolism begins to supplement aerobic — detected as ↑ CO₂ production relative to O₂ uptake (V-slope method or ventilatory equivalent method); occurs when cardiac output can no longer meet O₂ demand — reflects cardiac reserve <11 mL/min/kg = ↑ perioperative risk (Older P 1993) THE most clinically used CPET parameter for surgical risk; at or below AT, tissue O₂ delivery is adequate without lactate; below AT → anaerobic — reflects true cardiac limitation; Older et al. (1993): AT <11 mL/min/kg → 18% perioperative mortality vs 0.8% if AT ≥11 — landmark study in major abdominal surgery VE/VCO₂ slope Slope of minute ventilation vs CO₂ output during exercise — reflects ventilatory efficiency and dead-space ventilation >34 = ↑ risk; >45 = very high risk High VE/VCO₂ slope seen in heart failure, pulmonary hypertension, V/Q mismatch; independent predictor of perioperative complications even when AT is preserved METs (metabolic equivalents) 1 MET = resting O₂ consumption (3.5 mL/O₂/kg/min); functional capacity expressed in METs from clinical history (not CPET) — ""Can you climb two flights of stairs?"" ≈ 4 METs <4 METs = poor functional capacity = ↑ Quick clinical assessment without CPET; ESC/ESA guidelines: if patient can achieve ≥4 METs without symptoms → proceed to surgery without further cardiac investigation (unless RCRI ≥3) risk Who should have CPET? ESC/ESA 2022: patients with RCRI ≥2 undergoing major surgery + inadequate functional capacity assessment from history (unable to climb stairs, housebound); pre-bariatric surgery; pre-lung resection (to determine suitability for pneumonectomy — AT <10 = unacceptable risk for pneumonectomy); pre-cardiac surgery; the test takes 20–30 minutes and is non-invasive — far superior to echocardiography for functional assessment C. Perioperative Beta-Blockade 3 marks Rationale for beta-blockade: perioperative tachycardia → ↑ myocardial O₂ demand → subendocardial ischaemia in patients with fixed coronary artery disease; β-blockade → ↓ HR → ↑ diastolic filling time → ↑ coronary perfusion time → ↓ myocardial O₂ demand; theoretically should reduce perioperative MI History and evidence: Mangano et al. (NEJM 1996): atenolol perioperatively → ↑ 2-year survival; generated enormous enthusiasm for routine perioperative beta-blockade DECREASE trials (Poldermans — Rotterdam): dramatic benefit of bisoprolol perioperatively; later found to have significant data integrity issues → trials retracted (2011); this is one of the most important examples of research fraud affecting clinical guidelines POISE trial (Devereaux, NEJM 2008): the landmark definitive RCT; n=8,351; extended-release metoprolol started 2–4h before surgery → ↓ perioperative MI (4.2% vs 5.7%) BUT ↑ stroke (1.0% vs 0.5%), ↑ hypotension (15% vs 9.7%), ↑ total mortality (3.1% vs 2.3%); the stroke excess was attributed to perioperative hypotension from beta-blockade Current ESC/ESA 2022 recommendations: Class I (MUST): Continue chronic beta-blockers perioperatively — abrupt withdrawal → rebound tachycardia → ↑ MI risk; NEVER stop beta-blockers preoperatively Class IIb (MAY consider): initiate beta-blockade preoperatively in patients with ≥2 RCRI risk factors or known CAD undergoing high-risk surgery — but START at least 1 week before surgery (not on the day — POISE effect) and titrate to HR 60–80 bpm without hypotension; short-acting agent preferred (bisoprolol 2.5 mg, titrate up) Class III (DO NOT): do NOT start beta-blockade on the day of surgery in beta-blocker-naïve patients — ↑ stroke and mortality (POISE); do NOT use high fixed doses ★ Examiner's Pearl RCRI 6 factors: high-risk surgery, IHD, CCF, CVD, insulin-dependent DM, Cr >177 μmol/L. Score ≥3 → 11% MACE. CPET AT: the most clinically important parameter — <11 mL/min/kg = ↑ perioperative mortality (Older 1993). METs <4 = poor functional capacity. POISE trial: perioperative metoprolol → ↓ MI BUT ↑ stroke, ↑ hypotension, ↑ mortality. Current guideline: CONTINUE chronic beta-blockers (Class I); NEW beta-blocker — start ≥1 week before surgery, never on day of surgery. References: Lee TH et al. Derivation and prospective validation of a simple index for prediction of cardiac risk (Circulation 1999;100:1043-1049). Older P et al. CPET before major elective surgery (Chest 1993;104:701-704). Devereaux PJ et al. POISE trial (Lancet 2008;371:1839-1847). ESC/ESA Guidelines on Cardiovascular Assessment and Management of Patients Undergoing Non-Cardiac Surgery, 2022."