System Intra-abdominal Pressure (IAP) Effect CO₂ Absorption Effect Cardiovascular IAP 15 mmHg → IVC compression → ↓ venous return → ↓ CO; reflex peripheral CO₂ absorption → hypercapnia → sympathetic activation → ↑ vasoconstriction (↑ SVR) maintains MAP initially; at IAP >20 mmHg → HR, ↑ SVR (partially counteracts IVC compression effect); pH ↓ decompensated ↓ CO; ↑ CVP paradoxically (from abdominal compression) from respiratory acidosis Respiratory Diaphragm pushed cephalad → ↓ FRC → ↓ compliance → ↑ peak airway pressure CO₂ absorbed from the peritoneum → ↑ PaCO₂; increase minute → atelectasis; cephalad displacement of the carina (risk of right main bronchus ventilation by 15–25% to maintain normocapnia; ETCO₂ intubation when ETT was positioned correctly pre-inflation) underestimates PaCO₂ by 3–5 mmHg in healthy patients (V/Q mismatch widens this gap in sick patients) Renal IAP → ↓ renal cortical perfusion (renal artery compression + ↑ renal venous — pressure) → ↓ GFR → ↓ urine output intraoperatively (not indicative of hypovolaemia if urine output returns to normal after desufflation) Surgical Gas embolism (CO₂ injected directly into vessel during Veress needle insertion or — complications trocar placement); capnothorax (CO₂ tracking through diaphragm → pneumothorax); subcutaneous emphysema (CO₂ tracking into subcutaneous tissue → dramatically elevated ETCO₂, palpable crepitus)

Further ↓ FRC (abdominal viscera push diaphragm cephalad + IAP from pneumoperitoneum combined); peak airway pressures may reach 35–45 cmH₂O in steep Trendelenburg with pneumoperitoneum — especially in obese patients; manage with pressure-controlled ventilation (avoids high pressures), ↑ PEEP (8– 12 cmH₂O), and accepting slightly higher ETCO₂ if permissive hypercapnia is tolerated Cephalad redistribution of blood volume → ↑ cerebral blood flow → ↑ ICP; risk of cerebral oedema with prolonged steep positioning; raised intraocular pressure (IOP) — particularly concerning in pre-existing glaucoma; facial and conjunctival oedema (from ↑ venous pressure); post-operative airway oedema (from prolonged head-down → laryngeal oedema) — assess for stridor before extubation; consider leaving the ETT in situ longer if significant facial oedema is noted Brachial plexus injury (steep Trendelenburg with shoulder braces pushing into the supraclavicular region) — avoid shoulder braces where possible; use nonslip mattress and table friction instead; position arms alongside the body, well padded

Extreme (30–45°) steep Trendelenburg maintained for 3–4 hours; robot is docked over the patient → complete loss of patient access (cannot reach the head, cannot change patient position, cannot perform emergency airway manoeuvres) during surgery; pre-dock airway security is paramount: confirm ETT position with ETCO₂ waveform, chest auscultation, and bilateral breath sounds BEFORE docking; check ETT tie/tape security; tape eyes (cannot monitor or treat complications of eye during the docked phase)

Specific risks: endobronchial intubation from cephalad ETT migration after Trendelenburg (auscultate after final positioning); CO₂ embolism from large venous plexuses in the pelvis; significant blood loss requiring transfusion (but cannot access patient for lines if robot is docked — ensure adequate IV access before docking); haemodynamic instability during extended pneumoperitoneum in elderly prostatectomy patients with ischaemic heart disease

Post-operative: post-extubation stridor from laryngeal oedema → treat with nebulised adrenaline 1 mg in 4 mL 0.9% NaCl; consider re-intubation if severe; PONV high from peritoneal insufflation and opioids → TIVA preferred; bladder irrigation post-RARP may absorb significant volumes (dilutional hyponatraemia monitoring)

System Key Changes Anaesthetic Implication Respiratory ↓ FVC, ↓ FEV1 (~1% per year after 30); ↓ FRC; ↑ closing capacity (exceeds FRC at Rapid desaturation during apnoea; ↑ atelectasis tendency; 65 yrs upright, 44 yrs supine); ↓ hypoxic and hypercapnic ventilatory response; ↓ impaired aspiration clearance; higher FiO₂ may be mucociliary clearance; ↓ cough reflex required during surgery Cardiovascular ↓ Maximum heart rate (220 − age); ↓ cardiac reserve; diastolic dysfunction; ↑ SVR; ↑ Haemodynamic fragility; hypotension more likely with systolic hypertension; ↑ atrial fibrillation risk; ↓ baroreceptor sensitivity; ↓ induction; poor tolerance of rapid volume shifts; AF risk responsiveness to catecholamines (β-receptor downregulation) with surgery; blunted compensatory tachycardia Renal/Hepatic ↓ GFR (by 50% at 80 vs 30 years); ↓ renal tubular function; ↓ hepatic blood flow (by ↑ Drug accumulation for renally cleared drugs (morphine, 40%); ↓ hepatic enzyme activity gabapentin, some NMBs); prolonged action of hepatically metabolised drugs; drug dose reduction essential Neurological ↓ Brain volume (cortical atrophy); ↓ neurotransmitter synthesis; ↓ pain perception Reduced anaesthetic requirements (↓ MAC); cognitive threshold variation; ↑ anxiety; ↑ delirium susceptibility vulnerability; pre-operative cognitive assessment (baseline) Pharmacokinetics ↓ Albumin → ↑ free fraction of protein-bound drugs (warfarin, diazepam, propofol); ↑ Dose reduction for most sedatives and analgesics; start body fat:muscle ratio → ↑ Vd for lipophilic drugs (benzodiazepines, volatile agents); ↓ low and titrate total body water → ↓ Vd for water-soluble drugs (NMBs, morphine)

MAC decreases approximately 6% per decade of life after age 40; an 80-year-old requires approximately 25–30% less volatile agent than a 40-year-old for the same depth of anaesthesia; this is due to: ↓ neuronal density and ↓ synaptic connections in the aged brain; ↓ CNS neurotransmitter turnover; ↑ sensitivity of inhibitory pathways (GABA-A) and ↓ excitatory (NMDA) activity

Practical implications: overly deep anaesthesia is common in the elderly with standard adult volatile agent concentrations → hypotension, prolonged emergence, delirium; processed EEG (BIS target 40–60) is particularly valuable in elderly patients to avoid both over-sedation and underdosing

Propofol: Schnider TCI model automatically adjusts for age-related pharmacokinetic changes (reduces central compartment volume and clearance estimates with increasing age) → lower initial bolus and infusion rates are automatically calculated for elderly patients; still titrate carefully

POCD definition: Post-Operative Cognitive Dysfunction — a measurable decline in cognitive test scores (memory, concentration, executive function) in the weeks to months following surgery, compared to the individual's pre-operative baseline; it is DISTINCT from delirium (which is acute, fluctuating, and begins within days); POCD may persist for months or years in a subset of patients; associated with reduced quality of life, impaired return to work, and increased mortality ISPOCD1 (Moller JT, Lancet 1998; n=1218 patients ≥60 years having major non-cardiac surgery): POCD was present in 25.8% of patients at 1 week post-op and 9.9% at 3 months; risk factors identified: age ≥60; pre-existing cognitive impairment; lower educational attainment; second procedure and postoperative infections; anaesthetic technique (GA vs regional) was NOT significantly associated with POCD risk — this finding challenged the theory that GA causes POCD; ISPOCD2 confirmed these findings

Pathophysiology of POCD: neuroinflammation (surgical inflammation triggers neuroinflammatory cascades via the blood-brain barrier); sleep deprivation; hypotension episodes causing microischaemia; anaesthetic agents may contribute (some evidence that volatile agents and benzodiazepines increase neuroinflammation); exact mechanisms remain under investigation

The Hospital Elder Life Program (HELP; Inouye SK, NEJM 1999): a structured multi-component non-pharmacological intervention to prevent delirium in hospitalised elderly patients; implemented by trained volunteers and nursing staff; has been shown to reduce delirium incidence by 33% and falls by 32% in medical patients; widely adapted to surgical and ICU settings HELP Components (targeting modifiable delirium risk factors):

Cognitive orientation: daily reorientation (clock, calendar, date); cognitive exercises; encouraging family participation in orientation

Mobility: early mobilisation out of bed within 24 hours of surgery; daily walking programme if able; avoid physical restraints (increase delirium)

Vision: provision of glasses or magnifying glass; adequate room lighting; large-faced clocks and calendars visible

Hearing: provision of hearing aids; speaking clearly and loudly; amplifying devices

Sleep: non-pharmacological sleep promotion (warm milk, relaxation); avoid nighttime interruptions; noise and light reduction; scheduled medications to avoid nighttime disturbance; avoid benzodiazepines for sleep (worsen delirium)

Hydration/Nutrition: ensure adequate oral intake; dehydration is a major delirium trigger; dentures provided for eating

Pharmacological considerations: haloperidol 0.5–1 mg oral/IV for hyperactive delirium symptom management (not prevention); dexmedetomidine-based ICU sedation reduces delirium vs benzodiazepines; avoid benzodiazepines (particularly in elderly — increase delirium 3-fold); avoid anticholinergic drugs (hyoscine, diphenhydramine, TCAs — all worsen delirium); avoid polypharmacy

Drug Class Continue or Omit? Evidence/Rationale Beta-blockers CONTINUE if the patient is already POISE trial (Devereaux PJ, NEJM 2008; n=8351): high-dose metoprolol succinate started 2–4h (chronic) chronically established on a beta-blocker; do before surgery in patients NOT previously on beta-blockers → ↓ MI (4.2% vs 5.7%), but ↑ stroke NOT stop suddenly (rebound tachycardia, (1.0% vs 0.5%), ↑ bradycardia, ↑ hypotension, ↑ all-cause mortality (3.1% vs 2.3%); lesson: do NOT ischaemia, hypertension — withdrawal start high-dose beta-blockers immediately before surgery in beta-blocker-naive patients; only start syndrome); convert to oral dose day-of- in selected high-risk patients with documented CAD if there is time for dose titration over weeks surgery (small sip of water) before surgery ACE-inhibitors / OMIT on the morning of surgery (for most ACE-I/ARBs block the renin-angiotensin system → impair the vasopressor response to anaestheticARBs patients having major surgery with general induced vasodilation → profound refractory intraoperative hypotension (particularly with neuraxial or anaesthesia); the ESC/ESA 2022 guideline volatile agents); hypotension in this setting is severe and poorly responsive to standard recommends withholding ACE-I/ARB on the vasopressors (phenylephrine, ephedrine) — may require vasopressin; the VISION study confirmed day of major non-cardiac surgery ↑ intraoperative hypotension with pre-operative ACE-I/ARB; omitting on the morning of surgery reduces but does not eliminate this risk; restart post-operatively when patient is eating and drinking (haemodynamically stable) Statins CONTINUE throughout the perioperative Abrupt statin withdrawal causes a rebound inflammatory state (↑ CRP, ↑ plaque instability, ↑ period; do NOT omit thrombotic risk); statins have pleiotropic benefits (anti-inflammatory, plaque-stabilising) that are lost acutely with withdrawal; observational studies suggest statin continuation is associated with lower perioperative cardiac events; if patient is NBM: some centres give their regular statin with a sip of water (safe for most statins which have t½ >12 hours); hold if IV formulation not available and patient is genuinely nil by mouth for >24 hours then restart as soon as oral route is available Aspirin (75 mg — CONTINUE for most cardiac-risk patients; Aspirin provides primary and secondary cardiovascular event prevention; POISE-2 trial (Devereaux antiplatelet) CONSIDER stopping 7 days before for very- PJ, NEJM 2014; n=10,010): perioperative aspirin did NOT reduce MACE (major adverse cardiac high bleeding risk surgery (neurosurgery, events) in non-cardiac surgery patients and increased major bleeding; however: patients already on posterior eye surgery, closed-cavity surgery) aspirin for established secondary prevention (post-MI, post-stent) should CONTINUE aspirin perioperatively — the POISE-2 findings apply to patients where aspirin was being considered as a

NEW perioperative intervention

Clopidogrel / STOP 5 days before surgery (ticagrelor: 5 P2Y12 inhibitors cause irreversible (clopidogrel, prasugrel) or reversible (ticagrelor) platelet P2Y12 inhibitors days; clopidogrel: 5 days; prasugrel: 7 days); inhibition; withholding for 5–7 days allows sufficient new platelet generation to restore haemostasis;

EXCEPTION: patients with recent (<1 year) for DES: cardiology/interventional cardiology must agree on minimum safe DAPT duration before drug-eluting stent (DES) or <6 weeks bare- elective surgery (typically ≥12 months for DES with 2nd generation stents — can consider at 6 metal stent — discuss with cardiology; months with cardiologist approval for truly essential elective surgery) premature DAPT interruption → stent thrombosis → MI with high mortality Corticosteroids CONTINUE regular dose; add stress-dose Patients on chronic steroids have HPA axis suppression → inadequate cortisol response to surgical (chronic >5 mg hydrocortisone for major surgery stress → adrenal insufficiency; stress-dose coverage: hydrocortisone 25–50 mg IV at induction + 25 prednisolone/day mg 8-hourly for 24 hours (minor surgery); 50–100 mg IV at induction + 50 mg 8-hourly for 48–72 >3 months) hours (major surgery); taper back to the patient's usual dose over 2–3 days; DO NOT abruptly stop steroids (Addisonian crisis)

POISE trial key message: the HARM from starting beta-blockers (metoprolol 100 mg) in the immediate perioperative period in beta-blocker-naive patients OUTWEIGHS the cardiac benefit; do NOT routinely start beta-blockers within days of surgery; they may be started ONLY in high-risk patients if initiated weeks before surgery with careful dose titration; ALWAYS continue existing beta-blockers in patients already established on them

The hip joint capsule has a rich nerve supply — primarily from the articular branches (sensory only) of three main nerves; these branches do NOT innervate the quadriceps (which are supplied by the motor branches of the femoral nerve — these are separate from the articular branches targeted by PENG)

Anterior capsule: articular branches of the FEMORAL NERVE (from the nerve to the rectus femoris and nerve to the vastus intermedius — these are pure articular sensory branches, distinct from the motor branches to the quadriceps); articular branches of the ACCESSORY OBTURATOR NERVE (when present — in 20–30% of individuals); articular branches of the OBTURATOR NERVE

Posterior capsule: branches of the sciatic nerve (superior gluteal nerve, nerve to the quadratus femoris)

PENG block targets: the anterior capsule innervation at the level of the anterior inferior iliac spine (AIIS) and ipsilateral eminence (IPE) — where these articular branches converge before entering the joint capsule

Patient position: supine; hip in neutral or mild external rotation

Probe: curved array (low frequency 2–5 MHz) or high-frequency linear probe; placed in a transverse plane at the level of the anterior hip; angled to align with the ilio-pubic eminence (IPE)

Landmarks: identify the anterior inferior iliac spine (AIIS) — the bony prominence of the ilium at the superior aspect; identify the ilio-pubic eminence (IPE) — the junction of the ilium and superior pubic ramus; the femoral artery and femoral nerve are identified medially; the psoas tendon is identified as the round, bright (hyperechoic) structure overlying the anterior hip capsule between the AIIS and IPE

Injection: in-plane needle approach; the injection target is the plane BETWEEN the psoas tendon anteriorly and the anterior hip capsule (the iliofemoral ligament) posteriorly; 20–25 mL bupivacaine 0.25% or ropivacaine 0.375% is deposited in this interfascial plane; the injectate spreads along the plane superficial to the hip capsule, bathing the articular branches of the femoral, accessory obturator, and obturator nerves as they course along the capsule

Motor-sparing mechanism: the injection does NOT target the femoral nerve trunk → the motor branches to the quadriceps are NOT blocked; only the articular sensory branches from the capsular surface are anaesthetised; patients retain full quadriceps power and can walk immediately post-operatively

Feature PENG Block Femoral Nerve Block (FNB) Target Articular branches of femoral N, accessory obturator N, obturator N at AIIS/IPE Femoral nerve trunk at the femoral triangle (inguinal crease) level Motor NONE (motor-sparing — quadriceps function preserved) Quadriceps weakness (motor block of nerve to vastus lateralis, medialis, block intermedius) — falls risk; delays early mobilisation Analgesia Equivalent to FNB for anterior hip pain (surgical and fracture); may be less Good anterior hip analgesia; similar quality in many studies quality complete for posterior capsule pain (sciatic supply not included) Falls risk Minimal (quadriceps strength preserved) Significant — patients with FNB cannot be safely mobilised without supervised assistance; increased fall risk in hip fracture patients Adductor Partially preserved (obturator nerve articular branches blocked but main Not affected by FNB (FNB does not block the obturator nerve) strength obturator trunk usually not affected)

Lin DY et al. Pericapsular nerve group (PENG) block for hip arthroplasty (Anaesthesia 2021;76:1167–1173): RCT comparing PENG block vs placebo in total hip arthroplasty; PENG block significantly reduced: intraoperative opioid consumption; post-operative NRS pain scores at 24 hours; time to first analgesic request; PENG block group had preserved quadriceps function and achieved earlier mobilisation milestones vs placebo; no significant complications attributable to PENG block; conclusion: PENG block provides effective analgesia for THA with motor-sparing advantages consistent with an accelerated rehabilitation pathway

V/Q improvement mechanism: in ARDS, the dorsal (posterior) lung zones are the most severely consolidated and atelectatic (due to gravitational atelectasis — in the supine position, the heavy waterlogged lungs compress the dependent dorsal zones, which also receive the most blood flow due to gravity); in the prone position, the dorsal lung zones are now non-dependent → gravitational atelectasis is redistributed to the ventral (anterior) zones, which have less alveolar capacity; crucially, pulmonary blood flow redistributes less dramatically than ventilation in the prone position (the pulmonary vasculature is less responsive to gravity than the alveolar mechanics) → previously atelectatic dorsal lung regions open and are now both ventilated AND perfused → dramatic improvement in V/Q matching → ↑ PaO₂/FiO₂ ratio

More uniform stress distribution: the prone chest wall is stiffer (less compliant) than in the supine position — counterintuitively, this more uniform distribution of lung stress prevents overdistension of the non-dependent (now anterior/ventral) lung zones, which are already less consolidated; the dorsal zones, now nondependent, can be recruited at lower distending pressures; the result: more uniform alveolar inflation throughout the lung, less volutrauma to the small number of open alveoli

Improved secretion drainage: gravity assists secretion drainage from the posterior lung zones when prone (toward the main bronchus) → improved mucus clearance

Guérin C et al. PROSEVA (Proning Severe ARDS Patients) — NEJM 2013; n=466 patients with severe ARDS (PaO₂/FiO₂ <150 mmHg on FiO₂ ≥0.6, PEEP ≥5 cmH₂O): randomised to prone for at least 16 hours/day + lung-protective ventilation vs supine + LPV

Results: prone group: 28-day mortality 16.0% vs supine group 32.8% (absolute risk reduction 16.8%; relative risk 0.49; p<0.001); 90-day mortality 23.6% vs 41.0%; significantly greater improvement in PaO₂/FiO₂ in the prone group throughout the study; complications: higher rate of pressure ulcers, ETT displacement, and non-scheduled extubation in prone group (no difference in cardiac arrest during turning)

Indication for prone positioning: severe ARDS: PaO₂/FiO₂ <150 mmHg + FiO₂ ≥0.6 + PEEP ≥5 cmH₂O + adequate mechanical ventilation; initiated within 36 hours of ARDS diagnosis; minimum 16 continuous hours prone per session

Complication Mechanism Prevention Ischaemic Direct pressure on the orbit (from face-down position on an Head-specific prone support (Jackson frame, Mayfield head frame, padded optic unsupported face) → raised intraocular pressure → impaired optic horseshoe — ensuring NO pressure on the orbit or eyeball); confirm eye neuropathy nerve blood supply → optic nerve ischaemia → permanent position before draping (raise the head briefly and palpate to confirm the eye is (ION) blindness; prolonged prone anaesthesia (spine surgery >6 hours), not under any frame contact); check eyes every 30–60 minutes; maintain MAP hypotension, and anaemia increase risk; occurs in 0.1–0.2% of ≥80 mmHg; keep Hb ≥100 g/L; staged surgery if >6h anticipated prone spine cases but devastating when it does Brachial plexus Excessive arm abduction (>90°) in the prone position causes Arms alongside the body (preferred) or arms flexed at the elbow below injury traction on the brachial plexus (C5–T1 roots) between the clavicle shoulder level (<90° abduction); avoid the swimmer's position; pad all pressure and first rib; particularly the "swimmer's position" (one arm above the points (elbows, shoulders); check arm position after final prone positioning and head) → most common cause of brachial plexus injury in prone document spine surgery Facial pressure Prolonged pressure on face from headrest → ischaemic pressure Padded horseshoe or purpose-built prone head rest (ProneView, Dupaco); injuries ulcers on nose, cheeks, forehead, chin minimise face-to-surface contact area; check skin inspection whenever feasible during very long procedures Haemodynamic Turning from supine to prone (and back) → momentary venous Turning team of minimum 5 (ICU) or 6 (theatre) people; confirm ETT is secure compromise obstruction, arrhythmias from repositioning and line kinking, and has adequate length before turning; cross-clamp all unnecessary lines; during turning accidental ETT or IV line dislodgement senior anaesthesiologist controls the head and airway throughout the turn; have vasoactive drugs immediately available; continuous SpO₂, ETCO₂, and ECG monitoring during turning; post-turn: re-confirm ETCO₂ waveform, bilateral breath sounds, ETT position Accidental Most critical prone complication — re-intubating a prone patient is Secure the ETT with TWO separate securing methods (tape + tie, or a extubation extremely difficult; requires immediate log-roll back to supine before purpose-built tube-holder) before turning; ensure adequate ETT length (at any airway management least 3 cm beyond the teeth); a dislodged ETT in prone position = immediate log-roll back to supine then reintubation

Self-proning in awake non-intubated patients with hypoxaemia (first described at scale during COVID-19 pandemic): patients with SARS-CoV-2 pneumonia who were receiving HFNO or NIV were asked to lie prone voluntarily for 4–8 hours per day; multiple observational studies showed significant improvement in SpO₂ and oxygenation; may delay or avoid intubation in selected patients

Limitations: not tolerated by all patients; requires patient cooperation; does not provide the sustained 16-hour prone sessions shown in PROSEVA; not proven to reduce intubation rates in RCTs; but a safe, low-resource intervention that may provide short-term oxygenation improvement in pre-intubation COVID-19 patients

Probe Position View Structures Seen Primary Use and Angle Mid-Oesophageal Mid-oesophagus All four cardiac chambers simultaneously; Overall cardiac function; LV and RV size and function; valvular 4-Chamber (ME4C) (~30–35 cm); 0°; mitral valve; tricuspid valve; IAS; IVS assessment; ASD identification slight anteflexion Mid-Oesophageal Mid-oesophagus; LV and LA only; anterior and inferior LV walls; LV anterior and inferior wall motion; mitral valve anterior leaflet; LA 2-Chamber (ME2C) 90° mitral valve (2-chamber perspective) pathology Mid-Oesophageal Mid-oesophagus; LV outflow tract; aortic valve; proximal LVOT assessment; aortic valve morphology and stenosis/regurgitation; Long Axis 120–135° ascending aorta; posterior MV leaflet prosthetic aortic valve assessment (MELAX) Transgastric Short Transgastric (~45– LV cross-section at mid-papillary muscle Global LV function (all 16 segments simultaneously visible from a single Axis at Mid- 50 cm); 0°; neutral level; circular LV; anterior and posterior view); real-time ventricular wall motion; new regional wall motion Papillary Muscle position papillary muscles; RV (crescent-shaped, abnormalities = ischaemia; D-sign (septal flattening) for PE/RV strain (TG SAX) adjacent) Descending Aorta Mid-oesophagus; Descending thoracic aorta cross-section; Aortic atheroma (grading); aortic dissection; pleural effusion; identify Short Axis 0°; probe turned surrounding pleural space aorta for aortic cannula placement in cardiac surgery leftward (counterclockwise)

Effusion: pericardial effusion? Diastolic collapse of RV free wall = tamponade; anechoic fluid in the pericardial sac; measure dimension; respiratory variation of mitral inflow (pulsus paradoxus equivalent on Doppler)

Ejection: LV ejection fraction estimated by visual assessment of wall motion in ME4C and TG SAX; normal (>55%), mildly reduced (40–55%), moderately reduced (30–40%), severely reduced (<30% — walls barely move); hyperdynamic (walls touch in systole = EF >70%) Equalities (RV:LV ratio): normal RV:LV area ratio <0.6 in ME4C; D-sign in TG SAX (interventricular septal flattening — septal bowing into the LV forming a "D" shape when RV pressure exceeds LV) = RV pressure overload from massive PE, RV infarction, or pulmonary hypertension

Exits (IVC collapsibility and valvular assessment): IVC diameter >2.5 cm non-collapsing with respiration = elevated RA pressure = cardiogenic shock or obstructive shock; IVC <2 cm collapsing = low CVP = hypovolaemia; aortic and mitral valve structural assessment

Expected motion (wall motion assessment): regional wall motion abnormalities (hypokinesis, akinesis, dyskinesis) indicate myocardial ischaemia; new RWMA = acute coronary syndrome; global LV dysfunction = cardiomyopathy

Emergency TOE Finding Cardiac Pericardial effusion (anechoic fluid) + right atrial/RV diastolic free wall collapse (the low-pressure right heart chambers collapse when pericardial pressure tamponade exceeds diastolic filling pressure); swinging heart; respiratory variation in MV inflow >25% (pulsus paradoxus equivalent); dilated IVC (>2.5 cm, noncollapsing) Massive PE Acute RV dilation (RV:LV >1.0 in ME4C); McConnell's sign — regional RV wall motion abnormality: RV free wall akinesis with preserved RV apical function (unique to acute PE); D-sign in TG SAX (septal bowing into LV from acute RV pressure overload); LV underfilling (compressed by dilated RV); occasionally: direct thrombus visualisation in the pulmonary artery (MELAX or modified short axis views) LV Reduced EF visually (<30%); dilated LV; global hypokinesis; elevated LVEDP inferred from dilated LA; mitral regurgitation from papillary muscle dysfunction dysfunction; may coexist with new RWMA (MI as the cause) (cardiogenic shock) Air Characteristic "snowstorm" or "swirling" echobrightness in the right heart (microbubbles of air appear as hyperechoic masses in the RA and RV); small embolism amounts detectable before any haemodynamic compromise; TOE is the MOST SENSITIVE monitor for VAE; in sitting-position neurosurgery: even trivial (VAE) air entrainment is visible before the precordial Doppler signal changes

The traditional "coagulation cascade" model (intrinsic + extrinsic pathways → common pathway → thrombin → fibrin) is a laboratory construct that does not accurately represent in vivo clotting; the cell-based model (Hoffman M, 2003) describes coagulation in three overlapping phases occurring on cell surfaces:

Phase 1 — Initiation: occurs on tissue factor (TF)-bearing cells (fibroblasts, monocytes); vascular injury exposes TF → TF binds factor VIIa (pre-existing in plasma) → TF-VIIa complex activates factor X → Xa + Va → small initial thrombin burst (insufficient for full clot formation but enough to prime the system); factor IX is also activated by TF-VIIa

Phase 2 — Amplification: the small thrombin burst activates platelets (via PAR-1 receptors on the platelet surface) → activated platelets expose negatively charged phospholipid surface (phosphatidylserine) → coagulation complexes assemble on the platelet surface → cascade amplifies; thrombin activates factors

V, VIII, and XI

Phase 3 — Propagation: on the activated platelet surface: intrinsic tenase (IXa + VIIIa) → massive factor Xa generation → prothrombinase (Xa + Va) → massive thrombin burst → cleaves fibrinogen → fibrin; thrombin activates Factor XIII → cross-links fibrin → stable clot; THIS is the clinically important thrombin burst that forms the actual clot

Why this matters clinically: Factor VIIa (extrinsic initiation) and Factor VIII/IX (intrinsic amplification) are both essential; patients with haemophilia A (Factor VIII deficiency) have intact initiation but fail amplification → bleeding; recombinant FVIIa (NovoSeven) works by overwhelming the TF-VIIa pathway to generate enough thrombin even without Factor VIII/IX

Triggers: obstetric emergencies (amniotic fluid embolism, placental abruption, HELLP syndrome — massive TF release from placental and amniotic fluid); sepsis (LPS and cytokines upregulate TF on monocytes and endothelium); severe trauma (tissue injury → TF exposure); acute haemolytic transfusion reaction; malignancy (many tumour cells constitutively express TF); burns

Pathophysiology: systemic TF upregulation → continuous low-grade thrombin generation throughout the circulation → microvascular thrombi (fibrin deposits in small vessels → end-organ ischaemia: renal failure, cerebral dysfunction, hepatic failure) → CONSUMPTION of: fibrinogen (→ <1 g/L in severe DIC); platelets (→ <50×10⁹/L); clotting factors (V, VIII, XIII) → secondary fibrinolysis activation (plasmin dissolves the microthrombi but also destroys circulating fibrinogen and activates FDPs/D-dimers) → SIMULTANEOUS thrombosis and haemorrhage

Laboratory diagnosis: ↑ PT, ↑ APTT, ↑ TT (all clotting tests prolonged from factor consumption); ↓ fibrinogen (<1.5 g/L — most specific marker of DIC); ↑ Ddimers (fibrin degradation products — most sensitive marker); ↓ platelets (thrombocytopenia); fragmented red cells (schistocytes) on blood film — microangiopathic haemolytic anaemia from RBCs caught in fibrin strands

Treat the underlying trigger: the most important intervention — DIC will not resolve until the trigger is removed; in obstetric DIC → deliver the fetus and placenta; in septic DIC → antibiotics and source control; in haemolytic transfusion reaction DIC → stop the transfusion and treat the haemolysis Blood product replacement (guided by TEG/ROTEM or conventional coagulation tests): Fibrinogen concentrate 4–6 g IV or cryoprecipitate 10 units (when fibrinogen <1.5 g/L or FIBTEM MCF <10 mm) — the most urgently needed replacement; fibrinogen is the first clotting factor to be critically depleted in DIC FFP 10–15 mL/kg (factor replacement when PT/APTT >1.5× normal and there is active bleeding) Platelets (when <50×10⁹/L with active bleeding; or <20×10⁹/L even without active bleeding) Vitamin K 10 mg IV if concurrent warfarin or hepatic failure is contributing to factor deficiency

Recombinant Factor VIIa (rFVIIa / NovoSeven): 90–120 mcg/kg IV; bypasses the intrinsic pathway defects in DIC by overwhelming the extrinsic TF-VIIa pathway with supraphysiological concentrations of FVIIa → generates thrombin even in the absence of Factors VIII, IX, V; use: licensed for haemophilia with inhibitors; off-label for life-threatening haemorrhage refractory to all other measures (obstetric haemorrhage, major trauma); NOT recommended without adequate fibrinogen (>1 g/L) and platelets (>50×10⁹/L) — rFVIIa cannot work without substrate

Heparin in DIC: historically discussed as a treatment for the thrombotic component of DIC; not routinely recommended for acute haemorrhagic DIC; considered only in DIC predominantly manifesting as thrombosis (e.g., thrombotic DIC in purpura fulminans, malignancy-associated DIC) after very careful riskbenefit assessment

Step 1 — Self and Environment: confirm own identity, site, patient; check theatre environment and emergency equipment available

Step 2 — Electrical supply: connect mains power; check all monitoring equipment powered on and functional; check backup battery charge

Step 3 — Gas supplies: pipeline O₂, N₂O, and air pressure (400 kPa pipeline = 60 psi); check cylinder O₂ reserve cylinder is full (turn on, check pressure, turn off); check N₂O cylinder if applicable

Step 4 — Flowmeters: flowmeter tubes intact and correctly calibrated; bobbins spin freely; set to minimum at rest; check integrity of the rotameter assembly (no cracks)

Step 5 — Vaporisers: adequately filled; seated correctly on the back-bar (Selectatec® locking mechanism engaged); inter-lock functioning (cannot select two vaporisers simultaneously); not contaminated with wrong agent; vaporiser dial function at zero

Step 6 — Breathing system: assemble the circle breathing system; connect to machine; perform a leak test (close APL valve, occlude patient end → squeeze bag → confirm pressure maintained at ≥30 cmH₂O for ≥10 seconds without gas escape); confirm CO₂ absorber is functional (colour indicator fresh; weight appropriate)

Step 7 — Ventilator: switch on; test function; confirm appropriate settings (volume-control or pressure-control mode as required); test the disconnection alarm (pull the ventilator hose)

Step 8 — Monitoring: confirm SpO₂, ETCO₂, airway pressure, and agent monitoring are functioning and calibrated

Step 9 — Ancillary equipment: suction working; airway equipment available and checked; drugs prepared and labelled

Step 10 — Documentation: sign the machine check log; document time and initials

Principle of variable bypass (Tec 5, Tec 6, Tec 7 — Datex-Ohmeda; Mk 6 — GE): fresh gas flow (FGF) entering the vaporiser is split into two streams: a BYPASS FLOW (the larger portion — passes through the bypass chamber without contacting liquid anaesthetic) and a VAPORISING CHAMBER FLOW (the smaller portion — passes over or through the liquid anaesthetic where it becomes saturated with vapour); the two streams rejoin downstream; the output concentration is determined by the ratio of bypass flow to vaporising chamber flow (the "splitting ratio")

Splitting ratio: the fraction of total FGF directed through the vaporising chamber is controlled by the concentration dial; at the dial setting of 2% sevoflurane: the splitting ratio is adjusted so that the small saturated stream, when mixed with the large bypass stream, produces 2% sevoflurane in the output; the saturation vapour pressure (SVP) of the agent and the dial setting determine the mathematical splitting ratio required

Temperature compensation: as temperature falls, SVP falls → less vapour enters the vaporising chamber per unit of FGF → output concentration would fall; the vaporiser compensates with a bimetallic strip or temperature-sensitive valve — as temperature falls, the valve opens WIDER to allow a HIGHER proportion of FGF through the vaporising chamber, compensating for the lower SVP and maintaining the set output concentration constant; conversely at higher temperatures → the valve partially closes → maintains output

Flow compensation: at very high FGF rates (>15 L/min), the vaporising chamber may not achieve full saturation → the output concentration may be slightly lower than set; at very low FGF (<0.5 L/min), the output may be slightly higher than set (less dilution of the saturated vapour with bypass gas); Tec 5/6 vaporisers are calibrated for FGF 0.5–15 L/min

Agent-specific vaporisers: each vaporiser is calibrated for a specific volatile agent (SVP and MAC are agent-specific); filling the wrong agent into a vaporiser → catastrophic: e.g., desflurane (SVP 669 mmHg at 20°C) mistakenly filled into a sevoflurane vaporiser (SVP 157 mmHg) would result in delivery of a hypnotic overdose; colour-coding and agent-specific keyed fillers (Quik-Fil, Saf-T-Fill) prevent this

Safety System Design Prevents Pin Index Safety A unique arrangement of pins on the yoke (cylinder valve interface) for each gas cylinder; two pins project from Wrong gas cylinder being

System (PISS) the yoke in positions unique to each gas (O₂: positions 2,5; N₂O: 3,5; Air: 1,5); the cylinder valve has connected to the wrong gas corresponding holes; a cylinder can ONLY be connected to the correct yoke (O₂ cylinder cannot be connected to supply outlet; prevents the N₂O yoke) accidental substitution of N₂O for O₂ O₂ Failsafe When pipeline O₂ pressure falls below a threshold (approximately 200 kPa / 30 psi): an alarm sounds Delivery of a hypoxic gas System immediately; ALL gas flows to the flowmeters are automatically cut off (not just N₂O — ALL gases); the design mixture to the patient if the O₂ ensures that the patient cannot receive a hypoxic gas mixture if O₂ supply fails; on older machines: a pressure pipeline fails; also prevents regulator valve closes when O₂ pressure falls → blocks N₂O flow; on modern machines: electronic flowmeter N₂O only delivery without O₂ control automatically stops all flows; a reserve O₂ cylinder is mounted on the machine for this scenario Hypoxic Guard (O₂ A mechanical or electronic linkage between the O₂ and N₂O flowmeter controls that prevents the total gas mixture Accidental delivery of a Ratio delivered from containing less than a minimum O₂ concentration (typically 25%); on mechanical systems hypoxic gas mixture through

Monitor/Controller) (Ohmeda Link-25): a chain-and-sprocket mechanism links the O₂ and N₂O needle valves — increasing N₂O flow operator error on the automatically increases O₂ flow proportionally; on electronic systems: the O₂ concentration in the outflow is flowmeters (e.g., turning N₂O continuously measured and N₂O flow is automatically reduced if FiO₂ falls below 25% to maximum without proportionally increasing O₂) O₂ analyser An oxygen sensor (paramagnetic O₂ analyser — uses the paramagnetic properties of O₂ molecules) placed on Delivery of a hypoxic gas (paramagnetic) the inspiratory limb of the breathing circuit measures the inspired O₂ concentration continuously; if FiO₂ falls mixture to the patient despite below 21% (or a set alarm threshold) → alarm sounds immediately all upstream safety systems functioning — the final safety layer before the patient

Tool Patient Type Scale Details NRS (Numeric Communicative; 0–10 (0 = no Patient verbally rates pain; simple and quick; most widely used; 0–3 = mild; 4–6 = moderate; ≥7 = severe; Rating Scale) post-operative; pain; 10 = worst clinically meaningful change = ≥2 points; NRS ≤3 is the target for adequate analgesia adults; paediatric pain imaginable) ≥8 yrs VAS (Visual Communicative; 100 mm Patient marks a point on the line; ruler measures distance from left end = pain score in mm; more sensitive Analogue adults; requires horizontal line to change than NRS for research purposes; less practical at bedside Scale) literacy/visual (left = no pain, ability right = worst pain) Faces Pain Children 4–12 Six faces from Child points to the face that matches their pain; validated across cultures; revised version (FPS-R) uses Scale (FPS-R) years; adults with happy to crying faces without tears for better intercultural validity communication (scored 0–10) difficulty BPS Non- 3–12 (3 = no Three domains: Facial expression (1–4), upper limb position (1–4), compliance with mechanical ventilation (Behavioural communicative pain; 12 = (1–4); BPS ≥6 = clinically significant pain requiring treatment Pain Scale) adult ICU patients maximum pain) on ventilation CPOT Non- 0–8 Four domains: facial expression (0–2), body movements (0–2), muscle tension (0–2), compliance with (Critical-Care communicative ICU ventilator or vocalization (0–2); CPOT ≥3 = unacceptable pain level; validated in medical and surgical ICU Pain patients (intubated patients; PADIS 2018 recommends CPOT or BPS for pain assessment in non-communicative ICU patients Observation and non-intubated) Tool) DN4 (Douleur Chronic pain; 0–10 10 yes/no questions (7 symptoms, 3 clinical examination findings); score ≥4/10 = neuropathic pain likely; Neuropathique neuropathic pain validated for identifying neuropathic component of chronic pain (diabetic neuropathy, post-herpetic 4) screening neuralgia, CPSP)

An Acute Pain Service (APS) is a multi-disciplinary specialist team providing: consultant anaesthesiologist leadership; specialist pain nurses (pain sisters/APS nurses) who conduct daily ward rounds, troubleshoot analgesic failures, and educate nursing staff; dedicated pharmacist; physiotherapy input for rehabilitation pain management; psychology support for chronic pain patients admitted acutely; the APS is responsible for: managing all patient-controlled analgesia (PCA) infusions and epidural catheters in the hospital; developing and updating acute pain management protocols; monitoring adverse events (respiratory depression, PONV, inadequate analgesia); education of ward nursing staff in pain assessment and opioid safety

APS functions: daily review of all patients with epidurals, PCAs, or difficult acute pain management; 24-hour on-call support (pain nurse and pain anaesthesiologist available); adverse event monitoring and reporting; protocol development (multimodal analgesia pathways, procedure-specific protocols); training and education; quality improvement (NRS tracking, opioid consumption, adverse event rates)

IASP 2020 definition: CPSP is chronic pain that develops after a surgical procedure; it must: persist beyond the normal healing time (at least 3–6 months post-surgery); be distinct from pre-existing pain; be located in the surgical area or referred from it; significantly affect quality of life or daily function

Incidence: 10–50% of patients after major surgery develop some degree of CPSP; severe CPSP (significantly impacting function): 2–10%; highest incidence: thoracotomy (30–50% CPSP), limb amputation (phantom pain 50–70%), mastectomy (20–30%), inguinal hernia repair (10–12%); lowest after laparoscopic procedures

Pathophysiology — three phases:

Peripheral sensitisation: surgical tissue injury → prostaglandins, bradykinin, substance P, NGF released at the wound → sensitise peripheral nociceptors (threshold ↓, response ↑) → ↑ afferent firing

Central sensitisation: prolonged intense C-fibre activity activates NMDA receptors in the dorsal horn → glutamate-mediated windup → increased excitability of dorsal horn neurons → expansion of pain receptive fields → allodynia and hyperalgesia extend beyond the wound

Neuroplastic changes: persistent dorsal horn sensitisation → structural and functional changes in the CNS → chronic pain pathways established; this is the point at which pain transitions from a protective acute response to a maladaptive chronic condition

Risk factors: pre-operative: pre-existing pain at the surgical site (most powerful predictor); psychological factors (depression, anxiety, catastrophising — measured by Pain Catastrophizing Scale); genetic predisposition (COMT gene variants); younger age; female sex; intraoperative: nerve injury (direct or traction) during surgery; poor surgical technique; high-dose remifentanil infusion (OIH); post-operative: poorly controlled acute post-operative pain (NRS >6 in the first 24 hours is the most modifiable perioperative risk factor for CPSP)

Strategy Evidence Gabapentinoids Block α₂δ Ca²⁺ channel subunits → reduce presynaptic glutamate release → reduce central sensitisation → blunt windup in the dorsal horn; pre(pregabalin, operative pregabalin 150 mg + continued post-operatively reduces CPSP incidence in thoracotomy, breast surgery, and total hip/knee replacement gabapentin) pre- (multiple RCTs and meta-analyses); PROSPECT guidelines recommend peri-operative gabapentinoids for specific procedures with high CPSP risk operatively Ketamine (sub- NMDA antagonism → prevents central sensitisation directly; multiple RCTs (Lavand'homme 2005; Himmelseher 2005): intraoperative ketamine 0.2– anaesthetic) 0.5 mg/kg/hr reduces acute post-operative pain scores AND reduces CPSP incidence at 3 and 6 months after thoracotomy and colorectal surgery; effect is independent of its acute analgesic action — it specifically reduces the dorsal horn sensitisation that drives CPSP development Regional Blocks afferent nociceptive traffic to the dorsal horn throughout surgery → prevents the initial sensitisation trigger; well-designed neuraxial or anaesthesia peripheral nerve blocks that provide complete analgesia from incision → reduces acute pain AND reduces CPSP at 3–6 months in multiple procedures; thoracic epidural analgesia for thoracotomy dramatically reduces the 30–50% CPSP incidence

Minimising Surgical technique modification: nerve-sparing approaches (nerve-sparing radical prostatectomy; nerve identification and preservation during inguinal surgical nerve hernia repair — ilioinguinal, iliohypogastric nerve preservation reduces inguinal CPSP from 12% to <5%) injury Psychological Pre-operative cognitive behavioural therapy (CBT) targeting pain catastrophising reduces CPSP in patients with high pre-operative catastrophising pre-conditioning scores; mindfulness-based approaches; pain education (explaining the biology of pain transition to chronic pain)

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

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