Aortic stenosis for non-cardiac surgery

Surgical approach (non-cardiac surgery context)

• Not a single operation: principles apply to any non-cardiac procedure (e.g. hip fracture fixation, laparotomy, vascular, major abdominal, urology).
• Key surgical determinants of risk
  • Urgency: elective vs urgent vs emergency (time for echo/cardiology/valve intervention).
  • Surgical stress/bleeding: major intra-abdominal/vascular > orthopaedic > superficial.
  • Physiology: pneumoperitoneum, Trendelenburg, one-lung ventilation, major fluid shifts.
  • Post-op destination: HDU/ICU availability and need for invasive monitoring/vasopressors.
• Risk mitigation with surgeon
  • Consider less invasive/shorter procedure, regional/local infiltration, staged surgery, damage-control approach where appropriate.
  • Plan haemostasis: cell salvage, TXA (if appropriate), meticulous surgical technique, avoid prolonged hypotension/bleeding.

Anaesthetic management (template for non-cardiac surgery with AS)

• Type of anaesthesia: usually GA with invasive monitoring for moderate–severe AS; regional techniques may be used selectively with careful titration.
  • Neuraxial: avoid rapid sympathectomy; consider low-dose CSE/graded epidural if benefits outweigh risks and resources allow.
  • Peripheral nerve blocks: useful adjuncts to reduce opioid/volatile requirements (e.g. fascia iliaca for hip fracture).
• Airway: ETT often preferred (control ventilation, CO2, haemodynamics); SGA only for short, low-stress cases with minimal haemodynamic swings.
• Duration: depends on surgery; aim to minimise anaesthetic and surgical time; avoid prolonged hypotension/tachycardia.
• Pain: procedure-dependent; prioritise multimodal analgesia and regional blocks to blunt sympathetic surges while avoiding hypotension.
• Core haemodynamic aims: sinus rhythm, avoid tachycardia, maintain preload, maintain SVR/diastolic pressure, avoid myocardial depression.

Why aortic stenosis matters in non-cardiac surgery (pathophysiology)

• Fixed LV outflow obstruction → limited ability to increase cardiac output during stress/anaesthesia.
• LV hypertrophy → diastolic dysfunction; LV filling becomes preload- and atrial-contraction dependent.
• Coronary perfusion depends on diastolic aortic pressure; hypotension and tachycardia reduce supply while demand is high (LVH).
• Anaesthetic hazards: vasodilation (↓SVR), hypovolaemia, neuraxial sympathectomy, tachyarrhythmias/AF, myocardial depression, bleeding.

Definitions and severity (echo-based)

• Severe AS (typical): aortic valve area (AVA) < 1.0 cm² (or indexed <0.6 cm²/m²), mean gradient ≥ 40 mmHg, peak velocity ≥ 4.0 m/s.
• Moderate AS: AVA 1.0–1.5 cm²; mean gradient 20–39 mmHg; Vmax 3.0–3.9 m/s.
• Low-flow, low-gradient severe AS can occur (reduced stroke volume despite severe valve narrowing). Requires cardiology interpretation (DSE/CT calcium scoring).
• Symptoms that define high risk: exertional angina, syncope/presyncope, dyspnoea/heart failure, reduced exercise tolerance.

Preoperative assessment (history, exam, investigations)

• History: quantify functional capacity (METs), symptom triad (angina/syncope/dyspnoea), orthopnoea/PND, chest pain at rest, palpitations/AF, recent decompensation, falls (syncope).
• Examination: ejection systolic murmur radiating to carotids, slow-rising pulse, narrow pulse pressure (may be absent), signs of HF, volume status.
• ECG: LVH, strain, conduction disease, AF. Consider baseline troponin/BNP in high-risk pathways if locally used.
• Echo: ensure recent study and document severity, LV function, gradients, valve area, pulmonary pressures, other valve disease (MR), aortic root pathology.
  • Pragmatic: if no echo within ~12 months for known AS, or change in symptoms/signs, obtain echo if time allows (especially elective).
• Coronary disease: common co-morbidity; consider cardiology input if symptoms/ECG changes/high risk surgery.

Risk stratification and decision-making (elective vs urgent vs emergency)

• Key determinants: AS severity, symptoms, surgical urgency, surgical stress, physiological reserve, availability of HDU/ICU and invasive monitoring.
• Elective surgery
  • Asymptomatic severe AS: consider proceeding for low/intermediate-risk surgery with careful plan; for high-risk surgery, discuss cardiology and consider valve intervention first.
  • Symptomatic severe AS: generally defer elective non-cardiac surgery until valve treated/optimised (SAVR/TAVI) unless benefits outweigh risk and no alternative.
• Urgent/emergency surgery (e.g. hip fracture, laparotomy)
  • Proceed with enhanced monitoring and haemodynamic goals; obtain focused echo if feasible without delaying life/limb-saving surgery.
  • Early senior anaesthetist involvement; plan vasopressors, invasive lines, post-op critical care.
• Bridging options in selected cases: balloon aortic valvuloplasty (temporary) or expedited TAVI/SAVR if surgery can wait and risk is prohibitive.

Anaesthetic goals (what you are trying to achieve)

• Rhythm: maintain sinus rhythm; treat AF promptly (rate control often poorly tolerated; consider cardioversion if unstable).
• Rate: avoid tachycardia (shortens diastole → ↓coronary perfusion) and avoid significant bradycardia (CO depends on HR when SV fixed).
• Preload: maintain euvolaemia; avoid hypovolaemia (bleeding/vasodilation) and avoid overload (pulmonary oedema with diastolic dysfunction).
• Afterload: maintain SVR and diastolic pressure; hypotension is dangerous—treat early.
• Contractility: avoid myocardial depressants in excess; consider inotrope only if low output with adequate SVR/preload.
• Oxygenation/ventilation: avoid hypoxia, hypercarbia, acidosis (increase PVR and myocardial demand).

Monitoring and access

• Standard monitoring + invasive arterial line before induction for moderate–severe AS or any major surgery.
• Large-bore IV access; consider rapid infuser if bleeding risk.
• Central venous access: consider if major surgery/vasopressor infusion anticipated; CVP is a poor guide to volume but useful for access.
• Cardiac output monitoring: consider (especially major surgery) but interpret cautiously in fixed obstruction; trends more useful than absolute values.
• TOE: rarely for routine non-cardiac surgery, but may be valuable in high-risk major surgery with severe AS if expertise available.

Induction and maintenance (practical approach)

• Preparation: vasopressor drawn up and running plan (e.g. metaraminol/phenylephrine boluses; noradrenaline infusion if needed), defib pads available, discuss haemodynamic targets with team.
• Induction principles: slow, titrated induction; avoid sudden vasodilation and myocardial depression; ensure adequate preload.
  • Agents: etomidate or carefully titrated propofol; opioid (fentanyl/alfentanil/remifentanil) to blunt response; consider ketamine in selected patients but avoid tachycardia.
  • Muscle relaxant: choose haemodynamically stable agent; avoid histamine release.
• Airway: gentle laryngoscopy; treat sympathetic response (opioid, lidocaine, beta-blocker cautiously, deepen anaesthesia) while avoiding hypotension.
• Maintenance: volatile at low–moderate MAC with opioid infusion, or TIVA; avoid excessive vasodilation; maintain sinus rhythm and stable BP.
• Ventilation: avoid high intrathoracic pressures and excessive PEEP that reduce venous return; maintain normocapnia.

Haemodynamic management (what to do when things go wrong)

• Hypotension: treat immediately—check depth, bleeding, preload, rhythm; give alpha-agonist early to restore SVR/diastolic pressure.
  • First-line often metaraminol or phenylephrine; if persistent/major surgery: noradrenaline infusion.
  • If low output with adequate SVR/preload: consider dobutamine/adrenaline cautiously with senior help (tachycardia risk).
• Tachycardia: treat pain/light anaesthesia/hypovolaemia; consider short-acting beta-blocker (e.g. esmolol) cautiously; avoid dropping BP.
• Bradycardia: may reduce CO; treat causes; consider glycopyrrolate/atropine if appropriate; pacing if severe with instability.
• Atrial fibrillation: loss of atrial kick can precipitate pulmonary oedema/hypotension; if unstable → synchronised cardioversion; if stable → cautious rate control and optimise preload/SVR.
• Myocardial ischaemia: increase diastolic pressure (vasopressor), reduce HR, correct anaemia/hypoxia, treat pain; consider GTN cautiously (may drop preload/SVR).

Regional and neuraxial techniques (exam-relevant nuance)

• Traditional teaching: neuraxial anaesthesia can be hazardous in severe AS due to sympathectomy → ↓SVR/↓preload → hypotension and ischaemia.
• Modern practice: not absolutely contraindicated, but requires careful patient selection, incremental dosing, invasive BP monitoring, immediate vasopressor availability, and senior oversight.
• Prefer: peripheral nerve blocks + light GA, or GA with multimodal analgesia; if epidural used, dose slowly and avoid high block.

Postoperative care

• Destination: HDU/ICU for severe AS, symptomatic patients, major surgery, significant intra-op instability or vasopressor requirement.
• Analgesia: avoid uncontrolled pain (tachycardia/HTN) and over-sedation (hypoventilation/hypercarbia). Use regional blocks, paracetamol, cautious opioids; NSAIDs individualised (renal/CABG risk).
• Fluid balance: aim euvolaemia; monitor for pulmonary oedema; early mobilisation and VTE prophylaxis as appropriate.
• Monitoring: ECG for arrhythmia/ischaemia; consider postoperative troponin surveillance in high-risk patients per local pathway.

Special scenarios

• Hip fracture with severe AS
  • Time-critical surgery; optimise rapidly (echo if not delaying), arterial line, vasopressors ready, consider fascia iliaca block; GA often chosen for control; neuraxial only if graded and resourced.
• Laparoscopy
  • Pneumoperitoneum ↑SVR and can reduce venous return; hypercarbia increases HR; use lower insufflation pressures, careful ventilation, and close BP control.
• Major haemorrhage risk
  • Early blood availability, cell salvage if appropriate, maintain diastolic pressure; avoid permissive hypotension strategies used in trauma—often inappropriate in severe AS.