Aortic Stenosis for the Anaesthesiologist - A Comprehensive Guide

1. Overview and Epidemiology

• Congenital bicuspid aortic valve - stenosis typically manifests in the 4th-5th decade of life; occurs in 1-2% of the population
• Senile/calcific degenerative AS - most common cause overall; calcium deposits on normal cusps in patients aged 60+
• Rheumatic AS - less common in developed countries; rarely isolated and usually associated with aortic regurgitation or mitral valve disease

2. Pathophysiology - What the Anaesthesiologist Must Understand

The Fixed Obstruction

Pressure-Volume Loop in AS

Compensatory Mechanisms and Their Limits

1. Concentric LV hypertrophy - parallel replication of sarcomeres maintains stroke volume by generating the needed transvalvular pressure gradient. LV can generate systolic pressures up to 300 mmHg.
2. Increased LVEDP - despite normal LVEDV until late disease, end-diastolic pressure is elevated early due to reduced compliance from hypertrophy and fibrosis.
3. Diastolic dysfunction - impaired LV filling; ventricular filling becomes critically dependent on atrial systole (the "atrial kick" may contribute up to 40% of total cardiac output in AS).

The Pathophysiologic Triad (End-Stage)

• Angina - myocardial oxygen demand increases (hypertrophy) while supply decreases (compressed intramyocardial vessels from high intracavitary pressures)
• Syncope - inability to increase CO during exertion + vasodilation in exercising muscle; arrhythmias
• Heart failure / dyspnoea - elevated LVEDP backs up into pulmonary vasculature

• Angina: ~5 years survival
• Syncope: ~3 years survival
• Heart failure: ~1-2 years survival

Key Anaesthetic Implications of Pathophysiology

3. Preoperative Assessment

Clinical Evaluation

• Symptoms: exertional dyspnoea, angina, syncope, or near-syncope
• Signs: slow-rising, low-amplitude (pulsus parvus et tardus) carotid pulse; harsh late-peaking systolic ejection murmur best heard at right upper sternal border, radiating to carotids; absent A2; paradoxically split S2
• ECG: LV hypertrophy with strain pattern, left axis deviation, left bundle branch block
• Echocardiography: mandatory - confirms AVA, mean gradient, peak jet velocity, LV function, concurrent valve lesions

Risk Stratification for Non-Cardiac Surgery

• Asymptomatic severe AS + preserved EF: noncardiac surgery can proceed with acceptable risk with appropriate haemodynamic monitoring
• Symptomatic severe AS: aortic valve replacement (surgical or TAVR) should be considered before elective noncardiac surgery
• Asymptomatic AS + EF < 50% undergoing high-risk surgery: European guidelines recommend prior valve replacement
• High-risk patients ineligible for replacement: percutaneous balloon aortic valvuloplasty may be considered as a bridge

Acquired von Willebrand Syndrome

4. Haemodynamic Goals - The Core of AS Anaesthesia

5. Monitoring

Minimum Monitoring

• Standard ASA/international monitors (SpO₂, ECG, NIBP)
• Note: ST-segment and T-wave changes on ECG may be baseline abnormalities from LV hypertrophy, complicating ischaemia detection

Strongly Recommended / Often Mandatory

• Pre-induction invasive arterial line (radial): essential in severe AS. Pulse pressure is typically narrowed (may be ≤50 mmHg despite normal LVEF). Even brief hypotension is poorly tolerated. Allows beat-to-beat monitoring and facilitates vasopressor titration.
• Transesophageal echocardiography (TEE): gold standard for intraoperative monitoring. Assesses:
  • LV preload (LVEDA)
  • LV contractility and wall motion abnormalities
  • Valvular function and gradient
  • Haemodynamic response to interventions
  • Best views: midesophageal aortic valve short-axis and transgastric long-axis for Doppler gradients

TEE Views for Aortic Valve Assessment

PA Catheter

• Rarely required in patients with preserved ventricular function
• Risk: arrhythmias during insertion can severely compromise coronary perfusion in AS; CPR is ineffective across a stenotic valve
• Consider only in selected patients with severely impaired LV function

6. Anaesthetic Technique

General Anaesthesia

• Use dose-reduced agents - virtually all induction agents produce vasodilation and hypotension
• Preferred agents: etomidate (minimal haemodynamic effects) or a carefully titrated ketamine (maintains SVR)
• Slow, controlled induction with vasopressor (phenylephrine) immediately available
• Phenylephrine is the vasopressor of choice for acute hypotension in AS:
  • Pure alpha-agonist increases SVR/diastolic BP without increasing heart rate (unlike ephedrine, which causes tachycardia)
  • Restores coronary perfusion pressure across the fixed obstruction
  • Vasopressin and norepinephrine are alternative options

• Volatile agents: use with caution - concentration-dependent vasodilation, myocardial depression, and potential loss of sinus rhythm
• Keep concentrations low; supplement with opioids/neuraxial techniques where appropriate
• Tachycardia (e.g., from laryngoscopy) should be treated immediately with beta-blockade (esmolol) or deepening anaesthesia
• Significant hypertension should also be treated promptly as it increases myocardial O₂ demand
• SVT with haemodynamic compromise: immediate synchronised cardioversion

• Norepinephrine, vasopressin, and phenylephrine are preferred over ephedrine (which causes tachycardia)
• Vasodilators (GTN, SNP) should be used with extreme caution or avoided - these patients are very sensitive to afterload reduction

Regional Anaesthesia (Neuraxial)

• Mild-moderate AS (generally asymptomatic): may tolerate spinal or epidural anaesthesia
• Severe AS: neuraxial blockade is a relative contraindication but not absolute - decision must be individualised based on disease severity, LV function, and case urgency
• Epidural preferred over single-shot spinal because:
  • Slower, more titratable onset of sympatholysis
  • Allows more timely correction of hypotension
  • Continuous spinal catheters offer a similar advantage
• A vasopressor must be immediately available for any neuraxial technique in AS
• The acquired von Willebrand syndrome in these patients should be excluded/managed before neuraxial blockade

7. Specific Perioperative Scenarios

Cardiac Surgery - Aortic Valve Replacement (AVR)

• Baseline valve assessment and LV function
• Annulus measurement for valve sizing (critical to avoid patient-prosthesis mismatch)
• Post-bypass assessment of valve function, paravalvular regurgitation, and biventricular function

• After relieving the obstruction, LV may develop "suicide ventricle" (LVOTO from hypertrophy becoming dynamic) - diagnose with TEE and treat with volume and vasoconstrictors
• Watch for new conduction defects post-AVR

TAVR (Transcatheter Aortic Valve Replacement)

• Originally performed under GA with TEE guidance
• Trend toward monitored anaesthesia care (MAC) or moderate sedation with TTE monitoring, which improves efficiency without compromising safety
• GA with TEE is still preferred for:
  • High risk of coronary occlusion
  • Risk of annular rupture
  • Reducing contrast load in high-risk patients
  • Secondary valve sizing measurements
• Valve sizing: multidetector CT (MDCT) is the preferred modality; 2D TEE/TTE underestimates annular size due to the elliptical shape of the aortic valve complex; 3D TEE is more accurate
• Intraprocedural TEE monitoring: baseline biventricular function, wire and device positioning, post-deployment assessment of transvalvular gradients and paravalvular regurgitation, and immediate recognition of complications (coronary obstruction, pericardial effusion, new RWMA, aortic injury)

8. Critical Intraoperative Events and Management

9. Summary: The "4 DON'Ts" in AS Anaesthesia

1. Don't vasodilate - drop in SVR cannot be compensated; immediate coronary underperfusion
2. Don't allow tachycardia - reduces diastolic filling time and increases MVO₂ in an already oxygen-starved myocardium
3. Don't lose sinus rhythm - atrial kick contributes up to 40% of CO; loss is an emergency
4. Don't hypovolaemia - stiff, non-compliant LV requires adequate preload; small volume changes cause large haemodynamic shifts

Sources

• Morgan & Mikhail's Clinical Anesthesiology, 7e, Ch. 21 (Valvular Heart Disease), pp. 768-771
• Miller's Anesthesia, 10e, Ch. 50 (Valvular Heart Disease) and Ch. 28 (Preoperative Assessment), pp. 3907-3909, 7649-7656
• Barash, Cullen, and Stoelting's Clinical Anesthesia, 9e, Ch. 39 (Valvular Heart Disease), pp. 3307-3310
• Place A et al. "Peri-operative risk of non-cardiac surgery in patients with aortic stenosis: a systematic review and meta-analysis." Anaesthesia. 2026 Apr. PMID: 41388337