Aortic Stenosis

• Obstruction to left-ventricular outflow from narrowing of the aortic valve, generating a systolic pressure gradient between the LV and the aorta.
• A normal aortic valve area is 3–4 cm²; obstruction becomes haemodynamically significant below about 1 cm².
• In UK adults the cause is almost always calcific degeneration.

To drive flow across the narrowing the LV develops concentric hypertrophy, which holds cardiac output steady for years. When it can no longer compensate, stroke volume falls — and the gradient can paradoxically drop even though the valve remains severely stenosed — and the patient decompensates.

See Valve morphology & aetiology (Assessment approach) for the echo appearances of each.

It is not a grade of aortic stenosis — it sits at the very start of the same calcific spectrum. It is common and rises with age, and matters mainly as a cardiovascular risk marker; roughly 2% of patients per year progress to stenosis. Routine echocardiographic surveillance is not recommended. GuidelineRing L, et al. Echocardiographic assessment of aortic stenosis: a practical guideline from the British Society of Echocardiography. Echo Res Pract 2021;8:G19–G59.

• An active, atherosclerosis-like disease — not simple wear and tear — evolving over years to decades.
• Begins as aortic sclerosis: calcium at the cusp attachments and coaptation lines, with no obstruction to flow.
• Deposits then accumulate focally; leaflets stiffen and lose mobility and the orifice narrows, each leaflet involved separately and asymmetrically.
• Most sclerotic valves never progress — only ~2% per year develop stenosis.
• Once stenosis is established, a peak-velocity rise >0.3 m/s per year marks rapid progression and predicts a worse outcome.

Sources: Lindman et al. 2016 (Nat Rev Dis Primers); Otto & Prendergast 2014 (NEJM); Ring et al. 2021 (BSE, Echo Res Pract).

Pumping against the obstruction places a chronic pressure load on the left ventricle, and the LV adapts in ways visible on the same echo used to grade the valve:

• Concentric LVH — increased wall thickness and LV mass on 2D, as the ventricle hypertrophies to generate the pressure needed to drive flow across the valve.
• Diastolic dysfunction — the stiff, hypertrophied LV fills at high pressure (graded on mitral inflow and E/e'), becoming dependent on the atrial kick and on adequate filling time.
• Fixed stroke volume — the obstruction caps forward output, so the LVOT VTI cannot augment to meet a fall in afterload or a rise in demand.

Clinically, these produce the classic triad of angina, exertional syncope and dyspnoea, with heart failure the end stage once compensation fails.

The hypertrophied LV stays symptom-free for years; once symptoms appear (angina, exertional syncope, breathlessness), untreated survival falls sharply — so symptom onset is the key trigger for valve replacement.

Echo features that mark severe / high-risk disease and prompt referral:

• Severe: peak velocity ≥4 m/s, mean gradient ≥40 mmHg, or valve area <1.0 cm².
• Very severe: peak velocity ≥5 m/s or mean gradient ≥60 mmHg.
• Impaired LV: ejection fraction <50%.
• Rapid progression: peak-velocity rise >0.3 m/s per year.

Why it matters in critical care: severe AS tolerates hypotension, tachyarrhythmia and vasodilatation poorly, so recognising it on a bedside scan directly changes peri-operative and ICU management (see At the bedside).

Source: Otto & Prendergast 2014 (NEJM).

↪ Indications and timing of AVR/TAVI are on the clinical Aortic Stenosis page.

Work through it in a logical order: define the valve and its aetiology, build severity from qualitative to quantitative measures, assess the secondary and associated effects, then integrate everything with the clinical picture.

Interrogate from every available window and report the highest velocity/gradient. Continuous-wave alignment is harder on TOE, so transthoracic windows usually give the best gradients.

A non-imaging dual-crystal CW transducer (pencil/Pedoff probe) gives a higher signal-to-noise ratio and easier transducer manipulation, and is recommended for recording the AS jet velocity. Provided the AS is not severe (<3 m/sec with good leaflet opening) a dual imaging-Doppler probe is acceptable. Care should be taken where the aetiology is a bicuspid aortic valve and the AS is severe, as it can be challenging to align accurately with a narrow jet; here colour Doppler can occasionally help.

IMAGE TO SOURCE — photo: standalone Pedoff / pencil CW probe [photo]

• Zoom on the valve and set depth and sector width to fill the screen with the region of interest.
• Optimise gain, focal position and tissue harmonics for clear leaflet definition.
• Use the highest frame rate that is practical (narrow the sector, reduce the depth).
• Position the patient well — left lateral for the parasternal and apical windows, right lateral decubitus for the right parasternal window.
• Use the ECG for timing and avoid foreshortening the LVOT and apex.

↪ For how each cusp appears across these views and the full root anatomy, see Cardiac & Coronary Anatomy.

Assess the valve systematically in the zoomed PLAX and PSAX views, then step out to the LVOT and root. Each feature points towards a mechanism.

The cusps

Shape & motion clues

Surrounding structures

• In short axis, two functional cusps open to a "fish-mouth" (oval) orifice — judge cusp number in systole, not diastole.
• Systolic doming of the leaflets on the long-axis view (pliable cusps bowing into the aorta).
• An eccentric diastolic closure line on M-mode or the long-axis view.
• A raphe (fused commissure) can make a bicuspid valve look trileaflet in diastole — always confirm in systole.
• Commonest fusion is the right and left coronary cusps; look for associated root or ascending-aorta dilatation.

[VIDEO: PSAX bicuspid valve — fish-mouth systolic opening with a raphe]

A bicuspid valve has two working cusps instead of three. First the plain-English bit:

• A raphe is a seam — a fibrous ridge where two cusps that should have been separate are fused together. It looks like a fake third cusp line, so a bicuspid valve can appear trileaflet in diastole. Always count the cusps that actually open in systole.

They are classified two ways.

1. By which cusps are fused (the practical, day-to-day description):

2. By Sievers type — simply, how many raphes the valve has:

In short: RL / RN / LN names which cusps are fused; the Sievers type counts the raphes.

• Dense calcification throws bright echoes and acoustic shadows that obscure the cusps and commissures, so a calcified bicuspid and tricuspid valve can look identical.
• The same shadowing makes planimetry of the orifice unreliable.
• Judge cusp number in systole, and use TOE or 3D for clearer leaflet definition when the transthoracic view is ambiguous.

Grade it semiquantitatively, best seen on the zoomed short-axis view (the long-axis, A3C and A5C also help):

• Mild — small, isolated echo-dense spots.
• Moderate — multiple larger spots.
• Severe — extensive thickening and calcification of all cusps.

Echo cannot reliably separate dense fibrosis from calcium and underestimates the true burden, so CT quantifies it better. Calcification grade carries prognostic weight, and bicuspid valves calcify earlier than tricuspid.

↪ CT aortic-valve calcium scoring (sex-specific Agatston thresholds) is used to arbitrate discordant low-gradient cases — see Discordant & low-flow, low-gradient AS.

M-mode is a supportive, qualitative tool in AS — it does not grade severity, but it gives a quick read on leaflet motion and the level of obstruction.

• Cusp separation — the maximal systolic leaflet separation; <12 mm suggests significant obstruction (a crude marker, not a severity measure).
• Thickened, calcified leaflets throw multiple dense echoes and open poorly.
• LV ejection time can be read from how long the cusps stay open.
• Early systolic partial closure of the valve points to dynamic subvalvular obstruction rather than valvular AS.

IMAGE TO SOURCE — real echo: M-mode of the aortic valve showing reduced cusp separation [trace]

In practice: colour to find the jet, CW for the transvalvular velocities, PW for the LVOT — together they drive the gradient and the continuity equation.

Colour Doppler is qualitative — it does not grade severity, but it finds the jet and guides the CW interrogation.

• Normal — brief, laminar, low-velocity flow with little or no aliasing.
• Aortic stenosis — a turbulent, aliased mosaic jet from the valve; where laminar flow turns turbulent marks the level of obstruction (valvular, sub- or supravalvular).
• Use it to aim the CW beam, especially for eccentric jets, and to spot a second or paravalvular jet.
• Screen for coexisting aortic and mitral regurgitation at the same time.

Find and aim with colour, then switch to CW for the numbers.

[VIDEO: colour Doppler of turbulent flow across the aortic valve]

On CW from an apical window the AS jet is a systolic envelope below the baseline, framed by the aortic valve opening and closing clicks.

• Timing — starts after isovolumetric contraction (after the QRS and first heart sound) and ends before isovolumetric relaxation; confined to ejection.
• Shape with severity — mild AS peaks early and looks triangular; severe AS is rounded and peaks in mid-systole as ejection lengthens.

A late-peaking, dagger-shaped envelope instead points to dynamic obstruction (see fixed vs dynamic).

Trace the dense outer (modal) edge of the CW waveform; ignore the faint linear transit-time artefact.

• Sweep speed 50–100 mm/s.
• Average three or more beats (at least five consecutive in atrial fibrillation); avoid the post-ectopic beat.
• Interrogate from multiple windows and keep the highest signal.

Both appear below the baseline from an apical window, so they are easily confused. The MR jet is longer, higher-velocity and later-peaking; the AS jet is confined to ejection, framed by the aortic valve clicks.

Reading the timing in practice — put the ECG on screen and use a fast sweep (100 mm/s):

• AS leaves a gap after the QRS (the isovolumetric contraction time) before flow starts; the jet then sits between the aortic opening and closing clicks and stops before diastole.
• MR begins at the QRS / first heart sound (mitral closure) with no gap, and runs on past the aortic closing click into early diastole, until mitral opening.
• So MR is longer at both ends — it fills the isovolumetric periods AS cannot, and on an overlaid trace its envelope encloses the AS one.

Quick rule: a gap after the QRS with the signal ending at the aortic click = AS; a signal that starts with the QRS and spills past the aortic click = MR.

Valvular aortic stenosis is a fixed obstruction; subaortic obstruction (most often HOCM) is dynamic. The two are separated by the shape of the CW envelope and by how the gradient responds to loading.

• Fixed AS — a rounded, roughly symmetric envelope that peaks in mid-systole; the gradient is stable beat-to-beat.
• Dynamic (HOCM) — a concave-upward, late-peaking “dagger” as obstruction builds through mid-to-late systole.
• Response to load — dynamic obstruction increases with anything that empties the LV or boosts contractility (Valsalva strain, standing, the beat after an ectopic); fixed AS barely changes.
• Post-ectopic beat (Brockenbrough–Braunwald) — in HOCM the gradient rises but the aortic pulse pressure falls; in fixed AS both rise.
• A fixed subaortic membrane gives a high gradient with near-normal leaflets and a coarse, “rough” systolic trace — localise the velocity step-up below the valve on colour/PW.

In practice — a late-peaking dagger should stop you before you call severe AS: image the subaortic area and LV, and provoke the gradient (Valsalva) to expose dynamic obstruction.

IMAGE TO SOURCE — real echo: CW comparison of fixed (rounded) vs dynamic (late-peaking dagger) obstruction [trace]

Not all LV outflow obstruction is valvular aortic stenosis. The CW trace looks broadly similar wherever the obstruction sits, so localise it by where the velocity steps up on pulsed and colour Doppler.

Build the grade by layering the modalities from qualitative to quantitative — no single measure stands alone.

Severity thresholds, from aortic sclerosis through to very severe — read the core measures together. GuidelineRing L, et al. Echocardiographic assessment of aortic stenosis: a practical guideline from the British Society of Echocardiography. Echo Res Pract 2021;8:G19–G59.

Typical surveillance intervals by severity. TextbookRing et al. Echocardiographic assessment of aortic stenosis. Echo Res Pract 2021.

Peak aortic jet velocity (Vmax) is the highest velocity through the stenotic valve, recorded with continuous-wave (CW) Doppler — the single best-validated marker of AS severity.

• Why it tracks severity — conservation of mass: as the orifice narrows the velocity must rise, so Vmax follows the obstruction.
• Waveform — with worsening AS the jet is higher and peaks later in systole; the envelope becomes more rounded as ejection is prolonged.
• Link to gradient — Vmax converts to the transvalvular pressure gradient through the simplified Bernoulli equation, ΔP = 4V².

IMAGE TO SOURCE — real echo: labelled CW jet across a stenotic aortic valve [trace]

Alignment is everything: the CW beam must run parallel to the jet — an intercept angle ≤15° keeps velocity underestimation under 5%. Record from the same window on serial studies so changes are real, not positional.

Sweep every available window and keep the single highest signal:

Use CW Doppler — the high velocities in AS (3–6 m/s) exceed the Nyquist limit of pulsed-wave. A dedicated non-imaging pencil (Pedoff) probe gives the best signal and alignment thanks to its small footprint.

Optimise the trace: raise the wall filter, drop the Doppler gain, set sweep speed to 100 mm/s and the velocity scale ~1 m/s above the expected jet.

Trace the outer edge of the dense modal envelope (exclude fine linear over-shoot artefact). This single trace yields Vmax, the VTI (for the continuity equation) and the mean gradient.

Average ≥3 beats in sinus rhythm and ≥5 in AF; avoid the beat after an ectopic. Take the maximal Vmax across all windows, regardless of which window produced it.

IMAGE TO SOURCE — real echo: CW from multiple windows, showing selection of the highest velocity [trace]

Peak velocity (Vmax) is measured directly — there is no equation for Vmax itself.

It converts to a peak instantaneous pressure gradient through the simplified Bernoulli equation: ΔP = 4V².

Use the expanded form ΔP = 4(V²max − V²LVOT) when the LVOT velocity is >1.5 m/s or the AV velocity is <3.0 m/s — otherwise ignoring the proximal velocity overestimates the gradient.

The Doppler peak instantaneous gradient is higher than the peak-to-peak gradient measured at cardiac catheterisation — they are not interchangeable.

Typical values used to grade severity. TextbookRing et al. Echocardiographic assessment of aortic stenosis. Echo Res Pract 2021.

The mean gradient is the average pressure difference across the valve through systole, derived from the CW Doppler velocities — a flow-dependent but well-validated marker of severity.

• Why velocity rises — conservation of mass: as the orifice narrows, the flow velocity must increase proportionately.
• From velocity to pressure — the gradient is derived from the velocities using the simplified Bernoulli equation, ΔP = 4V².
• How it's taken — record the maximal transaortic signal with CW Doppler and trace the envelope; the machine integrates it to the mean gradient over the ejection period.

IMAGE TO SOURCE — real echo: machine-traced CW envelope returning the mean gradient [trace]

Good alignment of continuous wave (CW) Doppler is essential for determining mean gradient

Should always be recorded from the same acoustic window as the previous exams

• Transthoracic
• Apical 5-chamber (use with steep left lateral position) / Apical 3-chamber / Subcostal short axis / Right parasternal, suprasternal, and sometimes subcostal approaches using a small, dedicated CW Doppler transducer (pencil probe or Pedoff transducer).
• Transoesophageal
• Deep transgastric 5-chamber view / Transgastric long axis view

Text

Typical values used to grade severity. GuidelineRing et al. Echocardiographic assessment of aortic stenosis. Echo Res Pract 2021.

The transvalvular pressure gradient is derived from velocity using the simplified Bernoulli equation: ΔP = 4V².

Use the expanded form ΔP = 4(V²max − V²LVOT) when the proximal (LVOT) velocity is >1.5 m/s or the aortic velocity is <3.0 m/s — otherwise ignoring the proximal velocity overestimates the gradient.

This is the peak instantaneous gradient, which is higher than the peak-to-peak gradient measured at catheterisation — the two are not interchangeable.

The mean gradient cannot be taken from the mean velocity; the machine integrates 4V² across the traced CW envelope.

In practice — trace the dense outer edge of the envelope and let the software return the mean gradient; always report peak velocity and mean gradient together.

The velocity ratio (dimensionless index, DVI) is the ratio of the LVOT VTI to the aortic-valve VTI.

• What it does — expresses severity as a ratio, sidestepping the error-prone LVOT diameter measurement the continuity equation depends on.
• Threshold — a value below 0.25 indicates severe AS, independent of body size.

Good alignment of continuous wave (CW) Doppler is essential for determining velocity ratio

Should always be recorded from the same acoustic window as the previous exams

• Transthoracic
• Apical 5-chamber (use with steep left lateral position) / Apical 3-chamber / Subcostal short axis / Right parasternal, suprasternal, and sometimes subcostal approaches using a small, dedicated CW Doppler transducer (pencil probe or Pedoff transducer) /
• Transoesophageal
• Deep transgastric 5-chamber view / Transgastric long axis view /

IMAGE TO SOURCE — real echo: paired PW (LVOT) and CW (AV) traces for the velocity ratio [trace]

It is acceptable to use either velocity or VTI in the equation:

orVTI_LVOT/VTI_AS }

The dimensionless index trades away an absolute, validated valve area to dodge the one big LVOT-diameter error — so it is a cross-check, reached for when that diameter is the weak link (poor PLAX, heavy calcification), rather than the reference measure.

The continuity equation gives the effective aortic valve area from one simple idea: in a single heartbeat the same volume of blood that passes through the LVOT must pass through the valve. If you know the flow on one side and the velocity on the other, you can solve for the area you cannot measure directly.

• Conservation of mass — stroke volume is identical at the LVOT and at the valve, so CSA(LVOT) × VTI(LVOT) = AVA × VTI(AV). As the orifice narrows, velocity must rise to keep that volume constant, and the equation reads that rise back as a smaller area.
• Why it is the reference measure — because it weighs the valve against the patient’s own LVOT flow, it stays valid when the gradient falls in a low-output state — which is exactly why it is the arbiter in low-flow, low-gradient AS.
• What you measure — the LVOT diameter in a zoomed PLAX (cross-sectional area = π(d/2)²), the LVOT velocity-time integral by pulsed-wave in the apical 5-chamber, and the aortic-valve VTI from the continuous-wave jet aligned to flow; average several cycles in AF.
• What it actually gives — the effective orifice area at the vena contracta, slightly smaller than the anatomical area because the jet keeps narrowing just beyond the leaflets. That effective area is the clinically validated number — the severity thresholds are built on it.

In practice — the result is only as good as its weakest input, the squared LVOT diameter; see the equation below and the pitfalls that follow.

Aortic valve area comes from three Doppler measurements, each taken from the window that best lines the beam up with flow:

In practice — the LVOT diameter is squared, so it dominates the error budget; a clean, on-axis PLAX measurement matters more than any other single step.

IMAGE TO SOURCE — real echo: montage of PLAX LVOT diameter, PW LVOT VTI and CW AV VTI [echo]

In patients at the extremes of size, indexing for body surface area (BSA) has been proposed, with a cut-off value of less than 0.6 cm²/m² BSA indicating critical AS.

This can be helpful in patients with an unusually small BSA.

Planimetry measures the anatomical valve-orifice area directly, by tracing it on a short-axis image.

• How — trace the orifice at the leaflet tips in mid-systole, on a 2D PSAX view or a 3D zoom acquisition.
• Strength — a direct anatomical measure, independent of flow and pressure, so it can help in low-flow or ambiguous-gradient cases.
• Limitation — heavy calcification blurs the orifice and TTE planimetry is unreliable; TOE/3D is better. Not a routine measurement — reserved for selected patients.

IMAGE TO SOURCE — real echo: PSAX planimetry of the aortic-valve orifice [echo]

IMAGE TO SOURCE — real echo: 3D TOE planimetry of the aortic valve [echo]

• Transthoracic
• Text
• Transoesophageal
• Text

Measure the LVOT diameter at the cusp insertion (annulus), inner-edge to inner-edge, mid-systole, in a zoomed PLAX view, excluding eccentric calcification; do not assume 2 cm. Because CSA uses the radius squared, a 1 mm error is roughly a 0.1 cm² error in AVA.

Underestimating LVOT diameter overestimates severity; an elliptical LVOT assumed circular overestimates severity (consider 3D planimetry of the LVOT area). A PW sample placed too close to the valve underestimates severity; too far into the LV overestimates it. Do not use the inner phantom envelope seen within the CW trace.

Pressure recovery is the reconversion of kinetic energy across the narrowed valve back to potential energy in the ascending aorta. It must be taken into account in patients with an ascending aortic diameter of less than 30 mm, otherwise the gradient may be significantly overestimated.

Contamination with an adjacent mitral regurgitation jet, failing to take an elevated proximal (LVOT) velocity into account, and changes in cardiac output and blood pressure all distort severity. Doppler malalignment of more than 15-20 degrees underestimates Vmax and gradient (and so underestimates severity).

Severity is underestimated in low cardiac output states (LV dysfunction, significant MR/MS) and with sequential stenoses, and overestimated in high cardiac output states. Velocity and gradient are flow-dependent and may underestimate severity in low-flow/low-output states.

Severity is flow-dependent, so it should be graded with the blood pressure controlled. Uncontrolled hypertension adds afterload that blunts transvalvular flow, lowering the velocity and gradient and underestimating severity; the distortion can run either way, so a reading taken at high pressure is simply unreliable.

If the systolic pressure is high at the time of the study, repeat the assessment once it has been brought down towards a target of 130–140 mmHg systolic. GuidelineRing L, et al. Echocardiographic assessment of aortic stenosis: a practical guideline from the British Society of Echocardiography. Echo Res Pract 2021;8:G19–G59.

Beat-to-beat variation in filling changes transvalvular flow, so a single beat is unreliable. Average 5–10 consecutive beats for the peak velocity, mean gradient and the LVOT and AV velocity–time integrals.

Alternatively, match beats: pair an LVOT trace and an AV trace that follow a similar preceding R–R interval, so the continuity equation uses comparable flow on both sides.

• A valve area in the severe range — ≤1.0 cm² (indexed ≤0.6 cm²/m²).
• A low gradient — mean <40 mmHg, peak velocity <4 m/s.
• Low transvalvular flow — stroke-volume index (SVi) <35 mL/m².

So the valve is genuinely severe, but the low flow keeps the gradient down — it is easily under-graded as moderate.

• The gradient and velocity are not direct measures of the valve; they reflect how much blood is driven across it — the flow.
• For a given valve, more flow produces a higher gradient and less flow a lower one.
• In critical illness — shock, sepsis, impaired LV function, post-arrest — stroke volume falls, so transvalvular flow and the gradient fall with it, and a severe valve is read as moderate.
• Because valve area is independent of flow, it remains the reliable measure of severity when the gradient is not.

When the valve area is severe (≤1.0 cm²), the gradient and flow do not always agree. There are four recognised combinations of gradient, flow and ejection fraction — three are severe, one usually is not:

Both have a severe valve area with a low gradient because the flow is low. They differ in why the flow is low, told apart by the ejection fraction:

• Classical LFLG — reduced EF (<50%): a weak, dilated ventricle cannot generate an adequate stroke volume, so flow and gradient are low.
• Paradoxical LFLG — preserved EF (≥50%): a small, hypertrophied, stiff ventricle fills poorly, so stroke volume is low despite a normal EF.

[IMAGE: side-by-side ventricles — dilated thin-walled weak LV (classical) vs small thick-walled stiff LV (paradoxical)]

• Do not assign a definitive grade in a haemodynamically unstable patient — the gradient will mislead.
• Recognise the pattern and rely on the valve area, the 2D appearance (heavy calcification, restricted opening) and the stroke-volume index.
• Optimise haemodynamics, then re-image once flow is restored.
• Definitive confirmation is an elective, outpatient process — not a bedside one.
• When stable, the elective sort-out is by ejection fraction: reduced EF → dobutamine stress echo; preserved EF → CT aortic-valve calcium score (neither is a bedside test).

LV size, systolic function (assess long-axis too — it may be impaired despite a normal EF), hypertrophy / indexed LV mass; degree of pulmonary hypertension; the other valves and the aortic root / ascending aorta. Moderate AS with more than mild AR should be treated as severe valve disease. Severity is underestimated in low-output states (LV dysfunction, significant MR/MS) and with sequential stenoses, and overestimated in high-output states.

IMAGE TO SOURCE — real echo: PLAX showing concentric LVH and dilated LA secondary to AS [echo]

Heavy calcification with restricted cusp motion (without significant calcification, important AS is unlikely); a late-peaking / slow-acceleration CW envelope; very high gradients (very severe Vmax ≥5, mean ≥60); Vmax progression >0.3 m/s/year; LVEF <55% (intervention cut-off <50%); GLS more positive than −14%; indexed LV mass >110 g/m² (men) / >99 g/m² (women); pulmonary hypertension; low SVi (<35) and AVA <0.8 cm². GuidelineRing L, et al. Echocardiographic assessment of aortic stenosis: a practical guideline from the British Society of Echocardiography. Echo Res Pract 2021;8:G19–G59.

IMAGE TO SOURCE — real echo: GLS bullseye / strain example, plus LV-mass measurement [echo]

A severely stenotic valve is a fixed obstruction: the LV cannot increase output across it, and the hypertrophied, stiff ventricle depends on tight loading conditions. Small changes a normal heart shrugs off can tip it into a spiral of hypotension, falling coronary perfusion and arrest. ReviewChacko M, Weinberg L. Aortic valve stenosis: perioperative anaesthetic implications. BJA Educ 2012;12(6):295–301.

• Preload — keep it up; the stiff LV needs good filling. Treat hypovolaemia, but watch for pulmonary oedema.
• Afterload — maintain SVR. Vasodilators — and the vasodilatation of induction agents or neuraxial block — drop coronary perfusion pressure dangerously; have a vasopressor ready.
• Rhythm — keep sinus rhythm; the atrial kick contributes a large share of filling to a stiff LV. Treat new AF urgently.
• Rate — avoid tachycardia (shortens diastolic filling and coronary perfusion) and severe bradycardia (a fixed stroke volume means output falls).

Vmax and the mean gradient are flow-dependent. In a low-output state — sepsis, poor LV, post-arrest — transvalvular flow falls and the gradient drops, so severe AS can read as moderate or even mild.

• Look at the valve and the area, not just the gradient: a calcified, barely-opening valve with AVA <1.0 cm² and a low gradient is low-flow, low-gradient severe AS until proven otherwise.
• Check the stroke-volume index (SVi <35 mL/m² = low flow) and LV function.
• Resolve it with dobutamine stress echo (if EF is low) or a CT calcium score — not by trusting the gradient.

• New AF or tachyarrhythmia — loss of the atrial kick plus short filling causes an abrupt fall in output; restore rate or rhythm urgently.
• Sepsis / vasoplegia — low SVR drops coronary perfusion across the fixed lesion; early vasopressor, cautious with vasodilators.
• Induction & intubation — sympatholysis and positive-pressure ventilation cut preload and SVR; pre-optimise, induce slowly, vasopressor ready.
• Neuraxial anaesthesia — sympathetic block causes the same afterload and preload drop; use with great caution.
• Non-cardiac surgery — severe symptomatic AS markedly raises perioperative risk; in selected cases consider valve intervention first.
• Decompensation / cardiogenic shock — vasopressors to hold perfusion, avoid pure vasodilators; balloon valvuloplasty or urgent TAVI as a bridge.