Skip to textbook content
Doctor’s PassportTextbook
TopicsAll topics

Loading topic navigation…

Textbook navigation
TopicsAll topics

Loading topic navigation…
← Cardiology indexChapter sections
OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
Full textbook13 sectionsOpen only what you need
Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Aortic regurgitation

Cardiology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

RapidFull
!
Time-critical presentation

Acute severe aortic regurgitation can cause abrupt pulmonary oedema and shock with few classic peripheral signs. Call 999, obtain immediate echocardiography and involve cardiothoracic surgery urgently, particularly after endocarditis, aortic dissection or trauma.

Overview

Distinguish acute from chronic aortic regurgitation, quantify severity and LV response, and act before irreversible ventricular dysfunction develops.

AR results from leaflet failure, aortic-root dilatation or both. Chronic regurgitation allows adaptive LV enlargement and a large stroke volume; acute regurgitation abruptly raises LV diastolic pressure, impairing forward output and causing pulmonary oedema.

Assessment integrates mechanism, quantitative regurgitation, LV dimensions and function, aortic dimensions and symptoms. An apparently normal LVEF may already represent declining contractility in a volume-loaded ventricle, so trends matter.

Surgical repair or replacement is the definitive therapy for severe disease with symptoms or LV/aortic triggers. Transcatheter treatment is not the routine equivalent of TAVI for native pure AR and is reserved for selected inoperable patients at expert centres.

Key points

  • Chronic AR produces LV volume overload, eccentric dilatation and a wide pulse pressure; symptoms can appear late after prolonged compensation.
  • An early diastolic decrescendo murmur at the left sternal edge is typical; leaning forward in expiration can make it clearer.
  • Acute severe AR may have a short, soft murmur and normal pulse pressure because the LV has had no time to dilate.
  • Echo grades regurgitation using several measures; severe markers include vena contracta over 6 mm, regurgitant volume at least 60 mL/beat or EROA at least 0.30 cm2.
  • Symptomatic severe AR and severe AR with LV systolic impairment or excessive LV dilatation require valve-surgery assessment.
  • Measure the aortic root and ascending aorta: bicuspid valve, connective-tissue disease and dissection can determine the operation as much as the valve lesion.
  • Vasodilators treat coexisting hypertension or heart failure when surgery is not yet possible; they do not replace timely surgery in operable severe AR.
  • New dyspnoea, falling LVEF or rising LV end-systolic size during surveillance should trigger valve-team review before irreversible damage.

Aetiology

01

Primary leaflet disease

Bicuspid morphology, degenerative change, rheumatic disease or leaflet prolapse can prevent complete diastolic coaptation. Bicuspid disease also warrants assessment of the root and ascending aorta.

02

Aortic root dilatation

Hypertension, age-related aortic disease and heritable connective-tissue aortopathy can enlarge the annulus or root, pulling otherwise mobile leaflets apart and creating central regurgitation.

03

Infective endocarditis

Infection can perforate, tear or destroy a cusp and cause abrupt severe regurgitation. Fever, embolic features or positive cultures make this a time-critical cause rather than routine chronic valve disease.

04

Dissection, trauma or iatrogenic injury

An aortic dissection may disrupt commissural support, while trauma or a valve procedure can damage a leaflet. These causes often present acutely with pulmonary oedema or shock.

Pathophysiology

  1. 1
    Diastolic backflow

    Incomplete valve closure allows blood to return from the aorta into the LV during diastole. Severity depends on the regurgitant opening, pressure gradient and duration of diastole.

  2. 2
    Chronic volume compensation

    With gradual disease, the LV dilates eccentrically and increases total stroke volume to preserve forward flow. The large stroke volume and rapid diastolic run-off produce a wide pulse pressure.

  3. 3
    Ventricular decompensation

    Continuing volume load raises wall stress and eventually impairs contractility. Forward output falls while LV filling and pulmonary venous pressures rise, causing exertional limitation and heart failure.

  4. 4
    Acute haemodynamic decompensation

    In acute severe regurgitation, a non-dilated, relatively non-compliant LV cannot accommodate the sudden volume. Diastolic pressure rises sharply, may close the mitral valve early, and can cause pulmonary oedema, hypotension and shock.

Clinical features and red flags

Chronic compensated AR

A forceful displaced apex, collapsing pulse, wide pulse pressure and long early diastolic murmur reflect a large chronic regurgitant volume.

Chronic decompensation

Exertional breathlessness, reduced stamina, orthopnoea or angina indicates loss of compensation and prompts rapid reassessment.

Acute severe ARRed flag

Sudden pulmonary oedema, hypotension and tachycardia after endocarditis, dissection, trauma or iatrogenic injury may occur without classic peripheral signs.

Austin Flint murmur

A low-pitched mid-diastolic apical murmur can occur when a severe AR jet functionally impedes mitral inflow; it does not prove mitral stenosis.

Aortic disease cluesRed flag

Unequal pulses, tearing chest/back pain, connective-tissue phenotype or rapid aortic enlargement suggests associated aortopathy or dissection.

Endocarditis clues

Fever, new regurgitant murmur, embolic features or positive blood cultures require urgent endocarditis assessment and early surgical discussion.

Investigations

  1. 01
    Transthoracic echocardiographyFirst step
    Why
    Define mechanism, quantify AR, measure LV size/function and examine the aortic root.
    Interpretation and limitations
    Use an integrated assessment; severe features include vena contracta over 6 mm, regurgitant volume at least 60 mL, regurgitant fraction at least 50% or EROA at least 0.30 cm2.
  2. 02
    Transoesophageal echocardiography
    Why
    Clarify mechanism, endocarditis, dissection complications or repair anatomy when TTE is limited.
    Interpretation and limitations
    Particularly valuable in acute severe AR, but should not delay emergency surgery when the diagnosis and instability are clear.
  3. 03
    Cardiac MRI
    Why
    Quantify regurgitant fraction and LV volumes when echo is equivocal or discordant.
    Interpretation and limitations
    Serial CMR can provide reproducible ventricular volumes; interpret alongside symptoms and echo rather than as an isolated threshold.
  4. 04
    ECG and chest radiograph
    Why
    Assess LV hypertrophy, rhythm, pulmonary oedema, cardiac size and aortic contour.
    Interpretation and limitations
    Chronic severe AR may show LV enlargement; acute severe AR can produce oedema without cardiomegaly.

Differential diagnosis

01

Pulmonary regurgitation

Its early diastolic murmur is usually loudest at the upper left sternal edge and may increase with inspiration. A high-pressure pulmonary regurgitation murmur can accompany pulmonary hypertension; echocardiography identifies the affected valve.

02

Mitral stenosis

A low-pitched apical mid-diastolic rumble with an opening snap supports mitral obstruction. An Austin Flint murmur from severe AR can mimic it, so valve imaging is decisive.

03

Patent ductus arteriosus

PDA produces a continuous, often machinery-like murmur around the left infraclavicular area rather than an isolated early diastolic murmur; Doppler demonstrates persistent aortopulmonary flow.

04

High-output or stiff-artery pulse pressure

Anaemia, thyrotoxicosis or marked arterial stiffness can widen pulse pressure and produce forceful pulses, but do not create holodiastolic aortic flow reversal or a regurgitant valve jet.

Management

01acuteAcute severe aortic regurgitationFirst stepSudden severe AR causes pulmonary oedema, hypotension or shock.+
  1. 1Use ABCDE care, continuous monitoring, urgent TTE/TOE and immediate cardiology, critical-care and cardiothoracic-surgical involvement.
  2. 2Search simultaneously for dissection, endocarditis, trauma or procedure complication; obtain blood cultures promptly if infection is plausible.
  3. 3Support oxygenation and perfusion in critical care; avoid reflex bradycardia and recognise that intra-aortic balloon counterpulsation is contraindicated because it worsens regurgitation.
  4. 4Proceed to emergency surgery when severe acute AR is confirmed and treat the cause; medical therapy is only a bridge.
02chronic-symptomaticSymptomatic chronic severe ARSevere AR is associated with breathlessness, reduced exercise tolerance, angina or heart failure.+

Complications

01

Progressive LV failure

Long-standing severe volume overload can cause increasing LV dilatation, fibrosis and systolic dysfunction. Symptoms and ejection-fraction decline may appear only after substantial remodelling, so serial trends matter.

02

Pulmonary oedema and shock

Acute severe AR abruptly raises LV and left-atrial pressure while reducing forward output, producing life-threatening pulmonary oedema, hypotension and multi-organ hypoperfusion.

03

Myocardial ischaemia and arrhythmia

Reduced aortic diastolic pressure can impair coronary perfusion while the enlarged LV has high oxygen demand. Angina may occur, and ventricular arrhythmia can complicate advanced LV dysfunction, although neither is specific to AR.

04

Progressive aortic disease

When root or ascending-aortic disease underlies regurgitation, continuing enlargement increases the risk of dissection or rupture and may determine the need for combined aortic surgery.

Monitoring and follow-up

  • In asymptomatic severe AR suitable for intervention, review symptoms and repeat echocardiography every 6–12 months.
  • Trend LVEF and LV end-systolic diameter/index rather than acting on one borderline measurement.
  • Measure aortic root and ascending-aortic diameters consistently and shorten follow-up if growth accelerates.
  • Check BP at each review and renal function/electrolytes after ACE-inhibitor or diuretic initiation and dose changes.
  • Ask about exercise capacity, orthopnoea, nocturnal dyspnoea and angina; new symptoms override a previously reassuring schedule.
  • After intervention, monitor prosthetic or repaired-valve function, LV reverse remodelling and any residual aortic disease.

Special situations

Acute AR looks different

Peripheral collapsing signs require time and a large stroke volume to develop. In acute severe AR the pulse pressure may be normal and the murmur short despite life-threatening haemodynamics.

LVEF can be misleadingly normal

Ejection into both aorta and low-pressure LV diastolic flow can preserve the percentage initially; serial LV end-systolic size helps identify failing compensation.

The aorta may drive treatment

Bicuspid valve and heritable aortopathy require systematic aortic measurement; combined aortic surgery may be indicated even when valve symptoms are modest.

IABP is harmful

Balloon inflation during diastole raises aortic diastolic pressure and can increase regurgitant flow, so it is contraindicated in significant AR.

Vasodilators are not definitive therapy

Afterload treatment is useful for hypertension or inoperable heart failure, but it has not replaced surgery for operable symptomatic severe disease.

Use more than jet area

Colour-jet appearance changes with gain, BP and direction; vena contracta, flow reversal, quantitative volume/fraction and ventricular response should agree.

Common pitfalls

  1. 01

    Waiting for a wide pulse pressure before recognising acute severe AR.

  2. 02

    Grading severity from colour-jet area alone.

  3. 03

    Following LVEF without LV end-systolic size, serial trend or aortic dimensions.

  4. 04

    Using symptom improvement on diuretics as a reason to postpone indicated surgery.

  5. 05

    Using intra-aortic balloon counterpulsation in significant AR.

Practice

Two practice questions

Your practice draft is saved in this browser.

Question 1 of 2
0 correct
CardiologyOriginal SBA

Acute regurgitation after infection

A febrile patient develops sudden pulmonary oedema and a new early diastolic murmur. Echo shows severe acute AR from leaflet destruction. What is the definitive route?

Choose one answer, then submit
← Rapid synopsisBack to overviewAll Cardiology topics →
Sources and review status6 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • NICE NG208: Heart valve disease presenting in adultsUK referral, intervention and surveillance principles.
  • ESC/EACTS 2025 valvular heart disease guidelineContemporary surgical triggers and aortic assessment.
  • ESC: Chronic aortic regurgitationIntegrated severity criteria and multimodality imaging.
  • NHS: Heart valve diseaseSymptoms and routes to urgent care.
  • eMC: Ramipril SmPCLicensed adult hypertension dosing and safety monitoring.
  • eMC: Furosemide tablets SmPCAdult oedema dosing and cautions.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draft
05
CT or MR aortography
Why
Measure the thoracic aorta and diagnose suspected acute aortic syndrome.
Interpretation and limitations
An acute-dissection protocol is time-critical; aortic diameter, growth, genotype and family history guide combined aortic surgery.
  • 06
    Blood cultures and inflammatory tests when indicated
    Why
    Investigate infective endocarditis before antibiotics when the patient is stable enough for sampling.
    Interpretation and limitations
    Obtain multiple culture sets promptly; never delay antibiotics or surgery in septic shock for perfect sampling.
    • 1
    Confirm severity and LV/aortic measurements with expert echo, using CMR if quantification is discordant.
  • 2Refer promptly to the valve team for surgery if operative benefit is expected; assess the coronary arteries and the entire thoracic aorta.
  • 3Choose repair in selected expert-centre anatomy or valve replacement, adding root/ascending-aortic surgery when indicated.
  • 4Use diuretics for congestion and treat hypertension while awaiting intervention, but do not let symptom relief postpone surgery.
    • 03asymptomaticAsymptomatic severe AR surveillanceSevere AR is present without clear symptoms and LV function is preserved.+
    1. 1Record baseline LVEF, LV end-systolic diameter and indexed size, LV volumes and aortic dimensions; ask about actual exercise capacity.
    2. 2EscalationUnder NICE NG208, consider referral for intervention when LVEF is less than 55%, LVESD is more than 50 mm or indexed LVESD is more than 24 mm/m2; also escalate for serial decline/dilatation or when the aorta itself meets an intervention threshold.
    3. 3If no trigger exists, monitor clinically and by echo every 6–12 months while intervention remains suitable; use the same measurement method where possible.
    4. 4Bring review forward for new symptoms, pregnancy planning, rapid aortic growth or a meaningful LV trend.
    04hypertensionBlood-pressure and congestion managementDefinitiveChronic AR coexists with systolic hypertension or congestion while definitive timing is assessed.+
    1. 1Measure BP accurately and treat persistent hypertension, generally with an ACE inhibitor/ARB or dihydropyridine calcium-channel blocker selected for the individual.
    2. 2If fluid overloaded, use a loop diuretic at the lowest effective dose and monitor renal function and electrolytes.
    3. 3Avoid deliberately slowing the heart excessively in severe AR because a long diastole can increase regurgitant volume; treat another compelling indication carefully.
    4. 4Reassess symptoms and LV response; medical control does not cancel a surgical trigger.
    Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
    Treats coexisting hypertension or heart failure when appropriate; it does not correct the regurgitant valve.

    Ramipril

    For hypertension, usually 2.5 mg orally once daily initially; use 1.25 mg once daily when the renin–angiotensin system is strongly activated, then titrate at 2–4-week intervals to a maximum 10 mg/day.

    Check creatinine and potassium before and 1–2 weeks after starting or titrating; avoid in pregnancy and previous ACE-inhibitor angioedema, and use caution in renal-artery stenosis.

    Controls congestion while the cause and intervention timing are addressed.

    Furosemide

    For chronic oedema, 40 mg orally in the morning is a usual initial adult dose; maintenance may be 20 mg daily or 40 mg on alternate days, adjusted to response.

    Monitor weight, BP, renal function, sodium and potassium; over-diuresis can cause hypotension and renal injury. It does not delay a surgical indication.

    Clinical stateAwaiting review
    JurisdictionUnited Kingdom