Diastolic backflow from aorta into LV from leaflet or root pathology — wide pulse pressure, decrescendo diastolic murmur.
Also known as: AR, aortic insufficiency, AI, aortic regurg
Overview
Retrograde flow of blood from the aorta into the left ventricle during diastole due to incompetent aortic valve leaflets or dilation of the aortic root. May be acute (catastrophic) or chronic (compensated for years).
Epidemiology
Chronic AR is most often degenerative in older adults and bicuspid-related in younger patients. Acute AR is uncommon but life-threatening, most often from endocarditis or aortic dissection.
Try two board-style Aortic Regurgitation questions
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Question 1CardiovascularMedium
A 48-year-old man with chronic severe aortic regurgitation has a wide pulse pressure with bounding peripheral pulses, head bobbing, and an apical low-pitched mid-diastolic rumble. The rumble is best explained by which mechanism?
ATurbulent flow across a stenotic mitral valve
BTricuspid inflow through a stretched annulus
CRegurgitant aortic jet impinging on the anterior mitral leaflet
DHigh-velocity flow across a calcified aortic valve
Reveal answer & full explanation
Correct answer: C — Regurgitant aortic jet impinging on the anterior mitral leaflet
ATurbulent flow across a stenotic mitral valve
BTricuspid inflow through a stretched annulus
CRegurgitant aortic jet impinging on the anterior mitral leaflet✓
DHigh-velocity flow across a calcified aortic valve
Why Regurgitant aortic jet impinging on the anterior mitral leaflet is correct
The Austin-Flint murmur (an apical low-pitched mid-to-late diastolic rumble) of chronic severe aortic regurgitation (AR) is produced when the regurgitant aortic jet strikes the anterior mitral leaflet, causing relative functional mitral stenosis
The peripheral signs (Corrigan/water-hammer pulse, de Musset head bob, Quincke nail-bed pulsations) reflect wide pulse pressure
Why the others are wrong
A) Turbulent flow across a stenotic mitral valve — true rheumatic mitral stenosis produces an opening snap, which is absent in pure AR; the Austin-Flint murmur mimics mitral stenosis but is functional
B) Tricuspid inflow through a stretched annulus — tricuspid inflow does not explain an apical diastolic rumble in this clinical context
D) High-velocity flow across a calcified aortic valve — aortic stenosis produces a systolic ejection murmur, not a diastolic rumble
Question 2CardiovascularMedium
A 34-year-old man presents with several months of exertional fatigue and a sensation of a forceful heartbeat that is worse when he lies on his left side. He has a history of a bicuspid aortic valve. Blood pressure is 158/46 mm Hg and pulse is 78/min with bounding, collapsing peripheral pulses and visible nail-bed pulsation. On auscultation there is an early, soft, decrescendo diastolic murmur best heard at the left sternal border while he leans forward in expiration. Which of the following is the most likely diagnosis?
APulmonary regurgitation
BPatent ductus arteriosus
CAortic regurgitation
DMitral stenosis
Reveal answer & full explanation
Correct answer: C — Aortic regurgitation
APulmonary regurgitation
BPatent ductus arteriosus
CAortic regurgitation✓
DMitral stenosis
Why Aortic regurgitation is correct
Wide pulse pressure with a low diastolic BP (158/46) plus bounding, collapsing (water-hammer/Corrigan) pulses and Quincke nail-bed pulsation are the hallmark peripheral signs of chronic AR.
The early decrescendo diastolic murmur at the left sternal border, accentuated by sitting forward in expiration, is the classic AR murmur from retrograde diastolic flow across an incompetent valve.
A bicuspid aortic valve is the most common cause of AR in young adults in the US, and the forceful heartbeat when lying on the left side reflects the volume-overloaded, eccentrically hypertrophied LV.
Why the others are wrong
Mitral stenosis produces a low-pitched mid-diastolic rumble at the apex with an opening snap and loud S1, not an early decrescendo murmur at the left sternal border, and does not cause a wide pulse pressure.
Pulmonary regurgitation also gives a diastolic murmur at the left upper sternal border (Graham Steell) but accompanies pulmonary hypertension with a loud P2 rather than a wide pulse pressure and water-hammer pulses.
Patent ductus arteriosus causes a continuous machinery murmur at the left infraclavicular area, not a purely diastolic murmur, even though it can also widen the pulse pressure.
Per ACC/AHA valvular heart disease guidelines, the diagnosis of AR is confirmed and severity graded by transthoracic echocardiography.
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Regurgitant volume returns to the LV in diastole, producing combined volume and pressure overload. Chronic AR causes progressive LV dilation and eccentric hypertrophy with preserved stroke volume and EF for years. Acute AR leaves the LV unprepared — small chamber cannot accommodate regurgitant volume → rapid rise in LVEDP, pulmonary edema, and cardiogenic shock.
Clinical presentation
Symptoms
Chronic: asymptomatic for decades; eventual exertional dyspnea, orthopnea, fatigue, palpitations (forceful heartbeat lying on left side)
Acute: severe dyspnea, pulmonary edema, hypotension, chest pain
Angina (especially nocturnal) from reduced diastolic coronary perfusion
Signs / physical exam
Wide pulse pressure with low diastolic BP (chronic)
Bounding peripheral pulses (water-hammer / Corrigan), de Musset (head bobbing), Quincke (nail bed pulsation), Duroziez (femoral bruit), Traube (pistol-shot femoral)
Early decrescendo diastolic murmur best heard at left sternal border with patient leaning forward in expiration
Acute AR: tachycardia, narrow pulse pressure, soft S1, pulmonary edema, often without classic peripheral signs
Classic findings
Wide pulse pressure (e.g., 160/40) and the constellation of eponymous peripheral pulse signs in chronic AR.
Differential diagnosis
Mitral stenosis — Diastolic rumble at apex with opening snap; Graham Steell murmur of pulmonary regurgitation in severe MS can mimic AR
Pulmonary regurgitation (Graham Steell) — Diastolic murmur at left upper sternal border; loud P2, signs of pulmonary HTN rather than wide pulse pressure
Patent ductus arteriosus — Continuous machinery murmur, not purely diastolic; widened pulse pressure but heard at left infraclavicular area
Aortic dissection — Acute tearing chest/back pain with new AR murmur and pulse deficit; MUST exclude before anticoagulating
Acute mitral regurgitation — Holosystolic murmur with rapid pulmonary edema; not a diastolic murmur
High-output state (anemia, thyrotoxicosis, AV fistula) — Wide pulse pressure and bounding pulses, but no decrescendo diastolic murmur
Diagnostic workup
Diagnostic criteria
Severe AR by echo: vena contracta >0.6 cm, regurgitant volume ≥60 mL, regurgitant fraction ≥50%, effective regurgitant orifice ≥0.30 cm², pressure half-time <200 ms, holodiastolic flow reversal in descending aorta.
Labs
CBC, BMP, BNP
Blood cultures × 3 if endocarditis suspected
Inflammatory markers and syphilis serology if root involvement
Acute vs chronic aortic regurgitation — physiology and management contrasts.
Treatment
First-line
Acute severe AR: emergent surgical valve replacement; IV diuretics (furosemide) and afterload reduction with sodium nitroprusside as bridge; AVOID beta-blockers (block compensatory tachycardia) and IABP (worsens AR)
Chronic asymptomatic AR with preserved LVEF: serial echo every 6-12 months; no proven medical therapy to delay surgery
Hypertension in chronic AR: dihydropyridine CCB (amlodipine, nifedipine) or ACEi/ARB (lisinopril, losartan)
Endocarditis prophylaxis only for high-risk lesions (prosthetic valve, prior endocarditis, certain congenital lesions)
Second-line / adjunct
Surgical aortic valve replacement (SAVR) — Class I for symptomatic severe AR regardless of LVEF, OR asymptomatic severe AR with LVEF ≤55% OR LV end-systolic diameter >50 mm (or >25 mm/m² indexed)
Aortic root or ascending aorta replacement when diameter ≥5.5 cm (≥5.0 cm if bicuspid with risk factors, ≥5.0 cm if Marfan, ≥4.5 cm if undergoing AVR for other reasons)
TAVR generally not standard for pure AR (off-label) — surgical AVR is preferred
Complications
Left ventricular failure and dilated cardiomyopathy
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