1) Aortic regurgitation occurs when the aortic valve fails to close properly during diastole, allowing blood to flow back into the left ventricle from the aorta. 2) Chronic aortic regurgitation can increase left ventricular volume and pressure, potentially leading to heart failure. Symptoms may include dyspnea, orthopnea, and leg swelling. 3) Evaluation involves auscultating a characteristic decrescendo diastolic murmur and measuring widened pulse pressure. Echocardiography can quantify the regurgitant volume and assess left ventricular size and function. 4) Treatment depends on severity and chronicity. Mild cases may require monitoring but severe or symptomatic

1. AORTIC
REGURGITATION
DR SIVARANJANI
1st yr Post Graduate
Department of General Medicine

2. Aortic Valve Anatomy
● Aortic Valve is composed of three cusps of equal size, each of
which is surrounded by a sinus
● Cusps are separated by three commissures and supported by a
fibrous annulus
● Each cusp is crescent shaped and capable of opening fully to allow
unimpeded forward flow, then closing tightly to prevent
regurgitation

3. Anatomy
● Free edge of each cusp curves upward from the commissure and
forms a slight thickening at the tip or midpoint, called the
Arantius nodule.
● When the valve closes, these three nodes meet in the centre.
● Overlap of Valve tissues along the lines of closure produces a
tight seal and prevents backflow during Diastole.
● Doesn’t have chordae tendinae, papillary muscles unlike mitral
valve.

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5. TYPES AND ITS
ETIOLOGY
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6. Classification
● COMMON CAUSES OF ACUTE AR
 Aortic Dissection
 Rupture of Sinus of Valsalva
 Infective Endocarditis
● Chronic AR can be a Valvulopathy or Aortic
root issue or its combination.
● VALVULOPATHY
 Congenital problem (Bicuspid or
Quadricuspid)
 Rheumatic problem (MS/MR>MS/AR)
 Valve leaflet problem (Trauma)
 Endocarditis, Radiation
 Myxomatous Prolapse
 Ankylosing spondylitis
 Syphilis
COMMONEST AORTIC ROOT ISSUES:
 Behcet’s syndrome
 Aortic dissection
 Medial Degeneration
 IgG4 disease
 Aortitis
 Marfan’s disease
 Ehler danlos Syndrome
 Syphilis
 Hypertension
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Ehler Danlos Syndrome

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9. PATHOGENESIS
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10. Pathogenesis
● The LV diastolic pressure is equal
to 10 mm Hg and Aortic Diastolic
pressure is 80 mm Hg.
● Aortic valve opens after IVC and
closes after reduced ejection.
● In case of regurgitation, all the
blood will go from aorta to LV.
● This is known as DIASTOLIC LEAK.
● Preload increases and LVEDV
increases.
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11. Pathogenesis
● When EDV is increased, the contractility increases and after load further
increases (Frank Starling law) and EF also increases.
● This will raise the systolic blood pressure, and due to diastolic leak, the
diastolic pressure falls. Pulse pressure will be high.
● LV undergoes eccentric hypertrophy with dilatation and it allow this
chamber to eject a larger stroke volume without requiring any increase in
the relative shortening of each myofibril.
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13. Pathogenesis
● Severe AR may occur with a normal effective
forward stroke volume and a normal LV ejection
fraction (LVEF = total [forward plus regurgitant]
stroke volume/end-diastolic volume)
● Through the operation of Laplace’s law, LV
dilation increases the LV systolic tension
required to develop any given level of systolic
pressure.
● In chronic AR, thus Preload and Afterload
increases.
● As LV function deteriorates, LVEDV raises,
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14. ● In patients with acute severe AR, the LV is unprepared for the
regurgitant volume load and cannot dilate sufficiently to maintain
stroke volume, and LV diastolic pressure rises rapidly with
associated marked elevations of LA and PA wedge pressures, which
closes the mitral valve prematurely.
● Pulmonary edema and/or cardiogenic shock may develop rapidly.
● Myocardial ischemia may occur due to increased O2 demand by LV
dilatation and hypertrophy.
● The combination of increased O2 demand and reduced supply may
cause myocardial ischemia, particularly of the sub endocardium,
even in the absence of epicardial coronary artery disease (CAD).
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15. Symptoms
● Asymptomatic for decades.
● Uncomfortable awareness of the heartbeat, especially on lying
down, may be an early complaint (due to increased LV size).
● Exertional dyspnea, usually the first symptom of diminished cardiac
reserve. The dyspnea is followed by orthopnea, paroxysmal nocturnal
dyspnea, and excessive diaphoresis.
● Nocturnal angina (Bradycardia-Prolongs diastole-Increased AR-
increased O2 demand)
● Systemic fluid accumulation, including congestive hepatomegaly and
ankle edema in late course.
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16. Markers of Severity
● LOW EF
● HIGH ESV
● HIGH LVEDP
● Normal or slight widening of pulse pressure.
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17. Signs of Aortic Regurgitation
CORRIGAN’S PULSE OR WATER HAMMER
PULSE/COLLAPSING PULSE:
Bounding and forceful and subsequently
collapsing.
It is associated with increased stroke
volume of LV and decrease in peripheral
resistance, leading to widened pulse
pressure.
This is exaggerated by raising the
patient’s arm above the level of the heart.
It is associated with wide pulse pressure
(systolic – diastolic BP >80 mmHg)
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18. ● LIGHTHOUSE SIGN:
Alternate flushing and blanching of forehead.
● ALFRED DE MUSSET’s SIGN:
Head nodding with each heart beat.
● BECKER’s SIGN:
Visible pulsations of retinal arterioles during fundoscopy.
● ROSENBACH SIGN:
Palpable liver pulsations with every heart beat.
● GERHARDT’s SIGN or SAILER SIGN:
Palpable splenic pulsations.
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19. ● LANDOLFI SIGN:
Change in pupillary size in accordance with cardiac cycle.
● ASHRAFIAN SIGN:
Pulsatile pseudo-proptosis.
● MULLER SIGN:
Visible pulsations of uvula.
● MAYEN’s SIGN:
Fall in diastolic BP of more than 15 mm Hg with
elevation of arm.
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20. ● CORRIGAN’s NECK SIGN or DANCING CAROTIDS:
Dancing Carotid Artery.
● QUINCKE’s SIGN:
Capillary pulsations of nail bed, with light compression
of nail bed.
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21. ● DUROZIEZ’s SIGN:
Intermittent to and fro femoral artery systolic and diastolic murmur generated by
light compression with the bell of the stethoscope.
● TRAUBE’s SIGN:
Pistol shot systolic and diastolic booming sound over femoral artery.
● SHERMAN SIGN:
Dorsalis pedis pulse unexpectedly prominent in age > 75 years.
● SHELLY SIGN:
Pulsations of the cevix.
● HILL SIGN:
Most specific for AR. Lower limb systolic BP exceeding brachial systolic BP by >60
mmHg.
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LINCOLN SIGN – Pulsatile popliteal.

24. ARTERIAL PRESSURE:
● Rapid Upstroke, Rapid Downstroke, ill sustained peak, High volume pulse –
Collapsing pulse.
● Carotid Artery pulse – Pulsus bisferiens
(two systolic waves separated by a trough)
● Due to ejection of rapid jet of blood through the
Aortic valve. During the peak of flow, Bernouli’ s effect
on the walls of ascending aorta causes a sudden decrease
In lateral pressure on the inner aspect of the wall.
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25. BLOOD PRESSURE:
● Wide Pulse pressure will be seen.
● Hill’s sign.
ON PALPATION:
● LV impulse – Heaving and displaced laterally and inferiorly.
● Rocking motion of precardium.
● Diastolic thrill palpable along left sternal border.
● Systolic thrill may palpable along supra sternal notch and transmitted
along carotids.
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26. AUSCULTATION
● S1 will be soft because of premature closure of
valves
● S2 will be soft in valvular causes, loud in aortic
root causes.
● S3 – only heard in LV failure.
● S4 – not heard.
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27. MURMUR:
● High pitched, soft blowing decrescendo Early
diastolic murmur starting with A2.
● Sitting and leaning forward position.
● With diaphragm of stethoscope.
● Breath held in forced expiration.
● Best heard in left 3rd intercoastal space.
ADDITIONAL MURMUR:
● Ejection systolic murmur – flow murmur, best heard
at the base of heart, transmitted along carotids.
AUSTIN FLINT MURMUR:
● Soft, low pitched rumbling Mid diastolic murmur.
● Diastolic displacement of anterior mitral valve
leaflet by AR stream. Intensified by handgrip.
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29. Other murmurs
● Early diastolic murmur radiating to axilla – COLE CECIL MURMUR
● Murmur due to retroversion of leaflet – KEY HODGKIN’S MURMUR
● Murmur due to perforation of valve leaflets due to infective endocarditis
– COOING DOVE MURMUR
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30. Electrocardiogram
● In patients with chronic severe AR, ECG signs of LV hypertrophy are
common.
● In addition, these patients frequently exhibit ST-segment depression
and T-wave inversion in leads I, aVL, V5, and V6 (“LV strain”).
● Left axis deviation and/or QRS prolongation may also be present.
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31. Echocardiogram
● Detection of dilation of the aortic annulus and root, aortic dissection or
primary leaflet pathology.
● With severe AR, the central jet width assessed by color flow Doppler
imaging exceeds 65% of the width of the LV outflow tract, the regurgitant
volume is ≥60 mL/beat, the regurgitant fraction is ≥50%, and there is
diastolic flow reversal in the proximal portion of the descending thoracic
aorta.
● (TTE) forms the cornerstone of longitudinal follow-up and allows for the
early detection of changes in LV size and/or function.
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32. ● Cardiac magnetic resonance (CMR) imaging allows for accurate assessment
of aortic size and contour. It can also be utilized to screen for LV fibrosis
as assessed with late gadolinium enhancement.
● Both CMR imaging and cardiac computed tomography (CT) can provide
detailed assessment of aortic valve and root anatomy.
● Transesophageal echocardiography (TEE) can also provide detailed
anatomic assessment of the valve, root, and portions of the aorta.
● There is increasing experience with the use of three-dimensional
echocardiography to measure LV volumes.
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33. Chest Xray
● In chronic severe AR, the apex is
displaced downward and to the left in
the frontal projection.
● When AR is caused by primary
disease of the aortic root,
aneurysmal dilation of the aorta may
be noted, and the aorta may fill the
retrosternal space in the lateral view.
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34. Cardiac cathetarization
● Can be done to confirm aortic root causes.
● Coronary angiography is performed routinely in appropriate patients
prior to surgery, although this anatomic information can also be
gained with coronary CT angiographic techniques
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35. Treatment
● Patients with acute severe AR may respond to intravenous diuretics and
vasodilators (such as sodium nitroprusside)
● Operation is indicated urgently.
● Beta blockers are best avoided so as not to reduce the CO further or slow
the heart rate, thus allowing more time for diastolic filling of the LV.
● Surgery is the treatment of choice and is usually necessary within 24 h of
● diagnosis.
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36. Treatment of chronic AR
● The onset of symptoms, or LV systolic dysfunction, is an indication for surgery.
● Medical treatment with diuretics and vasodilators (ACE inhibitors, ARBs,
calcium channel blockers, or hydralazine) may be useful as a temporizing
measure.
● Patients with syphilitic aortitis should receive a full course of penicillin
therapy.
● Beta blockers and the ARB losartan may be useful to retard the rate of
aortic root enlargement in young patients with Marfan’s syndrome and
aortic root dilation.
● Beta blockers lowers blood pressure in patients with chronic AR and
hypertension. They can also lessen the sense of forceful heart action that
many patients find uncomfortable.
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37. Surgical treatment
● After the onset of LV dysfunction but prior to the development of severe
symptoms.
● Aortic valve replacement (AVR) is indicated for the treatment of severe AR
in symptomatic patients irrespective of LV function.
● In Asymptomatic patients with severe AR and progressive LV dysfunction
defined by
 an LVEF <55% on serial studies,
 an LV end-systolic dimension >50 mm (>25 mm/m2), or
 an LV diastolic dimension >65 mm.
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38. ● Transcatheter aortic valve implantation (TAVI) is not recommended
for patients with severe AR who are surgical candidates.
● Technical success with TAVI in patients with chronic AR is limited by
the degree of aortic annular dilation.
● AVR with a suitable mechanical or tissue (biological) prosthesis is
generally necessary in patients with rheumatic AR.
● Patients with acute severe AR require prompt (24–48 h) surgical
treatment, which may be lifesaving.
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