Aortic regurgitation is a condition where the aortic valve leaks, allowing blood to flow back into the left ventricle during diastole. It can be caused by valvular issues like congenital defects, endocarditis, or rheumatic fever, or aortic root diseases like dilation or dissection. In the pathophysiology, the incompetent aortic valve leads to left ventricular volume overload and increased systolic stroke volume but decreased diastolic pressure. In chronic severe aortic regurgitation, patients develop left ventricular hypertrophy and dilation over many years to compensate, while in acute cases pulmonary edema and heart failure can develop rapidly. Physical exam findings include a widened pulse pressure, diastolic

1. AORTIC REGURGITATION
Jose James
Final Year MBBS
M1 Unit

2. Introduction
•Aortic regurgitation (AR), also known as Aortic
insufficiency (AI), is the leaking of the aortic
valve of the heart that causes blood to flow in
the reverse direction during ventricular diastole,
from the aorta into the left ventricle. As a
consequence, the cardiac muscle is forced to
work harder than normal.

3. Etiology
Valvular
• Congenital (BAV)
• Endocarditis (acute)
• Rheumatic fever
(*with Mitral involvement)
• Myxomatous (prolapse)
• Traumatic Syphilis
• Ankylosing spondylitis
Root disease
• Root Dilation(80% idiopathic)
• Aortic dissection (acute)
• Cystic medial degeneration
• Marfan’s syndrome
• Nonsyndromic familial aneurysm
Aortitis
Trauma (acute)
Hypertension

4. Pathophysiology
Incompetent closure of the aortic valve
Diastolic reflux through the aortic valve can lead to left
ventricular volume overload (increased preload)
Increase in systolic stroke volume (due to ventricular overload)
and low diastolic aortic pressure (due to aortic regurgitation)
Increased SYSTOLIC and Decreased DIASTOLIC Blood Pressure
WIDE PULSE PRESSURE

5. • The LV does not have sufficient
time to dilate in response to the
sudden increase in volume.
• LV end-diastolic pressure
increases rapidly(>40mmhg),
causing an increase in
pulmonary venous pressure and
altering coronary flow dynamics.
• Patient develops dyspnea and
pulmonary edema. In severe
cases, heart failure may develop.
• Gradual left ventricular volume
overload that leads to a series of
compensatory changes, including
LV enlargement and eccentric
hypertrophy.
• Patients may remain
asymptomatic during this period.
• The effective forward CO usually
is normal or only slightly reduced
at rest, but often it fails to rise
normally during exertion.
ACUTE AR CHRONIC AR

6. Clinical Features
•(3/4)Pts with Pure/Predominant Valvular AR-Men.
•Women-Primary Valvular AR who have associated
rheumatic mitral valve disease
In acute severe AR,LV diastolic pressure rises rapidly
with associated marked
elevations of LA and PA wedge pressures.
•Pulmonary edema and/or cardiogenic shock may
develop rapidly.

7. In Chronic severe AR-Long latent period, relatively
asymptomatic for as long as 10–15 years.
•Palpitation-early complaint.(esp. on lying)
•Exertional dyspnea-symptom of diminished cardiac
reserve.
•Orthopnea, paroxysmal nocturnal dyspnea, and
excessive diaphoresis, Anginal chest pain with severe
AR.

8. On Physical Examination
ACUTE AR
•Signs of CHF or shock
•Tachycardia
•Peripheral
vasoconstriction
•Cyanosis
•Pulmonary edema
•*Arterial pulsus alternans
CHRONIC AR
•Manifestations are due to
widened pulse pressure.
•Diastolic pressures are
often lower than 60 mm
Hg, with pulse pressures
often exceeding 100 mm
Hg

9. Signs in Chronic AR
•Becker sign - Visible systolic pulsations of the retinal
arterioles
•Corrigan’s sign - Dancing Carotids
•Corrigan pulse ("water-hammer" pulse) - Abrupt
distention and quick collapse on palpation of the
peripheral arterial pulse
•de Musset sign - Bobbing motion of the patient's head
with each heartbeat
•*Hill sign - Popliteal cuff systolic blood pressure 40
mm Hg higher than brachial cuff systolic blood
pressure(>60-severe)

10. •Duroziez sign - Systolic murmur over the femoral
artery with proximal compression of the artery, and
diastolic murmur with distal compression.
•Quincke sign - Visible pulsations of the fingernail bed
with light compression of the fingernail
•Traube sign ("pistol-shot" pulse) - Booming systolic
and diastolic sounds auscultated over the femoral
artery
•Rosenbach’s sign—Pulsations of liver
•Gerhardt’s sign—pulsations over enlarged spleen

11. PALPATION
•LV impulse is Hyperdynamic & displaced
*laterally and inferiorly
•A diastolic thrill may be palpable along
the left sternal border.

12. AUSCULTATION
•Soft S1 (only in acute AR due to premature
closure of MV)
•A high frequency early decrescendo diastolic
murmur in aortic area.
•Duration of murmur >2/3 of diastole
indicates severity.
•*Austin Flint murmur

13. Investigations
ECG
• In patients with chronic severe AR, the ECG signs of LV hypertrophy
become manifest.
2D Echocardiogram with Doppler
• LV size is increased in chronic AR. A rapid, high-frequency diastolic
fluttering of the anterior mitral leaflet produced by the impact of the
regurgitant jet is a characteristic finding.
Chest X-ray
• The apex is displaced downward and to the left in the frontal
projection.
Cardiac Catheterization and Angiography
• Dilated LV, Aortic Regurgitation, Dilated Aortic Root

14. Treatment
ACUTE AR
•Diuretics
•IV Nitroprusside
•SURGERY(recommended)
*Beta-Blockers and Intra-
aortic balloon counter
pulsations are
Contraindicated
CHRONIC AR
•Vasodilators- Hydralazine,
DHPs, CCB
•Penicillin prophylaxis in
syphilitic
•Beta-Blocker in Aortic root
Dilation
•SURGERY-Valve
replacement/repair

15. Take Home Message.
•Blood leaks across aortic valve
•Primary Valve Disease OR Primary Aortic Root Disease
•Increased preload, stroke volume
•High Pitched Blowing Early Decrescendo diastolic
murmur in 2nd Aortic area.(root dilation better heard in
1st Aortic Area).
•Wide pulse pressure symptoms(>60)- Corrigan pulse
and Sign
•Treatment (severe disease): Surgery

16. THANK YOU