1. Aortic Insufficiency Acute and Chronic
The etiology, pathophysiology, and clinical manifestations of chronic and acute insufficiency are different, as is the therapy

2. Aortic Regurgitation Etiology
In the past rheumatic fever and syphilis were major causes of
aortic regurgitation, but these diseases have diminished in
frequency in recent years due to the availability of antibiotics.
As these two infectious diseases have diminished, diseases of
the connective tissue and anatomic abnormalities of the valve
have become more frequent causes.

3. Chronic Aortic Regurgitation
Congenital Etiology
Aortic Valve Prolapse - myxomatous valve
Bicuspid Aortic Valve
Coarctation of the Aorta – dilation of the aorta
Connective Tissue Disorders – loss of structural support
Marfan’s Syndrome, Ehlers-Danlos Syndrome etc.
Idiopathic Cystic Medial Necrosis
Ventricular Septal Defect – loss of cusp support

4. Chronic Aortic Regurgitation
Acquired Etiology
Rheumatic Heart Disease – fibrosis and retraction
Syphilitic Aortitis – dilation of the aorta
Dissecting Aneurysm – disruption of support
Bacterial Endocarditis
Systemic Lupus
Traumatic Aortic Insufficiency
Hypertension – dilation of the aorta

5. Acute Aortic Insufficiency
Infective Endocarditis
Dissecting Aneurysm
Rupture of the Aortic Leaflets
trauma
myxomatous valve

6. Dilated Aortic Root

7. Aortic Dissection

8. Valvular Abnormalities
Nodular Rheumatic Disease Aortic Root Dilation
Endocarditis

9. Aortic Regurgitation Pathophysiology
Chronic Aortic Regurgitation
Represents a volume overload(AS=pressure overload)
The LV responds by dilating(SV LVEDV but LVEDP =)
Eccentric hypertrophy occurs (sarcomeres replicate in series). In AS concentric LVH occurs as the sarcomeres replicate in parallel
In the late stages of AR as LV failure occurs the ventricle continues to dilate LVEDP

10. Aortic Regurgitation Pathophysiology

11. Aortic Regurgitation Pathophysiology

12. Aortic Regurgitation Pathophysiology
Acute Aortic Insufficiency
The volume overload will be suddenly imposed on a left ventricle unable to dilate acutely
As a result, marked elevation of the left ventricular end-diastolic pressure occurs
Such sudden hemodynamic changes produce pulmonary venous hypertension and acute pulmonary edema

13. Aortic Regurgitation Clinical Manifestations
History
Chronic Aortic Regurgitation
Dyspnea (orthopnea, PND, exertional dyspnea)
Angina when it occurs is usually nocturnal (due to the bradycardia and low diastolic blood pressure)
Acute Aortic Regurgitation
There is sudden cardiovascular collapse, with congestive heart failure and hypotension

14. Aortic Regurgitation Clinical Manifestations
Physical Examination
Chronic AR Acute AR
Systolic BP Systolic BP =
Diastolic BP Diastolic BP =
Aortic Pulse Pressure Aortic Pulse Pressure =
Heart Rate = Heart Rate
S1 = (in CHF ) S1
S2 = S2
S3 absent(except CHF) S3 present
S4 usually not present S4 never present

15. Aortic Regurgitation Clinical Manifestations
Physical Examination (Auscultation)
The AR murmur is a diastolic murmur that begins after A2
It is a decrescendo murmur heard best with the patient sitting up and leaning forward
The severity of the murmur correlates better with the duration than with the intensity of the murmur
In acute AR the murmur is also a decrescendo murmur but is of short duration since the LVEDP is elevated and pressure equalizes rapidly between LV and the aorta

16. Murmur of Aortic Regurgitation
S S 1

17. Aortic Regurgitation Clinical Manifestations
Physical Examination
Austin Flint Murmur occurs in severe AR. Created by rapid outflow across a partially closed MV. The MV is normal but partially closed due to rising LVDP.
Corrigan’s Pulse (water hammer pulse) pulse that rapidly rises and falls
de Musset’s Sign – bobbing of the head
Traube’s Sign – booming systolic and diastolic sounds over the femoral artery

18. Aortic Regurgitation Clinical Manifestations
Physical Examination
Muller’s Sign – systolic pulsations of the uvula
Durozier’s Sign – systolic murmur over the femoral artery when compressed proximally, and a diastolic murmur when it is compressed distally
Quicke’s Sign – flushing and blanching of the nail beds when lightly compressed

19. Aortic Regurgitation Laboratory Evaluation

20. Aortic Regurgitation Laboratory Evaluation
Chronic Acute
Normal size LV with pulmonary
vascular congestion
LVE with normal pulmonary
vasculature

21. Aortic Regurgitation Echocardiography

22. Aortic Regurgitation Echocardiography

23. Aortic Regurgitation Cardiac Catheterization

24. Aortic Regurgitation Natural History
Chronic AR
Mortality increases with onset of symptoms
4 year survival with angina, 2 years with CHF
It is imperative to intervene before irreversible LV dysfunction occurs
Acute AR
These patients suffer early death if they do not undergo emergent surgical intervention

25. Aortic Regurgitation Management
Medical Management
SBE prophylaxis is important
Afterload reduction will reduce the regurgitant volume
Avoidance of atrial fibrillation and bradycardia are important as these are poorly tolerated
Serial echocardiographic follow-up to monitor LV function

26. Aortic Regurgitation Management
Surgical Management
Not indicated in asymptomatic patients with good exercise tolerance and good LV function
Surgical treatment is advised in patients with severe AR who are symptomatic and who have impaired LV function
Long term results reveal 80-90% three year survival in patients with preserved LV function, and 40-60% three year survival in patients with poor LV function
Every effort should be made to operate on patients before irreversible LV dysfunction occurs