Aortic Insufficiency Acute and Chronic

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

2. Aortic RegurgitationEtiology 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. Aortic RegurgitationPathophysiology • 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

9. Aortic RegurgitationPathophysiology

10. Aortic RegurgitationPathophysiology

11. Aortic RegurgitationPathophysiology • 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

12. Aortic RegurgitationClinical 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

13. Aortic RegurgitationClinical 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

14. Aortic RegurgitationClinical 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

15. Murmur of Aortic Regurgitation Murmur of Aortic Regurgitation S 2 S 1

16. Aortic RegurgitationClinical 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

17. Aortic RegurgitationClinical 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

18. Aortic RegurgitationLaboratory Evaluation

19. Aortic RegurgitationLaboratory Evaluation Chronic Acute Normal size LV with pulmonary vascular congestion LVE with normal pulmonary vasculature

20. Aortic RegurgitationEchocardiography

21. Aortic RegurgitationEchocardiography

22. Aortic RegurgitationCardiac Catheterization

23. Aortic RegurgitationNatural 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

24. Aortic RegurgitationManagement • 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

25. Aortic RegurgitationManagement • 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