Aortic InsufficiencyAcute and Chronic

The etiology, pathophysiology, and clinical manifestations of chronic and acute insufficiency are different, as is

the therapy

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 valvehave become more frequent causes.

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

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

Acute Aortic Insufficiency

• Infective Endocarditis

• Dissecting Aneurysm

• Rupture of the Aortic Leaflets– trauma– myxomatous valve

Dilated Aortic Root

Aortic Dissection

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

Aortic RegurgitationPathophysiology

Aortic RegurgitationPathophysiology

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

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

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

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

S 2 S 1

Murmur of Aortic RegurgitationMurmur of Aortic Regurgitation

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

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

Aortic RegurgitationLaboratory Evaluation

Chronic Acute

Normal size LV with pulmonaryvascular congestion

LVE with normal pulmonaryvasculature

Aortic RegurgitationLaboratory Evaluation

Aortic RegurgitationEchocardiography

Aortic RegurgitationEchocardiography

Aortic RegurgitationCardiac Catheterization

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

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

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