Medicine. For mbbs undergraduates. Aortic regurgitation. Valvular heart disease

2. Etiology
Valvular Root
Congenital (bicuspid) Aortic dissection
Endocarditis Marfan’s syndrome
Rheumatic fever Cystic medial degeneration
Myxomatous (prolapse) Bicuspid aortic valve
Traumatic Non-syndromic familial aneurysm
Syphilis Aortitis
Ankylosing spondylitis Hypertension

3. Acute AR Chronic AR
Infective endocarditis Bicuspid aortic valve
Aortic dissection Rheumatic
Trauma SLE
Degenerative
Hypertension
Syphilitic aortitis
Ankylosing spondylitis
Marfan syndrome

6. The total stroke volume ejected by the LV is increased in patients with
AR.
In AR the entireLV stroke volume is ejected into a high-pressure zone, the
aorta.
An increase in the LV end-diastolic volume (increased preload)
constitutes the major hemodynamic compensation for AR.
The dilation and eccentric hypertrophy of the LV allow this chamber to
eject a larger stroke volume
Therefore, severe AR may occur with a normal effective forward stroke
volume and a normal LVEF together with an elevated LV end-diastolic
pressure and volume.
However, through the operation of Laplace’s law, LV dilation increases the
LV systolic tension required to develop any given level of systolic
pressure. Ultimately, these adaptive measures fail. As LV function
deteriorates, the end-diastolic volume rises further and the forward
stroke volume and EF decline. Deterioration of LV function often
Pathophysiology

7. The reverse pressure gradient from aorta to LV, which drives the AR flow,
falls progressively during diastole, accounting for the decrescendo
nature of the diastolic murmur.
In patients with acute severe AR, the LV is unprepared for the regurgitant
volume load.
LV compliance is normal or reduced, and LV diastolic pressures rise
rapidly, occasionally to levels >40 mmHg. The LV pressure may exceed
the LA pressure toward the end of diastole, and this reversed pressure
gradient closes the mitral valve prematurely.
Myocardial ischemia may occur in patients with AR because myocardial
oxygen requirements are elevated by LV dilation, hypertrophy,
and elevated LV systolic tension, and coronary blood flow may be
compromised

9. History
 Approx. 3/4th of pure/predominant AR – men
 Acute AR – cardiogenic shock and pulmonary oedema
 Chronic AR – long latent period
 Palpitations, esp. on lying down
 Exertional dyspnoea, 1st symptom of diminished cardiac
reserve
 Orthopnoea, PND, excessive diaphoresis
 Angina (nocturnal angina)
 Systemic fluid accumulation- congestive hepatomegaly
& pedal oedema

10. Physical findings
 Corrigan’s pulse – ‘water-hammer’ pulse
 Quincke’s pulse – alternate flushing & paling of skin at
the root of nail, when pressure applied to the tip of
nail
 Traube sign – pistol shot sound over femoral artery
 Duroziez’s sign – to and fro murmur over femoral
artery
 Widened pulse pressure , this widening is less in acute
AR

11. Palpation
 Apex beat – shifted down & laterally; heaving
 Systolic expansion & diastolic retraction of apex
 Diastolic thrill- left sternal border
 Systolic thrill- suprasternal notch, transmitted along
carotids

12. Auscultation
 A2 absent
 Systolic ejection murmur – BAV
 Occasionally, S4
 Diastolic murmur-
 high pitched, blowing, decrescendo
 3rd ICS, left sternal border
 Louder and longer in severe AR
 Louder along left border than right – primary valvular disease
 End expiration, sitting up & leaning forward
 Cooing – eversion of the valvular cusps
S1 S2 S1

13.  Mid systolic ejection murmur – isolated AR
 Base of heart
 Transmitted along the carotid arteries
 Austin Flint murmur – severe AR
 Soft, low pitched, rumbling
 Mid to late diastolic murmur
 Intensified by strenous & sustained hand grip
 Due to diastolic displacement of anterior leaflet of mitral valve

14. Investigations
 ECG
 Signs of left ventricular hypertrophy
 ST depression & T wave inversion (L1, aVL ,V5 ,V6) “LV
strain”

16.  Echocardiography
 Size of LV increased, systolic fuction normal initially
 A rapid, high-frequency diastolic fluttering of the
anterior mitral leaflet produced by the impact of the
regurgitant jet is characteristic
 Cause of AR

17.  Colour flow doppler imaging
 Central jet width > 65% of LV outflow
 Regurgitant volume >= 60ml/beat
 Regurgitant fraction >= 50%
 Diastolic flow reversal in proximal descending thoracic aorta
SEVERE AR

18. Chest X ray
 Chronic severe AR
 Apex shifted to left & down
 Left anterior oblique and lateral – shifted posteriorly,
encroaching on to spine
 Aortic root disease
 Aneurysmal dilatation
 Aorta filling retrosternal space in lateral view

20.  Cardiac catheterisation and angiography
 Cardiac MRI

21. Treatment
 Acute AR
 IV diuretics and vasodilators
 Intraaortic balloon counterpulsations contraindicated
 Β blockers better avoided
 Surgery is the treatment of choice and necessary in 24
hours

22.  Chronic AR
 Diuretics , vasodilators
 Vasodilators 1st choice as anti-hypertensives
 Cardiac arrhythmias and systemic infections promptly
treated
 Penicillin therapy – syphilitic aortitis
 Β blockers and ARBs retard the rate of aortic root
enlargement in Marfan syndrome & aortic root
dilatation

23. Surgery
 Asymptomatic until development of myocardial or LV
dysfunction
 If surgery delayed, normal function cannot be restored
 Therefore, regular follow with echocardiography in 6-
12months
 AVR is treatment of choice
 severe AR and progressive LV dysfunction defined by an
LVEF <50%, an LV endsystolic dimension >50 mm, or an
LV diastolic dimension >65 mm.

24.  AVR with mechanical or tissue prosthesis – Rheumatic
disease
 Primary surgical repair – Infective endocarditis,
Traumatic
 Narrowing the annulus or by excising a portion of the
aortic root without replacing the valve – Aneurysmal
dilatation

26. Thank you