Aortic regurgitation
Pathogenesis
• Regurgitation of blood through aortic valve causes left ventricle to
dilate as cardiac output increases to maintain the demands of
circulation
• Eventually stroke volume of left ventricle doubles
• As disease progress left ventricular failure lead to rise in left
ventricular end diastolic pressure and pulmonary edema
Management
• Treatment for underlying conditions like endocarditis or syphilis
• Aortic valve replacement is indicated if condition causes symptoms
• Chronic aortic regurgitation remain asymptotic for years because
compensatory ventricular dilation and hypertrophy occurs they
should be advised if any symptoms of breathlessness or angina
• Asymptotic should be followed up annually
• If hypertension present non rate limiting vasodialtors like nefidipine
be used
Tricuspid regurgitation
Clinical features
• Symptoms are usually non-specific, with tiredness related to reduced
cardiac output, and oedema and hepatic enlargement due to venous
congestion.
• The most prominent sign is a 'giant' v wave in the jugular venous
pulse (a cv wave replaces the normal x descent).
• Other features include a pansystolic murmur at the left sternal border
and a pulsatile liver. Echocardiography may reveal dilatation of the RV.
If the valve has been affected by rheumatic disease, the leaflets will
appear thickened and, in endocarditis, vegetations may be seen.
Management
• Tricuspid regurgitation due to right ventricular dilatation often improves
when the cardiac failure is treated. Patients with a normal pulmonary
artery pressure tolerate isolated tricuspid reflux well, and valves damaged
by endocarditis do not usually need to be replaced. Patients under- going
mitral valve replacement, who have tricuspid regurgitation due to marked
dilatation of the tricuspid annulus, benefit from valve repair with an
annuloplasty ring to bring the leaflets closer together. Those with
rheumatic damage may require tricuspid valve replacement.

Presentation aortic regurgitation ppt.pptx

  • 1.
  • 2.
    Pathogenesis • Regurgitation ofblood through aortic valve causes left ventricle to dilate as cardiac output increases to maintain the demands of circulation • Eventually stroke volume of left ventricle doubles • As disease progress left ventricular failure lead to rise in left ventricular end diastolic pressure and pulmonary edema
  • 5.
    Management • Treatment forunderlying conditions like endocarditis or syphilis • Aortic valve replacement is indicated if condition causes symptoms • Chronic aortic regurgitation remain asymptotic for years because compensatory ventricular dilation and hypertrophy occurs they should be advised if any symptoms of breathlessness or angina • Asymptotic should be followed up annually • If hypertension present non rate limiting vasodialtors like nefidipine be used
  • 6.
  • 7.
    Clinical features • Symptomsare usually non-specific, with tiredness related to reduced cardiac output, and oedema and hepatic enlargement due to venous congestion. • The most prominent sign is a 'giant' v wave in the jugular venous pulse (a cv wave replaces the normal x descent). • Other features include a pansystolic murmur at the left sternal border and a pulsatile liver. Echocardiography may reveal dilatation of the RV. If the valve has been affected by rheumatic disease, the leaflets will appear thickened and, in endocarditis, vegetations may be seen.
  • 8.
    Management • Tricuspid regurgitationdue to right ventricular dilatation often improves when the cardiac failure is treated. Patients with a normal pulmonary artery pressure tolerate isolated tricuspid reflux well, and valves damaged by endocarditis do not usually need to be replaced. Patients under- going mitral valve replacement, who have tricuspid regurgitation due to marked dilatation of the tricuspid annulus, benefit from valve repair with an annuloplasty ring to bring the leaflets closer together. Those with rheumatic damage may require tricuspid valve replacement.