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Aortic Valve Diseases fdsfgsrdfd (1).pptx
- 1. Dr Muhammad Saeed MBBS;FCPS(Cardiology) Assistant Professor Of Cardiology HBS Medical College& Hospital Islamabad Aortic Valve Diseases
- 2. Aortic Stenosis Inaortic stenosis aortic valve orifice is usually narrowed slowly. Left ventricle contracts forcefully to push the blood through the narrowed aortic valve orifice and becomes increasingly hypertrophied. Increase in cardiac output during exercise is limited by fixed valvular obstruction.
- 3. Causes Of AorticStenosis BicuspidAorticValve RheumaticAortic Stenosis Calcific Degenerative Aortic Stenosis
- 6. Pathophysiology Of AorticStenosis In chronic severe aortic stenosis left ventricular out put is maintained by the presence of left ventricular hypertrophy which may sustained a large pressure gradient across the aortic valve for many years without a reduction in cardiac output, left ventricular dilatation or the development of symptoms.
- 7. Critical obstructionof left ventricular outflow tract is usually characterized by: i)A peak systolic gradient exceeding 50 mmHg in the presence of normal cardiac output. ii) An effective aortic orifice area less than about 0.8 cm2 in an average adult i.e. 0.5 cm2/m2 of BSA.An aortic area of 1.0 to 1.5 cm2 is consided moderate AS, and an orifice of 1.5 to 2.00 cm2 is considered as mild AS. Atrial contraction plays particularly an important role in filling the left ventricle in severe AS.
- 8. Although thecardiac output is at rest is within normal limits in most patients in severeAS , it often fails to rise normally during exertion. Late in the course of the disease cardiac out put, stroke volume and therefore left ventricular pressure gradient all declines. Compensatory left ventricular concentric hypertrophy increases the left ventricular mass which increases left ventricular demand. Coronary perfusion is decreased and wall stress produces sub endocardial ischemia. There is supply demand mismatch causing ischemia.
- 9. Symptoms 1) Breathlessness: i)onexertion. ii) Orthopnea/ PND iii) Pulmonary edema 2) Angina on exertion: i) It may be due to myocardial supply demand mismatch, or ii) May be due to underlying coronary artery disease. 3)Syncope and dizziness on exertion. It may commonly due to reduced cerebral perfusion that occurs during exertion. 4)Sudden death
- 10. Signs 1)The ArterialPulse: Arterial pulse is anacrotic pulse( a notch on upstroke) and it is slow rising, small and peaking late on palpation of carotid pulse. Coarse systolic vibrations are also felt so called carotid shudder. 2) Blood Pressure: Blood pressure may normal or it may reduce in long standing AS.
- 11. Signs 3) ExaminationOf Precordium: A) Inspection/ Palpation: i) Apex: Apex is heaving in character, initially not displaced. ii) Systolic thrill ( palpable murmer) in second intercostal space on either side of sternum,in suprasternal notch and is frequently transmitted along the carotid.
- 12. B)Auscultation: i) HeartSounds: First Heart sound is normal. Second Heart sound may be single because of calcification and immobility of aortic valve. Paradoxical splitting of second heart sound if LBBB on ECG. Fourth heart sound is usually present. ii) Systolic Murmur: It is late peaking and the best heard at the base of heart, but is often well transmitted both along the carotids and to the apex.
- 13. Investigations 1) ECG: i)Theprincipal ECG change is left ventricular hypertrophy.T wave inversion and ST segment depression in leads with upright QRS complexes are common( left ventricular strain). ii) ECG changes of left atrial enlargement i.e. increase duration in lead II and late negativity of p wave inV1.
- 14. 2)X-Rays Chest: i)Heart is usually of normal size or slightly enlarged, with rounding of left ventricle border and apex. Long standing AS with systolic dysfunction may cause cardiac enlargement. ii) Post stenotic dilatation of ascending aorta. iii) Left atrium may be slightly enlarged in patients with severe AS.
- 15. Echo Cardiography TrueBicuspid AorticValve has two cusps and can be assessed on echocardiography. Degenerative Calcific Aortic valve appears as three leaflet structures with marked thickening and calcification of leaflets.
- 16. Echo – Assessmentof Severity Doppler Echocardiography: Doppler echocardiography is essential for assessment of physiological significant aortic stenosis. In case of clinically significant aortic stenosis, gradient is likely to exceed 50mmHg.
- 17. Echo – Assessmentof Severity
- 19. AS-Echocardiographic- Assessment of HeartChambers Because of long standingAortic valvular Stenosis there will be effects on heart chambers. LeftAtrium will be enlarged. LeftVentricular Hypertrophy. LeftVentricular Chamber dimension initially will be normal but with long standing aortic valve stenosis LV size will increase with systolic dysfunction.
- 20. Cardiac Catheterization Coronaryangiography in patients who have symptoms of effort angina greater than 45 years of age in male and greater than 55 years of age in female.
- 21. Treatment 1) MedicalTreatment: i)Patients with severe AS should be advised to avoid vigorous athletic and physical activity. ii) Symptomatic patients are usually candidate of surgery. iii) Diuretic but should carefully used. iv)ACE inhibitors but carefully should be used. v) Digoxin in patients withAF or in systolic dysfunction. 2) Balloon aortic vavuloplasty: In children and adolescent in symptomatic severe As with pliable aortic valves 3)Surgical AorticValve replacement.
- 22. Aortic Regurgitation Inaortic regurgitation aortic valve is not closed during diastole and large volume of blood comes back to left ventricle during diastole. When regurgitation is marked the stroke out put of left ventricle is doubled or trebled. The left ventricle dilates and hypertrophies and initially compensates for hypertrophy.
- 23. Causes AR maybe caused by primary disease of aortic valve and/or the wall of aortic roots. Valvular AR: i) Rheumatic fever ii) Infective endocarditis. iii)Trauma iv) Congenital bicuspid aortic valve. v) Structural deterioration of a prosthetic valve. Aortic Root Disease: i)Age related( degenerative ) aortic dilatation. ii)Cystic Medial Necrosis of aorta either isolated or in Marfan syndromes.
- 24. iii)Aortic dilatation related toBicuspid aortic valve. iv) Syphilitic aortitis. v)Ankylosing spondylitis. vi) Aortic Dissection.
- 25. Chronic Aortic Regurgitation Pathophsiology: Severe AR may occur with a normal effective forward stroke volume and a normal ejection fraction with compensatory eccentric hypertrophy of left ventricle. In compensatedAR there is sufficient wall thickness. Left ventricular systolic function is maintained through the combination of chamber dilatation and hypertrophy. Long standing AR may lead to further LV dilatation and systolic dysfunction with reduction of ejection fraction.
- 26. Chronic AR --Symptoms 1) In mild to moderateAR patient may be asymptomatic and in compensated severeAR also. 2) Patient may have awareness of heart beat( Palpitation). 3) Dyspnea: Complaints of exertional dyspnea,orthopnea, and paroxysmal nocturnal dyspnea usually develops gradually. 4) Angina Pectoris: Late in the course.
- 27. Signs 1) Arterialpulse is High volume, collapsing( Corrigan pulse). 2) BP: Systolic arterial blood pressure is elevated, and diastolic pressure is abnormally low(Wide pulse pressure).
- 28. 4)Examination OfPrecordium: Inspection/Palpation: Apex is diffuse, displaced laterally, inferiorly and hyperdynamic. Auscultation: i) Soft first heart sound. ii) A2 may be soft. iii)Left sided S3 in systolic dysfunction. iv)A harsh systolic outflow murmur caused by increased left ventricular stroke volume and this often radiates to the carotids.
- 29. v) Highfrequency, blowing, early diastolic murmur will be audible. The murmur is best audible with the diaphragm of the stethoscope while the patient is sitting up and leaning forward, with the breath d in expiration.
- 30. Investigations 1) ECG: Chronicsevere AR results in left axis deviation and a pattern of left ventricular diastolic volume overload, characterized by an increase in initial forces( prominent Q wave in leads I,Avl andV3- V6. Latter on prominent QRS complexes in lateral leads and tallT waves and then ST depression.
- 31. 2) X-RaysChest: i) Enlarged Cardiac shadow. ii) Dilatation of ascending aorta. Severe aneurysmal dilatation of aorta suggests aortic root disease( Marfan syndrome).
- 32. 3) Echocardiography: AorticRegurgitation may be caused by primary disease of aortic valve and / or the wall of aortic root. Valvular Aortic Regurgitation: Cause of Valvular aortic regurgitation can be assessed on 2D echo. Aortic Root Disease: AR secondary to marked dilatation of ascending aorta is now more common than primary valvular disease and can be assessed on 2D echocardiography.
- 33. Aortic Regurgitation- Assessmentof Severity Doppler Echocardiography: The pressure half time of regurgitant jet, defined as the time in milliseconds required for the initial transvalvular diastolic gradient to decline to one half of its peak value, can be calculated and is inversely related to the severity of aortic regurgitation.
- 34. Aortic Regurgitation- Assessment ofseverity Color Doppler echocardiography: Using color flow imaging the regurgitant jet can be visualized in the left ventricular outflow tract. By measuring the width or the cross- sectional area of the regurgitant jet in the LV outflow tract and indexing this to the width or cross-sectional area of LV outflow tract can be used for severity of AR. If regurgitant jet is greater than 65 % index to LV out flow tract width then it is severe AR.
- 35. Aortic Regurgitation- Assessment OFHeart Chambers Chronic AR:Left ventricle is dilated in long standing hemodynamically significant ChronicAR with preserved LV systolic function. However with long standing ChronicAR further LV dilatation and systolic dysfunction occur with decreased EF. Acute AR:InAcuteAR LV dimensions are normal with decreased EF.
- 36. Treatment MedicalTreatment: i) ArterialVasodilatorslike nifedepine. ii) Diuretics iii)ACE inhibitors. iv) B Blockers should be avoided due to negative inotropic effect. v) Digoxin. SurgicalTreatment: Aortic valve replacement in patients with symptomatic severe aortic regurgitation.
- 37. Acute Aortic Regurgitation Causes: 1) Infective Endocarditis. 2) Aortic Dissection. 3)Trauma. 4) Failure of prosthetic valve. 5) Rupture Of sinus ofValsalva. Pathophsiology: In acuteAR left ventricle has no time for compensatory eccentric hypertrophy and the regurgitant volume fills a ventricle of normal size that cannot accommodate the combined large regurgitant volume and inflow from left atrium. Because ability of total stroke volume to rise acutely is limited, forward stroke volume declines. The sudden increase in left ventricular filling causes the left ventricular diastolic pressure to rise rapidly above the left atrial pressure during the early diastole. Severe acuteAR may cause profound hypotension and cardiogenic shock and severe dyspnea due to elevated left atrial pressure.
- 38. Clinical Features: Symptoms: i) Acute dyspnea due to pulmonary edema. ii) Circulatory collapse due to low cardiac output. Signs: Peripheral signs of AR are not present like in chronic AR. Apex will be hyper dynamic and not displaced. S1 may be soft. Loud P2. S3 and S4. Early diastolic murmur is low pitched and short duration as compare to chronic AR. Austin flint murmur may be present.
- 39. Investigations: 1) ECG:ECG may or may not show left ventricular hypertrophy. 2)X-Rays Chest: Cardiac shadow is not enlarged and evidence of pulmonary edema in lung fields. 3) Echocardiography: Premature closure of mitral valve. Left ventricle is not dilated. Steep doppler velocity. Treatment: MedicalTreatment: Inotropic drugs like dopamine and dobutamine. Vaodilators Drugs. Surgery: Aortic valve replacement.