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Mitral stenosis
Mitral stenosis is commonly caused by rheumatic heart disease which leads to inflammation and fusion of the mitral valve leaflets, reducing the mitral valve orifice area. Severe mitral stenosis, defined as a mitral valve area less than 1.0 cm2, can cause pulmonary hypertension, pulmonary edema, atrial fibrillation, and right heart failure as the heart tries to maintain sufficient cardiac output against the back pressure. Physical exam may reveal signs of pulmonary hypertension like a loud pulmonary component to S2, as well as a tapping apex, opening snap, and mid-diastolic rumble on cardiac auscultation. Echocardiography can determine the severity of mitral stenosis and assess
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Mitral stenosis
- 1. MITRAL STENOSIS K. KavindyaM. Fernando JMJ 1
- 2. Mitral stenosis • Mitralvalve – Consist of fibrous annulus, – Anterior & posterior leaflets – Chordae tendinae, – Papillary muscle JMJ 2
- 3. Mitral stenosis • Commonestcause :rheumatic heart disease • Infections with group A beta hemolytic streptococci • More common in women • Inflammation leads to commissural fusion and a reduction in mitral valve orifice area JMJ 3
- 4. Pathophysiology • Normal valvearea: 4-6 cm2 • Mild mitral stenosis: – MVA 1.5-2.5 cm2 – Minimal symptoms • Moderate mitral stenosis – MVA 1.0-1.5 cm2 usually does not produce symptoms at rest • Severe mitral stenosis – MVA < 1.0 cm2 JMJ 4
- 5. To maintain sufficientcardiac output 1. Left arterial pressure increases 2. Left arterial hypertrophy and dilation 3. Pulmonary veins, pulmonary arterial and R/ heart pressure increases 4. Increase of pulmonary capillary pressure 5. Followed by development of – pulmonary oedema – Atrial fibrillation with tachycardia – Loss of coordinated atrial contraction JMJ 5
- 6. To maintain sufficientcardiac output 6. This is prevented by (Reactive pulmonary hypertension) – Alveolar and capillary thickening – Pulmonary arterial vasoconstriction 7. Pulmonary hypertension leads to – R/ ventricular hypertrophy, dilation and failure with subsequent tricuspid regurgitation JMJ 6
- 7. Symptoms • Palpitation • Systemicemboli JMJ 7 • Dyspnoea • Pulmonary infections (Recurrent bronchitis) • Haemoptysis • Cough • R/ heart failure • Fatigue • Abdominal and lower limb swelling Atrial fibrillation Pulmonary Hypertension
- 8. Signs • Face :Mitral fascies • Pulse : atrial fibrillation • RV : Heaving, sustained • Apex: Localized, tapping • Sounds: Loud S1, Loud P2 (if pulmonary hypertension), opening snap • Murmurs: Mid diastolic rumble at apex JMJ 8
- 9. Mitral Stenosis: Physical Exam •First heart sound (S1) is accentuated & snapping • Opening snap (OS) after aortic valve closure • Low pitch diastolic rumble at the apex • Pre-systolic accentuation (esp. if in sinus rhythm) S1 S2 OS S1
- 10. Signs (Face) • Severemitral stenosis with pulmonary hypertension • Mitral fascies / malar rash • Bilateral • Cyanotic or dusky pink discolouration • Over the upper cheeks • Due to atriovenous anastomosis & • Vascular stasis JMJ 10
- 11. Signs (Pulse) • Smallvolume pulse • Usually regular in early stages, • If the patient is in sinus rhythem • In severe disease, may develop atrial fibrillation • Irregularly irregular pulse JMJ 11
- 12. Signs (Jugular Veins) •If R heart failure develops • obvious distension of jugular veins • If pulmonary hypertension or tricuspid stenosis is present • ‘a’ Wave will be prominent JMJ 12
- 13. Signs (Palpation) • Tappingimpulse felt parasternally on left side • Palpable 1st heart sound • Combined with left ventricular backward displacement • Produced by an enlarging left ventricle • Sustained parasternal impulse • Due to R ventricular hypertrophy JMJ 13
- 14. Signs (Auscultation) • Loud1st heart sound – If the mitral valve is pliable – It will not occur in calcified mitral stenosis • Opening snap – Valve suddenly opens with the force of the increased L arterial pressure • Low pitched ‘rumbling’ mid diastolic murmur – Best heard with bell held lightly – At the apex with the patient lying on the left side JMJ 14
- 15. Signs (Auscultation) • Ifthe patient is in sinus rhythm – Murmur becomes louder at the end of diastole – As a result of atrial contraction – (Pre- systolic accentuation) JMJ 15
- 16. How to determinethe severity of mitral stenosis • Presence of pulmonary hypertension – Recognized by R/ ventricular heave & loud pulmonary component of 2nd heart sound – And signs with R heart failure : Oedema, hepatomegaly – Graham Steell murmur JMJ 16
- 17. How to determinethe severity of mitral stenosis • Closeness of the opening snap to the 2nd heart sound ∞ severe MS • Length of mid-diastolic murmur ∞ severity • As the valve cusps become immobile – Loud 1st heart sound softens – Opening snap diasppears – When pulmonary hypertension occurs : P2 intensity increase, mid diastolic murmur become quieter JMJ 17
- 18. Investigations • Chest X-ray •Electrocardiogram • Echocardiogram • Cardiac magnetic resonance • Cardiac catheterization JMJ 18
- 19. Investigations –X-ray • Smallheart with an enlarged L/ atrium • Pulmonary venous hypertension • Calcified mitral valve– on penetrated or lateral view • Signs of pulmonary oedema or pulmonary hypertension JMJ 19
- 20. Investigations –ECG • Sinusrhythm in ECG shows a bifid P wave – Owing to delayed L/atrial activation • Atrial fibrillation may be present • ECG features of R/ventricular hypertrophy – Right axis deviation – Perhaps tall R wave in lead V1 JMJ 20
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- 23. Investigations –Echocardiogram • Transthoracicechocardiography – To determine L/ R/ atrial and ventricular size – The sevirity of MS • Transoesophageal Echocardiography (TOE) – To detect the presence of L/ atrial thrombus JMJ 23
- 24. Treatment • Need notreatment other than prompt therapy of attacks of bronchitis • Early symptoms like dyspnea - diuretics • Onset of atrial fibrillation :digoxin, anticoagulants (to prevent atrial thrombus and systemic embolism) • If pulmonary hypertension or symptoms of pulmonary congestion : surgical therapy JMJ 24
- 25. Treatment • Operative therapies –Trans-septal balloon valvotomy – Closed valvotomy – Open valvotomy – Mitral valve replacement JMJ 25
- 26. Treatment: Trans-septal balloon valvotomy •Catheter introduced into R atriam via femoral vein • Under local anasthesia • Inter atrial septum is punctured • Catheter enter into left atrium then to mitral valve • Balloon is inflated, briefly to split the valve commissures JMJ 26
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- 28. Treatment: Trans-septal balloon valvotomy •Complications – Regurgitation may result • Contraindications – Heavy calcification – More than mild mitral regurgitation & thrombus in the L/atrium • TOE is done before this procedure JMJ 28
- 29. Treatment: Closed valvotomy •For the patients with – mobile, – non calcified and – non regurgitant mitral valves • Fused cusps forced apart by a dilator (introduced through the apex of L/ ventricle) • Cardiopulmonary bypass is not needed for this operation JMJ 29
- 30. Treatment: Open valvotomy •Often preferred to closed valvotomy • Cusps are carefully dissected apart under direct vision • Cardiopulmonary bypass is requied JMJ 30
- 31. Treatment: Mitral valvereplacement • It is necessary if – Mitral regurgitation is present – Badly diseased or badly calcified stenotic valve, – Moderate or severe mitral stenosis & thrombus in L atrium despite anticoagulation • Artificial valve >20 yrs • Anticoagulants are necessary JMJ 31
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