MITRAL STENOSIS

CASE SHEET Name: Age: Sex: Occupation: Place: Chief complaints: (with duration in chronological order) o Breathlessness o Orthopnoea and PND o Hemoptysis o Palpitation o Fatigue o Recurrent bronchitis H/O presenting illness. H/O Breathlessness: Duration Onset Progression / Episodic Grade according to NYHA classification Aggravating, relieving factors Orthopnoea PND Associated symptoms cough, expectoration, pain, wheeze H/O hemoptysis: Duration Episodes Amount Colour (fresh / altered blood) Postural, diurnal variation Aggravating, relieving factors Associated with cough & sputum Followed by malaena

H/O palpitation: Duration Severity Exertional or paroxysmal Aggravating, relieving factors Associated with chest pain, syncope H/O chest pain: Duration Site Nature Onset Aggravating, relieving factors Associated with sweating, syncope Related to food intake H/O syncope: Onset Duration No. of episodes Total / partial loss Recovery Conscious & memory before and after the episode Associated with fits, bladder & bowel disturbance Relation with exertion / posture / vomiting H/O cough: Duration Dry / productive Diurnal variation Postural variation Seasonal variation Aggravating, relieving factors Fatigue Daily activities affected

(cardiac failure history): H/O abdominal distention puffiness of face swollen feet diminished urine output right hypochondrial pain easy fatiguability loss of weight (rheumatic fever history): H/O fever with sore throat fleeting joint pain & swelling involuntary movements nodules under the skin any injection given every 21 days H/O voice changes H/O dysphagia Past H/O: Previous similar illness History suggestive of rheumatic fever HT, DM, coronary heart disease, dyslipidemia, TB H/O cyanotic spells H/O squatting episodes H/O exposure to STIs (syphilis, HIV) Previous cardiothoracic surgery Family H/O: Consanguinity Similar illness H/O congenital heart disease HT, DM, CAD, dyslipidemia Personal H/O: Diet Smoking Alcohol

Treatment H/O: Any diagnosis given Reason for hospitalization if any On any drugs? Menstrual and obstetric history for females General examination: Consciousness Orientation Comfortable / dyspneic at rest Built Nourishment Anaemia ( SBE) Jaundice Cyanosis (congenital cyanotic heart disease, acute pulmonary edema) Clubbing (SBE, congenital cyanotic heart disease) Pedal edema (edema CCF, constrictive pericarditis, pericardial effusion, tricuspid valve disease) Generalised lymphadenopathy Mitral facies pinkish purple patches on cheeks, peripheral cyanosis, malar flush Skin petechiae, Oslers nodules, rheumatic nodules Skeletal system polydactyly, cubitus valgus Vital signs: Pulse rate, rhythm, volume, character, nature of vessel wall, radialradial delay, radio-femoral delay, felt equally in all peripheral pulses on both sides (In mitral stenosis small volume pulse) BP: (measured in which limb in which position) Respiratory rate: (Cheyne-Stokes breathing cardiac failure) Temperature: (elevated in SBE)

Examination of the cardiovascular system: Inspection: Tracheal position Apical impulse Dyspneic at rest or not Neck veins prominence Chest wall symmetry Kyphosis, scoliosis Precordial bulge Pulsations over precordium Carotid pulsation Dilated vessels Scars, sinuses Epigastric pulsations Palpation: Tracheal position Apex beat: Site Character (in MS heaving due to palpable S1) Thrill (MS diastolic thrill) Parasternal heave (MS left parasternal heave) Palpable heart sounds (MS palpable S2) Thrills over the precordium Carotid thrill Epigastric pulsations Percussion: Heart borders Upper border of liver Traubes space Auscultation: - mitral area, tricuspid area, pulmonary area, aortic area, second aortic area Heart sound S1, S2 Loudness, splitting Additional heart sounds S3, S4

Murmur Loudness Diastolic / Systolic / Continuous Grade Best heard with diaphragm / bell Best heard in which position sitting / leaning forward/ left lateral In inspirational or expirational apnea Radiation Other sounds Pericardial rub Ejection click Opening snap Venous hum [in MS: loud S1, opening snap, mid-distolic murmur. Murmur is described as loud-pitched, rumbling mid-diastolic murmur with pre-systolic accentuation in mitral area heard with bell of stethoscope with patient in left lateral position with breath held in expiration. Ejection systolic murmur in pulmonary area if there is pulmonary artery hypertension Functional tricuspid regurgitation produces pan-systolic murmur in tricuspid area.] Examination of other systems: Respiratory system: Tachypnoea, orthopnoea Crepitations at lung bases due to left heart failure Hydrothorax (from CCF) Abdomen: Liver soft & tender hepatomegaly in CCF Spleen palpable in SBE Ascites CCF Central nervous system: Hemiplegia TIA Sydenhams chorea

Provisional Diagnosis: Acquired / Congenital / Ischaemic Anatomical mitral, tricuspid, aortic, pulmonary Structural abnormality stenosis, regurgitation Etiology rheumatic / syphilitic / others In sinus rhythm or not Complications pulmonary hypertension, CCF, infective endocarditis NYHA classification DISCUSSION Causes of mitral stenosis: Rhuematic heart disease Congenital parachute mitral valve (all chordae inserted into a single left ventricular papillary muscle) Hunters syndrome Hurlers syndrome Lutembachers syndrome (acquired MS of rheumatic origin + ASD) Carcinoid syndrome Amyloidosis Drugs Methysergide Collagen vascular disease Endomyocardial fibrosis Mucopolysaccharidosis Mitral valve leaflets are diffusely thickened (by fibrous tissue/ calcification)
1.

mitral commissures fuse chordae tendinae fuse valvular cusps become rigid Narrowing of orifice

2.

Pathophysiology: Obstruction to left ventricular outflow Increased pressure in left atrium Increased pressure in pulmonary veins

Pulmonary artery hypertension Right ventricular hypertrophy Right ventricular failure Functional tricuspid regurgitation Pathological types of MS: Button hole Fish mouth Funnel type

Pulmonary edema (if no PAH) Normal left atrial pressure: 4 - 12 mm Hg Normal pulmonary arterial pressure: 25 / 10 mm Hg Pulmonary arterial pressure in pulmonary hypertension: 35 / 15 mm Hg

3.

4. Causes of pulmonary hypertension in MS: Passive backward transmission of elevated left atrial pressure Pulmonary arteriolar constriction triggered by left atrial & pulmonary venous hypertension (reactive pulmonary hypertension) Interstitial edema in the walls of the small pulmonary vessels Organic obliterative changes in the pulmonary vascular bed
5.

Carvallos sign:

With severe PHT, a pansystolic murmur produced by functional TR may be audible along the left sternal border. Usually louder during inspiration and diminishes during forced expiration. May be confused with PSM of mitral regurgitation. Graham steel murmur: In severe PHT, a high-pitched decrescendo diastolic blowing pulmonary regurgitation murmur may be heard along the left sternal border due to dilatation of pulmonary valve ring. This may be indistinguishable from aortic regurgitation.
6.

Mitral facies: Pinkish purple patches on cheeks Low cardiac output in MS causes vasoconstriction leading to peripheral cyanosis (seen in lips, tip of nose and cheeks) Malar flush due to vasodilatation (vascular stasis) in malar area All these features constitute mitral facies.
7. 8.

9.

Malar flush is seen in: Mitral stenosis Myxoedema High altitude Cushings syndrome Thyrotoxicosis Chronic alcoholism Polycythemia Carcinoid syndrome Menopausal syndrome Pheochromocytoma SLE

Dyspnoea is usually nocturnal in MS coz: Venous return increases in supine position Mobilisation of edema fluid from extravascular to intravascular compartment in supine position Adrenergic drive is reduced during sleep

Heart rate increases during REM sleep Reduction of vital capacity in supine position Elevation of left atrial pressure & fall in PaO2 during sleep

10. Hemoptysis in MS is due to: Pulmonary apoplexy (due to rupture of thin walled dilated pulmonary veins usually as a consequence of sudden rise in left atrial pressure) Pulmonary congestion in PND Pulmonary edema pink frothy sputum Pulmonary infarction frank hemoptysis Recurrent bronchitis Bronchiectasis Winter bronchitis (chronic bronchitis) blood stained mucoid sputum Anticoagulant therapy (rare) Pulmonary hemosiderosis (rare) 11 .Protective mechanisms to prevent pulmonary edema in MS: High pulmonary vascular resistance (pulmonary hypertension) Capillary-alveolar-interstitial barrier Broncho-pulmonary venous shunts 12. Chamber involvement in MS: LV RV RA Left ventricle does not fail in MS as mitral valve lies proximal to it. Therefore, in the presence of LVH or failure there may be associated valvular diseases like MI, AI, AS, systemic hypertension, ischaemic heart disease or cardiomyopathy 13. Grading of parasternal heave: Grade I: visible but not palpable Grade II: visible and palpable but obliterable Grade III: visible and palpable but not obliterable 14. Factors influencing the intensity of S1:

Position of valve cusps at the onset of systole: - Wide open: loud S1 - Close to each other: muffled S1 P-R interval: Short P-R loud Prolonged P-R muffled Pliability of valve cusps(calcification loss of pliability muffled S1) Ventricular muscle mass (LVH booming S1) Heart rate (tachycardia short P-R loud S1) Intervening media between heart & stethoscope (emphysema / pericardial effusion / obesity muffled S1) 15. Loud S1in MS: Cusps are kept open until the onset of ventricular systole and kept wider. So when it closes rapidly it produces a louder sound than normal. 16. Muffled S1 in MS: When MS is associated with: Mitral incompetence or severe aortic incompetence Mitral valve calcification Acute rheumatic carditis (due to prolonged P-R interval) Digitalis overdose (due to prolonged P-R interval) Acute myocardial infarction (produces varying intensity of S1) Rotation of heart due to gross RVH & consequently right ventricle forming the apex Emphysema, obesity, thick chest wall Coincidental ASD Severe pulmonary artery hypertension Cardiomyopathy 17. Loud S1: Mitral stenosis Tricuspid stenosis High output states anemia, fever, exercise, pregnancy Atrial myxoma

Short P-R interval (except in WPW syndrome) Sinus tachycardia due to any cause Normally in children

18. Soft S1: Calcified mitral stenosis Mitral regurgitation Tricuspid regurgitation Calcified tricuspid stenosis Left ventricular dysfunction Acute aortic regurgitation Prolonged P-R interval (except in Ebsteins anamoly) 19. Murmur in MS: - Accentuated by exercise - Low-pitched because produced mainly by flow and not by gradient - Softens on inspiration because blood is sequestered in the lungs during inspiration. So left atrium gets less blood. So flow is less. - Best heard in expiration because lung has less blood and more blood goes to left atrium. 20. MS murmur can be made louder: Left lateral position LV brought closer to chest wall Increased flow: - Coughing - Exercise - Administering amyl nitrate: causes increased venous return and cardiac output Breath held in expiration Bell of stethoscope with a good air seal by light pressure 21. MS murmur may be soft in: Obesity Emphysema Large right ventricle pushing left ventricle posteriorly Coincidental ASD

Low flow: Severe pulmonary artery hypertension Associated AS or TS Cardiomyopathy Atrial fibrillation

22. Murmur in MS is mid-diastolic & not early-diastolic: Isovolumetric relaxation period is the interval between closing of the aortic valve (S2) and opening of the mitral valve. Diastolic murmur of MS is heard as soon as the blood flows from the left atrium to the left ventricle after opening of mitral valve (i.e., in the mid-diastole). There is no blood flow in the isovolumetric relaxation period & hence the murmur is mid-diastolic and not early-diastolic. 23. Mitral diastolic murmur organic or functional? Functional MS has the following features: Pulse normal volume Diastolic thrill in mitral area absent S1 not very loud Presystolic accentuation absent Opening snap absent Features of LVH 24. Bell of stethoscope is used to hear low-pitched sounds like: Murmur of MS and TS S3 or S4 Foetal heart sounds Venous hum 25. Presystolic accentuation: - Due to movement of mitral leaflet towards left atrium which compromises the size of the orifice - Occurs in the last part of ventricular diastole (last rapid filling phase) which coincides with the atrial systole. Atrial systole increases the blood flow across the stenotic valve and thus there is accentuation of the diastolic murmur.

26. Absent presystolic accentuation: Atrial fibrillation Left atrial failure Big left atrial thrombus 27. Differential diagnosis for mid-diastolic murmur: Mitral stenosis Tricuspid stenosis (loudest at lower left sternal edge, features of RVH not present) Carey-Coombs murmur functional murmur of valvulitis (absence of loud S1, opening snap & diastolic thrill) Flow murmurs of: - ASD (no LA enlargement, no Kerely B lines, wide fixed splitting of S2) - VSD - PDA - MR (left ventricular enlargement) - TR Ritans murmur in complete heart block Austin-Flint murmur of AR (no presystolic accentuation, S1 not loud, opening snap absent, isometric hand grip increases the murmur) Left atrial myxoma (associated wt loss, fever, anemia, systemic emboli, increased IgG, IL-6) Ball valve thrombus Cortriatriatum 28. Flow mid-diastolic murmur differential diagnosis: Right side: ASD TR Total anomalous pulmonary venous connection (TAPVC) Left side: VSD PDA MR AR 29. Opening snap:

 High-pitched loud snapping or clicking sharp sound due to sudden tensing of the cusps. Follows A2 by 0.05 0.12s Present in early diastole (at the end of isovolumetric relaxation period) Loudest between apex beat and left sternal border Best heard after expiration with patient in standing position Accentuated by exercise Best heard with diaphragm To differentiate between OS & S2 splitting: Ask the patient to stand. This increases the venous return. Thus, S2-OS gap increases whereas A2P2 gap decreases. 30. Causes of opening snap: Lower left parasternal region: TS TR ASD Just internal to apex: MS Posterior cuspal type of MR VSD PDA 31. Absent OS: Mild MS Calcified mitral valve MS with MR Severe MS Congenital MS 32. Opening snap indicates: MS is organic Valve cusps are pliable Significant MS

High AV pressure gradient Severe AI, gross MI, Gross PHT, AF, LAF, SBE absent. Decreased S2-OS gap indicates tightening of stenosis MS is already amenable to surgery

33. D/D of OS: Splitting of S2 S3 Pericardial knock 34. Auscultation in MS:

35. Pliable mitral valve cusps: - Short, sharp, accentuated S1 - Presence of opening snap 36. Parts of a valve: - Leaflet - Annulus - Chordae tendinae - Papillary muscle - Subjacent myocardium

37. Severity of MS: According to valve area and symptoms: (normal mitral valve area: 4 6 cm2) valve area > 2.5 cm2 mild 1.5 2.5 cm2 moderate 1 1.5 cm2 severe / critical < 1 cm2 According to A2-OS interval: mild: 0.10 0.12 s severe: 0.05 0.07 s According to gradient across stenotic mitral valve: (normal valve gradient : 0mm Hg) mild: < 5 mm Hg moderate: 5 15 mm Hg severe: > 15 mm Hg Duration of the diastolic murmur is directly proportional to the severity . Other signs of severity: symptomatic patient RVH and pulmonary hypertension in ECG cardiomegaly in chest X-ray 38. Changes when AF develops in MS: Heart rate is about 100 150 / min Irregularly irregular pulse with varying volume & a pulse deficit of > 10 Varying intensity of S1; OS not heard Absent a wave in JVP Presystolic accentuation of the diastolic murmur disappears CCF may precipitate and embolic manifestations may appear

symptoms none dyspnoea on severe exertion PND -/+ pulmonary edema orthopnoea

39. Complications of MS: Due to back pressure: Pulmonary edema: in the early phase of MS due to sudden surge in flow across markedly narrowed mitral valve, when LA pressure is > 25 mm Hg; less common in long-standing MS because of thickening of alveolar capillary membrane. Pulmonary artery hypertension ( long-standing PHT causes hemosiderosis and ossification) RVF TR Arrythmias AF (left atrial enlargement leads to myofibrillar disarray each myofibril produces its own beat) Atrial flutter Infection Infective endocarditis Bronchopulmonary infection Embolism Cerebral embolism Pulmonary embolism Renal hypertension Leriches syndrome: claudication of thigh (due to embolism at branching of common iliac artery) + impotence Angina like pain (PHT due to hypoxia; hypotension; decreased cardiac output) Pressure effects Ortners syndrome: compression of left recurrent laryngeal nerve by enlarged left atrium, tracheobronchial lymph nodes and dilated pulmonary artery leading to hoarsness of voice Dysphagia Collapse of left lung Bromchiectasis (pressure on left main bronchus) Erosion of spine leading to paraplegia Others hemoptysis, recurrent RTIs, jaundice, cardiac cirrhosis 40. Damped MS / Silent MS:

Development of pulmonary hypertension diminishes the cardiac output (throttle effect) and results in temporary sympyom-free period (period of illusion). The MDM may not be audible and thus known as silent MS / damped MS. 41. Juvenile mitral stenosis: - Occurs below 18 years of age - Pin-point mitral valve - Atrial fibrillation is rare - Valve calcification is uncommon 42. Investigations for MS: Blood TC, DC, ESR ASO titre Chest X-ray ECG Echocardiogram: thickened mobile cusps reduced rate of diastolic filling reduced valve area Doppler study: for estimation of the transvalvular gradient and of the mitral orifice size presence and severity of accompanying MR extent of restriction of valve leaflets, their thickness degree of distortion of the subvalvular apparatus anatomical suitability for balloon mitral valvotomy Cardiac catheterization to determine the haemodynamic status of the patient. 43. Chest X-ray findings: Slight increase in the transverse diameter of heart (due to RVH) Double density sign shadow witih shadow outer & upper border due to left atrial enlargement; inner & lower border due to right atrial enlargement.

 Splayed carina; elevation of left upper lobe bronchus (LA enlargement) Straightening of the left heart border MITRALISATION due to: small aortic knuckle convexity due to dilated pulmonary artery left atrial appendage becomes more prominent & produces a convexity Kerley B lines (dense, short, horizontal lines most commonly seen in the costophrenic angles when pulmonary venous pressure is between 20 30 mm Hg) Kerley A lines ( straight, dense, lines upto 4cm in length and running towards the hlum when pulmonary venous pressure is > 30 mm Hg) If pressure still rises alveolar pulmonary edema produces parahilar Bats wing shadowing Mitral valve calcification Evidence of PHT dilated pulmonary arteries at hilum with peripheral pruning

44. ECG findings in MS: Left atrial enlargement: P mitrale P wave is broad and bifid occupying > 0.11 s in lead II or biphasic P wave in v1. Right ventricular hypertrophy: right axis deviation dominant R waves in right oriented leads R wave > 5mm in amplitude in v1 dominance of S wave in left precordial leads sum of R wave in v1 and S wave in v6 > 10 terminal S waves in all standard leads Features of atrial fibrillation: absent P waves varying R-R intervals

45. Management of MS: General salt free diet, rest Medical Antifailure measures: * physical activity * salt-restricted diet * diuretics * digitalis for slowing the ventricular rate of patients with AF ( or can use beta blockers / nondihydropyridine Ca blockers such as verapamil / diltiazem) Treatment of AF: anticoagulation RF prophylaxis: IE prophylaxis Treatment of complications Surgical: Closed mitral valvotomy / commissurotomy ( without cardiopulmonary bypass) Open mitral valvotomy / commissurotomy ( with cardiopulmonary bypass) Percutaneous balloon valvuloplasty Mitral valve reconstruction Mitral valve replacement

46. Criteria / indications for balloon mitral valvuloplasty: Symptomatic ( NYHA class II, III or IV) Mitral valve area <= 1.5cm2 Isolated MS No significant MR Non-calcified, mobile valves / subvalvular apparatus Left atrium free of thrombus

47. Complications of valvuloplasty : Embolic events Cardiac perforation Development of MR Iatrogenic, residual ASD which later closes or decreases in size 48. Indications for valvotomy: Progressive symptomatic deterioration inspite of medical treatment MS with complications Asymptomatic patients with a single attack of thromboembolic manifestation Mitral valve orifice < 1cm2 49. Contraindications of closed valvotomy: MS with significant MI MS with left atrial thrombus Valvular calcification Presence of active rheumatic carditis Extremely tight stenosis Mitral valve distorted by previous operation 50. Prosthetic valves: Mechanical ( requires life-long anticoagulation) ball & cage valve ( Starr-Edwards prosthesis) tilting disc valve ( Bjork-Shiley valves) bileaflet ( St.Jude) Biological porcine bioprosthesis pericardial xenograft prosthesis 51. Bioprosthetic valve: Low incidence of thromboembolic phenomenon

 Not usually used in young patients < 35 years because of rapid degeneration Useful in: pregnancy contraindication to use of anticoagulants older patients > 70 years of age 52. Tilting disc preferred to caged ball valve coz: Occupies less space and hence useful in patients with small ventricle Incidence of hemoptysis is less common 53. Sound of prosthetic valves: Ball valves opening sound louder than closing sound Tilting disc valves only closure sound heard Bileaflet closure sound heard well 54. To determine the dominant lesion:MS with MR Features A) Symptoms: Hemoptysis, systemic embolisation, symptoms of CCF, pulmonary congestion, chest pain B) Signs: 1) Pulse low volume, within normal features of AF limit ( not more common low vol), collapsing low sysyolic BP left 5th ICS, normal lt 6th ICS,1/2 MS > MR MR > MS

2) 3)

BP Apex

inch outside lt MCL ( RVH )

4) 5) 6)

inch outside lt MCL(LVH)

Left parasternal heave S1 OS Diastolic murmur

+++ snapping present & the lesion is organic classical murmur of MS

+ soft / muffled absent short MDM without presystolic accentuation (due to functional MS) classical PSM of MR with radiation LVH + LAH LVH usually present

7)

8)

Systolic murmur

classical PSM of MR not heard LAH + RVH LVH usually not present

C) Investigation: 1) Chest X-ray 2) 3) ECG Echocardiography

thick, immobile LA enlargement cusps with with hyperdynamic diminished rate of LV diastolic filling