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MITRAL STENOSIS - Complete Exam Answer

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PHYSICAL SIGNS

A. General Examination

• Cyanotic lips and face
• Malar flush - dusky pink discoloration over the upper cheeks due to arteriovenous anastomoses and vascular stasis
• Mild jaundice

• Pulse is low in volume
• Peripheral pulse may be absent if embolism develops
• Pulse rhythm is irregularly irregular with varying volume in atrial fibrillation
• Blood pressure may be mildly reduced; mean of three readings to be taken if atrial fibrillation is present

• Jugular venous pressure (JVP) is raised when congestive heart failure develops
• Jugular venous pulse shows three patterns:
  1. Prominent 'a' waves - due to vigorous right atrial systole, seen when there is pulmonary hypertension WITHOUT atrial fibrillation
  2. Absence of 'a' waves - in atrial fibrillation
  3. Prominent V waves (C-V waves) and rapid 'y' descent - when there is development of functional tricuspid regurgitation

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B. Inspection and Palpation of Precordium

• Normally NOT shifted in pure MS
• Has a tapping character - this is the palpable S1 (closing snap) at the apex
• Apex beat is SHIFTED when MS coexists with mitral regurgitation (MR), aortic stenosis (AS), systemic hypertension, ischemic heart disease (IHD), or myocarditis

• Felt at the apex
• It is a palpable vibration felt on the chest wall when you place the heel of your hand there
• A thrill is to touch what a murmur is to hear

• Present if there is pulmonary arterial hypertension

• Present when there is right ventricular hypertrophy or left atrial enlargement
• It is a palpable lifting impulse felt along the left sternal border

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AUSCULTATION - Auscultatory Findings in Mitral Stenosis

1. Loud First Heart Sound (S1)

• In mitral stenosis, the forces that open and close the mitral valve increase as left atrial pressure increases. Together with the wide closing excursion of the leaflets, this makes S1 loud and palpable (tapping apex beat)
• When associated with atrial fibrillation, the intensity of S1 varies
• Low intensity of S1 in MS may be due to:
  1. Calcification of the mitral valve
  2. Congenital MS
  3. Dominant associated mitral/aortic regurgitation

2. Loud Second Heart Sound (S2) and Loud P2

• Loud S2 is a sign of pulmonary hypertension
• The second heart sound is closely split and the pulmonary component (P2) is loud
• Palpable P2 at the pulmonary area indicates significant pulmonary arterial hypertension

3. Mitral Opening Snap (OS)

• OS is a sharp, snappy sound heard during early diastole, following aortic valve closure (A2) by 0.05-0.12 seconds
• Mechanism: Produced due to sudden (abrupt) opening of the dome of the stenosed mitral valve with the force of increased left atrial pressure during diastole
• It is the most important auscultatory sign of valvular involvement in MS
• Absent OS indicates calcification of the body of the leaflets
• The A2-OS interval is inversely proportional to the severity of MS - the shorter the interval, the more severe the stenosis
• Best heard: During expiration, just medial to the cardiac apex with the diaphragm of the stethoscope
• Other conditions with OS: Mitral regurgitation (10%), tricuspid stenosis, atrial septal defect

4. Mid-Diastolic/Presystolic Murmur (MDM)

• Turbulent blood flow through stenosed mitral valve produces a characteristic low-pitched, rumbling, mid-diastolic murmur, sometimes accompanied by a thrill
• Best heard with the bell of the stethoscope held lightly at the apex with the patient lying on the left lateral decubitus position
• Duration varies with the severity of stenosis. In severe MS, the mid-diastolic murmur is long and merges with the presystolic murmur to produce a holodiastolic murmur

• Left lateral position using bell of stethoscope while holding expiration
• Auscultate after walking (isotonic exercise)
• Squatting (increased peripheral resistance)

• In the early phase of MS, a presystolic murmur may be the only auscultatory abnormality
• Mechanism of presystolic murmur:
  1. Atrial contraction
  2. Persistent atrioventricular gradient
  3. Left ventricular contraction in presystole reducing mitral funnel

• Atrial contraction contributes to increased gradient in presystole
• Hence mid-diastolic murmur is accentuated by exercise
• In sinus rhythm, the murmur becomes louder during atrial systole
• During long R-R interval in atrial fibrillation, it is still termed as presystolic accentuation

• Atrial fibrillation
• Mild MS
• Prolonged PR interval
• Bradycardia
• Left ventricular dysfunction (elevated LVEDP)

• Thick chest wall and emphysema
• Dampened MS - severe pulmonary hypertension throttling the left-sided input
• Low cardiac output
• Marked RV enlargement with RV occupying the apex

5. Systolic Murmur

• When pulmonary hypertension develops, it leads to right ventricular hypertrophy and dilatation with secondary tricuspid regurgitation
• This produces a systolic murmur and giant "v waves" in the venous pulse
• If MS coexists with mitral regurgitation, it produces a loud pansystolic murmur that radiates toward the axilla, heard at the lower left sternal border
• Functional tricuspid regurgitation produces a pansystolic murmur, accentuated during inspiration (de Carvallo's sign)

6. Graham Steell Murmur (Murmur of Pulmonary Regurgitation)

• High-pitched early diastolic decrescendo murmur heard along the left sternal border
• Indicative of severe pulmonary hypertension

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Box 1.35: Summary of Auscultatory Findings in Mitral Stenosis

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GRADES OF MITRAL STENOSIS (Table 1.64)

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STAGES OF MS (Table 1.65)

1. Presence of pulmonary hypertension
2. More closeness of the opening snap to the second heart sound (short A2-OS interval)
3. Lengthy mid-diastolic murmur

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INVESTIGATIONS

Radiological / Chest X-Ray Findings in Mitral Stenosis

Due to Enlargement of Left Atrium:

1. Enlarged left atrial appendage - causes filling up of normal concavity between pulmonary artery shadow and the left ventricle
2. Double atrial shadow - border of enlarged left atrium together with right atrial border gives an appearance like "atrium within an atrium"
3. Straightening of left heart border - Mitralization of heart (due to left atrial appendage enlargement, large pulmonary artery, hypoplastic aorta, and underfilled left ventricle)

Consequences of Left Atrial Enlargement:

• Pushing of left main bronchus upward - causing wide carinal angle (splaying of carina)
• Pushing esophagus backward - visible in lateral view of chest X-ray
• Left shift of aorta - Bedford sign
• Walking man sign - shift of left bronchus forwards (Fig. 1.43B)

Pulmonary Venous/Capillary Hypertension:

• Grade 1: Cephalization - prominence of veins of upper lobe of lung (pulmonary venous pressure ≤20 mm Hg); also called inverted moustache sign/antler's horn sign
• Grade 2: Kerley lines (A, B, C) - pulmonary venous pressure 20-25 mm Hg; also shows peribronchial and perivascular cuffing
  • Kerley A lines: Linear opacities extending from the periphery to hila; caused by distension of anastomotic channels between periphery and central lymphatics
  • Kerley B lines: Short horizontal lines situated perpendicularly to the pleural surface at the lung base; represent edema of interlobar septa
  • Kerley C lines: Reticular opacities at lung base, representing Kerley B line en face
• Grade 3: Banning opacities - pulmonary venous pressure >25 mm Hg

Pulmonary Arterial Hypertension:

• Prominent pulmonary outflow tract
• Enlarged pulmonary arteries (diameter of right descending pulmonary artery >14 mm in women and >16 mm in men)
• Pruning of peripheral pulmonary vessels

Right Ventricle Changes:

• Right ventricular hypertrophy - in presence of cardiomegaly, acute angle is observed between apex of enlarged heart and diaphragm
• Sternal contact sign - earliest and most sensitive sign in the lateral X-ray is obliteration of Holzknecht's space (retrosternal space)

Other X-ray Findings:

• Right atrial enlargement
• Calcification of mitral valve/pericardium/MacCallum patch
• Pulmonary hemosiderosis

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Electrocardiogram (ECG)

• Enlargement of left atrium - "P mitrale" (broad, notched P waves)
• Right ventricular hypertrophy
• Tall R waves in V1-V3
• P mitrale
• Atrial fibrillation

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Echocardiogram

• Thickening of mitral valve area
• Valvular leaflet thickening
• Thickening and shortening of chordae tendineae
• Fusion of commissures
• Calcification of leaflets and chordae
• Diastolic doming (due to commissural fusion)

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WILKINS SCORE (Table 1.66)

1. Leaflet thickness
2. Leaflet mobility
3. Leaflet calcification
4. Chordal (subvalvular) involvement

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Transesophageal Echocardiography (TEE)

• To assess mitral regurgitation (MR) severity
• To rule out left atrial appendage (LAA) thrombus

Doppler

• Provides definite evaluation of MS
• Shows pressure gradient across mitral valve, pulmonary artery pressure, and left ventricular function

Cardiac Catheterization

• Not usually needed
• Used to assess coexisting conditions such as coronary artery disease, pulmonary artery pressure, mitral stenosis, and regurgitation

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COMPLICATIONS OF MITRAL STENOSIS (Table 1.67)

1. Atrial Fibrillation (AF)

• The most common complication of MS
• Prevalence and incidence varies according to age and roughly parallels the age of the patient (e.g., second decade - 10%; sixth decade and beyond - 80%)

1. Decreasing diastolic filling time - leads to increased LA pressure
2. Loss of atrial contribution to LV filling - leads to increased LA pressure
3. LA thrombus leading to systemic embolization

2. Systemic Embolism

• Source of emboli: Left atrial thrombus, vegetations of infective endocarditis (rare)
• Factors predisposing to systemic embolism in MS: Atrial fibrillation, spontaneous echo contrast in left atrium, size of left atrium, age, and low cardiac output
• Clinical features: Depends on the localization of emboli:
  • Cerebral - strokes, abscess
  • Coronary - leads to chest pain
  • Renal - leads to hypertension
  • Leriche syndrome - claudication of thigh (due to embolism at branching of common iliac artery) + impotence
  • Ball valve or free-floating thrombus may produce syncope in specific body position, variability in physical findings, and requires urgent surgery

3. Infective Endocarditis

• May develop infrequently with isolated mitral stenosis

4. Ortner's Syndrome (Cardiovocal Syndrome)

• A very rare complication of severe pulmonary hypertension secondary to mitral stenosis
• Characterized by paralysis of left recurrent laryngeal nerve due to compression between the enlarged tense pulmonary artery and the aorta at ligamentum arteriosum
• Produces hoarseness of voice

5. Dampened MS

• Development of pulmonary hypertension diminishes the cardiac output (throttle effect) and results in temporary symptom-free period (period of illusion)
• The MDM may not be audible; only OS will be present

Other Complications (from Table 1.67):

• Thrombus formation
• Hemoptysis
• Dysphagia
• Lower lobe pneumonia
• Right heart failure
• Pulmonary edema
• Pulmonary infarction
• Cardiac cirrhosis
• Pulmonary hemosiderosis

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MANAGEMENT OF MITRAL STENOSIS

Medical Management

• MS with minor symptoms is treated medically
• Rheumatic fever prophylaxis to be given
• Infective endocarditis prophylaxis is NOT necessary
• Indications for anticoagulation:
  1. Atrial fibrillation (persistent or paroxysmal)
  2. Embolic events
  3. Left atrial thrombus
  4. Left atrial diameter >55 mm
  5. Spontaneous echo contrast
• Restrict/decrease sodium intake
• Diuretics: Early symptom such as mild dyspnea (due to pulmonary congestion) is usually treated with low doses of diuretics
• Beta-blockers or non-dihydropyridine (DHP) calcium channel blockers (e.g., verapamil or diltiazem) to reduce heart rate (even in sinus rhythm, more useful in atrial fibrillation)
• Digoxin if atrial fibrillation with right heart failure; atrial fibrillation also needs anticoagulation to prevent atrial thrombus and systemic embolization

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Surgical Management

1. Trans-septal Balloon Mitral Valvotomy (BMV) / Percutaneous Balloon Valvuloplasty (PBV)

• Treatment of choice
• Also known as Percutaneous Balloon Valvuloplasty (PBV)
• Procedure: Under local anesthesia, a catheter is passed through the femoral vein into the right atrium. The interatrial septum is punctured and the catheter is passed into the left atrium and across the mitral valve. A balloon is passed over the catheter across the valve and briefly inflated to split the valve commissures
• Indications: Pliable mitral valves with little involvement of the subvalvular apparatus and minimal mitral regurgitation
• Contraindications: Moderate or severe mitral regurgitation, severe calcification, severe subvalvular fibrosis, thrombus in left atrium or ventricle, recent embolism, bleeding disorders, and interatrial septal thickness >3 mm (relative contraindication)
• Complications: Mitral regurgitation may be severe enough to need surgery (2%), mortality (1-2%), cardiac perforation (1%), and cerebral embolism (1%)

2. Closed Mitral Valvotomy (CMV)

• Indication: Left atrial thrombus, mitral valvular calcification, severe subvalvular disease, or moderate or severe mitral regurgitation
• Contraindication: Left atrial thrombus, mitral valvular calcification, severe subvalvular disease, or moderate or severe mitral regurgitation
• Advantage: Cardiopulmonary bypass is NOT required and good result is obtained for 10 years or more
• Disadvantage: The valve cusps may refuse necessitating another operation

3. Open Mitral Valvotomy (OMV)

• Usually performed and preferred over closed valvotomy or mitral valve replacement
• Procedure: Under direct view, the valvular cusps are carefully separated from each other and commissures are incised
• Advantage: Less chances of traumatic mitral regurgitation; concurrent annuloplasty can be done for mitral regurgitation; removal of LA thrombus (if present), calcium in leaflets, amputation of LA appendage, and separation of fused chordae can also be done along with this surgical procedure
• Disadvantage: Needs cardiopulmonary bypass

4. Mitral Valve Replacement (MVR)

• Mitral stenosis associated with mitral regurgitation
• Severely damaged or severely calcified stenotic valve which cannot be reopened without producing significant mitral regurgitation
• Moderate or severe mitral stenosis and presence of thrombus in the left atrium even after anticoagulation therapy

• Mechanical prosthesis if age is <65 years
• Bioprosthesis if age is >65 years
• Artificial valves usually work successfully for >20 years
• Anticoagulants are usually given postoperatively to prevent thrombus formation and its embolization

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Management Algorithm for Clinically Significant Mitral Stenosis (MVA <1.5 cm²)

• If NO symptoms: Assess high risk of embolism or hemodynamic decompensation
  • If NO risk: Exercise testing → If symptoms develop: Assess CI or unfavorable characteristics for PMC
  • If high risk: Consider PMC or Surgery
• If YES symptoms: Check contraindication (CI) to PMC
  • If CI to PMC: Surgery
  • If NO CI to PMC: Assess CI or high risk for surgery
    • If NO CI for surgery: Assess favorable anatomical characteristics
      • If favorable anatomy: Assess favorable clinical characteristics → If Yes: PMC; If No: Surgery
      • If not favorable anatomy: Surgery
    • If CI for surgery: PMC

• CI: Contraindication; MS: mitral stenosis; PMC: percutaneous mitral commissurotomy
• Contraindications in the left atrium: new-onset atrial fibrillation
• High risk of hemodynamic decompensation: Systolic pulmonary pressure >50 mm Hg at rest
• Need for major non-cardiac surgery; desire for pregnancy
• High thromboembolic risk: History of systemic embolism, dense spontaneous contrast in the left atrium

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Key Points to Remember for Exam:

• Normal mitral valve area: 4-6 cm²; symptoms begin when MVA <2.5 cm²; severe MS when MVA <1 cm²
• Shortest A2-OS interval = most severe MS
• Opening snap absent = calcified mitral valve
• S1 soft = calcified or congenital MS
• Graham Steell murmur = severe pulmonary hypertension
• Wilkins score ≤8 = suitable for balloon valvuloplasty
• Most common complication = atrial fibrillation
• Most common cause = rheumatic fever
• Ortner's syndrome = hoarseness of voice due to left recurrent laryngeal nerve compression
• Period of illusion (Dampened MS) = pulmonary hypertension throttles left-sided input, symptoms temporarily improve

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MURMURS IN MITRAL STENOSIS - Full Explanation

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First, Understand the Basic Problem

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The Cardiac Cycle - What Happens When

SYSTOLE                    |        DIASTOLE
S1 -----> S2               |  S2 ----> (OS) ----> MDM ----> Presystolic ---> S1
(Mitral closes)  (Aortic closes)       (Mitral opens)  (Mid-diastolic)  (Atrial kick)

• S1 = Mitral valve CLOSES = start of systole
• S2 = Aortic valve CLOSES = start of diastole
• OS = Mitral valve forcefully OPENS = early diastole
• MDM = Blood rushes through narrow valve = mid diastole
• Presystolic accentuation = Atrial contraction pushes more blood = just before S1

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HEART SOUNDS in MS

S1 - LOUD

• In normal hearts, the mitral valve drifts close slowly before snapping shut
• In MS, left atrial pressure is HIGH, so the valve leaflets are held open wide right until systole begins
• Then they snap shut from a wide-open position = loud closing snap
• The wide excursion of the leaflets + high closing force = loud, palpable S1

1. Mitral valve is heavily calcified (rigid leaflets cannot snap)
2. Congenital MS
3. Associated severe mitral/aortic regurgitation

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S2 - LOUD P2 (Pulmonary Component)

• In MS, blood backs up behind the blocked mitral valve
• LA pressure rises → pulmonary vein pressure rises → pulmonary artery pressure rises → pulmonary hypertension
• High pressure in pulmonary artery makes the pulmonary valve close with MORE force
• So P2 becomes loud and you can feel it (palpable P2) at the pulmonary area

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Opening Snap (OS) - Early Diastole

• A sharp, high-pitched clicking sound heard in early diastole, just after S2 (A2)
• It occurs 0.05 to 0.12 seconds after A2

• In MS, the mitral valve leaflets are fused at the commissures (edges)
• When diastole begins, high LA pressure suddenly forces the dome of the valve to bulge downward into the LV
• This sudden abrupt opening/snapping of the dome = Opening Snap
• It is like a parachute suddenly snapping open

• Because it directly tells you the valve is involved but still MOBILE (not yet calcified)
• Absent OS = calcified body of leaflets (valve is too stiff to snap)

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THE MURMURS IN MS

Murmur 1: Mid-Diastolic Murmur (MDM) - THE MAIN MURMUR

• Blood is flowing through a NARROWED valve slowly over a long period
• Slow turbulent flow = low frequency = rumbling quality
• Compare: High-pitched murmurs = fast, high-pressure flows (like aortic regurgitation)

• After the OS, blood starts flowing from LA to LV through the narrow valve
• This creates the rumbling murmur in MID-DIASTOLE

• Patient lying on LEFT LATERAL DECUBITUS position
• Use the BELL of stethoscope (bell picks up low-frequency sounds)
• Hold lightly at the apex
• Best heard during expiration

1. Left lateral position - brings heart closer to chest wall
2. Bell of stethoscope held lightly
3. After exercise/walking - increases heart rate, increases flow across valve = louder murmur
4. Squatting - increases peripheral resistance → increases venous return → more blood crosses valve → louder murmur
5. Holding expiration

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Murmur 2: Presystolic Murmur (PSM)

• At the very END of diastole, just before S1
• This is when the atrium contracts (atrial kick) and pushes extra blood through the narrow valve

1. Atrial contraction - forcefully squeezes blood through the narrow valve
2. Persistent atrioventricular gradient - there is still a pressure difference between LA and LV
3. LV contraction begins in presystole, which reduces the mitral funnel opening even more, creating more turbulence

• The mid-diastolic murmur gets louder at the end (presystolic phase) due to atrial contraction
• In the diagram: MDM starts softly and gets LOUDER just before S1

1. Atrial fibrillation - there is no organized atrial contraction, so no atrial kick, so no presystolic murmur
2. Mild MS - gradient is too low
3. Prolonged PR interval - atrial contraction too early
4. Bradycardia - long diastole, pressure equalizes before presystole
5. Elevated LVEDP (LV dysfunction) - back pressure from LV reduces gradient

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How Severity Affects the Murmur Pattern:

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Murmur 3: Systolic Murmur

• MS → pulmonary hypertension → RV works harder → RV dilates and hypertrophies
• The tricuspid valve annulus stretches due to RV dilatation
• Tricuspid valve becomes incompetent (regurgitant) - NOT because the valve itself is diseased, but because the ring is stretched = FUNCTIONAL
• Blood leaks back from RV → RA during systole = pansystolic murmur at lower left sternal border
• Key feature: Increases on inspiration = de Carvallo's sign (inspiration increases venous return to right side)
• Also produces giant V waves in the jugular venous pulse

• If MS coexists with MR, there is a loud pansystolic murmur radiating to the axilla

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Murmur 4: Graham Steell Murmur

• A high-pitched, early diastolic, decrescendo murmur
• Heard along the left sternal border

• Severe MS → severe pulmonary hypertension
• High pulmonary artery pressure causes the pulmonary valve to leak (regurgitate) during diastole
• High-pressure regurgitation = high-pitched
• Starts immediately after P2 and decreases in intensity = decrescendo pattern

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COMPLETE PICTURE - The Auscultation Sequence in MS

SYSTOLE          |              DIASTOLE                           | SYSTOLE
                 |                                                 |
LOUD S1 -------> LOUD S2 (A2+P2) ----> OS ----> MDM (rumble) ----> PSM ----> LOUD S1
                                 0.05-0.12s      (gets louder      (presystolic
                                 gap             towards end)       accentuation)

• Loud S1 = Flexible leaflets, high LA pressure
• Loud P2 = Pulmonary hypertension
• OS present = Valve is mobile (not calcified)
• Short A2-OS = Severe MS (high LA pressure)
• Long MDM = More severe MS
• PSM absent = Atrial fibrillation OR mild MS
• Graham Steell = Severe pulmonary hypertension
• Pansystolic murmur = Tricuspid regurgitation or coexistent MR

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SIMPLE MEMORY TRICK

"LLOS-MDM-PSA"

• Loud S1
• Loud P2
• Opening Snap
• Mid-Diastolic Murmur
• PreSystolic Accentuation

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