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Dr. Swarnalatha Devi MD
Professor of Medicine
MITRA VALVULAR DISEASE
MITRAL STENOSIS
 Aetiology and pathophysiology
 Mitral stenosis is almost always rheumatic in origin,
although in the elderly it can be caused by heavy
calcification of the mitral valve apparatus.
 There is also a rare from of congenital mitral
stenosis.
AETIOLOGY
 Rheumatic heart disease.
 Congenital—parachute mitral valve.
 Hunter”, hurler” syndrome.
 Drugs---methysergide.
 Carcinoid syndrome.
PATHO PHYSIOLOGY
 In rheumatic mitral stenosis, the mitral valve orifice is
slowly diminished by progressive fibrosis, calcification of
the valve leaflets, and fusion of the cusps and subvalvular
apparatus.
 The flow of blood from left atrium to left ventricle is
restricted and left atrial pressure rises, leading to pulmonary
venous congestion and breathlessness.
 There is dilatation and hypertrophy of the left atrium, and
left ventricular filling becomes more dependent on left atrial
contraction.
PATHOPHYSIOLOGY
 Any increase in heart rate shortens diastole when
the mitral valve has to open it produces further
rise in left atrial pressure;
 Situations that demand an increase in cardiac
output will also increase left atrial pressure.
 Exercise and pregnancy are therefore poorly
tolerated.
 The mitral valve orifice is 4 -5 cm2 in diastole and
may be reduced to 1 cm2 or less in severe mitral
stenosis.
 Patients usually remain asymptomatic until the
stenosis is approximately 2 cm2 or less.
 At first, symptoms may occur only on exercise, in
severe stenosis, left atrial pressure is permanently
elevated so breathlessness occurs even at rest due
to.Chronic pulmonary venous congestion.
 Low cardiac output may cause fatigue.
 Pulmonary hypertension may lead to right ventricular
hypertrophy and dilatation, tricuspid regurgitation and
right heart failure.
 Less than 20% of patients remain in sinus rhythm;
many of these have a small fibrotic left atrium and
severe pulmonary hypertension.
 All patients with mitral stenosis, and particularly those
with atrial fibrillation, are at risk from left atrial
thrombosis and systemic thromboembolism.
.
SYMPTOMS
 Dyspnoea.
 Palpitations.
 Fatigue.
 Hemoptysis.
 Recurrent bronchitis.
CLINICAL EXAMINATION
 MITRAL FACIES.
 SMALL VOLUME PULSE.
 LEFT PARASTERNAL HEAVE.
 TAPPING APICAL IMPULSE (PALPABLE S1)
 Loud S1 ,opening snap,(in pliable valve). This is due
to diastolic buckling of anterior mitral or tricuspid
leaflet due to elevated left or right atrial pressure.
 A low pitched ,rough ,rumbling mid diastolic murmur
with pre systolic accentuation best heard over apex,
with bell of stethoscope in left lateral position,in
expiration.
 ESM over pulmonary area if there is PAH. Pan
systolic murmur in tricuspid area in functional TR.
© Continuing Medical
Implementation
…...bridging the care gap
Mitral Stenosis: Physical Exam
 First heart sound (S1) is accentuated and 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
INVESTIGATIONS
 ECG—”P” MITRALE AND RIGHT
VENTRICULAR HYPERTROPHY.
 ATIAL FIBRILLATION ---ABSENT P WAVES
,VARYING R-R INTERVALS.
 X—RAY CHEST—LEFT ATRIAL
ENLARGEMENT
 STRAIGHTENING OF LEFT BORDER
 KERLY A, B LINES
 R A O WITH BARIUM SWALLOW-
COMPRESSION BY LEFT ATRIUM
© Continuing Medical
Implementation
…...bridging the care gap
A 75 year old woman with loud first heart
sound and mid-diastolic murmer
 ECHO CARDIOGRAM—THICKENED
,IMMOBILE CUSPS, REDUCED RATE OF
DIASTOLIC FILLING. REDUCED VALVE
AREA.
 CARDIAC CATHETERISATION—
PRESSURE GRADIENT BETWEEN LA AND
LV
Mitral Stenosis
SEVERITY
 ACCORDING TO VALVE AREA----
 -4-6 cm2-----------NORMAL
 > 2.5 cm2-----------NO SYMPTOMS
 1.5—2.5 cm2---MILD -DYSPNOEA ON EXERTION
 1-1.5 cm2---MODERATE- PND +P .EDEMA
 <1cm2---SEVERE /CRITICAL -ORTHOPNEA –CLASS 1V
 ACCORDING TO A2—OS INTERVAL
 IN SEVERE MS---- THIS PERIOD IS
SHORTENED.—0.05-0.07 SEC
 MILD MS— 0.10-0.12 SEC
 ACCORDING TO PRESSURE GRADIENT
ACROSS MITRAL VALVE—
 MILD-<5 mm Hg
 MODERATE—5—15 mm Hg
 SEVERE-->15 mm Hg
 DURATION OF DIASTOLIC MURMUR IS
DIRECTLY PROPORTIONAL TO THE
SEVERITY
COMPLICATIONS
 HEMOPTYSIS---
 Due to pulmonary apoplexy.
 Acute LVF—pulmonary edema.
 Pulmonary congestion.
 Recurrent bronchitis.
 Pulmonary infarction.
 ATRIAL FIBRILLATION--
 2/3 will have AF
 Pulse is irregularly irregular
 No a waves in JVP
 Intensity of S1 is variable
 AF precipitates---CCF, thrombo embolic
phenomenon
 Infective endocarditis.
 Pressure symptoms----ortners syndrome----
compression of recurrent laryngeal nerve by left
atrium.
 Left bronchus--bronchiectasis.
DIFFERENTIAL DIAGNOSIS
 Left atrial myxoma.
 Cortriatritum.
 Ball valve thrombus of left atrium.
 Flow murmurs of VSD, ASD, PDA.
 Carey-coombs murmur.
Medical Management
 Anti failure measures.
 Anticoagulation in atrial fibrillation.
 Rheumatic fever prophylaxis.
 Infective endocarditis prophylaxis.
SURGICAL TREATMENT
 Closed mitral valvotomy/commissurotomy—(with
out cardio pulmonary by pass).
 Open mitral valvotomy/commissurotomy (with aid
of cardio pulmonary by pass).
 Per cutaneous balloon valvuloplasty.
 Mitral valve replacement.
 Closed mitral valvotomy—in pliable valve and ,no
mitral regurtitation
 Open mitral valvotomy---in this valve, sub valvular.
C hordae tendinae are loosened,
calcific deposits removed
Thrombi if present are removed.
 Percutaneous balloon valvuloplasty---in pregnant
women, Severe extracardiac disease.
 Criteria-
 -Significant symptoms
 Isolated MS.
 No mitral regurgitation.
 Mobile, non calcified valve.
Normal sub valvular apparatus
No thrombus in left atrium
VALVE REPLACEMENT----
 Associated MITRAL REGURGITATION
 Valve rigid, and calcified.
 Mechanical prosthesis—
 Caged ball valve(starr-edward prosthesis).
 TILTING DISK valves(st jude.Bjork-shiely valves)
THANK YOU

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2 MITRAL VALVE DISEASE.ppt

  • 1. Dr. Swarnalatha Devi MD Professor of Medicine
  • 3. MITRAL STENOSIS  Aetiology and pathophysiology  Mitral stenosis is almost always rheumatic in origin, although in the elderly it can be caused by heavy calcification of the mitral valve apparatus.  There is also a rare from of congenital mitral stenosis.
  • 4. AETIOLOGY  Rheumatic heart disease.  Congenital—parachute mitral valve.  Hunter”, hurler” syndrome.  Drugs---methysergide.  Carcinoid syndrome.
  • 5. PATHO PHYSIOLOGY  In rheumatic mitral stenosis, the mitral valve orifice is slowly diminished by progressive fibrosis, calcification of the valve leaflets, and fusion of the cusps and subvalvular apparatus.  The flow of blood from left atrium to left ventricle is restricted and left atrial pressure rises, leading to pulmonary venous congestion and breathlessness.  There is dilatation and hypertrophy of the left atrium, and left ventricular filling becomes more dependent on left atrial contraction.
  • 6. PATHOPHYSIOLOGY  Any increase in heart rate shortens diastole when the mitral valve has to open it produces further rise in left atrial pressure;  Situations that demand an increase in cardiac output will also increase left atrial pressure.  Exercise and pregnancy are therefore poorly tolerated.
  • 7.  The mitral valve orifice is 4 -5 cm2 in diastole and may be reduced to 1 cm2 or less in severe mitral stenosis.  Patients usually remain asymptomatic until the stenosis is approximately 2 cm2 or less.  At first, symptoms may occur only on exercise, in severe stenosis, left atrial pressure is permanently elevated so breathlessness occurs even at rest due to.Chronic pulmonary venous congestion.  Low cardiac output may cause fatigue.
  • 8.  Pulmonary hypertension may lead to right ventricular hypertrophy and dilatation, tricuspid regurgitation and right heart failure.  Less than 20% of patients remain in sinus rhythm; many of these have a small fibrotic left atrium and severe pulmonary hypertension.  All patients with mitral stenosis, and particularly those with atrial fibrillation, are at risk from left atrial thrombosis and systemic thromboembolism. .
  • 9. SYMPTOMS  Dyspnoea.  Palpitations.  Fatigue.  Hemoptysis.  Recurrent bronchitis.
  • 10. CLINICAL EXAMINATION  MITRAL FACIES.  SMALL VOLUME PULSE.  LEFT PARASTERNAL HEAVE.  TAPPING APICAL IMPULSE (PALPABLE S1)
  • 11.  Loud S1 ,opening snap,(in pliable valve). This is due to diastolic buckling of anterior mitral or tricuspid leaflet due to elevated left or right atrial pressure.  A low pitched ,rough ,rumbling mid diastolic murmur with pre systolic accentuation best heard over apex, with bell of stethoscope in left lateral position,in expiration.  ESM over pulmonary area if there is PAH. Pan systolic murmur in tricuspid area in functional TR.
  • 12. © Continuing Medical Implementation …...bridging the care gap Mitral Stenosis: Physical Exam  First heart sound (S1) is accentuated and 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
  • 13. INVESTIGATIONS  ECG—”P” MITRALE AND RIGHT VENTRICULAR HYPERTROPHY.  ATIAL FIBRILLATION ---ABSENT P WAVES ,VARYING R-R INTERVALS.  X—RAY CHEST—LEFT ATRIAL ENLARGEMENT  STRAIGHTENING OF LEFT BORDER  KERLY A, B LINES  R A O WITH BARIUM SWALLOW- COMPRESSION BY LEFT ATRIUM
  • 14. © Continuing Medical Implementation …...bridging the care gap A 75 year old woman with loud first heart sound and mid-diastolic murmer
  • 15.  ECHO CARDIOGRAM—THICKENED ,IMMOBILE CUSPS, REDUCED RATE OF DIASTOLIC FILLING. REDUCED VALVE AREA.  CARDIAC CATHETERISATION— PRESSURE GRADIENT BETWEEN LA AND LV
  • 16.
  • 18. SEVERITY  ACCORDING TO VALVE AREA----  -4-6 cm2-----------NORMAL  > 2.5 cm2-----------NO SYMPTOMS  1.5—2.5 cm2---MILD -DYSPNOEA ON EXERTION  1-1.5 cm2---MODERATE- PND +P .EDEMA  <1cm2---SEVERE /CRITICAL -ORTHOPNEA –CLASS 1V
  • 19.  ACCORDING TO A2—OS INTERVAL  IN SEVERE MS---- THIS PERIOD IS SHORTENED.—0.05-0.07 SEC  MILD MS— 0.10-0.12 SEC  ACCORDING TO PRESSURE GRADIENT ACROSS MITRAL VALVE—  MILD-<5 mm Hg  MODERATE—5—15 mm Hg  SEVERE-->15 mm Hg  DURATION OF DIASTOLIC MURMUR IS DIRECTLY PROPORTIONAL TO THE SEVERITY
  • 20. COMPLICATIONS  HEMOPTYSIS---  Due to pulmonary apoplexy.  Acute LVF—pulmonary edema.  Pulmonary congestion.  Recurrent bronchitis.  Pulmonary infarction.
  • 21.  ATRIAL FIBRILLATION--  2/3 will have AF  Pulse is irregularly irregular  No a waves in JVP  Intensity of S1 is variable  AF precipitates---CCF, thrombo embolic phenomenon
  • 22.  Infective endocarditis.  Pressure symptoms----ortners syndrome---- compression of recurrent laryngeal nerve by left atrium.  Left bronchus--bronchiectasis.
  • 23. DIFFERENTIAL DIAGNOSIS  Left atrial myxoma.  Cortriatritum.  Ball valve thrombus of left atrium.  Flow murmurs of VSD, ASD, PDA.  Carey-coombs murmur.
  • 24. Medical Management  Anti failure measures.  Anticoagulation in atrial fibrillation.  Rheumatic fever prophylaxis.  Infective endocarditis prophylaxis.
  • 25. SURGICAL TREATMENT  Closed mitral valvotomy/commissurotomy—(with out cardio pulmonary by pass).  Open mitral valvotomy/commissurotomy (with aid of cardio pulmonary by pass).  Per cutaneous balloon valvuloplasty.  Mitral valve replacement.
  • 26.  Closed mitral valvotomy—in pliable valve and ,no mitral regurtitation  Open mitral valvotomy---in this valve, sub valvular. C hordae tendinae are loosened, calcific deposits removed Thrombi if present are removed.
  • 27.  Percutaneous balloon valvuloplasty---in pregnant women, Severe extracardiac disease.  Criteria-  -Significant symptoms  Isolated MS.  No mitral regurgitation.  Mobile, non calcified valve. Normal sub valvular apparatus No thrombus in left atrium
  • 28. VALVE REPLACEMENT----  Associated MITRAL REGURGITATION  Valve rigid, and calcified.  Mechanical prosthesis—  Caged ball valve(starr-edward prosthesis).  TILTING DISK valves(st jude.Bjork-shiely valves)