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Rheumatic heart disease (RHD)

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Rheumatic heart disease (RHD) By : Dr. Sanjeev Rheumatic heart disease The sequelae of rheumatic fever consist of mitral, aortic and tricuspid valve disease The ... – PowerPoint PPT presentation

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Title: Rheumatic heart disease (RHD)


1
Rheumatic heart disease (RHD)
  • By Dr. Sanjeev

2
Rheumatic heart disease
  • The sequelae of rheumatic fever consist of
    mitral, aortic and tricuspid valve disease
  • The mitral valve involvement manifests
    predominantly as mitral regurgitation and less
    common as mitral stenosis
  • The aortic and tricuspid valve involvement
    presents exclusively as aortic and tricuspid
    regurgitation
  • Rheumatic aortic stenosis has never been
    described below the age of 15 years.

3
Terms
  • Regurgitation results from failure of a valve
    to close completely, thereby allowing reversed
    flow
  • Stenosis failure of a valve to open completely,
    thereby impeding forward flow
  • Pure only stenosis or regurgitation is present
  • Mixed both stenosis and regurgitation coexist
    in the same valve, but one of these defects
    usually predominates

4
Heart sounds
  • First heart sound when AV valve closed (mitral
    and tricuspid)
  • Second heart sound pulmonary and aortic valve
    closed
  • Third heart sound increase volume of blood
    within the ventricle
  • Fourth heart sound just after atrial
    contraction at the end of diastole and
    immediately before S1.

5
Mitral regurgitation
  • Is the commonest manifestation of acute as well
    as previous rheumatic carditis

6
Hemodynamics
  • When mitral regurgitation is present -----? blood
    leaks backwards through the mitral valve and into
    the left atrium when the heart contracts
    (systolic phase) ---? regurgitant volume of blood
    reaches the left atrium during ventricular
    systole, however, during diastole it can pass
    freely across the mitral valve ----? thus, mean
    atrial pressure normal or is only slightly
    increased (because left atrial pressure increases
    during systole, it drops during diastole) ----?
    there is thus no increase in pulmonary venous
    pressure and no pulmonary congestion --------?

7
Cont
  • ----? the increased volume of blood handled by
    the left atrium and left ventricle results in an
    increase in the size of both these chambers --?
    Mitral regurgitation provides two exits for the
    left ventricular blood flow --? the forward flow
    through the aortic valve into the systemic
    circulation and the backward leak into the left
    atrium --? the forward output becomes
    insufficient during exertion --? this decrease in
    the systemic output results in fatigue, the
    commonest symptom of significant MR --? absence
    of pulmonary congestion prevents occurrence of
    dyspnea unless the MR is severe or the left
    ventricular myocardium is failing ----?

8
Cont
  • With failing left ventricle, the left ventricular
    diastolic pressure increases, the left atrial and
    pulmonary venous pressure increases and pulmonary
    congestion appears --? there is an increase in
    pulmonary arterial pressure and features of
    pulmonary arterial hypertension appear.
  • Presence of features of pulmonary arterial
    hypertension in a patient having pure MR suggests
  • 1. severe MR or
  • 2. failing left ventricular myocardium, or
  • 3. acute MR

9
Cont
  • MR developing during acute RF is of sudden onset.
    In addition there is active myocarditis resulting
    in poorly functioning left ventricular
    myocardium. Thus the left ventricular failure can
    occur even with relatively moderate leaks during
    the acute illness.
  • The size of the left atrium also plays
    significant role in MR
  • With acute MR the left atrial size is normal and
    the increased volume reaching the left atrium
    increases the left atrial and the pulmonary
    venous pressure, resulting in pulmonary
    congestion and feature of left ventricular failure

10
Cont.
  • In long standing MR the left atrium increases in
    size to accommodate the regurgitant volume
    without increasing the left atrial pressure and
    features of LVF are absent.
  • Another adjustment consists of decrease in the
    systemic vascular resistance to help increase the
    forward flow.
  • R P/Q
  • where R is the vascular resistance (fluid
    resistance), P is the pressure difference, and Q
    is the rate of blood flow through it.

11
Cont
  • The maximum ejection of blood into the aorta
    takes place during early systole. The combination
    of these two factors results in an increased
    systolic and decreased diastolic pressure in the
    systemic circuit . The pulse pressure is,
    therefore, increased resulting in the small water
    hammer pulse of MR

12
Aetiology
  • Dilatation of valve ring (Acute rheumatic fever,
    Cardiomyopathy)
  • Damage to the valve cusp and chordae (Rheumatic
    heart disease, Infective Endocarditis)
  • Damage to the papillary muscle (myocardial
    ischaemia , infarction)
  • Mitral valve prolapse (congenital, degenerative,
    connective tissue disease such as Marfans
    syndrome).
  •  
  • Trauma Chest trauma can rarely cause breakage
    of the chords that hold the mitral leaflets in
    their normal position. Untethered leaflets swing
    widely, allowing valve leakage.

13
Clinical features
  • 1. Fatigue when cardiac output starts to fall
  • 2. Dysponea when pulmonary venous hypertension
    occurs, dysponea on exertion, orthopnea and
    paroxysmal nocturnal dysponea (PND) may ocuur
  • 3. Pulse rate increased to maintain an adequate
    cardiac output
  • 4. Features of left ventricular failure are
    absent and appear late unless the mitral
    regurgitation is acute, severe or left
    ventricular myocardium is failing

14
Cont..
  • 5. Heart size is dependent on the severity of MR
    as well as the status of the left ventricular
    myocardium.
  • 6. Apex beat is shifted down and out, farther
    than the normal position, due to ventricular
    dilatation
  • 7. Systolic thrill (lt10 ) due to the direction
    of the regurgitant stream which is backwards into
    the left atrium
  • 8. Systolic murmur is heard over the cardiac apex
    (mitral area) with following characteristic -
  • 1. Pansystolic murmur extending from s1 to s2
  • 2.High frequency murmur (diaphragm)
  • 3. murmur radiates towards the left axilla and to
    the back below the scapula

15
Cont
  • 9. First heart sound may be normal or diminished
    in intensity
  • 10. Severe MR, when a large amount of blood flows
    downs suddenly from the left atrium to the left
    ventricle during diastole, a third sound (s3) or
    ventricular gallop is produced. Immediately after
    such a third sound, a short mid diastolic murmur
    may also be heard.

16
Investigations
  • Chest X-Ray
  • ECG
  • Echocardiography
  • Doppler
  • Cardiac catheterization

17
Chest X-Ray
  • Backflow of blood due to incompetent mitral valve
  • Heart is enlarged transversely
  • The pulmonary vascular markings are typically
    normal, since pulmonary venous pressures are
    usually not significantly elevated.
  • Pulmonary vascular markings prominent (marked
    pul. HTN)

18
Cont
  • ECG Atrial fibrillation, left atrial enlargement
    (if patient is in sinus rhythm). left ventricular
    hypertrophy can be seen
  • Echocardiography Images mitral valve, left
    ventricular function and left atrial size. LA and
    LV will be dilated.
  • Doppler will quantify regurgitation
  • Cardiac catheterization can be done for pressure
    measurements

19
Differential diagnosis -
  • Atrial septal defect
  • Coarctation of aorta with MR (congenital)
  • Left ventricular fibroelastosis
  • Myocarditis

20
Management -
  • Medical Management
  • Low sodium diet
  • Diuretics (patient with orthopnoea and PND)
  • Vasodilator Sodium Nitroprusside or
    Nitroglycerine may be used in acute and/or severe
    MR.
  • ACE inhibitors are used for treatment of chronic
    MR (decreased the after load).

21
Cont
  • Digoxin is used for patients with atrial
    fibrillation or associated left ventricular
    failure.
  • Anticoagulant for patients with atrial
    fibrillation, for prevention of thromboembolism
    and who already developed features of systemic
    embolization to prevent further embolization.
  • Infective Endocarditis prophylaxis.
  • Prophylaxis for Rheumatic fever if MR is of
    rheumatic origin.

22
Cont
  • Surgical Management
  • Symptomatic patients despite optimal medical
    therapy
  • Asymptomatic or mildly symptomatic patient in
    presence of progressive LV dysfunction.
  • Mitral valve repair (Annuloplasty with valve
    Reconstruction) can be done if valvular cusps and
    basic architecture is preserved.
  • Otherwise markedly deformed, with shrunken,
    calcified leaflets requires mitral valve
    replacement with a prosthesis.

23
Complications
  • Atrial fibrillation (in case of severe MR and
    chronic long standing MR)
  • Systemic embolization
  • Infective endocarditis
  • Congestive heart failure
  • Pulmonary hypertension

24
Mitral stenosis
  • Normal size 5 sq. cm
  • Cardiac symptoms due to mitral stenosis start to
    be appear only when the valve is reduced to 2
    sq.cm
  • Severe stenosis lt 1 cm2
  • Aetiology
  • Acute RF with rheumatic endocarditis (99)
  • Some due to calcification of senile mitral valve
    apparatus
  • Congenital (very rare)

25
Pathophysiology -
  • Blood cannot flow freely from the left atrium to
    the left ventricle during diastole --? left
    atrial pressure as well as volume increases ---?
    increase in pressure and volume occurs in the
    pulmonary veins and capillaries ---? when the
    pulmonary venous pressure exceeds the plasma
    oncotic pressure, fluid from the vessels flow out
    into the interstitial space and alveoli of the
    lungs ---? leads to pulmonary arterial
    hypertension ---? right ventricle has to work
    more during systole to push the blood into the
    pulmonary artery ---? leads to right ventricular
    hypertrophy and later on to right ventricular
    dilatation --? if pulmonary HTN becomes severe,
    the amount of blood going to the left atrium from
    the right ventricle and pulmonary congestion
    tends to become less.

26
Clinical features -
  • Symptoms
  • 1. Dyspnoea (commonest symptom) due to
    pulmonary venous congestion.
  • Mild stenosis -?dyspnoea occurs on exertion or
    when the heart rate increases due to any reason.
  • Severe stenosis -?dyspnoea at rest
  • May develop orthopnoea and PND
  • 2. Cold extremities, with or without peripheral
    cyanosis and a smaller volume pulse --? decreased
    cadiac output in severe MS (recognized on the bed
    side)

27
Cont..
  • 3. Fatigue (due to low cardiac output)
  • 4. Palpitation (Atrial fibrillation, Sinus
    tachycardia)
  • 5. Haemoptysis (Pulmonary congestion, Pulmonary
    embolism)
  • 6. Cough, chest pain
  • 7. Symptoms of Thromboembolism
  • 8. Oedema, ascites (right heart failure)

28
Signs
  • Irregularly irregular pulse (atrial fibrillation)
  • Mitral facies (bluish pink hue over the malar
    prominences)
  • Auscultation Loud S1 , opening snap, mid
    diastolic murmur
  • Signs of raised pulmonary capillary pressure
    Basal crepitation, pulmonary oedema, and pleural
    effusion
  • Signs of pulmonary hypertension RV heave, loud
    P2
  • Signs of right heart failure E.g. Raised JVP,
    Hepatomegaly
  • Signs of systemic Thromboembolism E.g. Stroke,
    Acute limb ischaemia

29
Mitral Facies
30
Investigations
  •  ECG Atrial fibrillation,Left Atrial
    abnormality, Right ventricular enlargement
  • Echocardiogram Structural imaging of mitral
    valve, valve area, left atrial dimension,
    presence of thrombus in LA, pulmonary arterial
    pressure, RV dilatation.

31
  • Chest X-Ray
  • Straightening of the left border with fullness
    outwards bulging of the pulmonary conus
  • There is double border on the right side
  • Pulmonary vasculature increases
  • Normally, Heart is normal in transverse diameter
  • Cardiomegaly (rt. Ventricular enlargement)
  • Kerley B line

31
Dr S Chakradhar
32
Management
  • 1 . Medical management
  • Penicillin prophylaxis for rheumatic fever.
  • Prophylaxis for infective endocarditis.
  • Low sodium intake, diuretics.
  • If patient is in Atrial fibrillation ---- use
    digoxin ? low dose B-blocker.
  • Anticoagulation for at least 1 year for patients
    who suffered Thromboembolism and permanently to
    those with AF.

33
2. Surgical management
  • a. Mitral valvotomy
  • Symptomatic patients whose valve area is less
    than 1.0 cm2/m2 body surface area.
  • Two methods
  • 1. Percutaneous ballon mitral valvotomy and
  • 2. Surgical valvotomy Indicated in Re-stenosis
    , unsuccessful balloon valvotomy,.
  • Restenosis is frequent. This procedure cannot be
    done if there is significant regurgitation,
    calcification of the mitral valve or thrombus in
    left atrium.

34
b. Mitral valve replacement
  • This is procedure of choice in
  • Critical mitral stenosis i.e. lt 0.6 cm2/m2 body
    surface area
  • Significant mitral regurgitation
  • Calcified mitral valve leaflets

35
Complications
  • Atrial fibrillation
  • Systemic emboli
  • Pulmonary hypertension and
  • Heart failure

36
AORTIC STENOSIS
  • Aortic valve area 3 square cm

37
Aetiology
  • Infants ,children, adolescents
  • Congenital
  • Valvular aortic stenosis
  • Subvalvular aortic stenosis
  • Supravalvular aortic stenosis

38
Cont
  • Young adults to middle aged
  • Calcification and fibrosis of bicuspid aortic
    valve
  • Acute rheumatic fever with endocarditis

39
Pathophysiology -
  • When it gets narrowed, left ventricle has to pump
    harder to send blood across the narrowed aortic
    valve into the aorta -? increased work load
    -?left ventricular hypertrophy -? hypertrophied
    ventricle manages to maintain the cardiac output
    inspite of stenosis -? during atrial systole,
    plenty of blood comes to the left ventricle
    (atrial kick) -? left ventricle becomes more
    stretched due to such atrial kicks and as per
    Frank Starlings law, it now contracts more
    vigorously and thus more blood goes out of the
    ventricle into the aorta -? gradually , the
    oxygen demand of the left ventricle increases -?
    cause angina and sudden death -? if left
    ventricle is overworked for prolonged period -?
    LVF -? aorta blood will be less -?left
    ventricular end diastolic pressure and diastolic
    volume start to rise -?left arterial and
    pulmonary venous pressure increases and the
    patient starts to feel dyspnoeic ( pulmonary
    congestion and hypertension)

40
Clinical features -
  • Mild or moderate ----- Asymptomatic
  • Cardinal symptoms like (1, 2, and 3)
  • Exertional dyspnoea (signs of LVF)- initially
    exertional dyspnoea later PND.
  • Angina
  • Syncope due to inadequate blood flow through
    the stenosed aortic valve and arrhythmia.
  • Fatigue and palpitation
  • Apex beat heaving or forceful and sustained
    type (finger lifted up during systole, remains up
    for sometime and then falls down

41
Cont
  • 6. Auscultation three main signs
  • Aortic ejection sound or click heard over the
    cardiac apex by the diaphragm, in early systole,
    immediately after the first sound.
  • Aortic ejection murmur mid systolic murmur,
    heard over the right 2nd intercostal space by the
    side of the sternum, radiates to the neck towards
    both the carotids, and also called diamond shaped
    ejection systolic murmur.
  • Aortic component of the second sound is either
    late or soft

42
Cont
  • 7. Fourth heart sound due to increased
    stiffness of the left ventricle, the atrium
    contracts vigorously during atrial systole and
    pushes the a large amount of blood into the left
    ventricle, due to such strong atrial kick, S4
    becomes audible. It is a soft and low pitched
    sound and is heard just before S1. best heard
    over the cardiac apex by using the bell of the
    stethoscope.

43
Investigations -
  • ECG may show LV hypertrophy and ST depression
    and T wave inversion left bundle branch block is
    common
  • Chest X-Ray may show LV enlargement in PA view
    and calcification of aortic valve in lateral
    view.
  • Echocardiography will show abnormal aortic
    valve with left ventricular hypertrophy or
    dilatation.
  • Doppler echocardiography will estimate the
    pressure gradient

44
enlargement of the ascending aorta(white arrow).
left ventricle is enlarged (red arrow) and the
heart is mildly enlarged overall. The lateral
view on the right demonstrates calcifications in
the region of the aortic valve leaflets (circle).
generally, the aortic valve lies above a line
drawn from the carina to the junction of the
diaphragm with the anterior chest wall. The
mitral valve lies below the line.
45
Management
  • Strenuous physical activity should be avoided
  • Sodium restriction, digitalis and diuretics are
    used if there is heart failure.
  • Vasodilators should be avoided or used with
    extreme caution.
  • Asymptomatic stenosis in elderly conservative
    management is appropriate

46
Valve replacement in
  • Patients with calcified AS with critical
    obstruction (valve area lt0.5 cm2/m2 BSA).
  • Patients with symptomatic aortic stenosis
    (moderate to severe stenosis) even with normal
    cardiac output at rest.
  • Patients who exhibit LV dysfunction even they are
    asymptomatic.

47
Cont
  • Penicillin prophylaxis for rheumatic fever.
  • Prophylaxis for infective endocarditis.

48
Complications
  • Endocarditis
  • Cardiac arrhythmias atrial fibrillation,
    ventricular arrhythmias, complete heart block
  • Left ventricular failure

49
Differential diagnosis
  • Hypertrophic cardiomyopathy
  • Innocent systolic murmur eg. In anemia,
    thyrotoxicosis
  • Hypertension

50
AORTIC REGURGITATION
51
Definition
  • When the aortic valve is damaged and cannot close
    completely during diastole, blood from the aorta
    regurgitates into the left ventricle, such a
    state is called AR.
  • Clinically pure aortic regurgitation without
    associated mitral valve disease is rare and
    occurs in 5 8 patients

52
Pathophysiology
  • Blood regurgitates from the aorta into the left
    ventricle during diastole -?amount of blood
    regurgitating into the left ventricle depends
    upon
  • 1. size of the regurgitant hole in the aortic
    valve
  • 2. pressure gradiant between the aorta and the
    left ventricle during diastole
  • 3. duration of the diastole

53
Cont
  • When blood regurgitates from the aorta into the
    left ventricle during diastole it starts to
    dilate -? hypertrophy of left ventricle -? with
    progessive increase in the amount of regurgitant
    blood, the left ventriclar muscle fibre gets
    stretched further and as per Frank starlings
    law, these fibres contract more vigorously,
    thereby increasing the stroke volume -? but when
    the left ventricle is dilated too much and for a
    long period, its capacity to contract starts to
    decreased -? stroke volume also decreases and the
    volume overload in the left ventricle increases
    further during diastole -? peripheral
    vasodilation -? hands and feet are warm and
    diastolic pressure is very low (not clear why
    there is peripheral vasodilation) -?

54
Cont
  • later, when ventricular failure occurs, neuro
    hormonal activation leading to an increase in
    sympathetic vasoconstriction tone and increased
    intrinsic vascular stiffness and fall in cardiac
    output ----? when AR develops suddenly --? the
    left ventricular myocardium is failing and the
    left ventricular end diastolic pressure goes up
    -? increase in left atrial pressure and pulmonary
    congestion.

55
Clinical features -
  • 1. Palpitation (main symptom) due to increased
    force of contraction of the left ventricle
  • 2. Dyspnoea, orthopnoea and PND
  • 3. Sweating a lot when congestive failure
    develops
  • 4. Anigna pectoris due to
  • 1. low aortic diastolic pressure, due to which
    coronary blood flow is reduced
  • 2. increase in oxygen demand of the left
    ventricle as a result of left ventricular
    dilatation and hypertrophy

56
Cont.
  • 5. Peripheral physical signs of aortic
    insufficiency are related to the high pulse
    pressure and the rapid decrease in blood pressure
    during diastole due to blood returning to the
    heart from the aorta through the incompetent
    aortic valve -
  • 1. large-volume, 'collapsing' pulse also known
    as
  • Watson's water hammer pulse or
    Corrigan's pulse (rapid upstroke and collapse of
    the carotid artery pulse)
  • 2. De Musset's sign (head nodding in time with
    the heart beat)
  • 3. Quincke's sign (pulsation of the capillary bed
    in the nail)
  • 4. Hill's sign (a 20 mmHg difference in
    popliteal and brachial systolic cuff pressures)

57
Cont.
  • 5. Müller's sign (pulsations of uvula)
  • 6. Traube's sign - two sound heard over femoral
    arteries
  • 7. Duroziez sign - Systolic-diastolic murmur
    produced by compression of femoral artery with a
    stethoscope
  • 8. Pistol shot - Loud systolic sound over femoral
    arteries
  • 9. Gerhardt's sign (enlarged spleen and pulsation
    felt over the spleen)
  • 10. Rosenbach's sign (pulsatile liver)
  • 11. Landolfi's sign (alternating constriction
    dilatation of pupil)

58
Cont..
  • 6. cardiomegaly (inspection and palpation) apex
    beat shifted further down and out and is forceful
    and ill sustained (or hyperdynamic) in character.
  • Auscultation
  • 1. First and second heart sound both are normal
  • 2. Third heart sound or ventricle gallop (severe
    AR) due to large amount of blood suddenly coming
    to the left ventricle from the mitral and aortic
    valves during early diastole. Important sign in
    AR is early diastolic murmur high frequency
    murmur, an early diastolic murmur, decrescendo
    murmur and best heard over the left side of the
    mid sternum over the second aortic area

59
Cont
  • Many patients of AR have a mid diastolic rumbling
    murmur at the apex, as in MS, such murmur is
    called Austin Flint murmur --? when the blood
    regurgitates from the aorta into the left
    ventricle in AR, the regurgitant flow strikes the
    anterior leaflet of the mitral valve and gives
    rise to the Austin Flint murmur .

60
Investigations
  • ECG may show LV hypertrophy and ST depression
    and T wave inversion
  • Chest X-ray may show cardiac and aortic
    dilatation. There may be features of left heart
    failure.
  • Echocardiogram dilated LV with vigorous
    contraction. Vegetation may be visible if cause
    is infective endocarditis. There may be
    fluttering of AML (Anterior mitral leaflet)

61
Management
  • Remove the treatable cause like infective
    endocarditis, Rheumatic fever
  • Medical therapy low sodium diet, diuretics, and
    ACE inhibitors.
  • Surgery is advised if there is progressive LV
    dysfunction even when patient is asymptomatic or
    with mild symptoms.
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