Heart Vulvular diseases and heart sounds..............................BY urs N,D

1. `
 Topics :Diseases of the heart
valves, Heart sounds
Presented by :
Dr Barkam NAGARAJU
MD(General Medicine)

2. Diseases of the heart valves
Valve regurgitation
 Congenital
 Acute rheumatic carditis
 Chronic rheumatic
carditis
 Infective endocarditis
 Syphilitic aortitis
 Valve ring dilatation
Valve stenosis
 Congenital
 rheumatic carditis
 Senile degeneration
Causes of valve disease

3.  Rheumatic Heart Disease
 Acute rheumatic fever
 Chronic rheumatic heart disease

4. Pathogenesis
 Immune-mediated delayed response to infection
with specific strain of group A streptococci that
possess antigen which cross-react with cardiac
myosin & sarcolemmal membrane protein
 Ab against the streptococcal Ag mediate
inflammation in
endocardium,myocardium,pericardium,joint & skin
 Fibrinoid degeneration in the collagen of
connective tissues
 Aschoff nodules –only in the heart

5. Clinical features
 Streptococcal pharyngitis
 Fever,anorexia,lethargy,joint pain
 2-3 wks after initial attack of pharyngitis
 Arthritis
 Rashes
 Carditis
 Neurological changes

6. Jones criteria for the diagnosis of acute
Rheumatic fever
 Major manifestations
Carditis Erythema marginatum
Polyarthritis Subcutaneous nodules
Chorea
 Minor manifestations
Fever Raised ESR or CRP
Arthralgia Leucocytosis
Previous rheumatic fever First degree AV block
Plus
Supporting evidence of streptococcal infection;recent scarlet
fever, raised ASO or other streptococcal antibody titre,
positive throat swab culture

7. Investigations
 Positive blood culture
 Raised antistreptolysin O(ASO)
without evidence of recent streptococcal infection
 Isolated chorea
 pancarditis

8. Carditis
 Pancarditis
 Declines with increasing age
 (90% at 3yrs-30% in adolescent)
 Breathlessness
 Palpitation
 Chest pain
 Tachycardia
 Cardiac enlargement
 New or changed cardiac murmur

9. Carditis
 Soft MDM(Carey coombs murmur)
 AR 90%
 TV & PV rarely involved
 Pericarditis
 Cardiac failure
 ECG –conduction defect,ST-T changes

10. Arthritis
 Early feature
 Acute,painful,asymmetric and migratory joint
inflammation of the large joints
 Red, tender & swollen b/t a day & upto 4 wks
 Characteristically response to aspirin

11. Skin lesions
Erythema marginatum
 <5%
 Red macules which
fade in the centre
 Remain red at the
edges
 Trunk & proximities
but not the face
 May coalesce or
overlap
Subcutaneous nodules
 5-7%
 0.5-2 cm
 Firm & painless
 Extensor surface of
bone or tendon
 3 wks after onset of
other menifestations

12. Sydenham’s chorea(st Vitusdance)
 Late neurological manifestation
 3/12 after episode of ARF
 1/3 of cases
 More common in females
 Emotional lability
 Purposeless choreiform movements of the hands,feet or face
 Explosive & halting speech
 Spontaneous recovery within a few months
 1/4 of pts with Sydenham’s chorea –chronic rheumatic ht
disease

13. Investigations
 Evidence of a systemic illness(non-specific)
Raised WBC,ESR,CRP
 Evidence of preceding streptococcal infection(specific)
Throat swab culture(pt& family contact)
( + ) in 10-25% of cases
ASO titre >200(adults) ,>300(children)
1/5 of cases & most cases of chorea

14. Investigations
 Evidence of carditis
CXR
cardiomegaly,pulmonary congestion
ECG
Features of pericarditis,1st & 2nd Degree ht
block, low QRS voltage
Echo;
Cardiac dilatation,Valve abnormalities,
Pericardial effusion

15. Chronic rheumatic heart disease
 Mitral valve – more than 90 %
 Aortic valve
 Tricuspid valve
 Pulmonary valve
 Isolated mitral stenosis-25%
 Mixed mitral stenosis & regurgitation

16. Pathology
 Progressive fibrosis
 Predominantly involved heart valves
 Involvement of pericardium & myocardium
m/contribute to heart failure & conduction disorder
 Fusion of the mitral valve commissures &
shortening of the cordae tendinae –mitral
stenosis+/- mitral regurgitation
 Similar changes in other valves

17. Mitral valve disease
Mitral stenosis
causes
 Almost always rheumatic in origin
 Heavy calcification in elderly
 Congenital

18. Pathophysiology
 In rheumatic MS
progressive calcification of fusion of cups
fibrosis the valve leaflet & subvalvular
apparatus
Mitralvalve orifice
restricted flow from LA to LV
pulmonary venous congestion
(enlarged LA & LV filling mainly on LA
contraction)

19. Pathophysiology
Increase in heart rate
shortens diastole
Further rise in LA pressure
Demand an increase in cardiac output
Further increase in left atrial pressure

20. Pathophysiology
 MV orifice 5cm2
 1cm2 or less in severe MS
 Remain asymptomatic until MV orifice 2cm2
 At first,symptoms occur only on exercise
 Severe stenosis ; breathlessness at rest
 Reduced lung compliance due to chronic
pulmonary congestion
 Low cardiac output ;fatigue

21. Pathophysiology
Progressive dilatation of the LA
Atrial fibrillation
Tachycardia Loss of atrial contraction
Marked Haemodynamic deterioration
with rapid rise in LA pressure
Pulmonary oedema

22. Pathophysiology
More gradual rise in LA pressure
An increase pulmonary vascular resistance
Pulmonary hypertension
Right ventricular hypertropy & dilation
Tricuspid regurgitation
Rt heart failure

23. Pathophysiology
 In sinus rhythm
 < 20%
 Small LA
 Severe pulmonary hypertension
All pts with MS particularly in those with AF
LA thrombosis
systemic thromboembolism

24. Clinical features
Symptoms
 Breathlessness
 Fatigue
 Oedema
 Ascites
 Palpitation
 Haemoptysis
 Cough
 Chest pain
 Symptoms of
thromboembolic
complications
Signs
 AF
 Mitral facies
 Auscultation;
loud 1st heart sound
opening snap
Mid-diastolic murmur
 Signs of raised pulmonary
capillary pressure
crepitations,pulmonary
oedema,effusions
 Signs of pulmonary
hypertension
RV heave,loud P2

25. Investigations
ECG
 LAH(If not in AF)
 RVH
CXR
 Enlarged LA
 Signs of pulmonary venous
congestion
Echo
 Thickened immobile cusps
 Reduced valve area
 Reduced rate of diastolic
filling of LV
Doppler
 Pressure gradient across
the mitral valve
 Pulmonary arterial
pressure
 LV function
Cardiac catherization
 Assessment of
coexisting coronary
artery disease
&mitral regurgitation

26. Management
Medical treatment
 Pts with minor symptoms
Definitive treatment
 Pts remain symptomatic with medical treatment
 Balloon valvuloplasty
 Mitral valvotomy
 Mitral valve replacement

27. Medical treatment
Atrial fibrillation
 Anticoagulant
 Digoxin
 B blockers
 Rate limiting calcium antagonist
Heart failure
 Diuretics
Prophylaxis of infective endocarditis
 Antibiotics

28. Specific management
Mitral balloon valvuloplasty
 Treatment of choice
Criteria
significant symptoms
isolated MS
no or trivial MR
mobile non-calcified valve/subvalve apparatus on
echo
LA free of thrombus

29. Specific management
Closed or open mitral valvotomy
 No facilities or expertise for balloon valvuloplasty
 s/receive prophylactic antibiotics for IE
 Follow up 1-2 yrly
Mitral valve replacement
substantial mitral reflux
rigid or calcified

30. Mitral regurgitation
Causes
 Rheumatic disease
 Mitral valve prolapse
 After mitral valvotomy or valvuloplasty
 Dilation of LV and mitral valve ring
 Damage to valve cusps and cordae
 Damage to papillary muscle
 Myocardial infarction

31. Pathophysiology
Chronic Mitral regurgitation
Gradual dilation of the LA
with little in pressure gradual  LV diastolic
pressure& LA
pressure
No symptoms Breathlessness &
pulmonary oedema

32. Pathophysiology
Acute mitral regurgitation
Rapid rise in LA pressure
Marked symptomatic deterioration

33. Mitral valve prolapse
 Floppy mitral valve
 Congenital
 Degenerative myxoematous changes
 A features of connective tissue disorders

34. Pathophysiology (MVP)
Mildest form Regurgitation
haemodynamically
significant
Competent valve
during systole Infective
endocarditis
Bulge back to LA
Mid-systolic click click followed by Antibiotics
( no murmur) late systolic murmur

35. Clinical features
Symptoms
 Breathlessness
 Fatigue
 Palpitation
 Oedema
 Ascites
Signs
 AF/flutter/cardiomegaly
 Auscultation;
apical pansystolic
murmur
thrill
soft S1,apical S3
 Signs of raised pulmonary
venous congestion
(crepitations,pulmonary
oedema,effusions)
 Signs of pulmonary
hypertension & RHF
RV heave,loud P2

36. Investigations
ECG
 LAH(If not in AF)
 LVH
CXR
 Enlarged LA
 Enlarged LV
 Signs of pulmonary
venous congestion
 Pulmonary oedema
Echo
 Thickened immobile cusps
 Reduced valve area
 Reduced rate of diastolic
filling of LV
Doppler
 Detects & quantifies
regurgitation
Cardiac catheterization
 Dilated LA,LV,MR
 Pulmonary hypertension
 Assessment of coexisting
coronary artery disease

37. Treatment
Medical treatment
 Moderate severity
Definitive treatment
 Pts remain symptomatic with medical treatment
 Progressive radiological cardiac enlargement or
echo cardiac evidence of deteriorating LV function
 Mitral valve replacement/repair

38. Treatment
Atrial fibrillation
 Anticoagulant
 Digoxin
Heart failure
 Diuretics
 Vasodilators e.g ACEI
Prophylaxis of infective endocarditis
 Antibiotics

39. Treatment
Mitral valve repair
 MVP
 More advantage > MV replacement
 Prevent irreversible LV damage
 Those with CAD-CABG + MV repair by inserting
annuloplasty ring to overcome annular dilation & to
bring the valve leaflets closer together

40. Aortic valve disease
 2nd most frequently affected by rheumatic fever
 Commonly both mitral & aortic valves are affected
 In elderly structurally normal TV; similar process of
arthrosclerosis in arterial wall
 Haemodynamically significant AS develops slowly
 Age 30-60 rheumatic fever
50-60 bicuspid AV
70-90 degenerative AS
Aortic stenosis

41. Aortic stenosis(AS)
Causes
Infants,children,adolscents
 Congenital AS
 Congenital subvalvular AS
 Congenital supravalvular AS
Young adults and middle-aged
 Calcifications and fibrosis congenital bicuspid aortic valve
 Rheumatic AS
Middle-aged to elderly
 Senile degenerative aortic stenosis
 Calcifications of bicuspid aortic valve
 Rheumatic AS

42. Pathophysiology
Steadily increase pressure gradient across the AV
LV increasingly hypertrophied
Inadequate coronary blood flow
Angina

43. Pathophysiology
Fixed outflow obstruction
limit the increase in CO required by exercise
Effort related hypotension
Syncope
LV can no longer overcome outflow obstruction
Pulmonary oedema

44. Clinical features
Symptoms
Mild to moderate-
asymptomatic
 Exertional dyspnoea
 Angina
 Exertional syncope
 Sudden death
 Episodes of acute
pulmonary oedema
Signs
 Slow rising carotid pulse
 Narrow pulse pressure
 Thrusting apex beat(LV
overload)
 Harsh ejection systolic
murmur
 Soft S2
 Signs of pulmonary
venous
congestion(crepitations,pul
monary oedema)

45. Investigations
ECG
 LVH
 LBBB
CXR
 Normal
 Enlarged LV
 Dilated ascending aorta(PA )
 Calcified valve(lateral)
Echo
 calcified valve with restricted
opening
 Hypertrophied LV
Doppler
 Severity of stenosis
 Detection of associated
aortic regurgitation
Cardiac catheterization
 Assessment of coexisting
coronary artery disease
 Pressure gradient b/t LV &
aorta
CT/MRI
 Degree of valve calcification &
stenosis

46. Management
Asymptomatic
 Under review
Symptomatic –prompt surgery
 Moderately severe/ severe stenosis yearly doppler
echo
 Pts remain symptomatic with medical treatment
Elderly –relatively benign prognosis-medical
treatment

47. Management
AV replacement
 Severe stenosis with symptoms
 Asymptomatic - careful exercise test;symptoms on moderate
exertion
Valloon valvuloplasty
 congenital AS
 no long term value in elderly pts with calcified AS
Anticoagulants
 AF
 Coexisting mitral valve disease
 Valve replacement with mechnical prosthesis

48. Aortic stenosis in old patients
 Most common form
 Syncope,angina,heart failure
 Low pulse pressure
 Surgery –successful in those aged 80 without co-morbid condition
higher operative mortality
 Prognosis without surgery is poor if pt has symptoms
 Valve replacement –bioprosthetic valve

49. Aortic regurgitation
Aetiology
 Congenital
 Bicuspid or disproportionate cusps
Acquired
 Rheumatic disease
 Infective endocarditis
 Trauma
 Aortic dilatation(marfan’s
syndrome,aneurysm,dissectionsyphillis,ankylosing
spondylitis

50. Clinical features
Symptoms
Mild- moderate AR
 Often asymptomatic
 Awareness of heart beat
Severe AR
 Breathlessness
 Angina

51. Clinical features
Signs
 Pulse
 Large or collapsing pulse
 Low diastolic pressure& 
pulse pressure ,Bounding
peripheral pulses
 Capillary pulsations in nail
beds
 Femoral bruit(pistol shot)-
duroziez’s sign
 Head nodding with pulse
 De Musset ‘s sign
Murmur
 Early diastolic murmur
 Systolic murmur(stroke
volume)
 Austin flint murmur(soft
mid-diastolic murmur
Other signs
Displaced,heaving apex
beat
pre-systolic impulse
4th heart sound
pulmonary venous
congestion

52. Investigations
ECG
 Initially normal
 Later LVH
 T wave inversion
CXR
 Cardiac dilation
 Features of left heart
failure
Echo
 Dilated LV
 Hyperdynamic LV
 Fluttering anterior mitral
leaflet
Doppler
 detects reflux
Cardiac catheterization
 Dilated LV
 Aortic regurgitation
 Dilated aortic root
 Presence of coexisting
CAD

53. Management
Treat the underlying conditions
 Aortic valve replacement
aortic root replacement & CABG
symptomatic
Chronic AR without symptoms
 s/report if symptoms are developed
 Annually f/up with echocardiogram
AVR
 if evidence of increasing ventricular size
 If systolic dimension ≥55mmLV dilation
Control BP
 Nefidipine/ACEI

54. Tricuspid valve Disease
 Rheumatic in origin
 <5%
 Always association with mitral & aortic valve disease
 Isolated TV stenosis very rare
 TS & TR features of carcinoid syndrome
Tricuspid stenosis

55. Clinical features and investigations
 Symptoms of associated mitral & aortic valve disease
 Symptoms of right heart failure
 Raised JVP with a prominent a wave
 A slow y descent due to loss of normal rapid RV filling
 A mid-diastolic murmur at LLSE or RLSE
 High pitch > murmur of MS
 Increased by inspiration
 Hepatomegaly
 Presystolic pulsation (large a wave)
 Peripheral oedema
 Echo & Doppler ;similar appearance of mitral stenosis

56. Tricuspid regurgitation
Causes
Primary
 Rheumatic heart disease
 Endocarditis
 Ebstein’s congenital anomaly
Secondary
Rv dilatation( chronic LHF
RV infarction
Pulmonary hypertension( corpulmonale)

57. Clinical features
 Non-specific symptoms
 Tiredness
 Venous congestion
 A large systolic phase in JVP
 A cv wave replace normal x descent
 PSM at LSE
 Systolic pulsation of the liver

58. Investigations
Echocardiogram
 Dilation of the RV
 Thickened valve
 Vegetations in endocarditis
 Ebstein’s anomaly TV displaced towards the RV
apex
with consequent enlargement of the RA
associated with TR

59. Management
 Correct RV overload
 Normal pulmonary artery tolerate tricuspid
reflux well
 valve damage dut to IE not always needs valve
replacement
 repair of the valve with annuloplasty to bring the
leaflets together in patients undergoing MVR
 those with rheumatic damage m/require Tricuspid
valve replacement

60. Pulmonary valve Disease
Causes
 Carcinoid syndrome
 Usually congenital
 Isolated or associated with other abnormalities e.g TOF
Pulmonary stenosis

61. Clinical features
 ESM at left upper sternum
 Radiation to left shoulder
 Thrill
 Preceded ejection click
 Wide split S2
 Loud harsh murmur
 inaudible P2
  RV heave
 Prominent a wave in JVP

62. Investigations
ECG
 RVH
CXR
 Post-stenotic dilation in the pulmonary artery
Doppler echo

63. Management
 Mild to moderate isolated pulmonary stenosis
 Not usually progress
 Not required treatment
 Low risk for IE
 Severe Pulmonary stenosis
 ( resting gradient >50mmHg with normal CO)
 Percutaneous pulmonary balloon valvuloplasty
 Not available;surgical valvotomy
 Long term results very good
 Post operative pulmonary regurgitation is common
 Benign

64. Pulmonary regurgitation
 Rarely an isolated phenomenon
 Usually associated with pulmonary artery dilatation due to
pulmonary hypertension
 EDM at LSE in MS( Graham steel murmur)
 Pulmonary hypertension
2 to other disease of left heart
primary pulmonary vascular disease
Eisenmenger’s syndrome
 Trivial PR frequent doppler finding in normal individuals

65. Heart sounds
 Heart sounds are the noises generated by the
beating heart and the resultant flow of blood through it.
Specifically, the sounds reflect the turbulence created
when the heart valves snap shut. In
cardiac auscultation, an examiner may use
a stethoscope to listen for these unique and distinct
sounds that provide important auditory data regarding the
condition of the heart.
 In healthy adults, there are two normal heart sounds often
described as a lub and a dub (or dup), that occur in
sequence with each heartbeat. These are the first heart
sound (S1) and second heart sound (S2), produced by
the closing of the AV valves and semilunar
valves, respectively. In addition to these normal sounds, a
variety of other sounds may be present including heart
murmurs, adventitious sounds, and gallop
rhythms S3 and S4.

67. first heart tone
 S1[
 The first heart tone, or S1, forms the "lub" of "lub-dub" and is
composed of components M1 and T1. Normally M1 precedes
T1 slightly. It is caused by the sudden block of reverse blood flow
due to closure of the
atrioventricular valves, i.e. tricuspid and mitral (bicuspid), at the
beginning of ventricular contraction, or systole. When the
ventricles begin to contract, so do the papillary muscles in each
ventricle. The papillary muscles are attached to the tricuspid and
mitral valves via chordae tendineae, which bring the cusps or
leaflets of the valve closed; the chordae tendineae also prevent
the valves from blowing into the atria as ventricular pressure rises
due to contraction. The closing of the inlet valves prevents
regurgitation of blood from the ventricles back into the atria. The
S1 sound results from reverberation within the blood associated
with the sudden block of flow reversal by the valves.[1] If M1
occurs slightly after T1, then the patient likely has a dysfunction of
conduction of the left side of the heart such as a left bundle
branch block.

68. The second heart tone
 S2
 The second heart tone, or S2, forms the "dub" of "lub-dub" and is
composed of components A2 and P2. Normally A2 precedes P2 especially
during inspiration when a split of S2 can be heard. It is caused by the
sudden block of reversing blood flow due to closure of the semilunar
valves (theaortic valve and pulmonary valve) at the end of ventricular
systole and the beginning of ventricular diastole. As the left
ventricle empties, its pressure falls below the pressure in the aorta. Aortic
blood flow quickly reverses back toward the left ventricle, catching the
pocket-like cusps of the aortic valve, and is stopped by aortic valve
closure. Similarly, as the pressure in the right ventricle falls below the
pressure in the pulmonary artery, the pulmonary valve closes.
The S2 sound results from reverberation within the blood associated with
the sudden block of flow reversal.
 Splitting of S2, also known as physiological split, normally occurs during
inspiration because the decrease in intrathoracic pressure increases the
time needed for pulmonary pressure to exceed that of the right
ventricular pressure. A widely split S2 can be associated with several
different cardiovascular conditions, including right bundle branch
block, pulmonary stenosis, and atrial septal defect

69. Third heart sound S3
 Third heart sound
 Rarely, there may be a third heart sound also called a protodiastolic
gallop, ventricular gallop, or informally the "Kentucky" gallop as
an onomatopoeic reference to the rhythm and stress of S1 followed by S2
and S3 together (S1=Ken; S2=tuck; S3=y).
 "lub-dub-ta" or "slosh-ing-in" If new, indicates heart failure or volume
overload.
 It occurs at the beginning of diastole after S2 and is lower in pitch than S1
or S2 as it is not of valvular origin. The third heart sound is benign in
youth, some trained athletes, and sometimes in pregnancy but if it re-
emerges later in life it may signal cardiac problems, such as a failing left
ventricle as in dilated congestive heart failure (CHF). S3 is thought to be
caused by the oscillation of blood back and forth between the walls of the
ventricles initiated by blood rushing in from the atria. The reason the third
heart sound does not occur until the middle third of diastole is probably
that during the early part of diastole, the ventricles are not filled sufficiently
to create enough tension for reverberation.
 .

70.  It may also be a result of tensing of the chordae
tendineae during rapid filling and expansion of the
ventricle. In other words, an S3 heart sound indicates
increased volume of blood within the ventricle. An S3
heart sound is best heard with the bell-side of the
stethoscope (used for lower frequency sounds). A left-
sided S3 is best heard in the left lateral decubitus
position and at the apex of the heart, which is normally
located in the 5th left intercostal space at the
midclavicular line. A right-sided S3 is best heard at the
lower-left sternal border. The way to distinguish
between a left and right-sided S3 is to observe whether
it increases in intensity with inspiration or expiration. A
right-sided S3 will increase on inspiration, while a left-
sided S3 will increase on expiration

71. Fourth heart sound
 S4
 S4 when audible in an adult is called a presystolic gallop or atrial gallop.
This gallop is produced by the sound of blood being forced into a stiff or
hypertrophic ventricle.
 "ta-lub-dub" or "a-stiff-wall"
 It is a sign of a pathologic state, usually a failing or hypertrophic left
ventricle, as in systemic hypertension, severe valvular aortic
stenosis, and hypertrophic cardiomyopathy. The sound occurs just after
atrial contraction at the end of diastole and immediately before
S1, producing a rhythm sometimes referred to as the "Tennessee" gallop
where S4 represents the "Ten-" syllable. It is best heard at the cardiac apex
with the patient in the left lateral decubitus position and holding his breath.
The combined presence of S3 and S4 is a quadruple gallop, also known as
the "Hello-Goodbye" gallop. At rapid heart rates, S3 and S4 may merge to
produce a summation gallop, sometimes referred to as S7.
 Atrial contraction must be present for production of an S4. It is absent
in atrial fibrillation and in other rhythms in which atrial contraction does not
precede ventricular contraction.

72. `
Thank you