`
 Topics :Diseases of the heart
valves, Heart sounds
Presented by :
Dr Barkam NAGARAJU
MD(General Medicine)
Diseases of the heart valves
Valve regurgitation
 Congenital
 Acute rheumatic carditis
 Chronic rheumatic
carditis
 In...
 Rheumatic Heart Disease
 Acute rheumatic fever
 Chronic rheumatic heart disease
Pathogenesis
 Immune-mediated delayed response to infection
with specific strain of group A streptococci that
possess ant...
Clinical features
 Streptococcal pharyngitis
 Fever,anorexia,lethargy,joint pain
 2-3 wks after initial attack of phary...
Jones criteria for the diagnosis of acute
Rheumatic fever
 Major manifestations
Carditis Erythema marginatum
Polyarthriti...
Investigations
 Positive blood culture
 Raised antistreptolysin O(ASO)
without evidence of recent streptococcal infectio...
Carditis
 Pancarditis
 Declines with increasing age
 (90% at 3yrs-30% in adolescent)
 Breathlessness
 Palpitation
 C...
Carditis
 Soft MDM(Carey coombs murmur)
 AR 90%
 TV & PV rarely involved
 Pericarditis
 Cardiac failure
 ECG –conduc...
Arthritis
 Early feature
 Acute,painful,asymmetric and migratory joint
inflammation of the large joints
 Red, tender & ...
Skin lesions
Erythema marginatum
 <5%
 Red macules which
fade in the centre
 Remain red at the
edges
 Trunk & proximit...
Sydenham’s chorea(st Vitusdance)
 Late neurological manifestation
 3/12 after episode of ARF
 1/3 of cases
 More commo...
Investigations
 Evidence of a systemic illness(non-specific)
Raised WBC,ESR,CRP
 Evidence of preceding streptococcal inf...
Investigations
 Evidence of carditis
CXR
cardiomegaly,pulmonary congestion
ECG
Features of pericarditis,1st & 2nd Degree ...
Chronic rheumatic heart disease
 Mitral valve – more than 90 %
 Aortic valve
 Tricuspid valve
 Pulmonary valve
 Isola...
Pathology
 Progressive fibrosis
 Predominantly involved heart valves
 Involvement of pericardium & myocardium
m/contrib...
Mitral valve disease
Mitral stenosis
causes
 Almost always rheumatic in origin
 Heavy calcification in elderly
 Congeni...
Pathophysiology
 In rheumatic MS
progressive calcification of fusion of cups
fibrosis the valve leaflet & subvalvular
app...
Pathophysiology
Increase in heart rate
shortens diastole
Further rise in LA pressure
Demand an increase in cardiac output
...
Pathophysiology
 MV orifice 5cm2
 1cm2 or less in severe MS
 Remain asymptomatic until MV orifice 2cm2
 At first,sympt...
Pathophysiology
Progressive dilatation of the LA
Atrial fibrillation
Tachycardia Loss of atrial contraction
Marked Haemody...
Pathophysiology
More gradual rise in LA pressure
An increase pulmonary vascular resistance
Pulmonary hypertension
Right ve...
Pathophysiology
 In sinus rhythm
 < 20%
 Small LA
 Severe pulmonary hypertension
All pts with MS particularly in those...
Clinical features
Symptoms
 Breathlessness
 Fatigue
 Oedema
 Ascites
 Palpitation
 Haemoptysis
 Cough
 Chest pain
...
Investigations
ECG
 LAH(If not in AF)
 RVH
CXR
 Enlarged LA
 Signs of pulmonary venous
congestion
Echo
 Thickened imm...
Management
Medical treatment
 Pts with minor symptoms
Definitive treatment
 Pts remain symptomatic with medical treatmen...
Medical treatment
Atrial fibrillation
 Anticoagulant
 Digoxin
 B blockers
 Rate limiting calcium antagonist
Heart fail...
Specific management
Mitral balloon valvuloplasty
 Treatment of choice
Criteria
significant symptoms
isolated MS
no or tri...
Specific management
Closed or open mitral valvotomy
 No facilities or expertise for balloon valvuloplasty
 s/receive pro...
Mitral regurgitation
Causes
 Rheumatic disease
 Mitral valve prolapse
 After mitral valvotomy or valvuloplasty
 Dilati...
Pathophysiology
Chronic Mitral regurgitation
Gradual dilation of the LA
with little in pressure gradual  LV diastolic
pr...
Pathophysiology
Acute mitral regurgitation
Rapid rise in LA pressure
Marked symptomatic deterioration
Mitral valve prolapse
 Floppy mitral valve
 Congenital
 Degenerative myxoematous changes
 A features of connective tis...
Pathophysiology (MVP)
Mildest form Regurgitation
haemodynamically
significant
Competent valve
during systole Infective
end...
Clinical features
Symptoms
 Breathlessness
 Fatigue
 Palpitation
 Oedema
 Ascites
Signs
 AF/flutter/cardiomegaly
 A...
Investigations
ECG
 LAH(If not in AF)
 LVH
CXR
 Enlarged LA
 Enlarged LV
 Signs of pulmonary
venous congestion
 Pulm...
Treatment
Medical treatment
 Moderate severity
Definitive treatment
 Pts remain symptomatic with medical treatment
 Pro...
Treatment
Atrial fibrillation
 Anticoagulant
 Digoxin
Heart failure
 Diuretics
 Vasodilators e.g ACEI
Prophylaxis of i...
Treatment
Mitral valve repair
 MVP
 More advantage > MV replacement
 Prevent irreversible LV damage
 Those with CAD-CA...
Aortic valve disease
 2nd most frequently affected by rheumatic fever
 Commonly both mitral & aortic valves are affected...
Aortic stenosis(AS)
Causes
Infants,children,adolscents
 Congenital AS
 Congenital subvalvular AS
 Congenital supravalvu...
Pathophysiology
Steadily increase pressure gradient across the AV
LV increasingly hypertrophied
Inadequate coronary blood ...
Pathophysiology
Fixed outflow obstruction
limit the increase in CO required by exercise
Effort related hypotension
Syncope...
Clinical features
Symptoms
Mild to moderate-
asymptomatic
 Exertional dyspnoea
 Angina
 Exertional syncope
 Sudden dea...
Investigations
ECG
 LVH
 LBBB
CXR
 Normal
 Enlarged LV
 Dilated ascending aorta(PA )
 Calcified valve(lateral)
Echo
...
Management
Asymptomatic
 Under review
Symptomatic –prompt surgery
 Moderately severe/ severe stenosis yearly doppler
ech...
Management
AV replacement
 Severe stenosis with symptoms
 Asymptomatic - careful exercise test;symptoms on moderate
exer...
Aortic stenosis in old patients
 Most common form
 Syncope,angina,heart failure
 Low pulse pressure
 Surgery –successf...
Aortic regurgitation
Aetiology
 Congenital
 Bicuspid or disproportionate cusps
Acquired
 Rheumatic disease
 Infective ...
Clinical features
Symptoms
Mild- moderate AR
 Often asymptomatic
 Awareness of heart beat
Severe AR
 Breathlessness
 A...
Clinical features
Signs
 Pulse
 Large or collapsing pulse
 Low diastolic pressure& 
pulse pressure ,Bounding
periphera...
Investigations
ECG
 Initially normal
 Later LVH
 T wave inversion
CXR
 Cardiac dilation
 Features of left heart
failu...
Management
Treat the underlying conditions
 Aortic valve replacement
aortic root replacement & CABG
symptomatic
Chronic A...
Tricuspid valve Disease
 Rheumatic in origin
 <5%
 Always association with mitral & aortic valve disease
 Isolated TV ...
Clinical features and investigations
 Symptoms of associated mitral & aortic valve disease
 Symptoms of right heart fail...
Tricuspid regurgitation
Causes
Primary
 Rheumatic heart disease
 Endocarditis
 Ebstein’s congenital anomaly
Secondary
R...
Clinical features
 Non-specific symptoms
 Tiredness
 Venous congestion
 A large systolic phase in JVP
 A cv wave repl...
Investigations
Echocardiogram
 Dilation of the RV
 Thickened valve
 Vegetations in endocarditis
 Ebstein’s anomaly TV ...
Management
 Correct RV overload
 Normal pulmonary artery tolerate tricuspid
reflux well
 valve damage dut to IE not alw...
Pulmonary valve Disease
Causes
 Carcinoid syndrome
 Usually congenital
 Isolated or associated with other abnormalities...
Clinical features
 ESM at left upper sternum
 Radiation to left shoulder
 Thrill
 Preceded ejection click
 Wide split...
Investigations
ECG
 RVH
CXR
 Post-stenotic dilation in the pulmonary artery
Doppler echo
Management
 Mild to moderate isolated pulmonary stenosis
 Not usually progress
 Not required treatment
 Low risk for I...
Pulmonary regurgitation
 Rarely an isolated phenomenon
 Usually associated with pulmonary artery dilatation due to
pulmo...
Heart sounds
 Heart sounds are the noises generated by the
beating heart and the resultant flow of blood through it.
Spec...
first heart tone
 S1[
 The first heart tone, or S1, forms the "lub" of "lub-dub" and is
composed of components M1 and T1...
The second heart tone
 S2
 The second heart tone, or S2, forms the "dub" of "lub-dub" and is
composed of components A2 a...
Third heart sound S3
 Third heart sound
 Rarely, there may be a third heart sound also called a protodiastolic
gallop, ...
 It may also be a result of tensing of the chordae
tendineae during rapid filling and expansion of the
ventricle. In othe...
Fourth heart sound
 S4
 S4 when audible in an adult is called a presystolic gallop or atrial gallop.
This gallop is prod...
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Heart Vulvular diseases and heart sounds
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Heart Vulvular diseases and heart sounds

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

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Heart Vulvular diseases and heart sounds

  1. 1. `  Topics :Diseases of the heart valves, Heart sounds Presented by : Dr Barkam NAGARAJU MD(General Medicine)
  2. 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. 3.  Rheumatic Heart Disease  Acute rheumatic fever  Chronic rheumatic heart disease
  4. 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. 5. Clinical features  Streptococcal pharyngitis  Fever,anorexia,lethargy,joint pain  2-3 wks after initial attack of pharyngitis  Arthritis  Rashes  Carditis  Neurological changes
  6. 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. 7. Investigations  Positive blood culture  Raised antistreptolysin O(ASO) without evidence of recent streptococcal infection  Isolated chorea  pancarditis
  8. 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. 9. Carditis  Soft MDM(Carey coombs murmur)  AR 90%  TV & PV rarely involved  Pericarditis  Cardiac failure  ECG –conduction defect,ST-T changes
  10. 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. 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. 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. 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. 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. 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. 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. 17. Mitral valve disease Mitral stenosis causes  Almost always rheumatic in origin  Heavy calcification in elderly  Congenital
  18. 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. 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. 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. 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. 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. 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. 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. 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. 26. Management Medical treatment  Pts with minor symptoms Definitive treatment  Pts remain symptomatic with medical treatment  Balloon valvuloplasty  Mitral valvotomy  Mitral valve replacement
  27. 27. Medical treatment Atrial fibrillation  Anticoagulant  Digoxin  B blockers  Rate limiting calcium antagonist Heart failure  Diuretics Prophylaxis of infective endocarditis  Antibiotics
  28. 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. 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. 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. 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. 32. Pathophysiology Acute mitral regurgitation Rapid rise in LA pressure Marked symptomatic deterioration
  33. 33. Mitral valve prolapse  Floppy mitral valve  Congenital  Degenerative myxoematous changes  A features of connective tissue disorders
  34. 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. 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. 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. 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. 38. Treatment Atrial fibrillation  Anticoagulant  Digoxin Heart failure  Diuretics  Vasodilators e.g ACEI Prophylaxis of infective endocarditis  Antibiotics
  39. 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. 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. 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. 42. Pathophysiology Steadily increase pressure gradient across the AV LV increasingly hypertrophied Inadequate coronary blood flow Angina
  43. 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. 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. 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. 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. 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. 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. 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. 50. Clinical features Symptoms Mild- moderate AR  Often asymptomatic  Awareness of heart beat Severe AR  Breathlessness  Angina
  51. 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. 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. 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. 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. 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. 56. Tricuspid regurgitation Causes Primary  Rheumatic heart disease  Endocarditis  Ebstein’s congenital anomaly Secondary Rv dilatation( chronic LHF RV infarction Pulmonary hypertension( corpulmonale)
  57. 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. 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. 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. 60. Pulmonary valve Disease Causes  Carcinoid syndrome  Usually congenital  Isolated or associated with other abnormalities e.g TOF Pulmonary stenosis
  61. 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. 62. Investigations ECG  RVH CXR  Post-stenotic dilation in the pulmonary artery Doppler echo
  63. 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. 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. 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.
  66. 66. 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.
  67. 67. 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
  68. 68. 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.  .
  69. 69.  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
  70. 70. 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.
  71. 71. ` Thank you

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