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VALVULAR HEART DISEASE
By: MR.JAGDISH SAMBAD
M.Sc.Nursing in M.S.N.
Assistant Professor
Balaji College of Nursing.
Heart valves
• The heart contains two atrioventricular valves:
1. Mitral valve
2. Tricuspid valve
Two semilunar valve
1. Aortic valve
2. Pulmonary valve
Types of valvular heart disease
• Types of valvular heart
disease are defined
according to the valve
defect.
1. Stenosis – constriction
or narrowing
2. Regurgitation –
incomplete closure of
the valve leaflets
results in the backward
flow of blood.
Types of valvular heart disease
1. Mitral stenosis
2. Mitral regurgitation
3. Mitral prolapse
4. Aortic stenosis
5. Aortic regurgitation
6. Tricuspid stenosis
7. Tricuspid regurgitation
8. Pulmonary stenosis
9. Pulmonary regurgitation
Mitral stenosis
• Narrowing of the mitral valve
Etiology
• The majority of adult cause of mitral valve
stenosis result from rheumatic heart disease.
• Less common include:
- Congenital mitral stenosis
- Rheumatoid arthritis
- Systemic lupus erythromatous (SLE)
PATHOPHYSIOLOGY
Rheumatic endocarditis along with other causes
Scaring of the valve leaflets &the chorde tendinee
Contracture develop with adhesions between two leaflets
Funnel shape of the valve because of thickening and shorting of the structure
Obstruction of flow of blood from the mitral valve
Pressure gradient difference between LA & LV during diastole
Increase pressure and volume in LA
Increase pressure in pulmonary vasculature
Hypertrophy of pulmonary vessel in chronic congestion
Extertional dyspnea due to decrease pulmonary compliance
Reactive pulmonary hypertension
Right ventricular hypertrophy
Right ventricular failure
Clinical manifestation
• Dyspnea on extortion, orthopnea and PND.
• Acute pulmonary edema may be precipitate
by uncontrolled AF, exercise, chest infection,
anesthesia and pregnancy.
• fatigue is due to reduce cardiac out put
reserve and is common in mild or moderate
stenosis.
• Hemoptysis can occur for a Varity of reasons.
Cont..
• Alveolar capillary rupture (pink frontally
pulmonary oedema)
• Bronchial vein rupture (large hemorrhage)
• Blood stained sputum of chronic bronchitis
• Horse voice (left recurrent laryngeal nerve
compression- ortner’s sign )
• Dysphagia (esophageal compression)
• Left lung collapse (left main bronchus
compression )
Investigation
• History and physical examination
• ECG
• chest X-ray
• Cardiac catheterization- increase PcWP, LAP
• Echocardiogram
Management
• Asymptomatic patient need only infective
endocarditis prophylaxis
• Mild symptoms- sault intake restriction and
oral stenosis
• In AF digoxin beta blocker or CCB for the rate
control restoration of sinus rhythm may be
attempted if appropriate.
• Anticoagulants- at last 1 year for those with
thromboembolism and life long if in AF.
Surgical management
i. Closed valvotomy: fused cups separated by
dilator introduced through LV apex.
ii. Open valvotomy: with cardiopulmonary
bypass is preferred to closed valvotomy cups
separated under direct vision. Any fusion of
subvalvular apparatus is loosened.
iii. Mitral valve replacement(MVR)
- MVR if there is significant MR or the valve
is severely or heavily calcified.
Mitral regurgitation
Etiology
Acute MR Chronic MR
Infective endocarditis
Acute myocardial
infarction
Trauma
Chronic rheumatic heart
disease
Mitral valve prolapse
Left ventricular dilatation
Degeneration of valve cups
Hypertrophic
cardiomyopathy
Pathophysiology
Regurgitation mitral orifice
Volume overload on the LV
LV dilatation
LV is decompressed into the LA during diastole
Backward flow of blood in the LA
Volume overload in LA
LA enlargement
Raised left atrium pressure
Rise pressure in pulmonary vasculature
Pulmonary oedema
Clinical manifestation
Acute MR Chronic MR
Symptoms related to
pulmonary oedema and shock
Thready peripheral pulse
Cool and clammy extremities
Murmur is heard during
auscultation of heart sound
May remain asymptomatic for may year
until the development of some degree
of right ventricular failure.
Weakness
Fatigue
Dyspnea (due to decrease forward
cardiac output)
Paroxysmal nocturnal dyspnea
Peripheral oedema in later stage
Investigation
• History and physical
examination
• ECG
• chest X-ray
• Cardiac catheterization-
increase PcWP, LAP
• Echocardiogram
Medical management
• Infective endocarditis prophylaxis required
• Asymptomatic patient with mild MR managed
conservatively with serial echocardiograms.
• Vasodilators
Surgical management
• Mitral valve repair and
• Mitral valve replacement
Mitral valve prolapse
• MVP is the structural abnormality of the
mitral valve leaflets and the pupillary muscles
or chorade that allows the leaflets to prolapse
or back into the left atrium during systole.
• MVP is the most common from of valvular
heart disease in the united states.
Etiology
• Unknown but is related to diverse pathogenic
mechanism of the mitral valve.
• Secondary to MS & MR.
- MVP can occur in the presence, redundant mitral valve
leaflets elongated chorde tendineae (longer)
- Enlarged mitral annulus (right that is attached to the
mitral valve leaflets)
- MVP is usually benign but serious complications can
occur including mitral regurgitations, infective
endocarditis sudden death and cerebral ischemia.
Clinical manifestation
• Arrhythmias most commonly ventricular
premature contraction
• Ventricular tachycardia
• May cause palpitations
• Light headache and dizziness
• Chest pain may be due to abnormal tension
on the pupillary muscles. This chest pain does
not respond to Anti-Anginal treatment. E.g
nitrate, sorbitrate.
Management
• Recommend antibiotic prophylaxis for endocarditis.
• Monitor the patient treated with B-adrenergic blockers
to control palpitations.
• Advice the patient to adopt healthy eating pattern such
as avoiding caffeine, because if it is a stimulant and any
exacerbate symptoms.
• Counsel the patient who uses diet pills continuing
stimulants that these preparations will exacerbate
symptoms.
• Instruct the patient to take over the counter drug with
caution.
• Develop a planned aerobic exercise program and the
patient implement it.
Surgical management
• Mitral valve repair
• Mitral valve replacement in severe damage
and calcifications
Patient and family teaching
1. Teach patient the importance of antibiotic
prophylaxis for endocarditis before
undergoing any surgical procedure if the
patient has MVP.
2. Advise to patient to adopt healthy eating
pattern and to avoid caffeine because it is
stimulants and may cause exacerbate
symptoms.
3. Help to patient to develop and implement an
exercise program to maintain optimal health.
4. Instruct patient to contact 108 or health care
provider if symptoms develop or worsen.
Aortic stenosis
• Definition:
- Narrowing of the
aortic valve.
Incidence
• Commonest valve lesion in UK.
• Risk increase with the age
• 2% of people >65 years have echo feature of
aortic stenosis.
Causes
Acquired causes Congenital causes
Acquired degenerative calcific as
rheumatic fever, Paget disease of bone
end stage renal failure.
Bicuspid aortic valve 1-2% live births.
Bicuspid AV results in calcification and
fibrosis of leaflets with reduced valve
area.
Etiology
• As can occur at level of valve or above
supravalvular stenosis or below the aortic valve.
• Degenerative calcified as results from years of
normal stress on valve.
• IHD (increased BP, lipids, DM)
• Inflammatory changes occur with in valve with
calcium deposited causing immobility reduced,
excursions and reduced opening area.
• Rheumatic as due to adhesions and fusion of
commissures.
Pathophysiology
Progressive narrowing of aortic valve orifice.
Increase pressure on LV.
Worsening LVH to minimum stroke volume
Stiff, non- compliant ventricle
Elevated end diastolic pressure
More pressure on LA
Blood backflow into LA and pulmonary vasculature
Various clinical manifestations
Clinical manifestations
• Angina pectoris
• Dyspnea
• Syncope
• Dizziness
• Palpitations
• Heart failure
• Sudden death
• BP- narrow pulse pressure in advanced as systolic BP is
decreased.
• Systolic thrill felt at aortic area(2nd ICP on right side).
• Slow rising, small volume pulse-best felt at carotid.
Investigation
• History and physical examination
• ECG
• chest X-ray
• Cardiac catheterization- increase PcWP, LAP
• Echocardiogram
Medical management
• β- blocker reduce myocardial or demand and
may improve coronary blood flow.
• Loop diuretics for hypervolemia.
• Digoxin in case of heart failure.
• In severe as avoid drugs which reduce
afterload. E.g NTG, ACE-I as this may worsen
gradient and cause syncope.
Surgical management
• Balloon aortic valvuloplastiy
• Aortic valve replacement (AVR)
Aortic regurgitation
Causes
Valvular causes Other causes
Rheumatic fever
Infective endocarditis
Degenerative calcification
Trauma
Aortic root disease
Hypertension
Marfan’s syndrome
Spondylitis
Pathophysiology
Failure of aortic valve
More blood of LV stroke volume regurgitation into LV
Increase in stroke volume to maintain cardiac output
Increase in end-diastolic pressure
LV dilatation and hypertrophy
Back flow in pulmonary system
Clinical manifestation
Acute clinical feature Chronic clinical feature
Abrupt onset of profound
dyspnea
Transient chest pain
Progression to shock
Fatigue
Exertional dyspnea
Corrigan’s sign (Abnormal
pulse felt on coronary
artery)
Investigation
• History and physical examination
• ECG
• chest X-ray
• Cardiac catheterization- increase PcWP, LAP
• Echocardiogram
Medical management
• Asymptomatic mild/ moderate AR with normal LV
routine follow up every 1-2 year with echo.
• Asymptomatic severe AR with normal LV frequent
6 monthly follow up or sooner if symptoms
intervene.
• Loop diuretics and digoxin for CCF.
• Vasodilator, ACE-I, & calcium channel blocker
should be used in AR.
• Anginal chest pain can be treated with nitrates
but use beta blocker with caution.
Surgical management
• Balloon aortic valvuloplastiy
• Aortic valve replacement (AVR)
Tricuspid stenosis
Causes
• Rheumatic fever
• Congenital
• Fatigue
• Anorexia
• Peripheral oedema
On examination: wasting edema, hepatomegaly
Elevated jugular vein pressure, rumbling mid
systolic murmurs.
Investigation
• History and physical examination
• Echocardiography
• ECG: sinus rhythm with sign of RA
enlargement.
• CXR: enlarge RA but normal PA size.
Treatment
• Salt restriction and diuretic may markedly
improve symptoms. If co-existent MS is being
operated on surgical valvuloplastiy can help.
• Tricuspid valve replacement occasionally may
perform. Bio prosthetic valve give better
results than mechanical valve.
Tricuspid regurgitation
Causes
• Any cause of RV dilatation(MV disease
congenital heart disease, RV dysfunction etc..)
• Endocarditis
• Marfan's syndrome
• Rheumatic fever
Pathophysiology
Clinical manifestation
• Usually minimal as right side HF develop
patient complaints of :
• Ascites
• Edema
• Nausea
• Anorexia
• Abdominal pain
On examination: wasting, jaundice, oedema,
artificial flutter is common, elevated JVP, tender
pulsatile hepatomegaly, auscultation-S3 often
heard and increased expiration.
Investigation
• History and physical examination
• ECG: non specific, may show evidence of
underlying condition
• CXR: cardiomegaly in patient with functional
tricuspid regurgitation, pleural effusion.
• Echocardiogram: color Doppler confirm
diagnosis.
Treatment
• In absence of pulmonary hypertension. TR is
well tolerated and may not require well
tolerated and may not require specific
treatment.
• Symptoms of RV failure respond to diuretic
and fluid/salt restriction.
• TR secondary to valve pathology may require
valve replacement.
Pulmonary stenosis
Causes
• Congenital
• Rheumatic heart disease
• Extrinsic compression
Clinical manifestation
• Usually none
• If severe stenosis; exertional dyspnea and light
headiness.
• Examination: prominent “a” wave in JVP
occasionally thrill in 2nd left in ICS.
Investigations
• History and physical examination
• ECG: right ventricular hypertrophy and RV
overload
• CXR: dilated pulmonary arteries.
• Echocardiogram: confirms diagnosis and can
show level stenosis.
• Cardiac catheterization: to severity of
obstruction and hemodynamic effect.
Medical Treatment
• In general invasive intervention is
recommended when gradient across valve is
>50 mmhg at rest for when symptoms occur.
• Medical- supportive symptomatic treatment
of RV failure is diuretics & fluid restriction.
Surgical intervention
• Balloon valvuloplastiy
• Pulmonary valve replacement is indicated if
not suitable for medical treatments.
Pulmonary regurgitation
Causes
• Any cause of increased pulmonary BP
• Infective endocarditis
• Connective tissue disease-Marfan's syndrome
Clinical manifestation
• Often asymptomatic
• Symptoms increase when pulmonary BP
increase or right ventricular failure exists.
• Then get dyspnea on exertion, lethargy,
peripheral edema, abdominal pain.
• On examination: thrill in pulmonary area.
• Auscultation; murmur of PR is heard best in
3rd & 4th ICP on left adjacent to sternum and
increase during inspirations.
Investigation
• History and physical examination
• ECG: right ventricular hypertrophy
• CXR: enlarged pulmonary arteries and right
ventricle
• Echocardiogram: image may show RV
dilatation and hypertrophy. Abnormal septal
motion if RV volume overload.
Treatment
• Usually supportive treatment suffices treat RV
failure in use of diuretics.
• If pulmonary regurgitation is due to PV ring
dilation secondary to pulmonary HT, treating
cause of increased pulmonary BP can relive
and decrease the pulmonary regurgitation
severity.
• If severe right HF then pulmonary valve
replacement can be considered.
Prosthetic valve
• The two categories of prosthetic valve are:
Mechanical valve Biologic valve
MV are manufactured
form man made material
and consist of
combination of metal
alloys polite, carbon &
Dacron.
BV are constructed from
bovine porcine and
human cardiac tissue.
Mechanical valve
1. caged-ball valve: metal cage with several
stratus mounted on a circular ring hollow metal
or plastic ball inside cage.
2. tilting-disk valve
• Mobile lens-shaped disk attached to a circular
sewing ring by two offset transverse stratus:
pyrolytic carbon composition.
3. bi-leaflet valve
• Two pivoting semi-circular disk that open
centrally, mounted directly onto a swing ring.
Biological valve
Porcine heterograft Pericardial heterograft Homograft cadaver valve
Harvested aortic valve of pig
that is preserved in
glutraldehyde and mounted
on specially designed sewing
ring.
Three leaflets composed of
pericardium from 16 to 18
months old that are
preserved in glutraldehyde
and mounted on Dacron
covered frame
Harvested aortic valve from
human cadaver that is
initially needed for
replacement then sewn into
with special mounting
material.
Valvular heart disease

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Valvular heart disease

  • 1. VALVULAR HEART DISEASE By: MR.JAGDISH SAMBAD M.Sc.Nursing in M.S.N. Assistant Professor Balaji College of Nursing.
  • 2. Heart valves • The heart contains two atrioventricular valves: 1. Mitral valve 2. Tricuspid valve Two semilunar valve 1. Aortic valve 2. Pulmonary valve
  • 3. Types of valvular heart disease • Types of valvular heart disease are defined according to the valve defect. 1. Stenosis – constriction or narrowing 2. Regurgitation – incomplete closure of the valve leaflets results in the backward flow of blood.
  • 4. Types of valvular heart disease 1. Mitral stenosis 2. Mitral regurgitation 3. Mitral prolapse 4. Aortic stenosis 5. Aortic regurgitation 6. Tricuspid stenosis 7. Tricuspid regurgitation 8. Pulmonary stenosis 9. Pulmonary regurgitation
  • 5. Mitral stenosis • Narrowing of the mitral valve
  • 6. Etiology • The majority of adult cause of mitral valve stenosis result from rheumatic heart disease. • Less common include: - Congenital mitral stenosis - Rheumatoid arthritis - Systemic lupus erythromatous (SLE)
  • 7. PATHOPHYSIOLOGY Rheumatic endocarditis along with other causes Scaring of the valve leaflets &the chorde tendinee Contracture develop with adhesions between two leaflets Funnel shape of the valve because of thickening and shorting of the structure Obstruction of flow of blood from the mitral valve Pressure gradient difference between LA & LV during diastole Increase pressure and volume in LA Increase pressure in pulmonary vasculature Hypertrophy of pulmonary vessel in chronic congestion Extertional dyspnea due to decrease pulmonary compliance Reactive pulmonary hypertension Right ventricular hypertrophy Right ventricular failure
  • 8. Clinical manifestation • Dyspnea on extortion, orthopnea and PND. • Acute pulmonary edema may be precipitate by uncontrolled AF, exercise, chest infection, anesthesia and pregnancy. • fatigue is due to reduce cardiac out put reserve and is common in mild or moderate stenosis. • Hemoptysis can occur for a Varity of reasons.
  • 9. Cont.. • Alveolar capillary rupture (pink frontally pulmonary oedema) • Bronchial vein rupture (large hemorrhage) • Blood stained sputum of chronic bronchitis • Horse voice (left recurrent laryngeal nerve compression- ortner’s sign ) • Dysphagia (esophageal compression) • Left lung collapse (left main bronchus compression )
  • 10. Investigation • History and physical examination • ECG • chest X-ray • Cardiac catheterization- increase PcWP, LAP • Echocardiogram
  • 11.
  • 12. Management • Asymptomatic patient need only infective endocarditis prophylaxis • Mild symptoms- sault intake restriction and oral stenosis • In AF digoxin beta blocker or CCB for the rate control restoration of sinus rhythm may be attempted if appropriate. • Anticoagulants- at last 1 year for those with thromboembolism and life long if in AF.
  • 13. Surgical management i. Closed valvotomy: fused cups separated by dilator introduced through LV apex. ii. Open valvotomy: with cardiopulmonary bypass is preferred to closed valvotomy cups separated under direct vision. Any fusion of subvalvular apparatus is loosened. iii. Mitral valve replacement(MVR) - MVR if there is significant MR or the valve is severely or heavily calcified.
  • 14.
  • 15.
  • 17.
  • 18.
  • 19. Etiology Acute MR Chronic MR Infective endocarditis Acute myocardial infarction Trauma Chronic rheumatic heart disease Mitral valve prolapse Left ventricular dilatation Degeneration of valve cups Hypertrophic cardiomyopathy
  • 20. Pathophysiology Regurgitation mitral orifice Volume overload on the LV LV dilatation LV is decompressed into the LA during diastole Backward flow of blood in the LA Volume overload in LA LA enlargement Raised left atrium pressure Rise pressure in pulmonary vasculature Pulmonary oedema
  • 21. Clinical manifestation Acute MR Chronic MR Symptoms related to pulmonary oedema and shock Thready peripheral pulse Cool and clammy extremities Murmur is heard during auscultation of heart sound May remain asymptomatic for may year until the development of some degree of right ventricular failure. Weakness Fatigue Dyspnea (due to decrease forward cardiac output) Paroxysmal nocturnal dyspnea Peripheral oedema in later stage
  • 22. Investigation • History and physical examination • ECG • chest X-ray • Cardiac catheterization- increase PcWP, LAP • Echocardiogram
  • 23. Medical management • Infective endocarditis prophylaxis required • Asymptomatic patient with mild MR managed conservatively with serial echocardiograms. • Vasodilators
  • 24. Surgical management • Mitral valve repair and • Mitral valve replacement
  • 25. Mitral valve prolapse • MVP is the structural abnormality of the mitral valve leaflets and the pupillary muscles or chorade that allows the leaflets to prolapse or back into the left atrium during systole. • MVP is the most common from of valvular heart disease in the united states.
  • 26.
  • 27. Etiology • Unknown but is related to diverse pathogenic mechanism of the mitral valve. • Secondary to MS & MR. - MVP can occur in the presence, redundant mitral valve leaflets elongated chorde tendineae (longer) - Enlarged mitral annulus (right that is attached to the mitral valve leaflets) - MVP is usually benign but serious complications can occur including mitral regurgitations, infective endocarditis sudden death and cerebral ischemia.
  • 28. Clinical manifestation • Arrhythmias most commonly ventricular premature contraction • Ventricular tachycardia • May cause palpitations • Light headache and dizziness • Chest pain may be due to abnormal tension on the pupillary muscles. This chest pain does not respond to Anti-Anginal treatment. E.g nitrate, sorbitrate.
  • 29. Management • Recommend antibiotic prophylaxis for endocarditis. • Monitor the patient treated with B-adrenergic blockers to control palpitations. • Advice the patient to adopt healthy eating pattern such as avoiding caffeine, because if it is a stimulant and any exacerbate symptoms. • Counsel the patient who uses diet pills continuing stimulants that these preparations will exacerbate symptoms. • Instruct the patient to take over the counter drug with caution. • Develop a planned aerobic exercise program and the patient implement it.
  • 30. Surgical management • Mitral valve repair • Mitral valve replacement in severe damage and calcifications
  • 31. Patient and family teaching 1. Teach patient the importance of antibiotic prophylaxis for endocarditis before undergoing any surgical procedure if the patient has MVP. 2. Advise to patient to adopt healthy eating pattern and to avoid caffeine because it is stimulants and may cause exacerbate symptoms. 3. Help to patient to develop and implement an exercise program to maintain optimal health. 4. Instruct patient to contact 108 or health care provider if symptoms develop or worsen.
  • 32. Aortic stenosis • Definition: - Narrowing of the aortic valve.
  • 33.
  • 34. Incidence • Commonest valve lesion in UK. • Risk increase with the age • 2% of people >65 years have echo feature of aortic stenosis.
  • 35. Causes Acquired causes Congenital causes Acquired degenerative calcific as rheumatic fever, Paget disease of bone end stage renal failure. Bicuspid aortic valve 1-2% live births. Bicuspid AV results in calcification and fibrosis of leaflets with reduced valve area.
  • 36. Etiology • As can occur at level of valve or above supravalvular stenosis or below the aortic valve. • Degenerative calcified as results from years of normal stress on valve. • IHD (increased BP, lipids, DM) • Inflammatory changes occur with in valve with calcium deposited causing immobility reduced, excursions and reduced opening area. • Rheumatic as due to adhesions and fusion of commissures.
  • 37. Pathophysiology Progressive narrowing of aortic valve orifice. Increase pressure on LV. Worsening LVH to minimum stroke volume Stiff, non- compliant ventricle Elevated end diastolic pressure More pressure on LA Blood backflow into LA and pulmonary vasculature Various clinical manifestations
  • 38. Clinical manifestations • Angina pectoris • Dyspnea • Syncope • Dizziness • Palpitations • Heart failure • Sudden death • BP- narrow pulse pressure in advanced as systolic BP is decreased. • Systolic thrill felt at aortic area(2nd ICP on right side). • Slow rising, small volume pulse-best felt at carotid.
  • 39. Investigation • History and physical examination • ECG • chest X-ray • Cardiac catheterization- increase PcWP, LAP • Echocardiogram
  • 40. Medical management • β- blocker reduce myocardial or demand and may improve coronary blood flow. • Loop diuretics for hypervolemia. • Digoxin in case of heart failure. • In severe as avoid drugs which reduce afterload. E.g NTG, ACE-I as this may worsen gradient and cause syncope.
  • 41. Surgical management • Balloon aortic valvuloplastiy • Aortic valve replacement (AVR)
  • 43. Causes Valvular causes Other causes Rheumatic fever Infective endocarditis Degenerative calcification Trauma Aortic root disease Hypertension Marfan’s syndrome Spondylitis
  • 44. Pathophysiology Failure of aortic valve More blood of LV stroke volume regurgitation into LV Increase in stroke volume to maintain cardiac output Increase in end-diastolic pressure LV dilatation and hypertrophy Back flow in pulmonary system
  • 45. Clinical manifestation Acute clinical feature Chronic clinical feature Abrupt onset of profound dyspnea Transient chest pain Progression to shock Fatigue Exertional dyspnea Corrigan’s sign (Abnormal pulse felt on coronary artery)
  • 46. Investigation • History and physical examination • ECG • chest X-ray • Cardiac catheterization- increase PcWP, LAP • Echocardiogram
  • 47. Medical management • Asymptomatic mild/ moderate AR with normal LV routine follow up every 1-2 year with echo. • Asymptomatic severe AR with normal LV frequent 6 monthly follow up or sooner if symptoms intervene. • Loop diuretics and digoxin for CCF. • Vasodilator, ACE-I, & calcium channel blocker should be used in AR. • Anginal chest pain can be treated with nitrates but use beta blocker with caution.
  • 48. Surgical management • Balloon aortic valvuloplastiy • Aortic valve replacement (AVR)
  • 50. Causes • Rheumatic fever • Congenital • Fatigue • Anorexia • Peripheral oedema On examination: wasting edema, hepatomegaly Elevated jugular vein pressure, rumbling mid systolic murmurs.
  • 51. Investigation • History and physical examination • Echocardiography • ECG: sinus rhythm with sign of RA enlargement. • CXR: enlarge RA but normal PA size.
  • 52. Treatment • Salt restriction and diuretic may markedly improve symptoms. If co-existent MS is being operated on surgical valvuloplastiy can help. • Tricuspid valve replacement occasionally may perform. Bio prosthetic valve give better results than mechanical valve.
  • 54. Causes • Any cause of RV dilatation(MV disease congenital heart disease, RV dysfunction etc..) • Endocarditis • Marfan's syndrome • Rheumatic fever
  • 56. Clinical manifestation • Usually minimal as right side HF develop patient complaints of : • Ascites • Edema • Nausea • Anorexia • Abdominal pain On examination: wasting, jaundice, oedema, artificial flutter is common, elevated JVP, tender pulsatile hepatomegaly, auscultation-S3 often heard and increased expiration.
  • 57. Investigation • History and physical examination • ECG: non specific, may show evidence of underlying condition • CXR: cardiomegaly in patient with functional tricuspid regurgitation, pleural effusion. • Echocardiogram: color Doppler confirm diagnosis.
  • 58. Treatment • In absence of pulmonary hypertension. TR is well tolerated and may not require well tolerated and may not require specific treatment. • Symptoms of RV failure respond to diuretic and fluid/salt restriction. • TR secondary to valve pathology may require valve replacement.
  • 60. Causes • Congenital • Rheumatic heart disease • Extrinsic compression
  • 61. Clinical manifestation • Usually none • If severe stenosis; exertional dyspnea and light headiness. • Examination: prominent “a” wave in JVP occasionally thrill in 2nd left in ICS.
  • 62. Investigations • History and physical examination • ECG: right ventricular hypertrophy and RV overload • CXR: dilated pulmonary arteries. • Echocardiogram: confirms diagnosis and can show level stenosis. • Cardiac catheterization: to severity of obstruction and hemodynamic effect.
  • 63. Medical Treatment • In general invasive intervention is recommended when gradient across valve is >50 mmhg at rest for when symptoms occur. • Medical- supportive symptomatic treatment of RV failure is diuretics & fluid restriction.
  • 64. Surgical intervention • Balloon valvuloplastiy • Pulmonary valve replacement is indicated if not suitable for medical treatments.
  • 66. Causes • Any cause of increased pulmonary BP • Infective endocarditis • Connective tissue disease-Marfan's syndrome
  • 67. Clinical manifestation • Often asymptomatic • Symptoms increase when pulmonary BP increase or right ventricular failure exists. • Then get dyspnea on exertion, lethargy, peripheral edema, abdominal pain. • On examination: thrill in pulmonary area. • Auscultation; murmur of PR is heard best in 3rd & 4th ICP on left adjacent to sternum and increase during inspirations.
  • 68. Investigation • History and physical examination • ECG: right ventricular hypertrophy • CXR: enlarged pulmonary arteries and right ventricle • Echocardiogram: image may show RV dilatation and hypertrophy. Abnormal septal motion if RV volume overload.
  • 69. Treatment • Usually supportive treatment suffices treat RV failure in use of diuretics. • If pulmonary regurgitation is due to PV ring dilation secondary to pulmonary HT, treating cause of increased pulmonary BP can relive and decrease the pulmonary regurgitation severity. • If severe right HF then pulmonary valve replacement can be considered.
  • 70. Prosthetic valve • The two categories of prosthetic valve are: Mechanical valve Biologic valve MV are manufactured form man made material and consist of combination of metal alloys polite, carbon & Dacron. BV are constructed from bovine porcine and human cardiac tissue.
  • 71. Mechanical valve 1. caged-ball valve: metal cage with several stratus mounted on a circular ring hollow metal or plastic ball inside cage.
  • 72. 2. tilting-disk valve • Mobile lens-shaped disk attached to a circular sewing ring by two offset transverse stratus: pyrolytic carbon composition.
  • 73. 3. bi-leaflet valve • Two pivoting semi-circular disk that open centrally, mounted directly onto a swing ring.
  • 74. Biological valve Porcine heterograft Pericardial heterograft Homograft cadaver valve Harvested aortic valve of pig that is preserved in glutraldehyde and mounted on specially designed sewing ring. Three leaflets composed of pericardium from 16 to 18 months old that are preserved in glutraldehyde and mounted on Dacron covered frame Harvested aortic valve from human cadaver that is initially needed for replacement then sewn into with special mounting material.