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.
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.
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.
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
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.
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.
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.
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
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.
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.
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.
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.
