Anda di halaman 1dari 54

VALVULAR

HEART DISEASE
MITRAL STENOSIS
Causes:

Rheumatic heart
disease
Lutembachers
syndrome (acquired
mitral stenosis+atrial
septal defect)
Calcification and fibrosis
of the valve, valve ring
and subvalvular
apparatus in elderly
Malignant carcinoid Congenital
Pathophysiology
Symptoms:
Begin when the mitral valve orifice area <2 cm
2

(normal: 4-6 cm
2
)

dyspnoea
haemoptysis
weakness
fatigue
abdominal or lower limb swelling
palpitations



Signs:


Pulse:
Small-volume,
irregular pulse
Face:
Malar flush
Jugular veins: Obvious
distension of the jugular
veins if the right heart
failure develops
Palpation:
Tapping impulse felt
parasternally on the
left side

Auscultation:
Opening snap, rumbling
mid-diastolic murmur,
Loud S
1


Investigations:

Atrial fibrillation
P-mitrale (left atrial hypertrophy)
RVH
Progressive right axis deviation
ECG
Left atrial enlargement
Pulmonary oedema
Mitral valve calcification
CXR
Left and right atrial and ventricular size and
function
Severity of the stenosis
Echocardiography
Treatment:
Mild dyspnoea-low doses of diuretics
Onset of atrial fibrillation- digoxin and
anticoagulation
If pulmonary hypertension develops or the
symptoms of pulmonary congestion persist-
surgical relief of the mitral stenosis (trans-
septal balloon valvotomy, closed valvotomy,
open valvotomy, mitral valve replacement)

Mitral regurgitation
Mitral regurgitation (MR) can occur due to
abnormalities of the valve leaflets, the
annulus, the chordae tendineae or papillary
muscles, or the left ventricle.

The most frequent causes of mitral
regurgitation are degenerative (myxomatous)
disease, ischemic heart disease, rheumatic
heart disease, and infectious endocarditis.
Pathophysiology
With acute mitral regurgitation the normal compliance
of the left atrium does not allow much dilatation and
the left atrial pressure rises.

Thus, in acute mitral regurgitation the left atrial v-wave
is greatly increased and pulmonary venous pressure
rises to produce pulmonary oedema.

Since a proportion of the stroke volume is regurgitated,
the stroke volume increases to maintain the forward
cardiac output and the left ventricle therefore enlarges.
The Carpentier classification
uses mitral leaflet motion to divide patients into different
classes according to the mechanism of regurgitation which
can be useful when considering surgical intervention.
Symptoms
The increased stroke volume is sensed as a palpitation.

Dyspnoea and orthopnoea develop owing to pulmonary
venous hypertension occurring as a direct result of the
mitral regurgitation and secondarily to left ventricular
failure.

Fatigue and lethargy develop because of the reduced
cardiac output.

In the late stages of the disease the symptoms of right
heart failure also occur and eventually lead to congestive
cardiac failure.
Signs
Laterally displaced (forceful) diffuse apex beat and a systolic thrill (if
severe)

Soft first heart sound, owing to the incomplete apposition of the valve
cusps and their partial closure by the time ventricular systole begins

Pansystolic murmur, owing to the occurrence of regurgitation throughout
the whole of systole, being loudest at the apex but radiating widely over
the precordium and into the axilla

With a floppy mitral valve, there may be a mid-systolic click, which is
produced by the sudden prolapse of the valve and the tensing of the
chordae tendineae that occurs during systole. This may be followed by a
late systolic murmur owing to some regurgitation.

Prominent third heart sound, owing to the sudden rush of blood back into
the dilated left ventricle in early diastole (sometimes a short mid-diastolic
flow murmur may follow the third heart sound).
Investigations
1. Chest X-ray
The chest X-ray may show left atrial and left
ventricular enlargement.
There is an increase in the CTR, and valve
calcification is seen.
2. Electrocardiogram
left atrial delay (bifid P waves)
left ventricular hypertrophy

3. Echocardiogram
dilated left atrium and left ventricle.
There may be specific features of chordal or papillary
muscle rupture.

4. Cardiac catheterization
prominent left atrial systolic pressure wave, and when
contrast is injected into the left ventricle it is seen
regurgitating into an enlarged left atrium during
systole.

Treatment
Any evidence of progressive cardiac enlargement
generally warrants early surgical intervention by
either mitral valve repair or replacement.

In patients who are not appropriate for surgical
intervention, or in whom surgery will be
performed at a later date, management involves
treatment with ACE inhibitors, diuretics and
possibly anticoagulants.
Prolapsing (billowing) mitral valve
This is also known as Barlows syndrome or floppy
mitral valve.

It is due to excessively large mitral valve leaflets, an
enlarged mitral annulus, abnormally long chordae or
disordered papillary muscle contraction.

Its cause is unknown but it is associated with Marfans
syndrome, thyrotoxicosis, rheumatic or ischaemic heart
disease. It also occurs in association with atrial septal
defect and as part of hypertrophic cardiomyopathy.
Aortic Stenosis
Definiton
Chronic progressive disease that produces
obstruction to the left ventricular stroke
volume leading to symptoms of chest pain,
breathlessness, syncope and pre-syncope and
fatigue.
Type & Classification
i. Aortic valve stenosis includes calcific
stenosis of a trileaflet.
ii. Calcific aortic valvular disease (CAVD) is the
commonest
iii. Bicuspid aortic valve (BAV)


iv. Rheumatic fever
v. Other causes of valvular stenosis
vi. Valvar aortic stenosis
Supravalvular obstruction
Hypertrophic cardiomyopathy
Subvalvular aortic

Several forms of left ventricular
outflowtract obstruction
Pathophysiology
1. Obstructed left ventricular emptying leads to increased
left ventricular pressure and compensatory left
ventricular hypertrophy.
2. In turn, this results in relative ischaemia of the left
ventricular myocardium, and consequent angina,
arrhythmias and left ventricular failure.
3. The obstruction to left ventricular emptying is relatively
more severe on exercise. Normally, exercise causes a
many-fold increase in cardiac output, but when there is
severe narrowing of the aortic valve orifice the cardiac
output can hardly increase.
4. The blood pressure falls, coronary ischaemia worsens,
the myocardium fails and cardiac arrhythmias develop.
Left ventricular systolic function is typically preserved in
patients with aortic stenosis (cf. aortic regurgitation).
Symptoms
Usually no symptoms until aortic stenosis is
moderately severe (when the aortic orifice is
reduced to one-third of its normal size).
At this stage, exercise-induced syncope,angina
and dyspnoea develop.
When symptoms occur, the prognosis is poor
on average, death occurs within 23 years if
there has been no surgical intervention.
Signs
Pulse
The carotid pulse is of small volume and is slow-rising or
plateau in nature.

Precordial palpation
The apex beat is not usually displaced because hypertrophy
(as opposed to dilatation) does not produce noticeable
cardiomegaly.
However, the pulsation is sustained and obvious.
A double impulse is sometimes felt because the fourth
heart sound or atrial contraction (kick) may be palpable.
A systolic thrill may be felt in the aortic area.
Signs
Sig Features of aortic stenosis and aortic regurgitation.
EC, ejection click; EDM, early diastolic murmur; MSM, mid-systolic murmur; S1, first heart sound.
LSE, left sternal edge.
Auscultation
The most obvious : ejection systolic murmur that is usually
diamond-shaped (crescendo-decrescendo).
The murmur : usually longer when the disease is more severe. Not a
good guide to the severity of the condition lessened by a reduced
cardiac output. In severe cases, the murmur may be inaudible.

Other findings include:

Systolic ejection click
Soft or inaudible aortic second heart sound when the aortic valve
becomes immobile.
Reversed splitting of the second heart sound (splitting on expiration)
Prominent fourth heart sound,
Investigations
Chest X-ray
Cardiac magnetic resonance and cardiac CT
Electrocardiogram
Echocardiography
Cardiac catheterization




Treatment
a) The symptoms are a good index of severity
and all symptomatic patients should have
aortic valve replacement.
b) Patients with a BAV and ascending aorta >50
mm or expanding at >5 mm/year should be
considered for surgical intervention.
c) Asymptomatic patients : regular review for
assessment of symptoms and
echocardiography.
Treatment
d) Surgical intervention for asymptomatic
people + severe aortic stenosis:
Symptoms during an exercise test or with a drop in
blood pressure.
A left ventricular ejection fraction of <50%
Moderatesevere stenosis undergoing CABG,
surgery of the ascending aorta or other cardiac
valve.
Treatment
e) Antibiotic prophylaxis against infective endocarditis :
Provided that the valve is not severely deformed or heavily
calcified.

f) Critical aortic stenosis in childhood or adolescence can be
treated by valvotomy temporary relief from the
obstruction

g) Aortic valve replacement will usually be needed a few
years later. Balloon dilatation (valvuloplasty) has been
tried in adults, especially in the elderly, as an alternative to
surgery. Generally results are poor and such treatment is
reserved for patients unfit for surgery or as a bridge to
surgery (as systolic function will often improve).
Treatment
h) Percutaneous valve replacement
A novel treatment for patients unsuitable for
surgical aortic valve replacement is transcatheter
implantation with a balloon expandable stent
valve.
Valve implantation has been shown to be
successful (86%) with a procedural mortality of
2% and 30-day mortality of 12%. Further larger
and randomized studies with long-term follow-up
are required.
2-D
Echocardiogram (long-axis view) in
a patient with calcific aortic
stenosis. The calcium in the valve
generates abnormally intense
echoes. There is some evidence of
the associated left ventricular
hypertrophy.
Continuous-wave (CW) Doppler
signals obtained from the right
upper parasternal edge, where the
high-velocity jet from the stenotic
valve is coming towards the
transducer.
AV, aortic valve; LA, left atrium; MV, mitral
valve; LV, left ventricle; IVS, inter.
Cardiac Echograms
Aortic Regurgitation
Etiology
Acute aortic regurgitation Chronic aortic regurgitation
Acute rheumatic fever
Infective endocarditis
Dissection of the aorta
Ruptured sinus of Valsalva
aneurysm
Failure of prosthetic valve
Rheumatic heart disease
Syphilis
Arthritides : Reactive
arthritis, ankylosing
spondylitis, rheumatoid
arthritis
Hypertension (severe)
Bicuspid aortic valve
Aortic endocarditis
Marfans syndrome
Osteogenesis imperfect
Pathophysiology
Reflux of blood from the aorta through the
aortic valve into the left ventricle
1. Maintenance of cardiac output the total
volume pumped inti aorta must increase
enlargement of left ventricle
2. Aortic runoff during diastole diastolic bp
falls coronary perfusion decrease
3. Larger left ventricle less efficient greater
demand of
2
cardiac ischaemia develops
Symptoms
Signs
Pulse Sinus rhythm, large
volume, collapsing
BP Wide pulse pressure
Apex Displace, diffuse,
forceful
Murmur
s
1. High pitched, early
diastolic at left
sternal edge
2. Ejection systolic at
base and into neck
(high flow)
3. Mid diastolic
rumble at apex
(Austin flint)
Significant symptoms
occur late and do not
develop until left
ventricular failure occurs.
Common:
Pounding of the heart
Increased left ventricular
size and its vigorous
pulsation
Angina pectoris
Dyspnoea
Uncommon
Arryhthmias
Investigations
Chest X-Ray
Left vebtricular
enlargement
Possible of
dilatation of the
ascending aorta
Increase
cardiothoracic
ratio

ECG
Appearances of left ventricular
hypertrophy due to volume overload
Tall R waves and deeply inverted T waves
in the left-sided chest leads
Deep s waves in the right sided leads
Normally, sinus rhythm is present
Echocardiogram
Dilated left
ventricle
Hyperdynamic
left ventricle
Fluttering
anterior mitral
leaflet
Doppler detects
reflux


Treatment
Acute aortic regurgitation
Vasodilators
Inotropes

ACEi are useful for patients with left ventricular
dysfunction
Beta-blockers may slow aortic dilatation in
Marfan patients
Aortic surgery : mechanical prostheses, tissue
valves

Indication of Aortic Surgery
in acute severe aortic regurgitation e.g. endocarditis
in symptomatic (dyspnoea, NYHA class II-IV, angina)
patients with chronic severe aortic regurgitation
when asymptomatic with left ventricular ejection
fraction is 50%
when asymptomatic with left ventricular ejection
fraction >50% but with a dilated left ventricle (end-
diastolic dimension >70 mm or systolic dimension >50
mm)
when undergoing CABG, surgery of the ascending aorta
or other cardiac valve
Tricuspid stenosis
Aetiology:
Rheumatic in origin and seldom seen in
developed countries.
Occurs in fewer than 5% of pt. with rheumatic
heart disease and nearly always in association
with mitral and aortic valve stenosis.

Clinical features:
Predominate symptoms of aortic and mitral valve disease.
May cause symptoms of right heart failure-hepatic discomfort
and pulmonary edema.
Raised in JVP: prominent a wave and slow y descent due to
the loss of normal right ventricular filling.
Mid diastolic murmur best heard at lower left or right sternal
edge.
Usually high pitched than the murmur of mitral stenosis and
increased by inspiration.
Right heart failure causes hepatomegaly with presystolic
pulsation (large a wave), ascites and peripheral edema.
Doppler echo: the valve has similar appearance to those of
rheumatic mitral stenosis.
Management:
Surgery
Ballon vulvuloplasty
TRICUSPID REGURGITATION
Tricuspid
regurgitation is a
disorder in which
the heart's
tricuspid valve
does not close
properly, causing
blood to flow
backward (leak)
into the right
atrium when the
right ventricle
contracts
CAUSES OF TRICUSPID REGURGITATION

Primary
Rheumatic heart disease
Endocarditis
Ebsteins congenital anomaly
Secondary
Right ventricular dilation due to chronic left heart
failure (functional tricuspid regurgitation)
Right ventricular infarction
Pulmonary hypertension
SIGNS AND SYMPTOMS
Tiredness related to reduced forward flow
Oedema and hepatic enlargement due to venous
congestion
giant v wave in the jugular venous pressure
Pansystolic murmur at the left sternal edge
Pulsatile liver
ECHOCARDIOGRAPHY
Dilation of RV
In rheumatic disease, leaflets will appear thicken
In endocarditis, vegetations may be seen
MANAGEMENT
Tricuspid regurgitation due to right ventricular
dilation often improves when cause of RV
overload is corrected, with diuretic and
vasodilator treatment of congestive heart
failure
Leaflets with rheumatic damage may require
tricuspid valve replacement
Pulmonary Stenosis
Etiologies:-
Usually congenital (intact ventricular septum or
with ventricular septal defect [Fallots tetralogy]).
Rheumatic fever
Carcinoid syndrome
Rubella Infection on fetus

Pulmonary Stenosis
Signs and Symptoms:-
Right ventricular hypertrophy
Lesser degree of obstruction: fatigue, syncope,
and right heart failure symptoms eg: swelling of
lower limb, ascites and etc.
Auscultation:
Harsh midsystolic ejection murmur best heard on
inspiration.
Pulmonary closure sound will be delayed & soft




Pulmonary Stenosis
Investigations:
Chest X-ray: Prominent pulmonary artery
ECG: Right atrial and Right Ventricle hypertrophy
Doppler Echocardiogram: Flow of blood through
the pulmonary valve.
Treatment: Pulmonary valvotomy (Balloon or
surgery).







PULMONARY REGURGITATION
-Very rare
-Associated with pulmonary artery dilatation
due to pulmonary hypertension
- may complicate mitral stenosis, producing an
early diastolic decrescendo murmur at the left
sternal edge difficult to distinguish from
aortic regurgitation
-Trivial pulmonary regurgitation is a frequent
finding in normal individuals and has no
clinical significance.