2. 1.rheumatic heart disease:
Is the most common cause resulting from
adhesions and fusions of the commissures
and cusps.
2. congenitally abnormal aortic valve:
normal valve may be stenotic with
commissural fusion at birth but usually
not causing serious narrowing of the
aortic orifice during childhood.
3. The abnormal architecture induces
turbulent flow which traumatizes the
leaflets and leads to fibrosis , increased
rigidity, calcification of leaflets and
narrowing of the aortic orifice in
adulthood.
4. 3.senile aortic stenosis:
Age related AS degeneration and
calcification of previously normal
valve in elderly , usually smokers,
daibetics, hypertension and
hyperlipidemic.
5. 4.SLE and severe familial
hypercholesterolemia occasionally cause
aortic stenosis.
6. 7% of total cases of CHD
Increased pressure in the LF side of the
heart (LV hypertrophy)
Assessment… murmur ,thrill ,high BP, high
HR.
7.
8. Murmur is loudest
Loudness is
proportional to
severity
LVH
……………
9. Obstructed left ventricular outflow due to
aortic stenosis leads to increased left
ventricular pressure and compensatory
left ventricular hypertrophy.
Cardiac output at rest is maintained
within normal limits in most patients with
severe AS, it often fails to rise normally
during exertion.
10. late in the course of the disease , the
cardiac output and stroke volume decline
(due to LV dysfunction) resulting in
decline of pressure gradient across the
aortic valve and rise in pulmonary arterial
pressure.
11. Ischemia in AS:
due to hypertrophy , heart required more
blood for oxygenation that may be not be
possible in sever AS resulting in myocardial
ischemia even in the absence of coronary
artery disease.
12. High left ventricular pressure may compress
the coronary blood flow manifesting as
myocardial ischemia angina, and left
ventricular failure.
This ischemia become more severe on
exercise.
13. Severity of AS is determined by the valve
area and the pressure gradient across the
valve(usually by echo).
Normal aortic valve size is 3-4 cm.
Severe AS: critical obstruction to left
ventricular outflow is usually characterized
by a peak systolic pressure gradient
exceeding 50mmhg in the presence of a
normal cardiac output and aortic valve area
less than 0.8cm.
14. Moderate AS: aortic valve area less than 1.0 -
1.5cm.
Mild AS: 1.5-2.0 cm.
15. Symptoms:
1.long asymptomatic phase.
2.symptomatic AS manifests as:
angina
exercise induced syncope.
exertional dysphea and ultimately
heart failure and sudden death.
these symptoms appear when the aortic
orifice is reduced to one third of its normal
size.
16. Syncope attacks are due to markedly
decreased cerebral perfusion that occurs
during exertion due to systemic
vasodilatation in the presence of reduced
cardiac output due to fixed obstruction.
17. Angina occurs due to myocardial ischemia
which develops when left ventricular oxygen
demand exceeds supply .
Decreased coronary blood flow which does
not fulfill the requirement of the
hypertrophied heart particularly after
exercise.
Decreased coronary blood flow may be due
to compression of coronary arteries by the
hypertrophied myocardium.
18. Exertional dyspnea orthopnea and PND are
late symptoms in AS and reflect pulmonary
venous hypertension.
HEART FAILURE:
heart failure occurs due to both left
ventricular systolic and diastolic dysfunction.
19. Gastrointestinal bleeding GI bleeding may
develop in patients with severe AS ,often
associated with vascular malformations with
malformations associated with severe AS
20. INSPECTION OF PERCORDIUM:
Apex beat is not displaced , visible on its
normal position.
PALPATAION:
Apex beat is not displaced because
hypertrophy (in contrast to dilatation) does
not produce cardiomegaly.
Apex beat is heaving in character (forceful)
due to left ventricular hypertrophy(as result
of pressure overload).
21. A systolic thrill may be felt in the aortic
area or suprasternal notch and is
transmitted along the carotid arteries.
Right ventricular failure with
hepatomegaly , and edema precedes left
ventricular septum that encroaches the
right ventricular cavity causing
impairment of right ventricular filling
23. MURMUR:
Mid systolic murmur present at aortic area.
The murmur is usually rough in quality and
best heard in aortic area .
It radiates to the carotid artery and also the
precordium to the apex.(it usually produces
confusion that patient has two lesions AS and
MR ; however remember that systolic
murmur at apex is murmur of MR that
pansystolic while murmur of AS is mid
systolic ).
24. The murmur of AS is reduced in intensity
when standing due to reduced transvalvular
flow.
Longer the murmur severe is the aortic
stenosis .
However when the left ventricle fails the
stroke volume falls , the systolic murmur of
AS becomes softer, rarely it disappears
altogether.
25. PULSE: carotid pulse is low volume and
slowly rising .
Simultaneous palpation of the apex and
carotid artery reveals delay in carotid pulse
in severe AS.
JVP: prominent due to reduced compliance
of right ventricular due to pulmonary
hypertension or hypertrophy of the
ventricular septum.
26. CHESTCX RAY:
May be normal .
In critical AS the heart is usually normal in
size or slightly enlarged.
Dilation of ascending aorta on PA view in
commonly seen.
27. ECG:
Left ventricular hypertrophy.
Left ventricular pressure overload.
Left atrial enlargement.
28. ECHOCARDIOGRAPHY:
This shows thickened .calcified and immobile
aortic valve cusp.
Detects left ventricular hypertrophy , its
systolic and diastolic function.
Demonstrates the pressure across the valve
and the valve area.
Pressure more than 50mmhg or an aortic
area less than 0.8 cm2 indicates that the
aortic stenosis is severe enough to cause
patients symptoms.
29. Medical treatment is not effective for aortic
stenosis.
Patients who develops any of the three
symptoms( angina, syncope or heart
failure)is candidate for valve replacement.
Surgery is not indicated for asymptomatic
patients except those with declining left
ventricular function, very severe left
ventricular hypertrophy and very high
pressure or reduced valve area.
31. Medical treatment is given to those
patients who are inoperable (usually
comorbids).
Avoid physical activity.
Carefully follow up of the patient because
the disease is progressive.
Pressure increase by 4-8mmhg per year
while valve area decrease by 0.2-
0.3cm2m per year.
32. In mild AS, repeat echo every 2 years.
In asymptomatic patient severe AS echo
should be done every 6-12months.
Angina may be treated with bete-blockers
but cautiously because they may lead to
shock or heart failure.
ACE inhibitors in small does are indicated
in patients with symptomatic left
ventricular systolic dysfunction who are
not candidate for surgery.
33. Valve replacement is indicated early and
in following conditions:
All symptomatic patients including with
left ventricular dysfunction .
Asymptomatic patient with decling left
ventricular function.
Severe left ventricular hypertrophy.
Severely reduced valve area.
Patient of severe AS undergoing another
cardiovascular operation.