Aortic Stenosis

DR.MASHUK
Aortic Stenosis
 Introduction
 Aortic stenosis is a narrowing of the aortic valve opening that increases
resistance to blood flow from the left ventricle to the aorta.
Aortic Stenosis
 Causes
 Congenital aortic stenosis
 Calcification
 Fibrosis
 Senile degenerative aortic stenosis
 Rh heart disease
Aortic Stenosis
 Pathophysiology
 When the aortic valve becomes stenotic, resistance to systolic ejection
occurs and a systolic pressure gradient develops between the left ventricle
and the aorta. Stenotic aortic valves have a decreased aperture that leads to
a progressive increase in left ventricular systolic pressure. This leads to
pressure overload in the left ventricle, which, over time, causes an increase
in ventricular wall thickness (ie, concentric hypertrophy). At this stage, the
chamber is not dilated and ventricular function is preserved, although
diastolic compliance may be affected.
Aortic Stenosis
 Eventually, however, the left ventricle dilates. This, coupled with a
decrease in compliance, is associated with an increase in left ventricular
end-diastolic pressure, which is increased further by a rise in atrial systolic
pressure. A sustained pressure overload eventually leads to myocardial
decompensation. The contractility of the myocardium diminishes, which
leads to a decrease in cardiac output. The elevated left ventricular end-
diastolic pressure causes a corresponding increase in pulmonary capillary
arterial pressures and a decrease in ejection fraction and cardiac output.
Ultimately, congestive heart failure (CHF) develops.
Aortic Stenosis
 Clinical Presentation
 Breathlessness with activity
 Chest pain, angina-type
 Crushing, squeezing, pressure, tightness
 Pain increases with exercise, relieved with rest
 Fainting, weakness, or dizziness with activity
 Sensation of feeling the heart beat (palpitations)
 Sudden death
 In infants and children-Becoming tired or fatigued with exertion more
easily than others (in mild cases) and serious breathing problems that
develop within days or weeks of birth (in severe cases)
Aortic Stenosis
 Physical Findings
o Ejection systolic murmur
o Slow rising carotid pulse
o Narrow pulse pressure
o Crepitation present
o Thrusting apex beat
o Pulmonary edema
Aortic Stenosis
 Differential Diagnoses
 Subacute bacterial endocarditis
Aortic Stenosis
 Investigation
 Chest x-ray may normal
 Doppler echocardiography shows calcified valve with restricted opening
and hypertrophied left ventricle
 ECG shows left ventricular hypertrophy and left bundle branch block
 ETT
 Left cardiac catheterization
 Transesophageal echocardiogram (TEE)
Aortic Stenosis
 Management
 A) Medication
o Antibiotics like erythromycin
o Diuretics like Tab.Furosemide Initial: 20 to 80 mg per dose.
Maintenance: Increase in increments of 20 to 40 mg/dose every 6 to 8
hours to desired effect
o GTN tablet 500 µg.

 B) Surgical treatment
o An operation to widen the valve (valvotomy)
o Valve replacement.
o Stretching the stenosed valve (balloon valvuloplasty)
Aortic Stenosis
 Complications
 Aortic valve disease will eventually lead to decompensation with raised
end-diastolic pressure, increased pressure in the pulmonary system and
congestive heart failure.
 Damaged valves are susceptible to infective endocarditis.
 Calcified AS may produce small systemic emboli. The effect will depend
upon where they lodge.
 Sudden death occurs in less than 0.2% of patients per year.
Aortic Stenosis
 Prognosis
 Calcific AS is a chronic, progressive disease. The duration of the
asymptomatic phase varies widely between individuals.
 Sudden cardiac death is a frequent cause of death in symptomatic patients
but appears to be rare in truly asymptomatic patient, even in very severe
AS.
 In asymptomatic patients with severe AS, reported average event-free
survival at two years ranges from 20% to more than 50%.