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AORTIC STENOSIS
CLINICAL COMPETENCY
S.R.SRUTHI MEENAXSHI
AORTIC STENOSIS
Aortic Stenosis (AS) is narrowing of the
aortic valve resulting in obstruction of
blood flow from the left ventricle to the
ascending aorta during systole.
ETIOLOGY
Aortic stenosis
Williams syndrome
PATHOPHYSIOLOGY
Symptoms
The classic symptoms due to AS are heart failure(HF), syncope and angina.
However, these “classic” symptoms reflect end stage disease
Now, with earlier diagnosis by echocardiography and prospective followup of patients, the most
common presenting symptom are
1. Dyspnea on exertion or decreased exercise tolerance
2. Exertional dizziness
3. Exertional angina
Dyspnea and decreased exercise
tolerance
The most common symptom of AS is dyspnea , usually with exertion
2 factors can contribute : diastolic dysfunction , with an increase in LV filling pressure with exercise
and an inability of LV to increase the CO during exercise because of stiff AV obstructs flow
Systolic LV dysfunction is rare and overt HF is a late end stage finding,usually in who haven’t received
regular medical care .
Once overt HF occurs ,the patient may complain of SOB,easy fatiguability , debilitation and other s/s
of a low CO state.
AF ,which is uncommon in isolated AS ,often accompanies HF
Inspection : Carotid Pulse
The quality of the arterial pulse reflects the obstruction to blood flow into the peripheral arterial
circulation
The arterial pulse : as “parvus and tardus “ ie ,it is small or weak and rises slowly
Best appreciated in the carotid artery where the pulse is reduced in amplitude and delayed in
occurrence
The delay can be appreciated by simultaneous palpation of the apex (PMI) and the carotid
artery
There may be an associated carotid artery thrill or coarse vibration (“ shuddering”) due to the
marked turbulence of blood flow across the stenotic valve.
PALPATION OF PRECORDIUM
The cardiac impulse at the apex is sustained and is initially normal in location.
However, it becomes displaced late in the course of AS when left ventricular failure occurs
A systolic thrill : at the base of the heart (2nd ICS) ,especially during full expiration with the
patient leaning forward
Cardiac Auscultation :Heart sounds
S2: soft and single A2 ( due to AV closure ) is delayed and tends to occur simultaneously with P2
(due to PV closure )
S2 may become paradoxically split when the stenosis is severe and associated with LV
dysfunction
With increasingly severe, fixed AS and A2 closing sound may disappear
The presence of a normal split S2 is the most reliable finding to exclude severe AS in adults
The S1 is usually N.
However,an aortic ejection click, which is more commonly heard with congenital bicuspid valve,
may be heard after S1 ( when the leaflets are stiff ,but still somewhat compliant and mobile )
Vigorous LA contraction can lead to a S4
AS :Murmur
The hallmark finding is a crescendo – decrescendo ejection murmur ,heard best with the
diaphragm of the stethoscope at the right upper sternal border when a patient is sitting upright
leaning forward
The murmur typically radiates to one or both carotid arteries and has a harsh or grating quality
The intensity of systolic murmur does not correspond to the severity of AS .
The more severe the stenosis, the longer the duration of the murmur and the more likely it
peaks at late systole .
In elderly persons with calcific AS ,however the murmur may be more prominent at the apex
,because of radiation of its high frequency components( Gallavardian phenomenon) .
This may lead to its misinterpretation as a murmur of MR
The murmur is soft when stenosis is less severe ,grows louder as stenosis progresses, and
becomes longer and peaks in volume later in systole ( ie crescendo phase becomes longer and
decrescendo phase becomes shorter) as stenosis becomes more severe .
As LV contractility decreases in critical AS ,the murmur becomes softer and shorter.
The intensity of the murmur may therefore be misleading in these circumstances .
The murmur of AS typically increases with maneuvers that increase LV volume and
contractility (eg leg raising , squatting , Valsalva release) and decreases LV volume (Valsalva
maneuvers ) or increase afterload (isometric handgrip)
A high pitched, diastolic blowing murmur may be present if the
patient has associated aortic regurgitation
Rarely, right ventricular failure with systemic venous
congestion ,hepatomegaly and edema precede LV failure.
This probably due to the bulging of the interventricular septum
into the right ventricle, with impedence in filling ,elevated
jugular venous pressure , and prominent a wave ( Bernheim
effect)
Management
Patients with symptomatic severe AS should have prompt AV replacement
Old age is not a contraindication to valve replacement
Aortic balloon Valvuloplasty is useful in congenital aortic stenosis but is of no value in older
patients with calcific aortic stenosis
Anticoagulants are only required in patients who have Afib or those who have had a valve
replacement with a mechanical prosthesis.
Guide to Diagnosing and Managing Aortic Stenosis

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Guide to Diagnosing and Managing Aortic Stenosis

  • 2. AORTIC STENOSIS Aortic Stenosis (AS) is narrowing of the aortic valve resulting in obstruction of blood flow from the left ventricle to the ascending aorta during systole.
  • 3.
  • 4.
  • 9. Symptoms The classic symptoms due to AS are heart failure(HF), syncope and angina. However, these “classic” symptoms reflect end stage disease Now, with earlier diagnosis by echocardiography and prospective followup of patients, the most common presenting symptom are 1. Dyspnea on exertion or decreased exercise tolerance 2. Exertional dizziness 3. Exertional angina
  • 10. Dyspnea and decreased exercise tolerance The most common symptom of AS is dyspnea , usually with exertion 2 factors can contribute : diastolic dysfunction , with an increase in LV filling pressure with exercise and an inability of LV to increase the CO during exercise because of stiff AV obstructs flow Systolic LV dysfunction is rare and overt HF is a late end stage finding,usually in who haven’t received regular medical care . Once overt HF occurs ,the patient may complain of SOB,easy fatiguability , debilitation and other s/s of a low CO state. AF ,which is uncommon in isolated AS ,often accompanies HF
  • 11. Inspection : Carotid Pulse The quality of the arterial pulse reflects the obstruction to blood flow into the peripheral arterial circulation The arterial pulse : as “parvus and tardus “ ie ,it is small or weak and rises slowly Best appreciated in the carotid artery where the pulse is reduced in amplitude and delayed in occurrence The delay can be appreciated by simultaneous palpation of the apex (PMI) and the carotid artery There may be an associated carotid artery thrill or coarse vibration (“ shuddering”) due to the marked turbulence of blood flow across the stenotic valve.
  • 12.
  • 13.
  • 14. PALPATION OF PRECORDIUM The cardiac impulse at the apex is sustained and is initially normal in location. However, it becomes displaced late in the course of AS when left ventricular failure occurs A systolic thrill : at the base of the heart (2nd ICS) ,especially during full expiration with the patient leaning forward
  • 15. Cardiac Auscultation :Heart sounds S2: soft and single A2 ( due to AV closure ) is delayed and tends to occur simultaneously with P2 (due to PV closure ) S2 may become paradoxically split when the stenosis is severe and associated with LV dysfunction With increasingly severe, fixed AS and A2 closing sound may disappear The presence of a normal split S2 is the most reliable finding to exclude severe AS in adults
  • 16.
  • 17.
  • 18.
  • 19. The S1 is usually N. However,an aortic ejection click, which is more commonly heard with congenital bicuspid valve, may be heard after S1 ( when the leaflets are stiff ,but still somewhat compliant and mobile ) Vigorous LA contraction can lead to a S4
  • 20. AS :Murmur The hallmark finding is a crescendo – decrescendo ejection murmur ,heard best with the diaphragm of the stethoscope at the right upper sternal border when a patient is sitting upright leaning forward The murmur typically radiates to one or both carotid arteries and has a harsh or grating quality The intensity of systolic murmur does not correspond to the severity of AS . The more severe the stenosis, the longer the duration of the murmur and the more likely it peaks at late systole .
  • 21. In elderly persons with calcific AS ,however the murmur may be more prominent at the apex ,because of radiation of its high frequency components( Gallavardian phenomenon) . This may lead to its misinterpretation as a murmur of MR The murmur is soft when stenosis is less severe ,grows louder as stenosis progresses, and becomes longer and peaks in volume later in systole ( ie crescendo phase becomes longer and decrescendo phase becomes shorter) as stenosis becomes more severe .
  • 22.
  • 23. As LV contractility decreases in critical AS ,the murmur becomes softer and shorter. The intensity of the murmur may therefore be misleading in these circumstances . The murmur of AS typically increases with maneuvers that increase LV volume and contractility (eg leg raising , squatting , Valsalva release) and decreases LV volume (Valsalva maneuvers ) or increase afterload (isometric handgrip)
  • 24.
  • 25. A high pitched, diastolic blowing murmur may be present if the patient has associated aortic regurgitation Rarely, right ventricular failure with systemic venous congestion ,hepatomegaly and edema precede LV failure. This probably due to the bulging of the interventricular septum into the right ventricle, with impedence in filling ,elevated jugular venous pressure , and prominent a wave ( Bernheim effect)
  • 26. Management Patients with symptomatic severe AS should have prompt AV replacement Old age is not a contraindication to valve replacement Aortic balloon Valvuloplasty is useful in congenital aortic stenosis but is of no value in older patients with calcific aortic stenosis Anticoagulants are only required in patients who have Afib or those who have had a valve replacement with a mechanical prosthesis.