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- Heard in the aortic area when mild. When severe, heard over entire
Precordium
- Length of murmur is more important tha n the intensity
Discussion. Aortic stenosis is a reduction in the valve orifice size or a reduction of the
valve ring itself as part of underdevelopment of the entire left heart and may cause
serious difficulty in infancy. In the adult, however, stenosis is always associated with
abnormalities of the leaflet. The severity of the stenosis varies considerably and
determines the extent of compensatory responses, symptoms and therapy.
With mild aortic stenosis, in childhood or adolescence, the only finding may be a loud
ejection click heard at the apex and a short, early systolic murmur. The murmur of aortic
stenosis is a systolic ejection murmur that peaks in early systole when mild.
Moderate aortic stenosis. As the moderate obstruction develops, the murmur becomes
louder and longer. It is loudest at the aortic area, but may be transmitted to the
supraclavicular fossa, carotid vessels and the apex. The murmur is harsh, but ends well
before the aortic second sound. The sound at the apex may be normal.
With severe aortic stenosis, the valve is thickened and heavily calcified. The ejection
sound is no longer present and the aortic second sound (A2) is markedly diminished.
The murmur may be faint to very loud, but will always long and occupy almost all of
systole. An S4 may be present in Severe AS.
In severe AS, the aortic leaflets are fused and therefore don’t make a closure sound. All
you hear is P2. The murmur may be faint to very loud, but will always long and
occupy almost all of systole. The murmur of aortic stenosis is well transmitted to the
apex where it may have a pure or musical quality and may be mistaken as the patient
having both aortic stenosis and mitral regurgitation.
The severe AS murmur may also migrate into the neck and also may have an S4.
When severe, it often radiates to the carotid arteries, suprasternal notch and
clavicles. Even though it is an aortic sound, it can also be heard at the apex. As the
stenosis becomes more severe, the murmur peaks later in systole and the closure of the
aortic valve component of S2 decreases in intensity and is delayed. This results in a
paradoxical splitting of S2 with the closure of the aortic valve and the closure of the
pulmonic valve merging on inspiration.
NOTE: With Severe AS, the murmur often migrates into the neck.
as part of under development of the entire left heart. In the adult, however, stenosis is
always associated with abnormalities of the leaflet.
The slow rising of the carotid pulse, a classic sign of aortic stenosis in the young, is often
absent in elderly patients because of diminishing vascular compliance. Additionally, the
symptoms of severe aortic stenosis in the elderly such as angina pectoris, syncope, or
heart failure is confusing because it can result from coronary artery disease or
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cerebrovascular disease.
In the example shown here, you will hear the systolic ejection murmur in the aortic,
pulmonic and tricuspid areas, but in the mitral area (apex) you will hear only S1 and S2.
In other situations, you may hear an ejection sound in the early systole in the aortic area and
an S4, an ejection sound and a systolic murmur at the mitral area (apex). In severe
aortic stenosis, you may hear a systolic murmur at the apex. Don’t confuse this murmur
with the holosystolic murmur of mitral regurgitation. This pitch and quality of the murmur
of mitral regurgitation and aortic stenosis are quite different.
Practical Points regarding Aortic Stenosis
- Paradoxical splitting of S2 implies severe AS
- AS is severe if SEM peaks within the second half of systole
- Length of murmur is more important tha n the intensity
- At the apex, systolic murmur in the elderly can be MR, Galavardin or
Calcified annulus
Congenital bicuspid valve. The most common cause of aortic stenosis is a congenital
bicuspid formation of the valve leaflets. This may be severe at birth and cause serious
difficulties during infancy or childhood, but more commonly the stenosis is mild in infancy and childhood. With the passage of time, however, the obstruction tends to increase so that moderate stenosis is present during the fourth and fifth decade of life and severe stenosis develops during the fifth decade or later. This slow increase in severity of
stenosis is due to progressive sclerosis, thickening and eventual calcification of the
valve so that there is a progressive reduction in the orifice. This disorder is seen about
twice as frequently in men as in women. Other conditions associated with aortic
stenosis are rheumatic fever and aortic sclerosis.
Aortic stenosis in the aged. Occasionally, even the leaflets of a normal tricuspid aortic
valve may become rigid and cause stenosis. This develops in the 8th or 9th decades of
life and is only rarely severe.
Other causes. Practically the only other cause of aortic stenosis is rheumatic fever.
With this process, the severity of stenosis also tends to progress slowly. Eventually, the
obstructed valve is indistinguishable from the end state of the congenitally abnormal
longer as the severity increases. It is, therefore, more important to identify the length
than the intensity. Notice also that as the severity increases, the split S2 that is A2 and
P2 becomes paradoxical. As you recall from earlier lessons, A2 is the aortic component
and P2 is the pulmonic component of the second heart sound, S2.
Maneuvers affecting the Murmur. The murmur of AS may be accentuated by
maneuvers that increase stroke volume such as expiration, sitting up and leaning
forward or exercise. Maneuvers that will decrease the murmur of AS are standing
abruptly, inspiration, Valsalva or hand grip.
Palpation of the Pulse.
Initially, the pulse may be normal. With hemodynamically significant stenosis, the pulse
becomes low in volume and late in attaining its maximal excursion. This is the classic
“pulsus parvus et tardus (Latin for small and delayed).
Listening technique.
auscultating at the right upper sternal border (aortic area), followed by the left upper
sternal border (pulmonic area), and then proceed down the left sternal border (tricuspid
area) and finally the apex (mitral area). The stethoscope should be moved within the
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above areas by inching with the area to determine the point of maximum intensity.
Palpate the carotid pulse to identify S1 and the onset of systole.
In listening to mild aortic stenosis, listen to the murmur at the aortic area. When does it
start; stop and when is it loudest? These are clues that will help you determine if the
stenosis is mild, moderate or severe.
Best heard. Aortic stenosis is best heard in the aortic area. However, the ejection
murmur of aortic stenosis can also be heard at the apex. When severe, it often radiates
to the carotid arteries, suprasternal notch and clavicles. This murmur is often heard
over the clavicles illustrating the importance of bone in the transmission of sound.
Aortic area. The first and second heart sounds (S1 and S2) are normal with the first
heart sound being somewhat dominant in all areas. In some patients, there may be an
ejection click although one is not illustrated in this example. The systolic murmur is
grade III and ends well before the second sound.
Pulmonary area. There is a grade II murmur that is transmitted from the aortic area.
Tricuspid area. There is a grade II murmur that is also transmitted from the aortic area.
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Mitral area. The sound at the mitral area is normal in this patient. In some patients,
there may be an S4, an ejection click and/or a grade I systolic murmur. An S4 indicates
that the degree of aortic valvular obstruction is severe. If a murmur is heard, it is
transmitted from the aortic area and may have a slightly higher frequency.
Figure 5 Aortic stenosis. The Auscultatory Picture.
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