Page 208 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Aortic Stenosis
The normal opening area of the aortic valve is addition, the ejection period is lengthened
2.5–3.0 cm . This is sufficient to eject blood, causing a small and slowly rising pulse (pulsus
2
not only at rest (ca. 0.2 L/s of systole), but also parvus et tardus). At auscultation there is, in
on physical exertion, with a relatively low addition to the sound created by the strong
pressure difference between left ventricle and atrial contraction, a spindle-shaped rough sys-
aorta (P LV – P Ao ; → A1, blue area). In aortic ste- tolic flow murmur (→ A2, SM) and, if the valve
nosis ([AS] 20% of all chronic valvar defects) is not calcified, an aortic opening click (→ A2).
the emptying of the left ventricle is impaired. The transmural pressure of the coronary arter-
The causes of AS (→ A, top left) can be, in addi- ies is diminished in AS for two reasons:
tion to subvalvar and supravalvar stenosis, – The left ventricular pressure is increased
congenital stenosing malformations of the valve not only in systole but also during diastole,
(age at manifestation is < 15 years). When it
which is so important for coronary perfu-
Heart and Circulation due to a congenital bicuspid malformation of Coronary blood flow is thus reduced or, at least
sion (→ p. 216).
occurs later (up to 65 years of age) it is usually
– The pressure in the coronary arteries is also
affected by the poststenotically decreased
the valve that becomes stenotic much later
through calcification (seen on chest radio-
(aortic) pressure.
gram). Or it may be caused by rheumatic–in-
flammatory stenosing of an originally normal
during physical exertion, can hardly be in-
atic after the age of 65 is most often caused by
uses up abnormally large amounts of oxygen,
degenerative changes along with calcification.
myocardial hypoxia (angina pectoris) and myo-
7 tricuspid valve. An AS that becomes symptom- creased. As the hypertrophied myocardium
In contrast to mitral stenosis (→ p.194), cardial damage are consequences of AS
long-term compensation is possible in AS, be- (→ p. 218ff.).
cause the high flow resistance across the ste- Additionally, on physical exertion a critical
notic valve is overcome by more forceful fall in blood pressure can lead to dizziness,
ventricular contraction. The pressure in the transient loss of consciousness (syncope), or
left ventricle (P LV ) and thus the gradient P LV – even death. As the cardiac output must be in-
P Ao (→ A1,2), is increased to such an extent creased during work because of vasodilation
that a normal cardiac output can be maintain- in the muscles, the left ventricular pressure in-
ed over many years (P LV up to 300 mmHg). creases out of proportion (quadratic function;
Only if the area of the stenosed valve is less → A1). Furthermore, probably in response to
2
than ca. 1 cm do symptoms of AS develop, stimulation of left ventricular baroreceptors,
especially during physical exertion (cardiac additional “paradoxical” reflex vasodilation
output ↑→ P LV ↑↑). may occur in other parts of the body. The re-
The consequences of AS include concentric sulting rapidly occurring fall in blood pressure
hypertrophy of the left ventricle as a result of may ultimately be aggravated by a breakdown
the increased prestenotic pressure load of the already critical oxygen supply to the
(→ p. 224). This makes the ventricle less dis- myocardium (→ A). Heart failure (→ p. 224ff.),
tensible, so that the pressures in the ventricle myocardial infarction (→ p. 220), or arrhythmia
and atrium are raised even during diastole (→ p.186ff.), all of which impair ventricular
(→ A2, P LV , P LA ). The strong left atrium contrac- filling, contribute to this vicious circle.
tion that generates the high end-diastolic
pressure for ventricular filling causes a fourth
heart sound (→ A2) and a large a wave in the
left atrium pressure (→ A2). The mean atrial
pressure is increased mainly during physical
exertion, thus dyspnea develops. Poststenoti-
cally, the pressure amplitude and later also
198 the mean pressure are decreased (pallor due
to centralization of circulation; → p. 232). In
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
All rights reserved. Usage subject to terms and conditions of license.