Page 210 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Aortic Regurgitation
After closure of the aortic valve the aortic pres- and Musset’s sign, respectively). At ausculta-
sure (P Ao ) falls relatively slowly, while the pres- tion an early diastolic decrescendo murmur
sure in the left ventricle (P LV ) falls rapidly to (EDM) can be heard over the base of the heart,
just a few mmHg (→ p.179), i.e., there is now produced by the regurgitation, as well as a
a reverse pressure gradient (P Ao > P LV ). In aortic click and a systolic murmur due to the forced
valve regurgitation (AR, also called insufficien- large-volume ejection (→ A1, SM).
cy) the valve is not tightly closed, so that dur- The above-mentioned mechanisms allow
ing diastole a part of what has been ejected the heart to compensate for chronic AR for
from the left ventricle during the preceding several decades. In contrast to AS (→ p.198),
ventricular systole flows back into the LV be- patients with AR are usually capable of a good
cause of the reverse pressure gradient (regur- level of physical activity, because activity-
gitant volume;→ A).
associated tachycardia decreases the duration
Heart and Circulation anomaly (e.g., bicuspid valve with secondary Also, peripheral vascular dilation of muscular
of diastole and thus the regurgitant volume.
Causes. AR can be the result of a congenital
work has a positive effect, because it reduces
calcification) or (most commonly) of inflam-
the mean diastolic pressure gradient (P Ao –
matory changes of the cusps (rheumatic fever,
P LV ). On the other hand, bradycardia or periph-
bacterial endocarditis), disease of the aortic
eral vasoconstriction can be harmful to the pa-
root (syphilis, Marfan’s syndrome, arthritis
or atherosclerosis.
The compensatory mechanisms, however,
come at a price. Oxygen demand rises as a con-
The consequences of AR depend on the re-
7 such as Reiter’s syndrome), or of hypertension tient.
gurgitant volume (usually 20–80 mL, maxi- sequence of increased cardiac work (= pressure
mally 200 mL per beat), which is determined times volume; → A2, orange area). In addition,
by the opening area and the pressure difference the diastolic pressure, which is so important
during diastole (P Ao – P LV ) as well as the dura- for coronary perfusion (→ p. 216), is reduced
tion of diastole. To achieve an adequate effec- and simultaneously the wall tension of the
tive stroke volume (= forward flow volume) left ventricle is relatively high (see above)—
the total stroke volume (→ A2, SV) must be in- both causes of a lowered transmural coronary
creased by the amount of the regurgitant vol- artery pressure and hence underperfusion
ume, which is possible only by raising the end- which, in the presence of the simultaneously
diastolic volume (→ A2, orange area). This is increased oxygen demand, damages the left
accomplished in acute cases to a certain de- ventricle by hypoxia. Left ventricular failure
gree by the Frank–Starling mechanism, in (→ p. 224) and angina pectoris or myocardial
chronic cases, however, by a much more effec- infarction (→ p. 220) are the result. Finally, de-
tive dilational myocardial transformation. compensation occurs and the situation dete-
(Acute AR is therefore relatively poorly toler- riorates relatively rapidly (vicious circle): as a
ated: cardiac output ↓; P LA ↑). The endsystolic consequence of the left ventricular failure the
volume (→ A2, ESV) is also greatly increased. endsystolic volume rises, while at the same
According to Laplace’s law (→ p. 225), ventric- time total stroke volume decreases at the ex-
ular dilation demands greater myocardial pense of effective endsystolic volume (→ A2,
force as otherwise P LV would decrease. The di- red area), so that blood pressure falls (left heart
lation is therefore accompanied by left ventric- failure) and the myocardial condition deterio-
ular hypertrophy (→ p. 224f.). Because of the rates further. Because of the high ESV, both
flow reversal in the aorta, the diastolic aortic the diastolic P LV and the P LA rise. This can cause
pressure falls below normal. To maintain a pulmonary edema and pulmonary hyperten-
normal mean pressure this is compensated by sion (→ p. 214), especially when dilation of
a rise in systolic pressure (→ A1). This in- the left ventricle has resulted in functional mi-
creased pressure amplitude can be seen in the tral regurgitation.
200 capillary pulsation under the finger nails and
pulse-synchronous head nodding (Quincke’s
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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