Page 212 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

At auscultation the changes due to valvar
Defects of the Tricuspid defects of the right heart are usually louder
and Pulmonary Valves during inspiration (venous return increased).
– TS: First heart sound split, early diastolic tri-
In principle the consequences of stenotic or re- cuspid opening sound followed by diastolic
gurgitant valves of the right heart resemble murmur (tricuspid flow murmur) that in-
those of the left one (→ p.194–201). Differ- creases in presystole during sinus rhythm
ences are largely due to the properties of the (atrial contraction);
downstream and upstream circulations (pul- – TR: Holosystolic murmur of regurgitant
monary arteries and venae cavae, respectively). flow; presence (in adults) or accentuation
The cause of the rare tricuspid stenosis (TS) is (in children) of third heart sound (due to in-
usually rheumatic feverinwhich, as in tricuspid creased diastolic filling) and of the fourth
heart sound (forceful atrial contraction);
regurgitation (TR) of the same etiology, mitral – PS: Occurrence or accentuation of fourth
valve involvement usually coexists. TR may
Heart and Circulation aly, in which the septal leaflet of the tricuspid – PR: Early diastolic regurgitation murmur
also be congenital, forexample, Ebstein’s anom-
heart sound, ejection click (not in subvalvar
or supravalvar stenosis); systolic flow mur-
valve is attached too far into the right ventricle
mur;
(atrialization of the RV). However, most often
TR has a functional cause (dilation and failure
(Graham–Steell murmur).
of the right ventricle). Pulmonary valve defects
is usually congenital and often combined with
a shunt (→ p. 204), while pulmonary regurgita-
7 are also uncommon. Pulmonary stenosis (PS) Circulatory Shunts
tion (PR) is most often functional (e.g., in ad- A left-to-right shunt occurs when arterialized
vanced pulmonary hypertension). blood flows back into the venous system with-
Consequences. In TS the pressure in the out having first passed through the peripheral
right atrium (P RA ) is raised and the diastolic capillaries. In right-to-left shunts systemic ve-
flow through the valve is diminished. As a re- nous (partially deoxygenated) blood flows di-
sult, cardiac output falls (valve opening area, rectly into the arterial system without first
2
2
normally ca. 7 cm , reduced to < 1.5–2.0 cm ). passing through the pulmonary capillaries.
The low cardiac output limits physical activity. In the fetal circulation (→ A) there is
A rise in mean P RA to more than 10 mmHg leads – low resistance in the systemic circulation
to increased venous pressure (high a wave in (placenta!),
the central venous pulse; → p.179), peripheral – high pressure in the pulmonary circulation
edema, and possibly atrial fibrillation. The lat- (→ B2),
ter increases the mean P RA , and thus the ten- – high resistance in the pulmonary circula-
dency toward edema. Edemas can also occur tion (lungs unexpanded and hypoxic vaso-
in TR, because the P RA is raised by the systolic constriction; → C),
regurgitation (high v wave in the central ve- – right-to-left shunt through the foramen
nous pulse). Apart from the situation in Eb- ovale(FO) and ductus arteriosusBotalli (DA).
stein’s anomaly, serious symptoms of TR occur At birth the following important changes oc-
only when there is also pulmonary hyperten- cur:
sion or right heart failure (→ p. 214). PR in- 1. Clamping or spontaneous constriction of
creases the volume load on the right ventricle. the umbilical arteries to the placenta in-
As PR is almost always of a functional nature, creases the peripheral resistance so that
the effect on the patient is mainly determined the systemic pressure rises.
by the consequences of the underlying pulmo- 2. Expansion of the lungs and rise in the alveo-
nary hypertension (→ p. 214). Although, PS, lar P O lower the pulmonary vascular resis-
2
similar to AS, can be compensated by concen- tance (→ C), resulting in an increase in
tric ventricular hypertrophy, physical activity blood flow through the lungs and a drop in
202 will be limited (cardiac output↓), and fatigue the pressure in the pulmonary arteries
and syncope may occur. (→ B1,2).
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Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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