o_1977r8vv9vk1ts2ms0kd8pksa.pdf

542 D. Arduini, G. Rizzo
Fig. 36.2. Doppler tracing
from the pulmonary artery in
an IUGR fetus at 29 weeks'
gestation. The peak velocity is
37 cm/s (normal value for
gestation is 57 cm/s)
brain-sparing mechanism. However, peak velocities
and cardiac output progressively decline, rather than
rise with gestation as expected. The ventricular ejection
force decreases in both ventricles and the different
hemodynamic conditions in the vascular district
(reduced cerebral resistance for the left ventricle and
increased splanchnic and placental resistances for the
right ventricle) can explain this decline in cardiac
output. These changes may reflect decompensation of
a normally protective mechanism responsible for the
brain-sparing effect. According to this model, the fetal
heart adapts to placental insufficiency in a manner
that helps to maximize brain substrate and oxygen
supply. With progressive deterioration of the fetal
condition, this protective mechanism is overwhelmed
by the decreased cardiac output, which may explain
the reported changes in fetal peripheral vessels and
the venous circulation.
Fetal Venous Flows
Studies of inferior vena cava blood flow velocities have
demonstrated a characteristic pattern during fetal
heart failure [75, 76]. Changes in venous blood velocity
have been described during congestive heart failure
with decreased diastolic blood velocity and increased
reversal of flow during atrial contraction [76].
In IUGR fetuses an increase of reverse flow during
atrial contraction may be present in the most severely
compromised fetuses [23, 77] (Fig. 36.3). As a consequence
of these abnormal venous flow patterns, the
return of blood from the placenta to the heart is impaired,
further reducing the supply of oxygen and nutrients.
These findings are compatible with the decrease
in both cardiac output and aortic and pulmonary
peak velocities in deteriorating IUGR fetuses
[50, 66, 78]. These changes are an expression of the
sample phenomenon (i.e., cardiac decompensation)
that impairs both the filling and the output of the
heart. Concomitant changes are present in the ductus
Fig. 36.3. Doppler tracing from the inferior cava in an
IUGR fetus at 29 weeks' gestation. The percent reverse flow
in the inferior vena cava is 16.9% (normal value for gestation
is 7.4%)
venosus of IUGR fetuses, where the velocity during
atrial contraction is significantly reduced or reversed
[50, 62, 79] (Fig. 36.4).
It seems that the blood velocity waveform in the
hepatic vein is an earlier predictor of intrauterine
death than that of the ductus venosus [78]. This
might be due to the fact that the hepatic vein is
nearer the heart and blood flow from the right liver
lobe flows mainly to the right side of the heart, while
that from the ductus venosus flows mainly to the left
ventricle in the foramen ovale. The fetal left ventricle
in IUGR fetuses usually has to work against a lower
afterload than the right ventricle, due to brain spar-