o_1977r8vv9vk1ts2ms0kd8pksa.pdf

62 T. Kiserud
Fig. 5.10. Doppler recording of the ductus venosus blood
velocity without pulsation (a) due to the fetal position
bending forward and squeezing the ductus venosus outlet.
The wave has been completely reflected at the junction
with the inferior vena cava (see Fig. 9b). Seconds later, a
change in fetal position restores the dimension of the vessel
and the pulsatile flow pattern (b). (From [31])
Fig. 5.9. A distension of the ductus venosus (DV) inlet and
increased tone in the umbilical vein with reduced diameter
reduce the difference of impedance between the two sections.
Correspondingly, less reflection and more transmission
increase the likelihood that velocity pulsations are observed
in the umbilical vein (a). When the DVis squeezed
right up to the outlet, a larger proportion of the wave is
reflected at the level of outlet (b) leaving little wave energy
to be transmitted further down the transmission line.
No pulsation may then be observed at the DVinlet. (From
[31])
vessel and acts as a reservoir. The larger and more
compliant the reservoir is, the higher wave energy is
required to induce a visible pulsation of the blood
velocity (Fig. 5.11). Accordingly, pulsation should be
a rare event in late pregnancy, whereas the small vascular
dimensions in early pregnancy predispose for
pulsation. Pulsation in the umbilical vein is a normal
phenomenon particularly before 13 weeks of gestation
[56]. It follows that an increased tone of the vessel
wall (e.g. adrenergic drive, venous congestion)
and reduced diameter (e.g. hypovolaemia in fetal
hemorrhage) may be accompanied by pulsation in
the umbilical vein.
The effect of compliance is particularly well illustrated
by the physiological stricture of the umbilical
vein at the entrance through the abdominal wall.
Once the period of physiological umbilical herniation
has been completed at 12 weeks of gestation, there is
an increasing tightening of the umbilical ring causing
a constricting impact on the vein in quite a few fetuses
during the following weeks and months [42±
44]. The stricture causes a high velocity, which, interestingly,
often pulsates (Fig. 5.12) [45]. Although the
pulsation may be a velocity inflection caused by the
a-wave, probably a more common waveform would be
a smooth increment of velocity caused by the neighboring
umbilical arteries. The same phenomenon can
be traced in the umbilical cord with increased turgor,
angulation or extreme twisting [46]. Another example
is the pulsation commonly traced in the left branch