o_1977r8vv9vk1ts2ms0kd8pksa.pdf

The homeostatic significance of absent end-diastolic
velocity in relation to alterations in other components
of the fetal circulation and other parameters of fetal
well-being needs clarification. Some of these issues,
particularly those related to the diagnostic efficacy of
fetal Doppler indices, are discussed in Chap. 24.
Although some degree of overlap is inevitable, the focus
of this chapter is specifically on the umbilical arterial
AREDV. Reports provide considerable insight in
this area. Teyssier et al. [45] observed in an animal
model a hierarchic sequence in the decline of the
end-diastolic flow when fetoplacental vascular resistance
increased; flow in the aortic isthmus was affected
first, followed by flow in the descending aorta
and the umbilical artery. Preliminary clinical observations
tend to confirm this sequence [46].
Bekedam and associates [13] performed longitudinal
measurements of the umbilical arterial PI in 29
growth-restricted fetuses with antepartum late heart
rate decelerations. In 17 of these fetuses (59%), AEDV
preceded the occurrence of decelerations, with a median
interval of 12 days. Arduini and colleagues [47]
evaluated 37 fetuses without structural and chromosomal
abnormalities regarding the various maternal
and fetal factors that affect the time interval between
the occurrence of AEDV in the umbilical artery and
either the development of abnormal fetal heart rate
patterns or delivery. The interval between the first
occurrence of umbilical arterial AEDV and delivery
ranged from 1 to 26 days. Multivariate analysis revealed
that gestational age, the presence of hypertension,
and the appearance of umbilical venous pulsation
are the principal determinants of this time interval.
Finally, Weiner and associates [48] studied hemodynamic
changes in the middle cerebral artery and
the aortic and pulmonic outflow tracts, correlating
these changes with the computerized fetal heart rate
pattern in fetuses with AREDV in the umbilical artery.
They observed that when the middle cerebral artery
began to lose its compensatory vasodilatation
other ominous fetal cardiovascular signs emerged, including
decreases in the left cardiac output (p