o_1977r8vv9vk1ts2ms0kd8pksa.pdf

152 K. MarsÏ—l
Fig. 11.11. Absence of end-diastolic velocity in the descending
aorta of a growth-retarded fetus at 27 weeks' gestation
Fig. 11.12. Flow pulsatility index (P.I.), flow pulse amplitude,
and mean blood flow measured with an electromagnetic
flowmeter in the descending thoracic aorta of sheep
fetuses versus the vascular resistance of the lower body circulation
during progressive embolization of the hind limbs
and placenta. Solid circles show values obtained during angiotensin
II infusion. (Reprinted from [59], with permission)
lated to the increased neonatal nucleated red blood
cell counts that are considered a sign of intrauterine
hypoxia [58]. Doppler results from the fetal descending
aorta, umbilical artery, and maternal uterine arteries
were independent determinants of neonatal nucleated
red blood cell count.
In an experimental study on the fetal lamb, increasing
the placental and hind limbresistance by
embolization with microspheres caused a progressive
increase in the aortic flow PI [59]. In another study
on pigs, the aortic PI, recorded by Doppler ultrasonography,
was shown to correlate with the total
peripheral resistance calculated from the invasively
measured blood flow and pressure (r=0.64±0.87)
[60]. In the study by Adamson and Langille [59] the
aortic PI reflected not only the vascular resistance
but also the pulsatile flow and pressure pulsatility
(Fig. 11.12). Thus an increasing fetal aortic PI should
not be interpreted solely as an expression of increasing
placental vascular resistance.
When studying the aortic blood velocity waveforms
of lambfetuses during experimental asphyxia,
Malcus et al. [61] found a loss of aortic end-diastolic
flow velocities, a significant increase in the PI, and a
decrease in mean velocity. Concomitantly, increases
in the diameter and mean velocity were recorded in
the fetal common carotid artery [62], and there was a
slight decrease in the carotid artery PI. These changes
indicate a redistribution of flow, although the changes
occurred as relatively late phenomena in the development
of acute asphyxia.
An interesting observation on fetal aortic isthmus
has been reported, based on animal experiments [63]
and human studies [64]. With increased resistance to
flow in the placenta and fetal lower body, changes in
the diastolic flow velocity occurred earlier in the aortic
isthmus than in the descending aorta and umbilical
artery. In the sheep fetus during an acute increase
in placental vascular resistance, delivery of oxygen to
the brain was preserved despite a significant decrease
in arterial oxygen content as long as net flow through
the aortic isthmus was antegrade [65]. These reports
offer an interesting possibility of closely following the
process of centralization of flow. The suggested concept
awaits evaluation in prospective clinical studies.