o_1977r8vv9vk1ts2ms0kd8pksa.pdf

Reduced oxygen supply is the usual cause of fetal distress.
Although some of the cardiovascular responses
to reduced oxygen supply are similar, observations
obtained from studies in fetal lambs signify dramatic
differences in vascular responses to different types of
hypoxemic stress.
Oxygen delivery to the uterus is a function of uterine
blood flow and oxygen content of uterine blood,
whereas oxygen delivery from the placenta to the fea
Chapter 9 Fetal and Maternal Cardiovascular Physiology 125
Table 9.3. Umbilical blood flow and fetal oxygen consumption
Subject
Umbilical blood flow
(ml ´ min ±1´kg ±1 )
Human
Late gestation 120 ?
Midgestation 180 ?
Sheep
Late gestation 200 7.5
Midgestation 470 10.9
O 2 consumption
(ml ´ min ±1 ´kg ±1 )
Fig. 9.11. Partition of fetal energy requirement between
growth and oxidative metabolism during mid and late gestation.
(Reprinted from [106] with permission)
In relation to fetal weight, umbilical blood flow is
more than double the normal values for the mature
fetus (Table 9.3). Fetal oxygen consumption is greater
at midgestation than at late gestation, probably reflecting
accelerated rates of protein synthesis. At midgestation
the sheep fetus is growing at approximately
three times the rate of the mature fetus. The total energy
requirement during midgestation is 38% greater
than during late gestation, although the partition of
the fetal energy requirement between growth (37%)
and oxidative metabolism (63%) is similar (Fig. 9.11).
Regulation of Umbilical-Placental Circulation
The progressive rise in umbilical blood flow during
gestation is accomplished by the continuous increase
and growth of the number of fetoplacental vessels, as
evidenced by the increasing number of endothelial
cells in the fetoplacental microcirculation [34]. This
statement is consistent with the observations of a
progressive decrease in fetoplacental resistance to
flow of about 2.8% per day [110].
The umbilical arteries are not innervated beyond
the proximal 1±2 cm of the umbilical cord; they consist
of several components of circular or longitudinal
muscle and contain less collagen and elastin than the
systemic arteries [113]. Because of the lack of innervation,
the umbilical circulation has been considered
to be a passive circulation in which the flow rate is
determined by the mean effective perfusion pressure
(i.e., the arterial-venous pressure difference) [50].
Acute hypoxemia does not change the magnitude
of umbilical-placental blood flow, suggesting that
hypoxemia has little or no direct effect on the umbilical
placental circulation [114, 115]. However, umbilical-blood
flow may be altered by hypoxemia secondary
to changes in arterial blood pressure, fetal heart
rate, or the release of vasoactive agents into the systemic
circulation. The umbilical-placental vasculature
is constricted by certain vasoactive agents, such as
prostanoids, norepinephrine, angiotensin II, and bradykinin
[116, 117]. Although total umbilical-placental
blood flow did not change during hypoxia, the total
vascular resistance to flow increased significantly.
Paulick et al. [118] measured pressures at various
sites of the umbilical-placental circulation and calculated
vascular resistances to umbilical-placental blood
flow before and during acute hypoxemia. Total resistance
to flow was calculated from placental blood flow
and the change in pressure between the descending
aorta and IVC. As shown in Figure 9.12, this total resistance
comprises the individual resistance of: (1)
the umbilical arteries and placenta; (2) the umbilical
veins; and (3) the ductus venosus and liver. During
the control period those individual resistances accounted
for 82%, 11%, and 7%, respectively, of the
total resistance to umbilical-placental flow. Hypoxemia
increased resistance in the umbilical veins 2.3-
fold but did not affect resistance in the umbilical arteries
or placenta. Hepatic vascular resistance increased
and ductus venosus resistance decreased, so
the total liver/ductus venosus resistance did not
change. The increased placental outflow resistance,
which resides in the umbilical vein, may increase the
total surface area in the placenta, improving maternal-fetal
blood gas exchange.
Cardiovascular Responses to Stress