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126 J. Itskovitz-Eldor, I. Thaler<br />

Fig. 9.12. Sites of pressure<br />

measurements (arrows) and<br />

calculations of vascular resistance<br />

(R) to umbilical-placental<br />

blood flow. This total resistance<br />

comprises the following<br />

individual resistances: R [Ao-<br />

Uvp] resistance presented by<br />

the umbilical arteries plus placenta.<br />

R[UVp-PS] resistance<br />

across the unbilical veins. R<br />

[PS-IVS] combined resistance of<br />

the ductus venosus and liver.<br />

(Reprinted from [118] with permission)<br />

tus is a function of umbilical blood flow and oxygen<br />

content of umbilical venous blood. In general, maternal<br />

conditions affect uterine blood flow (hypotension,<br />

obstruction of the IVC) or uterine arterial blood oxygen<br />

content (hypoxia, anemia) without affecting umbilical<br />

blood flow significantly. Fetal conditions principally<br />

influence umbilical blood flow (umbilical cord<br />

compression, hemorrhage) but may also affect umbilical<br />

venous oxygen content (anemia, polycythemia)<br />

[119]. Oxygen delivery to the fetus can be reduced<br />

experimentally by administering a low-oxygen gas<br />

mixture to the mother [120] restricting uterine [53,<br />

97] or umbilical [59, 94] blood flows, fetal hemorrhage<br />

[92], or altering fetal hemoglobin concentration<br />

[120, 121] or its affinity for oxygen [122, 123].<br />

Acute Hypoxia<br />

Circulatory adaptation to acute hypoxic stress is accomplished<br />

by changes in the distribution of cardiac<br />

output secondary to the responses of the vasculature<br />

in the various organs. In general, blood flow to the<br />

priority organs (brain, heart) increase with maintenance<br />

of oxygen delivery, whereas blood flow and<br />

oxygen delivery to organs that are less essential for<br />

immediate survival decreases [115, 116, 124].<br />

Umbilical blood flow reduction is associated with<br />

decreased fetal cardiac output, which is closely related<br />

to the decrease in umbilical venous return; when flow<br />

is reduced by 50%, fetal cardiac output is reduced by<br />

about 20% [94]. With maternal hypoxemia or uterine<br />

blood flow reduction, fetal cardiac output may be<br />

maintained during mild hypoxemia but decreases by<br />

about 20% with more severe hypoxia [97, 114]. The<br />

changes in distribution of fetal cardiac output and actual<br />

organ blood flows associated with umbilical<br />

blood flow reduction show several similarities, as well<br />

as a number of significant differences, when compared<br />

with the findings during maternal hypoxemia<br />

or uterine blood flow reduction. In the latter situation,<br />

the proportion of cardiac output and the actual<br />

blood flow increase to the brain and myocardium but<br />

decrease to the lungs. Whereas the percentage of cardiac<br />

output and the actual blood flow to the carcass<br />

(skin, muscle, bone) and to the splanchnic organs decrease<br />

during maternal hypoxemia or uterine blood<br />

flow reduction, they increase during cord compression<br />

(Fig. 9.13). Thus although the total umbilicalplacental<br />

vascular resistance increases during cord<br />

compression, total fetal body vascular resistance does<br />

not change significantly [94]. Maternal hypoxemia<br />

and uterine blood flow reduction are associated with<br />

increased fetal body vascular resistance but with only<br />

a small change in umbilical-placental vascular resistance<br />

[97, 114, 118].<br />

It is possible that the increase in peripheral blood<br />

flow during umbilical blood flow reduction may serve<br />

as a mechanism for augmenting venous return to the

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