Fetal placental blood flow

In the placenta a volume of oxygen sufficient for fetal needs must diffuse across the membranes from maternal to fetal blood during the short time the two circulations are in close contact. This oxygen transfer is a function of several factors which include uterine and umbilical arterial 02 partial pressures, maternal and fetal placental blood flow rates, the 02 capacity and 02 affinity of maternal and fetal hemoglobin, the diffusing capacity of the placenta, the amount of C02 exchanged, and the vascular arrangement of maternal to fetal vessels. 

Normal values for the various determinants of 02 transfer are necessary for quantitative analysis of the exchange process. Some values— e.g., those for the maternal and fetal arterial 02 tensions, 02 capacities, and 02 affinities—are fairly well defined. Others—e.g., the diffusing capacity and maternal and fetal placental blood flows—are less well determined. 

Consumption. Our model predicts that the maternal and fetal end-capillary p02 difference would be less than 1 mm Hg. Experimentally the uterine vein to umbilical vein (V-v) po2 difference is from 10-15 mm Hg (41,42). Possible explanations for the large V-v difference are placental 02 consumption (22), uneven distribution of maternal and fetal placental blood flows (27), and vascular shunts (25, 26). 

Effect of Varying Fetal Placental Blood Flow. The effects of changes in umbilical flow, Qf, are shown in Figure 12. As umbilical flow increases, it can carry more 02, and the end-capillary p02 decreases until finally at infinitely rapid flow rates the po2 approaches umbilical arterial p02. A small end-capillary po2 difference becomes apparent at high values of Qf because of a diffusional limitation. The 02 transfer rate varies almost linearly with Qf over the range from 100-400 ml/min. Above... 

Effects of Changing Maternal and Fetal Placental Blood Flows Together. Figure 13 shows the effects of varying maternal and fetal blood... 

Ergot alkaloids contain lysergic acid (formula in A shows an amide). They act on uterine and vascular muscle. Ergo-metrine particularly stimulates the uterus. It readily induces a tonic contraction of the myometrium (tetanus uteri). This jeopardizes placental blood flow and fetal O2 supply. The semisynthetic derivative methylergometrine is therefore used only after delivery for uterine contractions that are too weak. 

During the antepartum period, oxytocin induces uterine contractions that transiently reduce placental blood flow to the fetus. The oxytocin challenge test measures the fetal heart rate response to a standardized oxytocin infusion and provides information about placental circulatory reserve. An abnormal response, seen as late decelerations in the fetal heart rate, indicates fetal hypoxia and may warrant immediate cesarean delivery. 

The effect of the sympathomimetic drugs on the pregnant uterus is Vciriable and difficult to predict, but serious fetal distress can occur, due to reduced placental blood flow as a result both of contraction of the uterine muscle (a) and arterial constriction (a). Pj-agonists are used to relax the uterus in premature labour, but unwanted cardiovascular actions can be troublesome. Sympathomimetics were particularly likely to cause cardiac arrhythmias (p, effect) in patients who received halothane anaesthesia (now much less used). 

Although furosemide has embryotoxic properties in some animal species, it has been widely used in pregnant women without any adverse effects. Nevertheless, it should be used with great caution, since hypovolemia can lead to reduced uterine and placental blood flow. Careful monitoring of fetal heart action is necessary. Furosemide passes the placenta and increases fetal urine production. It can also increase acid concentrations in maternal serum, fetal serum, and amniotic fluid, thus masking a useful index for the development of pre-eclampsia (24). Its use in pregnant women should therefore be restricted to the treatment of cardiac failure. 

Effect of Varying Maternal Placental Blood Flow. Figure 11 shows the dependence of end-capillary p02 on maternal placental flow, Qm. At large flow rates the p02 of end-capillary blood approaches that of the maternal artery. At lower rates of flow the equilibrated po2 value decreases because less 02 is available for exchange. The rate of 02 transfer follows a trend similar to that of end-capillary po2, except that increases in above 300-400 ml/min result in little additional 02 transfer because the rise in mean maternal p02 adds little 02 content to the flat part of the fetal oxyhemoglobin saturation curve. 

Wootton, R., I.R. McFayden and J.E. Cooper, 1977. Measurement of placental blood flow in the pig and its relation to placental and fetal weight. Biol. Neonate 31, 333-339. 

Figure 3. Diagrammatic representation of maternal and fetal placental exchange vessels with uniform dimensions and concurrent flows. As the blood flows along the capillaries, Ot diffuses in a one-dimensional plane from maternal to fetal blood.

Discussion of Assumptions of the Model. The pattern of maternal to fetal placental flow affects the amount of 02 transferred. It seems unlikely that the simple concurrent system shown in Figure 3 accurately represents the placental capillaries in sheep, a species in which the exchange vessels interdigitate in a nonuniform and complex manner (30, 31). The flow patterns are also complicated in humans where maternal blood enters the intervillous spaces from the base and flows upward and outward past fetal capillary loops in placental villi. Physiological studies also fail to reveal a simple geometric flow pattern. For... 

Effect of Varying Fetal Arterial 02 Tension. Placental exchange has usually been considered limited by either maternal and fetal blood flows or by diffusion. The present analysis suggests umbilical arterial p02 (Pf) is a third and very important factor, based on the observation... 

Role of Various Factors in Placental O2 Transfer. These experiments characterize the dependence of 02 transfer and umbilical venous po2 on maternal arterial p02> fetal placental flow rate, and fetal inflowing po2 on O2 exchange in a single cotyledon of the sheep placenta and on fetal placental flow in the rabbit placenta. Each factor was studied individually while the fetal placental circulation was isolated and perfused in situ. The present findings do not apply for an intact fetus whose blood recirculates between peripheral tissues and the placenta because compensations would tend to maintain 02 transfer equal to fetal 02 consumption in this latter instance. The present data take account of changes in only a single variable. 

If it is true that the rate of umbilical blood flow remains constant in spite of spontaneous fluctuations in 02 need and delivery, then there are important consequences for fetal homeostasis as recently discussed by Faber (50). A constant umbilical blood flow would assure that intravascular, hydrostatic pressures would remain constant in fetal placental capillaries, and the balance of maternal-fetal hydrostatic forces determining transplacental water movement would be maintained. The fetus would not gain or lose water as might otherwise happen if umbilical flow and pressure were to vary in response to different fetal 02 needs. The fetus could avoid becoming dehydrated during periods of increased 02 transport. 

---