Placental respiratory gas exchange and fetal oxygenation
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This document summarizes oxygen transport from the atmosphere to fetal tissues. It describes how oxygen diffuses across membranes in the lungs, placenta, and fetal tissues. While fetal oxygen levels are lower than maternal levels, high fetal cardiac output and blood flow to organs maintains oxygen delivery. The placenta facilitates gas exchange through a villous tree structure that increases surface area from stem to terminal villi. Fetal growth restriction is associated with a smaller, less developed placenta and lower umbilical oxygen levels. In response to acute hypoxia, the fetus redistributes blood flow to favor the brain and heart. Though oxygen therapy increases maternal oxygen levels, there is a smaller corresponding increase in fetal oxygen levels due to the placent
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Placental respiratory gas exchange and fetal oxygenation
- 1. PLACENTAL RESPIRATORY GAS EXCHANGE AND FETAL OXYGENATION
- 2. Transport of Oxygen from the atmosphere to the Fetal Tissues Transport from Atmosphere to alveoli Diffusion across Alveolar membrane Transport from lungs to placenta Diffusion across the placenta Transport from placenta to fetus Diffusion into the fetal tissues
- 4. Po2 & O2 Saturation = fetal blood < maternal blood (late third trimester) Therefore… the oxygenation of a third trimester fetus would define a state of severe hypoxia in post natal life?
- 5. For each of these organs, blood flow that is used to maintain a given oxygen consumption rate is about 2.5 x greater than in the adult. Fetal cardiac output compensates for the low level of oxygenation by maintaining a high ratio of blood flow to oxygen consumption through the circulation of individual fetal organs.
- 6. Development of Oxygen Transport Across the Human Placenta
- 7. Placental Villous Tree : 1. Stem villi – contains much less capillary volume 2. Intermediate villi – greater capillary diameter 3. Terminal Villi - larger surface area
- 8. Hypoxia of Fetal Growth Restriction
- 9. . Fetal Growth Restriction - associated with significantly Low umbilical venous oxygen saturation and Po2 values. The placenta is then noted to be SMALL, - under development of the villous tree, shifting the umbilical Oxygen uptake - reduction in the volume ratio of the Terminal compared with the Intermediate villi -large fraction of the oxygen that the fetus consumes is drawn across the Thick, oxygen consuming barrier of the Intermediate villi
- 10. Therefore…The Uterine-Umbilical Venous Po2 difference is inversely proportional to placental weight* * Development and Mechanisms of Fetal Hypoxia in severe Fetal growth Restriction, Placenta; Regnault, TRH, et al 2007 Structural changes in the placental vascular tree Increasing Impedance to flow Enlargement of the Umbilical Pulsatility Index
- 11. Fetal Response to Hypoxia
- 12. Acute Fetal Hypoxia = redistribution of cardiac output favoring the CNS and the heart = placental blood flow and cardiac output tend to remain constant The Limit as to a successful circulatory defense against Acute Hypoxia is reached is when the perfusion rate of the CNS And Heart has reached its maximum.
- 13. Oxygen Therapy
- 14. “Inhalation of oxygen by a pregnant patient can dramatically increase the Po2 of the maternal arterial blood but causes a small increase in fetal Po2.”
- 15. The conclusion is that, Po2 change of 410 mmHg in maternal arterial blood results in a Po2 increase of only 4 mmHg.* * Transfer of oxygen across the placenta, Meschia, G, 1977
- 16. “Oxygen therapy may show similar increments in the oxygen content of maternal AND Fetal blood. “ “ An Increase of 1 mM Total blood O2 in Maternal blood , results in an increase of 0.7 mM Total blood O2 in Fetal Blood.”
- 17. Thank You…
Editor's Notes
- Can be visualized as a sequence of six steps… Step 1: transport of o2 from the atmosphere to the alveoli is maintained by the respiratory muscles responsible in taking air in and out of the lungs to maintain the p02 of oxygen in the alveoli Step 2: the oxygen now diffuses from the alveoli into the maternal red blood cells that circulate though the lungs Step 3: Maternal blood will transport oxygen from the lungs to the gravid uterus (via the pulmonary veins, left atrium, left ventricle, aorta, uterine arteries and branches of the ovarian nad vaginal arteries
- Important aspect of fetal physiology is that during last third of gestation, fetal blood has much lower 02 sat and p02 values than maternal blood. At sea level, Maternal blood: fetal blood Po2 = 100 mmHg:35mmHg Maternal blood : fetal blood o2 sat = 96%:81%
- In the near term placenta (39weeks), the villous tree is subdivided into 3 parts, namely: …. The terminal villi has a larger surface area than the intermediate villi therefore creating greater capillary volume than the intermediate villi. But this villi only starts to form during the 23rd week of fetal life, therefore umbilical oxygen uptake at mid gestation occurs almost exclusively via the intermediate villi… As the gestation enters into the third trimester, terminal villi plays the larger role of capillary uptake of oxygen.
- ***Fetal cardiac output compensates for the low level of oxygenation by maintaining a high ratio of blood flow to oxygen consumption through the circulation of individual fetal organs. Significantly low because even the umbilical pulsatility index ( measure of blood velocity in the umbilicus ) is >2 SD above normal and an abnormal heart rate close to the limits of fetal viability
- Which brought one study on FGR models by Regnault et al in 2007 to a conclusion that… But this still does not explain the reason why the umbical-uterine venous po2 is below normal. Which brought them to a theoretical consideration that:
- The circulation of an otherwise, non anesthetized healthy fetus reacts to an acute decrease in umbilical venous and arterial Po2 in a predictable manner. The fraction of cardiac output directed toward the CNS and heart at the expense of other parts of the fetal body. The functional meaning of this relationship is that, to be able to mount a successful defense against hypoxia, the fetus must keep the flow of oxygen to the CNS and heart at a constant or nearly constant level. Between physiologic hypoxia and hypoxia that would later on result to petal growth restriction, causing redsitribution of cardiac output to the CNS and the heart has a broad range. Extensive studies have been done to fetal lamb, stating that ovine and human fetus reacts similary to acute hypoxic events, however, as dramatic the reponse of redistribution of flow to fetal lambs, therefore, the human fetus may not be able to produce a percentage increase in cerebral blood flow as dramatic as that of the species with a small brain.
- This observation seems to contradict the empiric knowledge that oxygen therapy can be effective in improving fetal oxygenation.
- It readily explains the small effect of oxygen therapy on fetal po2.
- If we focus on po2 and exclude other considerations, we could be tempted to conclude thatmaternal oxygen therapy has no significant effect on fetal oxygenation. However, oxygen therapy may also show significant increments of MATERNAL AND FETAL blood. Which may therefore conclude that Oxygen therapy is effective in increasing fetal oxygenation.