Foetal Physiology Flashcards
Describe how and where materno foetal exchange occurs
Materno-foetal exchange happens at the placenta. Umbilical arteries and umbilical vein branch into foetal capillaries within chorionic villi – giving a large surface area. Uterine arteries and uterine veins form maternal blood lakes in the intervillous spaces. Note this means oxygenated blood is carried via the umbilical vein and deoxygenated blood carried via the umbilical arteries.
How big is the diffusion barrier in the placenta? Is it always the same? How is a diffusion gradient established across this barrier?
The diffusion barrier at the placenta is small and decreases as pregnancy proceeds. A gradient of partial pressures is required but Maternal pO2 increases only marginally, therefore to make the gradient work, foetal pO2 must be lower than maternal pO2.
How does the foetus allow for its much lower partial pressure of oxygen?
Foetal blood has low pO2, approximately 4kPa compared to normal adult pO2 of 11 – 13kPa. However, there are factors increasing foetal O2 content: Foetal haemoglobin variant, foetal haematocrit (ratio of red cells to blood volume) is increased over that of an adult, increased maternal production of 2,3 DPG which is secondary to physiological respiratory alkalosis of pregnancy.
Describe foetal haemoglobin?
From week 12 the predominant form is HbF. This is created from 2 alpha subunits plus 2 gamma subunits. This gives greater affinity for oxygen because it doesn’t bind 2,3-DPG as effectively as HbA.
What is the double bohr affect?
The double Bohr effect speeds up the process of O2 transfer. As CO2 passes into intervillous blood, pH decreases and this decreases the affinity of maternal Hb for O2. At the same time, as CO2 is lost, pH rises increasing affinity of foetal Hb for O2.
Describe the role of progesterone in CO2 tranxfer and the double haldane effect
CO2 Transfer – progesterone-driven hyperventilation causes lower pCO2 in maternal blood giving a concentration gradient at the placenta so the maternal blood can remove foetal CO2. Double Haldane effect – as Hb gives up O2, it can accept increasing amounts of CO2. Foetus gives up CO2 as O2 is accepted so there is no alterations in local pCO2.
Why is the ductus venosus needed?
Ductus venosus – connects umbilical vein carrying oxygenated blood to the IVC which enters the right atrium. By ensuring shunting of blood around the liver, saturation is mostly maintained – Drops from 70% to 65.
Why is the foramen ovale needed?
Foramen ovale – right atrial pressure is greater than that in the left atrium. Forces leaves of the foramen ovale apart and blood flows into LA. Free border of septum secundum forms a “crest” – crista dividens. This creates streams of blood flow optimising flow to LA. Minor proportion flows to RV, mixing with blood from SVC (deoxygenated).
Why is the ductus arteriosus needed and is there any pulnonary venous return?
Ductus arteriosus – Shunts blood from RV and pulmonary trunk to aorta. Note it joins aorta distal to the supply to the head (and heart) minimising drop in O2 saturation. Left atrium – Small amount of pulmonary venous return – deoxygenated. Blood reaching left atrium has saturation approx. 60%. Heart and brain get majority of blood pumped from LV
What is special about the foetus’ response to hypoxia, and how can this response cause problems for the foetus?
The foetus has adaptations to manage transient decrease in oxygenation. HbF and increased concentration of Hb. Redistribution of flow to protect supply to heart and brain (reducing supply to GIT, kidneys, limbs). Foetal heart rate slows in response to hypoxia to reduce O2 demand. Foetal chemoreceptors detecting decreased pO2 or increased pCO2 causes Vagal stimulation leading to bradycardia. Chronic hypoxaemia (such as when mother smokes) causes growth restriction, behavioural changes and has an impact on development.
What hormones are necessary for foetal growth?
Hormones necessary for foetal growth: Insulin, IGFI and IGFII (IGF II nutrient independent, dominant in first trimester, IGF1 nutrient dependent, dominates in T2 and T3) and Leptin. Placental production – Plus EGF, TGFa.
What are the different types of growth that occur in the foetus and what occurs in malnutrition?
In the first 20 weeks, the main cellular growth mechanism is hyperplasia, in weeks 20-28 you have a mixture of hyperplasia and hypertrophy and in the final weeks it is predominantly hypertrophy. Malnutrition can cause symmetrical or asymmetrical growth restriction. Nutritional and hormonal status during foetal life can influence health in later life. Placental adaptive responses to alterations in hormonal and/or nutritional status.
What is the amniotic sac and what does it do?
Amniotic sac encloses embryo/foetus in amniotic fluid. Its function is protection and contributes to development of the lungs (practice breathing takes amniotic fluid into the lungs). Volume is about 10 ml at 8 weeks, approx. 1 litre at 38 weeks – Falls away post estimated delivery day.
How is amniotic fluid produced and recycled?
Foetal urinary tract – urine production by 9 weeks – Up to 800 ml/day in T3 which forms the amniotic fluid. Foetal lungs and Foetal GI tract absorb some with breathing and swallowing. Finally some is absorbed into the placenta and foetal membranes (intramembranous pathway).
What does amniotic fluid compose of?
98% water plus electrolytes, creatinine, urea, bile pigments, renin, glucose, hormones and foetal skin cells, lanugo (fine hair) and vernix caseosa (water proofing for the foetus).
