Session 9 not completed Flashcards
Where does maternofetal circulation take place?
Materno-fetal exchange happens at the placenta
Fetal circulation:
- Oxygenated blood carried via the umbilical vein
- Deoxygenated blood carried via the umbilical arteries
- Fetal capillaries within chorionic villi - Increase surface area
Maternal circulation:
- Uterine arteries • Uterine veins
- Maternal blood lakes in the intervillous spaces (cotyledons)
How does gas exchange occur at the placenta?
- Diffusion barrier - Small, and decreases as pregnancy proceeds
- Gradient of partial pressures required
- Maternal pO2 increases only marginally, therefore to make the gradient work, fetal pO2 must be lower than maternal pO2
- Fetal blood has low pO2 - approx. 4kPa compared to normal adult pO2 of 11 – 13kPa
- But there are factors that increase fetal O2 content
- Fetal haemoglobin variant
- Fetal haematocrit is increased over that in the adult.
Additional factors Promoting O2 exchange to the fetus at the placenta:
- Increased maternal production of 2,3 DPG - Secondary to physiological respiratory alkalosis of pregnancy
- Fetal haemoglobin
- Double Bohr effect
Structure of fetal haemoglobin?
- Predominant form from weeks 12 – term is HbF
- 2 alpha subunits plus 2 gamma subunits instead of 2 alpha subunits with 2 beta subunits (adult)
- Greater affinity for oxygen because it doesn’t bind 2,3-DPG as effectively as HbA
Synthesis of adult haemoglobin occurs at beginning of second trimester although mainly HbF
How does the transfer of O2 from mother to fetus use the double bohr effect?
- Speeds up the process of O2 transfer
- As CO2 passes into intervillous blood (from foetus), pH decreases. this causes the Bohr effect - Decreasing affinity of Hb for O2 as pH decrease so more likely to give it up
- At the same time, as CO2 is lost, pH rises • Bohr effect on other side • Increasing affinity of Hb for O2
How does CO2 transfer take place between mother and foetus?
- Maternal physiological adaptation to pregnancy
- Progesterone-driven hyperventilation
- Hence lower pCO2 in maternal blood which creates concentration gradient.
- Double Haldane effect - Oxygenation of blood in the lungs displaces carbon dioxide from maternal haemoglobin which increases the removal of carbon dioxide. Same happens in placenta, oxygenation of foetal blood in the placenta displaces carbon dioxide from from foetal haemoglobin which increases removal of carbon dioxide.
- As Hb gives up O2, it can accept increasing amounts of CO2
- Fetus gives up CO2 as O2 is accepted • No alterations in local pCO2
Describe the fetal circulation
- Receives oxygenated blood from mother via placenta in umbilical vein which enters right side of the heart.
- Lungs are non-functional so blood by-passes the lungs
- Returns to the placenta via umbilical arteries insert
Why are shunts required in the fetal circulation?
Ductus venosus
- DV connects umbilical vein carrying oxygenated blood to the IVC
- Blood enters right atrium
- By ensuring shunting of blood around the liver (liver is highly metabolically active), oxygen saturation is mostly maintained.
- Drops from 70% to 65
Foramen ovale - located in interatrial septum
- Right atrial pressure is greater than that in the left atrium
- Forces leaves of FO apart and blood flows into LA
- Free border of septum secundum forms a “crest” – crista dividens - Creates two streams of blood flow
- Majority flows to LA
- Minor proportion flows to RV, mixing with blood from SVC (deoxygenated). RV is muscular structure so needs to be used a bit to avoid atrophy and ensure proper development.
Left atrium • Small amount of pulmonary venous return. This is deoxygenated
- Blood reaching left atrium has saturation approx. 60% due to mixing from pulmonary venous return and some lost along circulation.
- Pumped by LV to aorta • Heart and brain get majority share of oxygen.
Ductus arteriosus
- Shunts blood from RV and pulmonary trunk to aorta
- Blood joins aorta distal to the supply to the head (and heart)
- Joins after branches of early aorta minimising drop in O2 saturation
What is the fetal response to hypoxia?
Fetus lives in hypoxic environment in order for gas to diffuse
Adaptations to manage transient decreases in oxygenation:
- HbF and increased [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
- Fetal chemoreceptors detecting decreased pO2 or increased pCO2
- Vagal stimulation leading to bradycardia - in adult normally you would have vagal inhibition leading to tachycardia
- Chronic hypoxaemia causes growth restriction and behavioural changes - Impact on development
Describe how hormones and nutrition affect foetal growth during pregnancy
- Hormones necessary for fetal growth:
- Insulin
- Insulin-like growth factor I (IGF1) and IGFII
- IGF II nutrient independent, dominant in first trimester
- IGF1 nutrient dependent, dominates in T2 and T3
- Leptin - Placental production
- Plus epidermal growth factor, tumor/transforming groth factor alpha
First 20 weeks, growth is facilitated mainly by hyperplasia, 20-28 weeks both hyperplasia and hypertrophy and after 28 weeks hypertrophy is the primary method of growth.
Effects of maternal nutrition on fetal growth during pregnancy:
- Malnutrition can cause symmetrical or asymmetrical growth restriction (areas left to preserve more important structures, mainly brain)
- Nutritional and hormonal statusof mother during fetal life can influence the adult that the foetus becomes health in later life - “developmental origins of health and disease hypothesis” - Mechanisms not well understood - likely to be placental adaptive responses to alterations in hormonal and / or nutritional status
What is amniotic fluid and how is it produced/recycled?
- Amniotic sac encloses embryo / fetus in amniotic fluid
- Protection
- Also contributes to development of lungs
- Volume - 10 ml at 8 weeks. Approx 1 litre at 38 weeks
- Falls away post expected date of delivery likely to be related to deteriorating function of placenta.
Production and recycling of amniotic fluid
• Vast majority of amniotic fluid from fetal urinary tract - urine production by 9 weeks - Up to 800 ml/day in T3
Small amount produced by the Fetal lungs and Fetal GI tract
• Placenta and fetal membranes contribute small volume through intramembranous pathway (predominant method of amniotic fluid production in early pregnancy.)
Composition: • 98% water • Plus electrolytes, creatinine, urea, bile pigments, renin, glucose, hormones and fetal cells, lanugo and vernix caseosa (waxy protective substance)
- Swallowed
- Absorbs water and electrolyes
- Debris accumulates in gut - substance called Meconium (green substance usually passed after birth in first bowel movement).
- Debris from AF plus intestinal secretions including bile - will be green as mecoium passed early. Sign of foetal distress if seen outside in amniotic fluid.
What is amniocentesis?
- Sampling of amniotic fluid - low risk and relatively non-invasive.
- Allows for collection of fetal cells
- Useful diagnostic test • E.g. fetal karotyping (can also be done from chorionic villi from placenta although much higher risk and more invasive)
Describe bilirubin metabolism for the fetus
- During gestation clearance of fetal bilirubin is handled efficiently by the placenta
- Fetus cannot conjugate bilirubin due to immaturity of liver and intestinal processes for metabolism, conjugation and excretion
- Physiological jaundice common at birth
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