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Flashcards in Session 9: Fetal Growth and Development Deck (42)
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1
Q

Define the Fetal Period

A

The fetal period is the stage of intra-uterine life from the end of the eighth week (beginning of ninth week) till term. During this time, systems laid down and structures created during the embryonic period grow and mature to fit the individual for birth and post-natal life. The fetal period involves preparation for the transition to independent life after birth.

  • The most important body systems for determining survival outside the uterus are the nervous system, respiratory system, cardiovascular system and urinary system.
  • Pre-Embryonic Period: Fertilisation => 3 weeks
  • Embryonic Period: 3 => 8 weeks
  • Fetal period: 8 => 38 weeks
  • Pregnancy weeks calculated from date of LMP (definable event) i.e. conception weeks +2 so term is 40 pregnancy weeks. However this system is inherently inaccurate.
  • The embryonic period is characterised by intense activity (morphogenesis) – organogenetic period. But absolute growth (increase in mass) is very small – except placenta! Growth and weight gain accelerate in fetal period.
2
Q

Describe the pattern of growth and weight gain acceleration? What is used to measure development in early pregnancy?

A

Growth and weight gain accelerate during pregnancy
Crown Rump Length (CRL) increases rapidly in the pre-embryonic, embryonic and early fetal periods. Weight gain is slow at first, but increases rapidly in the mid and late fetal period. CRL is a good measure of development in early pregnancy.

[*] Embryo

  • Intense morphogenesis and differentiation
  • Little weight gain
  • Placental growth most significant

[*] Early fetus

  • Protein deposition

[*] Late fetus

  • Adipose deposition (part of preparation for independent life after birth – important in thermoregulation).
3
Q

Describe how body proportion changes during pregnancy

A

Body Proportion: body proportions change dramatically during the fetal period

[*] At week 9, the head is approximately half of the crown rump length (A)

[*] Thereafter, body length and lower limb growth accelerates. At birth the head is approximately one quarter of the crown rump length (B, C)

[*] 9 weeks: CRL is ~5cm

[*] 12 weeks: CRL is ~8.5cm

[*] 20 weeks: CRL is ~19cm

[*] 28 weeks: CRL is ~28cm

[*] 38 weeks: CRL is ~36cm.

4
Q

Describe Fetal CO2 and the Lungs

A

Fetal CO2

[*] Maternal CO2 levels are lowered by hyperventilation stimulated by progesterone, which enable the fetus to have a relatively normal pCO2

Fetal Lungs

[*] The fetus makes breathing movements, which draw amniotic fluid into and out of the lungs 1-4 hours each day – ‘flushing lungs with amniotic fluid to keep cells nice and clear’. The lungs develop relatively late but exist by T3 although non-functioning.

[*] Surfactant is produced by type II pneumocytes from around week 20 but production is significantly increased after week 30 when the alveoli open in significant number and the surface area dramatically increases.

[*] Surfactant lowers the alveolar surface tension, such that inspiration is made with less effort post-natally.

[*] A deficiency, usually in pre-term infants, can lead to respiratory distress of the newborn.

5
Q

Describe embryonic development of the lungs

A

there are 4 phases of maturation, which influence the viability of premature infants. The lungs develop relatively late as they are not needed until birth.

[*] Embryonic development creates only the bronchopulmonary tree (airways, no gas exchanging parts)

[*] NB: transoesophageal septum separates GI tract from respiratory tract.

[*] Functional specialisation occurs in the fetal period – creation of a membrane of which gas exchange can occur across.

[*] Major implications for pre-term survival (threshold of viability – viability is only a possibility after 24 weeks).

[*] Survival depends on:

  • The presence of thin-walled air sacs for gas exchange
  • Presence of surfactant to lower surface tension and allow air sacs to expand.
6
Q

For the lungs and breathing, there are 4 stages of maturation. Describe the 1st Stage

A

Pseudoglandular (8-16 weeks): not viable, no air sacs, airways formed only as far as terminal bronchioles.

Duct systems begin to form within the bronchopulmonary segments created during the embryonic period.

7
Q

Describe the 2nd and 3rd stages of lung maturation

A

Canalicular (16-26 weeks):

  • Formation of respiratory bronchioles – budding from bronchioles formed during the pseudoglandular stage.
  • Still no gas exchange but may be viable at the end.
  • More vascular – vascularization of surrounding parenchyma
  • Some terminal sacs

Terminal Sac (26 wk-term): viability improves with age.

  • Terminal sacs begin to bud from the respiratory bronchioles.
  • Some primitive alveoli
  • Differentiation of pneumocytes
    • Type 1: Gas exchange
    • Type 2: Surfactant production from week 20
8
Q

Describe the final stage of lung maturation

A

Alveolar period: late fetal to 8 years (95% of alveoli are formed post-natally)

[*] During T2 and T3 gas exchange occurs at the placenta. At birth, the lungs are filled with amniotic fluid aspirated by fetal breathing movements from wk 12-14, together with secreted fluid. Most is expelled during vaginal birth - any remaining is absorbed. Lungs must be prepared to assume full burden of gas exchange at birth.

  • ‘Breathing’ movement: conditioning of the respiratory musculature
  • Fluid filled: crucial for normal lung development

[*] Pulmonary resistance falls as alveoli open at the first breath. Blood flow increases in the pulmonary vessels.

9
Q

Describe the development of the Nervous System

A

Nervous System: the first to begin development and the last to finish

[*] Whilst withdrawal from pain can be elicited at 15 weeks, thalamo-cortical projections do not reach maturity until week 29.

[*] Corticospinal (anatomical) tracts required for coordinated voluntary movements begin to form in the 4th month. Myelination of the brain only begins in the 9th month.

[*] Completion of myelination in corticospinal tracts is not complete until into the post-natal period (as evidence by increased infant mobility in the 1st year) but musculoskeletal movements are essential for fetal growth.

[*] No movement until week 8

[*] After week 6, a large repertoire of movements develops.

  • ‘Practicing’ for post-natal life.
  • E.g. suckling, breathing
10
Q

Describe the development of the Central Nervous System

A

[*] The brain is the fastest developing organ in the fetus and infant. On average it accounts for 12% of the body weight at birth, falling to around 2% in adults.

[*] During the fetal period, important changes occur – structurally and functionally.

  • Cerebral hemisphere becomes the largest part of the brain – gyri and sulci form after 5 months, as the brain grows faster than the head (cerebellar hemispheres grow larger than the skull)
  • Histological differentiation of cortex in the cerebrum and cerebellum
  • Formation and myelination of nuclei and tracts
  • Relative growth of the spinal cord and vertebral column
11
Q

Describe the development of the Sensory and Motor Systems

A

[*] Hearing and taste mature before vision.

[*] The organ of corti in the inner ear is well-developed in the fetus at 5 months but the retina is immature at birth. Little evidence exists for smell.

[*] The possibility of intra-uterine surgery on the fetus and invasive procedures in intensive care of the premature makes the development of somatic senses such as pain an important issue.

[*] Histological studies suggest that ascending tracts are present, though not myelinated, as early as 19 weeks.

12
Q

Describe the clinical relevance of the development of the Sensory and Motor Systems

A

Fetal movements (‘quickening’)

  • Fetal movements can be seen by ultrasound as early as 8 weeks, but not felt by the mother until about 17 weeks – can be up to 20 weeks in first pregnancy.
  • Low cost, simply method of ante-partum fetal surveillance
  • Reveals foetuses that require follow-up

Viability – is the brain sufficiently mature to control body functions e.g. breathing
Sensory awareness e.g. pain, sound

Maternal/neonatal nutrition and cortical development

13
Q

Describe the fetal cardiovascular system

A

[*] The fetal circulation is adapted to bring oxygenated blood from the placenta to the fetus via umbilical vessels – arranged to ensure oxygenated blood collected by umbilical vein at the placenta is circulated around the fetus.

[*] The fetal lungs receive only the blood needed to sustain their own growth and development.

[*] Rapid and profound changes take place in the circulation at birth, related to the onset of air breathing.

[*] The definitive fetal heart rate is achieved around 15 weeks. Fetal bradycardia is associated with fetal demise. In identified pregnancies, additional surveillance is carried out that will measure fetal heart rate and uterine contractions.

14
Q

Describe the fetal kidneys

A

[*] Fetal waste is ultimately excreted by the placenta.

[*] The functional fetal kidney is the metanephros

  • Ascent is completed and function begins around 10 weeks.
  • Kidneys have a lobulated form, until 4-5 years of age.
  • Glomeruli and some tubules are present at 10 weeks, pelvis, calyces etc by 23 weeks.
  • Histological differentiation of cortex and medulla is almost complete by 8 months.
  • Fetal urine is a major contributor to amniotic fluid volume.
  • Fetal kidney function is not necessary for survival during pregnancy, but without it there is oligohydramnios.
15
Q

Describe the bladder in the fetus

A
  • In the fetus and infant it lies in the abdominal cavity. Urine enters the bladder and is emptied into the amniotic fluid, to be swallowed by the fetus.
  • The bladder fills and empties every 40-60 minutes in fetus – can be seen on ultrasound scans.
  • This is used clinically to assess fetal urinary function.
16
Q

Describe the Fetal Glucose

A

[*] The fetus relies upon relatively high maternal blood glucose to drive glucose across the placenta and support fetal growth and development.

[*] Fetal insulin secretion commences at week 10.

17
Q

Describe the Fetal Endocrine System

A
  • Placental progesterone promotes fetal corticosteroid production especially near term; the steroid is vital for the fetal physiology, particularly in cardiovascular function.
  • Nervous system development, bone and hair growth are mediated via thyroid hormones active from week 12
18
Q

Describe the Fetal Liver

A

The liver stores large amounts of glycogen, which is reflected in changes in fetal abdominal circumference.

19
Q

Describe the factors, which influence the viability of the pre-term neonate

A
  • Threshold of viability: viability is only a possibility once the lungs have entered the terminal sac stage of development (after 24 weeks). Before then the lungs are not sufficiently developed to sustain life hence.
  • Brain development: viability is only possible if the brain is sufficiently mature to control body functions e.g. breathing
  • Respiratory Distress Syndrome

[*] Only affects infants born prematurely

[*] Insufficient surfactant production

[*] If pre-term delivery is unavoidable or inevitable

Glucocorticoid treatment (of the mother)

  • Increases surfactant production in Type II pneumocytes in the fetus => offers some protection during delivery.
20
Q

What techniques are used to assess the foetus?

A

[*] Ultrasound scan

  • Obstetric Ultrasound Scan (USS)
  • Safe
  • Can be used vaginally to query ectopic pregnancy but more routinely used trans-abdominally
  • Can be used early in pregnancy to calculate age and also rule out ectopic, determine number of foetuses etc.
  • Routinely carried out at ~20 weeks – assess fetal growth and fetal anomalies.

[*] Doppler ultrasound

[*] Non-stress Tests (NST)

  • Monitors heart-rate changes associated with fetal movement

[*] Biophysical profiles (BPP)

  • 5 measured variables (combines non-stress with ultrasound so looks at heart rate, breathing, movements, muscle tone and amniotic fluid level)

[*] Fetal movements kick chart

21
Q

What is classified as growth restriction? Differentiate between asymmetrical and symmetrical growth restriction

A

[*] A fetus is regarded as having ‘growth restriction’ if weight is below the 10th percentile for gestational age. Depending on the cause a fetus with growth restriction may be compromised in the uterine environment and require closer monitoring in order to allow the continuation of the pregnancy to term

[*] Symmetrical Growth Restriction

  • Growth restriction is generalised and proportional

[*] Asymmetrical Growth Restriction

  • Abnormal growth lags
  • Relative sparing of head growth
  • Tends to occur with deprivation of nutritional and oxygen supply to fetus
22
Q

Why is it important to estimate fetal age?

A

Estimation of fetal age: it is important to be able to distinguish between a fetus born prematurely, i.e. pre-term and one showing intra-uterine growth retardation (i.e. full term but small).

Age may be estimated by a range of methods of varying accuracy.

23
Q

How can you use duration of pregnancy to measure foetal age?

A
  • Fertilisation age
  • Age since mother’s last menstrual period
  • Confusion may arise from:
    • Irregular cycles (no such thing as a 28-day circulation, implantation bleeding can occur and may be reported as a period, recollection of date may be hazy)
    • Whether calendar months are used (may cause inaccuracies)
24
Q

What development criteria can you use to estimate foetal age?

A

Accurate measurements and predictions can be made in utero by ultrasound

  • Crown-rump (CR) length (used in T1)

Measured between 7 and 13 weeks to date the pregnancy and estimate the Estimated Due Date (EDD).
Scan in T1 also used to check location, number and viability
Becomes less accurate in later pregnancy.

  • Foot length
  • Biparietal diameter of head (used in T2/T3): the distance between the parietal bones of the fetal skull. Used in combination with other measurements to date pregnancies.
  • Abdominal Circumference and femur length used in combination with biparietal diameter for dating and growth monitoring, and is also useful for anomaly detection e.g. foetal growth retardation which may or may not be head-sparing.
  • 3- or 4-D ultrasound: new wave of obstetric ultrasonography but not likely to replace standard ultrasound scan – can be a complimentary tool.
  • Weight after delivery
  • Appearance after delivery
25
Q

How can Symphysis-Fundal Height be used to estimate foetal age?

A

Ante-natal assessment of fetal well-being involves regular measurements of uterine expansion, which is a crude measure of growth of fetus.

  • Distance between symphysis pubis to top of uterus (i.e. fundus). It can be measured with a tape measure (e.g. about 20cm at 20 weeks, 36 cm at 36 weeks then, plateaus).
  • Alternatively, the height of the fundus is assessed in relation to other structures such as the umbilicus or xiphisternum.
  • But can only be done when the uterus has moved into the abdomen - uterus is palpable above the pelvis after gestational week 12.
  • A lag of 4 cm or more of the fundal height is suggestive of intrauterine growth restriction/fetal growth restriction.
  • Sources of variability:
    • Number of fetuses
    • Volume of amniotic fluid
    • Extent of engagement of head
    • The lie of the fetus
26
Q

What is meant by Daily Rhythms`/

A

A fetus has daily rhythms of heart rate, breathing and activity which are good indicators of maturity and development of physiological functions.

Heart rate variability is a good index of developing control systems. This development process continues after birth for 3 or 4 months

27
Q

Describe how amniotic fluid changes during pregnancy

A

[*] Amniotic fluid volume reaches a maximum of 1L around 38 weeks, but may fall as labour nears.

[*] Cells within the amniotic fluid are derived from the amnion and from the fetus. Amniotic fluid also contains a variety of proteins. Biochemical and cytological studies of the fluid are made by amniocentesis and can be used to assess the presence of neural tube defects, chromosomal abnormalities such as Down’s Syndrome etc.

[*] In early pregnancy, amniotic fluid is derived probably by dialysis of fetal and maternal extracellular compartments with some exchange occurring across the fetal skin. With functional maturation of the fetal kidney, fetal urine contributes significantly to the volume in later pregnancy. The fetus also swallows amniotic fluid that is then processed through the fetal gut and kidneys. The gut and the kidneys cannot excrete – there is nowhere for excretory products to go.

[*] Amniotic fluid volumes are assessed by ultrasound.

28
Q

Describe Polyhydramnios and Oligohydramnios

A

An excess, polyhydramnios, is associated with fetal abnormality leading to inability to swallow - oesophageal or duodenal atresia (blind ended oesophagus etc) or CNS abnormalities (unable to coordinate swallowing movements). The fetus is not able to recycle the fluid.
A low volume of fluid, oligohydramnios, is suggestive of poor or absent renal function / renal impairment or reduced placental function (placental insufficiency) such as in pre-eclampsia. But oligohydramnios can be idiopathic with no identifiable pathology.

29
Q

Describe Quickening

A

[*] Maternal awareness of fetal movements from Week 17 onwards

[*] Low cost, simply method of ante-partum fetal surveillance

[*] Reveals foetuses that require follow-up

30
Q

Describe the classification of birth weights

A

many factors influence birth weight, not all pathological.

[*] <2,500g = Growth Restriction

Babies can have low birth-weight because:

  • They are premature OR
  • They are constitutionally small (no underlying pathology) OR
  • They have suffered growth restriction – associated with neonatal morbidity and mortality.

[*] 3,500g = Average

[*] >4,500g = Macrosomia

    • Maternal diabetes increases risk of macrosomia, which carries a larger risk of intrapartine complications e.g. shoulder dystocia
31
Q

Describe the effects of the fetus of poor nutrition during early and the changes, which occur at birth

A

Poor nutrition in early pregnancy

  • Neural tube defects e.g. DiGeorge Syndrome

Poor nutrition in late pregnancy

  • Asymmetrical growth restriction
  • Subsequent oligohydramnios
32
Q

Describe the processes involved in the control of amniotic fluid, volume and composition

A

Amniotic fluid surrounds the fetus, providing mechanical protection (shock absorber) and a moist environment so the fetus does not dehydrate, amongst other functions.

[*] ~10ml at 8 weeks

[*] ~1 Litre at 38 weeks

[*] Falls to ~300ml at 42 weeks

Amniotic fluid is turned over constantly

[*] Early in pregnancy

  • Formed from maternal fluids
  • Fetal extracellular fluid by diffusion across non-keratinised skin of the embryo – ‘fluid leaks out’.

[*] Later in pregnancy

  • Turnover via fetus

Amniotic fluid contains cells from the fetus and amnion. It includes a variety of proteins, and if sampled via an amniocentesis, can be diagnostically useful.

33
Q

How is amniotic fluid filtered? (Discuss the role of the fetal kidneys)

A

[*] The fetal kidneys (metanephros) produce urine which forms a major part of the amniotic fluid, particularly late in gestation.

[*] At 25 weeks the fetus produces ~100ml of hypotonic urine a day rising to about 500ml at term.

  • Adults only produce ~1L a day

[*] Fetus swallows amniotic fluid constantly so the gut absorbs water and electrolytes, leaving debris e.g. dead skin cells to accumulate together with debris from the developing gut, in the fetal large bowel (gut and kidneys cannot normally excrete)

[*] This is meconium, and is usually only secreted by a fetus in distress (such as fetal hypoxia).

[*] This way amniotic fluid is kept pure – this is how amniotic fluid is filtered.

34
Q

Describe the excretion of bilirubin

A

[*] Formed as a result of haemoglobin breakdown in the fetus and mother.

[*] Mother excretes bilirubin via bile – must be conjugated first so the fetus cannot excrete bilirubin via its gut. Bilirubin crosses placenta (after accumulating => generating a gradient) and is excreted by mother.

[*] The neonate may not immediately become able to deal with bilirubin (liver has never had to conjugate bilirubin before during pregnancy, so it takes a little bit of time for the liver to kick in), so neonate jaundice is not uncommon. This is normally physiological not pathological.

[*] Exposure to light (phototherapy stimulates the liver to begin conjugation.

35
Q

Compare the direction of blood flow in the adult to the fetus

A

In the adult, blood returning from the body is pumped by the right heart through the lungs and then by the left heart around the body.

In the fetus, blood from the umbilical vein returns from the placenta to combine with the venous drainage of the gut. In the absence of modification to the circulation, this oxygenated blood would pass through the liver and the lungs and mix with venous blood from the body and brain before it reaches the systematic arteries; thus losing most of its oxygen.

36
Q

Describe the foetal circulation in detail

A

[*] The fetus must cope with low pO2 blood arriving in the wrong place (blood would have lost much of its oxygen before reaching the brain) but this is not a major problem, as in the foetus the lower body is relatively small and not that active metabolically.

[*] Umbilical venous blood (~70% oxygen saturated) is shunted around the liver by the ductus venosus. It mixes with a small amount of desaturated venous blood from the lower body in the ascending inferior vena cava (the venous side of fetal circulation) so saturation drops to 65%.

[*] Mixing with venous blood from the brain, which arrives at the right atrium via the descending superior vena cava, is largely prevented by the crista dividens, which directs the oxygenated blood towards the foramen ovale, a hole between the right and left atrium, which allows blood to by-pass the right ventricle and the lungs and enter the left heart directly. Right atrial pressure > left.

[*] Dexoygenated blood from the brain passes through the right heart towards the lungs. The collapsed (fluid-filled, oxygen-deficient) lungs of the fetus offer a high resistance to blood flow (via hypoxic pulmonary vasoconstriciton) and most of the output of the right heart flows instead through the ductus arteriosus, which links the pulmonary artery with the aorta, joining the latter at a level below the arterial outflow to the brain.

[*] The oxygenated blood directed to the left heart via the foramen ovale is therefore mixed with very little blood from the lungs in the left atrium, and remains well oxygenated (~60%), so that the left ventricle can pump it out to the aorta and up to the brain. Oxygen content is ~ 7 mmol.l-1 which is enough to support brain growth and development.

[*] The remaining arterial flow joins the flow from the ductus arteriosus to supply the rest of the body (whose needs are less critical) and to return to the placenta (which has very low resistance) via the 2 umbilical arteries (branches of internal iliac arteries) for reoxygenation.

[*] In summary, flow goes left heart – right heart rather than vice versa. This pattern of circulation requires that the pressure in the left atrium should be lower than that in the right, so blood will flow the right way through the foramen ovale, and the pressure in the pulmonary artery is higher than that in the aorta, so flow in the ductus arteriosus will be in the right way. Both requirements are met in the fetus because of the high flow resistance of lungs (hypoxic pulmonary vasoconstriction)

37
Q

Describe Adaptations of the Foetal Circulation at birth

A

[*] At birth, a combination of physical trauma and cold temperatures induces the neonate to take its first breath. This leads to a dramatic reduction in pulmonary vascular resistance (removal of hypoxic pulmonary vasoconstriction) and a dramatic rise in arterial pO2.

[*] The fall in pulmonary vascular resistance causes left atrial pressure to rise in response to the right atrial pressure (greater venous return to LA), so closing the foramen ovale (pressure in LA>RA). This occurs within minutes.

[*] Smooth muscle sensitive to high pO2 in the wall of the ductus arteriosus contracts to close the ductus, so both fetal shunts are rapidly closed just by taking the first breath. Both shunts close off completely within a few weeks.

[*] Increased O2 saturation of blood and decreased [prostaglandins] (placenta has been removed) lead to constriction of both ductus arteriosus and the umbilical arteries.

[*] The ductus venosus variably remains open for several days after birth, but closes within two-three months. A sphincter in the vessel constricts shortly after birth, re-directing all blood through the liver sinusoids; this is again regulated by pO2 levels.

  • Stasis of blood in umbilical vein and ductus venosus
  • Clotting of blood
  • Closure due to subsequent fibrosis
38
Q

Describe Oxygen Diffusion across the placenta

A

Oxygen diffuses across the placenta from maternal blood across a thin barrier (haemochorial). The driving factor for this is the gradient of partial pressures between maternal and umbilical blood, as the placenta has a large area for and low resistance to diffusion. The barrier is small – fetal chorionic villi in contact with maternal blood.

[*] Maternal pO2 increased (partly due to hyperventilation in pregnancy) – but this effect is small.

[*] Umbilical venous pO2 entering the foetus must be much lower (compared to normal human adult). This is very important in creating the partial pressure gradient.

39
Q

How is the oxygen transport rate determined? What is fetal heart rate a good indicator of?

A

Oxygen transport rate is determined by the umbilical artery pO2, meaning the fetus gets the oxygen it needs.

[*] Fetal oxygen stores are very low (about 2 minutes worth), which can be a problem in a labour, particularly if the problem involves the placenta. Contraction of the myometrium can compress placenta blood vessels.

[*] Foetal heart rate is a good indicator of foetus O2 saturation.

40
Q

Even with the changes in the fetal circulation, the partial pressure of oxygen in the fetal blood is very low compared to the adult. The fetus is adapted to a degree of hypoxia that would be fatal in a normal adult. How is this achieved?

A

A different haemoglobin – fetal haemoglobin has a much higher affinity for oxygen, and will carry more at a lower pCO2.

  • Fetal pO2 is 4 kPa, human adult pO2 is 13.3 kPA
  • Fetus Hb does not have beta chains (replaced by a different globin => creates a different overall shape => changes its affinity for oxygen), which is better at these lower partial pressures of pO2. It does not readily bind 2,3DPG.
  • The higher affinity of fetal haemoglobin ‘sucks across’ the O2.
  • Fetal Hb is 70% saturated at 4kPa
  • Adult Hb is 45% saturated at 4kPa (insufficient to support life)
  • These adaptations mean that at 4kPa fetal bood contains ~7.5mmol of O2 per litre, a similar amount to what is normally in adult blood.

Higher haemoglobin levels – the neonate has a haemoglobin level of 18 -20 g.dl-1 (human adult is 12-14 g.dl-1)

41
Q

What is meant by the Double Bohr Effect?

A

Double Bohr Effect: an increase in pCO2 or [H+] concentrations results in Haemoglobin losing affinity for and releasing more oxygen. This is called the Bohr effect. This happens both in the maternal and fetal blood (partially because of acid-base changes), so is termed the Double Bohr Effect

The umbilical artery has a higher amount of pCO2 and lower pH compared to the umbilical vein. The uterine artery has a higher amount of pCO2 and lower pH compared to the uterine vein.

Fetus has a higher haematocrit than mum - more Hb and different (HbF).

42
Q

Describe the transfer of CO2

A

[*] Transfer of CO2 is also dependent on partial pressure gradients. However, the fetus cannot tolerate higher pCO2 than the mother due to acid base problems

[*] Placental transfer of CO2 therefore needs to be facilitated by lowering maternal pCO2. This is achieved by hyperventilation, stimulated by progesterone.