Fetal physiology Flashcards
Placenta purpose
Gas (O2/CO2) and nutrient transport, waste removal
Endocrine organ - maintenance of pregnancy and fetal development
Barrier to prevent immunologic attack by mum
Haemochorial placenta
Fetal and maternal blood do not mix directly
Fetal placental tissue is suspended in maternal blood
Basic structure of mature placenta
Fetal side: Chorionic plate and villi
Maternal side: Decidua basalis, intervillus space
Exchange area: Intervillus space
Intervillous space - maternal exchange area
Holds about 500-600mls
Placental perfusion ~500-800ml/min
Blood completely replaced ~2-3 min
Spiral arteries eject blood at ~70mmHg into intervillous space
Intervillous pressure low ~10mmHg
Gradient promotes efficient diffusion
Fetal placental villi are suspended in the intervillous space so are
bathed in maternal blood
Remember: Maternal and fetal circulations and thus blood do not
touch directly.
Villi - fetal part of the placenta
Site of gas/nutrient/waste exchange unit between mum & fetus
Gases diffuse across the villi
Intervillous pool
Location: Within the placenta, between chorionic villi.
Function: Facilitates the exchange of nutrients, gases, and waste between maternal and fetal blood.
Blood Supply: Maternal blood enters through spiral arteries.
Diffusion of Gases in Intervillous Pool
Oxygen Diffusion: From maternal blood in the intervillous pool to fetal blood in the chorionic villi.
Carbon Dioxide Diffusion: From fetal blood in the chorionic villi to maternal blood in the intervillous pool.
Exchange Mechanism: Passive diffusion driven by concentration gradients.
Importance: Ensures the fetus receives oxygen and expels carbon dioxide effectively, critical for fetal health.
Amniotic fluid functions
- Hydraulic brace – protective buffer (like CSF in your brain) – protects the cord from compression.
- Permits fetal body and breathing movements (fetal behaviour).
- Fluid reservoir – blood volume, electrolyte balance, fetal and
maternal fluid balance. - Nutrient reservoir – swallowing
In and Out of amniotic fluid
In: Amniotic fluid is made of fetal urine/lung liquid – but
mainly fetal urine
Out: swallowed, absorbed by placenta, umbilical cord,
skin (until mid-gestation when the skin starts to
keratinise)
Why does the fetus make body and breathing movement
Exercising muscles ready for birth
Movements also co-ordinate brain-body
connections
Growing lungs:
Lungs fluid filled with lung liquid
Respiratory muscle contractions moves lung fluid
Lung fluid movements stretches lungs develops
alveoli
If this is prevented, lungs don’t grow very well (lung
hypoplasia)
Why does the mature fetus not continue to do everything at once like the immature fetus?
From 32 weeks, the fetus significantly increases growth rate
(and thus energy demand)
Mum cannot supply significantly more food or oxygen (energy)
Solution: practice different movements at different times regulated by sleep states, so there is energy to grow and
exercise
Mature sleep states and behaviours
Mature fetuses compartmentalise behaviour relative to sleep state for energy management – to grow and be physically active at the same time.
These general behaviours go with these sleep states
Rapid eye movement (REM) sleep
^Fetal breathing movements (FBMS)
^Swallowing
^ Licking,
^ Eye movements
X Few body movements (atonia or sleep paralysis)
Non-REM (NREM) sleep
^ Body movements
X Fetal breathing movements (FBMS)
X Swallowing
X Licking,
X Eye movements
Fetus survival at low PaO2
The fetus has a low PaO2 but a high saturation (SaO 2) > 70% (left shifted oxygen dissociation curve)
Has more O2 than needed – usually a surplus
Needs a lot of O2 due to high metabolic demand (growth and organ
function). Nearly 2x the adult requirement
The fetal PaO2 is low only because oxygen diffuses down a gradient from mother to fetus.
The fetus cannot be higher than the lowest PO2 in mum (her venous PO2).
The fetus compensates for the low PaO2 to ensure good saturation.
How does the fetus compensate for a low PaO2
Different type of haemoglobin – alpha and gamma, can
hold 2x the amount of O2 than an adult.
Gamma Hb resistance to 2,3 DPG – the
organophosphate that encourages Hb to release O2
Acidity at tissues and within placenta encouraging
release of O2 from haemoglobin (Bohr effect)
Fetal haemoglobin
Hb structure allows Hb to hold 2x the amount of O2 vs.
adult
Adults = 4 moles of O2/1mole of Hb.
Fetus = 8 moles of O2/1mole of Hb
Fetal Hb has different protein structures
Adults: 2 alpha chains & 2 beta chains.
Fetus: 2 alpha chains & 2 gamma chains
Gamma chain differs in amino acid sequences; specifically has
serine not histidine at position 143.
Different amino acid sequence effects 2,3DPG binding
2,3 - DPG
2,3 DPG: Organophosphate from erythrocytes
2,3 DPG acts to reduce Hb O2 affinity
It encourages Hb release of oxygen
Adults: 2,3 DPG binds to the beta Hb protein mainly due to positively charged amino acid histidine 143
Fetus: in the gamma chain, histidine is replaced by serine which
has a neutral charge
Neutral charge reduces 2,3 DPG binding. It encourages Hb holding of O2
↑2,3 DPG binding = O2 release
↓2,3 DPG binding = O2 attraction
Bohr effect
Tissue respiration during metabolism = PCO2 ^ acidity
Bohr effect = in the presence of acid, Hb release O2
PaO2 gas diffusion gradient blood vessel (higher) to tissue (lower)
Haldane effect
Empty Hb preferentially takes up CO2.
PaCO2 gas diffusion gradient tissue (higher) to blood vessel (lower)
Bohr & Haldane in the placenta
Fetal CO2 diffusion into the in the pool acidifies maternal blood (Bohr)
Acidification causes maternal O2 release (Bohr) – diffusion to fetus
++ maternal increase in 2,3DPG throughout pregnancy to help O2 release
Empty maternal Hb takes up CO2 (Haldane), CO2 transported to maternal lungs
++ Fetuses ^ metabolism with advancing age
Mum compensates with changes in
breathing decreasing her CO2 (compensated
respiratory alkalosis) to increase gas
gradient
Adult oxygen dissociation curve
Describes PaO2 - SaO2 relationship and how haemoglobin acquires and releases O2 molecules
Fetal circulation and shunts
Umbilical cord
Ductus venosus - liver
IVC
Foramen ovale = atrium
Ductus arteriosus = lung bypass
Stream one - oxygenated blood from placenta
Placenta
Umbilical vein
Ductus venosus
IVC, no mixing
Right atrium
Foramen ovale
Left atrium
Left ventricle
Ascending Aorta
Umbilical cord has
2x arteries - carry deoxygenated blood to the placenta for oxygenation
1 x vein: carries oxygenated blood from the placenta to the fetus
Whartons jelly
Whartons jelly
Surrounds blood vessels and protects them from being
squeezed
Gelatinous substance similar to that found in eyeballs, contained
in a connective sheath
Rich source of stem cells
Umbilical cord
Ductus venosus (from liver to IVC)
The DV = duct between UV
and the IVC
Arterial blood is shunted
through the DV into the IVC
The DV duct is very narrow
DV is narrow = greater
pressure ejection (faster) of
arterial blood into IVC
DV to IVC
The IVC now has 2 streams of differently oxygenated blood
Oxygenated blood is travelling faster than the deoxygenated blood
The speed prevents mixing of the 2 streams of blood
Can do this effectively for the short distance from DV to right atrium
Foramen ovale
FO is a flap between left and right atria
FO flap kept open by higher pressures in right atrium due to high-speed arterial blood flow. DV ejection blood flow
This streams highest oxygenated blood into ascending aorta
Circulation that feeds organs with highest metabolic demand - brain and heart
Mixing in the right atrium
Stream one adds oxygenated blood to stream two in the right atrium
This increases the oxygen saturation of stream two
Stream two - returning deoxygenated blood
IVC and SVC
IVC, no mixing
Right atrium – pick up some O2 in the RA from stream 1
Right ventricle
Pulmonary artery
Most blood bypasses lung through ductus arteriosus
Descending aorta – pick up more O2 blood from the aortic arch spillover - aortic isthmus
Ductus arteriosus - lung bypass
Blood does not go to lung to be oxygenated
Lungs need some blood for growth, around 8% of cardiac output
Remaining blood is shunted past lungs and into the descending aorta via the ductus arteriosus.
De-oxygenated blood returning to the heart from IVC and SVC picks
up oxygen
In the right atrium
From aortic isthmus spill-over
Causes of hypoxia
Cord occlusion, cord knots, prolapse
Placenta: impaired formation, abruption, haemorrhage
Delivery in the wrong position – e.g. feet first
Premature closure of the ductus arteriosus
Maternal respiratory illness/anaemia
How do adults and fetuses
detect hypoxia?
Peripheral chemoreceptors – carotid and
aortic arch (fetus = carotid dominance)
Central (brain) chemoreceptors -
brainstem, midbrain
Collectively they detect changes in O2,
CO2 - pH
Initiate quick chemoreflex responses
Added to by slower acting factors (eg
endocrine, endothelial factors) to change
respiration and cardiovascular function
Fetal response to hypoxia
Fetal heart rate: Reduce heart rate to reduce metabolic demand -
protect the heart
Blood flow: Send more blood to key organs (e.g. brain, heart) to
support organs with higher metabolic demand
Reduce blood flow to liver: Increase blood flow from placenta (stream one) to key organs and stream more blood through foramen
ovale
Haemoconcentrate: reduce fluid in blood vessels – send it to extracellular space – this aggregates red blood cells and increases O2 delivery per unit of blood
Behaviour: Reduce energy/O2 demands such as body and breathing
movements
Fetal heart: Parasympathetic chemoreflex
Role for parasympathetic in
bradycardia can be demonstrated by
1. Cut the vagus nerves
2. Giving a parasympathetic
muscarinic receptor blocker like atropine.
Chemoreflex control can be
demonstrated by
1. Cutting carotid sinus nerve
Purpose of the fall in FHR?
1. Reduces cardiac work, protects the heart from injury during low O2
Prolonged bradycardia may also be caused by the heart becoming gradually hypoxic itself
Peripheral vascular resistance: Sympathetic chemoreflex
Role for sympathetic in
vasoconstriction can be
demonstrated by
1. Giving an alpha adrenergic
antagonist.
Chemoreflex control can be
demonstrated by
1. cutting carotid sinus nerve
Why does peripheral blood flow fall?
1. Sends blood flow to vital organs with highest metabolic demand
- Supports blood pressure when heart rate falls
Peripheral vasoconstriction
Blood pressure = determined by CO
(stroke volume and heart rate) +
peripheral resistance.
Fetal CO is mainly controlled by heart rate as immature heart structure limits stroke volume.
The fall in heart rate can cause a big change in BP.
Peripheral vasoconstriction supports BP during hypoxia.
Blood pressure is vital for blood flow and O2 delivery and CO2 removal
Blood flow to the brain : not a carotid chemoreflex
Endothelial activity
The change in blood flow to
the brain is not a chemoreflex
Cutting the carotid sinus nerve
does not change brain blood
flow.
It is not due to the increase in blood pressure
It is actively mediated by
vasodilatation due mainly to
endothelial vasodilators like
nitric oxide
This is demonstrated by using nitric oxide donor inhibitors
Haemoconcentration and shunting
Fetus will concentrate red blood cells.
Does this by removing fluid out of the blood vessels to the extracellular space.
This helps concentrate red blood cells, reduces diffusion area at the
tissue site
Ductus venosus – less blood to liver.
Greater streaming into IVC – due to increased flow
Less mixing in RA - due to increased flow
More well oxygenated blood (stream 1) crosses the foramen ovale
Energy conserving behaviour
Switch to non-REM brain activity or reduced brain activity
NREM lower metabolic state – conserves energy
Isoelectric (near complete suppression) if severe.
Activity and growth
Stop making breathing movements, licking, swallowing
Not chemoreflex as carotid denervation does not change them. Apnea is due to
brainstem centres.
Stop making body movements
Not chemoreflex. In fact the fetus makes some body movements to begin with to
try and move away from cord obstructions.
If hypoxia is prolonged and the fetus has adapted, some movements will return to help lungs and body prepare for birth but at the expense of somatic (body) growth
