NEWBORN 1. BP 2. Pulse rate 3. CO (L/min) 4. Cardiac Index (L/m2/min)

1. 70/45 2. 140 3. 0.6 4. 2.5-3

Gametes - Foetal Physiology Flashcards by Michelle Doody

First organ system developed - necessary to sustain viable embryo

circulatory system

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Critical period for development of circulatory system

day 20 - day 50

wk 3 - begins development

wk 4 - functioning heartbeat

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How far does the foetus need to be from blood supply to become hypoxic

150 um from blood supply

formation of new BVs through angiogenesis

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Function of ductus venosus

Links umbilical vein with IVC - allows blood to bypass foetal liver

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How is flow through ductus venosus regulated

By sphincter

50-80% of blood can avoid hepatic sinuses

If there is enough pressure on sphincter it will open (if there is an overload - uterine contractions compress BVs and more blood to foetal heart - overload)

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Function of foramen ovale

Links RA with LA

blood flow: RA → LA, then upwards to ascending aorta

makes sense - most oxygenated blood goes to brain & spinal cord, avoids oxygen rich blood going to pulmonary circulation

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What does ductus arteriosus link

how does it control blood flow

Links pulmonary artery with descending aorta

Decreased blood flow to non-functioning lungs

10% of foetal blood travels via lungs - growth and development of lungs

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Overview of foetal circulation

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Site of oxygenation in foetus

Placenta

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How does oxygen traverse the placental membrane

Difference in partial pressure

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proportion of blood that bypasses the immature foetal liver

80%

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Where is there mixing of blood

in RA

Speed ensures only a small amount of mixing

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What happens to the foramen ovale at birth

Removal of placenta results in decreased venous return - causes decreased RA pressure

Neonate takes their 1st breath - once opened there will be a decrease in pulmonary resistance - this contributes to decrease in RA pressure

=> more blood flow to pulmonary circulation - increase in LA blood flow

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Most common atrial septal defect

Patent foramen ovale

Alone - no haemodynamic importance as pressure in LA > RA so keeps it closed

With other defects e.g. cyanosis of skin and mucus membrane

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Closure of ductus arteriosus at birth - depends on

Oxygen

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pO2 in foetal ductus arteriosus

15-20 mmHg

by the time the blood goes to maternal sinuses - the pO2 will have dropped to about 15

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pO2 in neonatal ductus arteriosus

100 mmHg

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Critical point pO2 in relation to closure of DA

50 mmHg (pO2 is normally 100 mmHg in artery)

Bradykinin from lungs and PGs E2/F2

=> VasoC

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Primary function of DA

Bypass pulmonary circulation bevause oxygenation is not happening there

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Problems associated with patent ductus arteriosus (1 in 5500)

Infants - few problems

Adults - increased re-circulation, increased cardiac output

Decreased cardiac and respiratory reserves

(Less O2 blood being circulated - in an attempt to get enough O2 to tissues there is increased cardiac output - increased BP, decreased cardiac and resp reserves because HR and stroke vol will be increased so there won’t be reserve to increase it more during times of stress/exercise)

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When does the ductus venosus close

how does pressure in portal system change as a result

within 1-3 hours

Pressure in portal system increases by 6-10 mmHg to force blood through the liver

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NEWBORN

BP
Pulse rate
CO (L/min)
Cardiac Index (L/m2/min)

70/45
140
0.6
2.5-3

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ADULT

BP
Pulse rate
CO (l/min)
Cardiac index (L/m2/min)

120/80
70
5
2.5-3

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Newborn BP

70/45

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Newborn pulse rate

140

newborn CO

0.6 L/min

newborn CI

2.5-3 L/m2/min

Adult pulse rate

Adult CO

Adult Cardiac Index

2.5-3 L/m2/min

When do foetal respiratory movements decrease

In 3rd trimester PROTECTIVE MECHANISM * Decreased foetal growth * Decreased foetal waste in amniotic fluid * Decreased resp movements - decreased swallowing of wastes

Blood flow related to maternal sinuses

Uterine arteries to uterine vein

Placenta - organ type

Foeto-maternal organ

What are the foetal capillaries

Chorionic villi - dip into maternal sinuses but no direct contact Gas exchange across capillary wall

pO2 maternal sinuses

50 mmHg

pO2 foetal vein

30 mmHg

pO2 foetal artery

20 mmHg by the time blood has come back around again (offloaded O2 on its way)

pCO2 maternal sinuses

45 mmHg

pCO2 foetal vein

45 mmHg

pCO2 foetal artery

46 mmHg this small difference in pCO2 (compared with maternal sinuses - 45 mmHg) drives CO2 from foetal side into maternal circulation this change in CO2 causes a localised change in pH which allows further O2 to be carried by foetal blood

What difference drives O2 into foetal circulation

pO2 maternal sinuses (50 mmHg) - pO2 foetal vein (30 mmHg)

What happens in adults if pO2 drops to 60 mmHg

Peripheral chemoreceptors are triggered - causes hyperventilation to bring it back up to pO2

ADULT Hb 1. Name 2. Polypeptides 3. 2,3-DPG 4. Conc

1. Hb-A 2. α, β 3. 2,3-DPG binds well 4. 14.8g/100ml

FOETAL Hb 1. Name 2. polypeptides 3. 2,3-DPG 4. Conc

1. Hb-F 2. α, δ 3. 2,3-DPG binds poorly 4. 16.8g/100ml

How does foetus survive at low pO2

Oxygen dissociation curve shifts to left - little binding of 2,3-DPG =\> at any given pO2, foetal Hb carries 20-30% more O2 than adult Hb

Oxygen dissociation curve for foetal vs maternal blood

Uterine blood flow

Increased maternal CO Increased up to 500ml/min to uterus

How do oestrogen and progesterone affect blood flow

Oestrogens increase uterine vasodilation Progesterone increase uterine venoconstriction - diminishes rate at which blood leaves the area - pooling of blood

Double Bohr effect

Increase in pH shifts O2 dissociation curve to left

Alkaline conditions

Binds more O2 at any given pO2

Acidic conditions

Binds less O2 at any given pO2

What happens when CO2 dissolves to maternal circulation

Localised decrease in foetal pCO2 and increase in pH Foetal O2 dissociation curve shifts to left =\> at any pO2 foetus binds more O2 than mother

What happens when CO2 dissolves to maternal circulation

Localised increase in maternal PCO2 and decrease in pH Maternal O2 dissociation curve shifts to the right At any pO2 mother binds less O2 than foetus

What happens with the removal of placenta (foetus' supply of O2)

Hypoxia (foetus has been surviving in hypoxic conditions) and hypercapnia HYPERCAPNIA stimulates first breath Slight asphyxiation (lack of O2) at birth as neonate travels through birth canal Increase in pCO2 via central chemoreceptors - stimulation of first breath (air moves in // diaphragm contracts, volume in cavity increases, pressure decreases - Boyle's law - external ICs contract to pull ribcage out)

Pressure volume curve for baby's first/second breath

Neonate resp rate

40 breaths per min

Neonate TV

16 ml/min

Neonate minute vol

640 ml/min

Neonate FRC

1/2 adult value

FRC of neonate - consequence of a decrease in FRC

Rapid changes in blood gases can occur if resp is altered

Define FRC

Vol of lungs in lungs at the end of a normal exp - prevent fluctuation of gases - no yo yo like effect

How does surfactant affect the lungs

Increased compliance of lungs Decreased surface tension in alveolus Makes lungs compliant - easier to bring in air - reduces surface tension attraction of hydrogen molecules that want to collapse alveoli

When is surfactant produced What type of cells compose surfactant

At 28 weeks Type II alveolar epithelial cells Foetal cortisol stimulates production of surfactant

Function of phospholipids in surfactant How are they organised

PLs = amphipathic compounds Hydrophilic portion - reduces attraction of H+ to each other 2 parallel hydrophobic tails Line up in alveoli - tails face lumen of alveolus - repel water molecules

What hormone predominates in the last weeks of pregnancy What does it cause

Oestrogen reaches a peak causes myometrial weakness and irritability weak braxton hicks contractions may take place

What causes uterine contractions

As birth nears, oxytocin and PGs cause uterine contraction oestrogen allows for gap junction

Effect of emotional and physical stress on body

Activates hypothalamus Sets up a positive feedback mechanism to release more oxytocin

Initiation of parturition

Oestrogen from placenta mostly (less so from foetal ovaries) Increased rate of contractility - positive feedback - more PGs produced, increased sensitivity

Foetal and mother hypothalamic activities

What does cortisol stimulate

PG production by chorion/placenta Weak androgens (DHEAS) - upregulate PGs

Lactation

Milk ejection reflex