adaptations at birth Flashcards

1
Q

what is the starting point of fetal circulation

A

at the placenta which is embedded in the uterine wall and is partly maternal and partly foetal.

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2
Q

where does exchange between maternal and fetal circulations occur

A

At the placenta there is exchange of oxygen and nutrients

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3
Q

how is there exchange between maternal and fetal blood if the blood does NOT mix

A

fingerlike projections capillaries push into the pool of maternal blood separated by thin membranes (placental villi) deoxygenated blood containing waste products enters umbilical cord. is high in CO2, waste, diffuses into maternal circulation. Blood from mother high in O2, nutrients, diffuses into fetal capillaries and returns to umbilical cord via umbilical vein

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4
Q

how is o2 carried in the blood

A

1 - dissolved in plasma (2%)

2 - bound to Hb (98%)

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5
Q

what is adult Hb composed of

A

2 alpha 2 beta polypeptide chains.

each has a haem group containing porphyrin ring and ferrous Fe2+

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6
Q

when does Hb bind o2

A

when PO2 is high, binds O2 to haem group

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7
Q

when does Hb release O2

A

when O2 is low, O2 will dissociate

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8
Q

what is fetal Hb composed of

A

2 alpha 2 gamma polypeptide chains.

each has a haem group containing porphyrin ring and ferrous Fe2+

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9
Q

what synthesises Hb early in gestational life (before 6 weeks)

A

yolk sac synthesises Hb

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10
Q

what synthesises Hb in gestational life (between 8 weeks and 24wks -birth)

A

liver

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11
Q

what type of Hb is made in gestation

A

Fetal Hb (2xa, 2xg)

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12
Q

nearing birth (post 24weeks), what organ takes over Hb production

A

spleen

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13
Q

how does Hb production change as we near birth

A

starts to be produced by spleen
fall in gamma Hb
beta Hb starts to increase. at birth, bHb shoots up, gHb nosedives down

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14
Q

at birth what starts to take over production of Hb

A

bone marrow

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15
Q

difference between fetal and adult Hb

A

fetal contains gamma chains, adult contain beta chains

fetal Hb = higher affinity for o2, so binds o2 at lower PO2 and is saturated at lower O2.

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16
Q

what is the role of 2,3 DPG in o2 binding

A

2,3 DPG binds to deoxygenated Hb and promotes further release of the remaining O2 and it also makes it harder for O2 to bind.
shifts o2 dissociation curve to the right .’. releases 2 at higher PO2

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17
Q

what is the role of 2,3 DPG in o2 binding in pregnant women

A

30% increase in 2,3 DPG so their Hb has less oxygen and allows more O2 to be offloaded at the placenta and given to the fetus
Foetal Hb doesn’t bind 2,3-DPG as well as adult Hb does, therefore this further enhances HbF affinity to oxygen as the curve is shifted to the left.

18
Q

what happens to the blood coming into the umbilical vein from the mother

A

umbilical vein travels up to the liver.
50-60% bypasses hepatic circulation and is shunted to IVC via the ductus venosus.
Rest enters the portal vein.

19
Q

how does fetal circulation bypass the lungs

A

lungs are still developing. filled with fluid. not ready for gas exchange .’. lung capillaries are vasoconstricted.’. high pressure & resistance in pulmonary artery = high pressure in the RV .’. high pressure in right atria.
.’. blood is pushed through foramen ovale and into left atrium .’. enters left ventricle and is pumped out into aorta

20
Q

how does fetal circulation stop blood in RV going to lungs

A

RV -> pumped into pulmonary artery.
ductus arteriosus connects the pulmonary artery to the aorta .’. blood entering pulmonary artery is shunted into the aorta .’. blood prevented from going to lungs

21
Q

what big events happen at birth

A

placental circulation ceases
baby starts to breathe (fluid in lung pushed out)
foramen ovale closes
ductus arteriosus closes

22
Q

how does placental circulation close after birth

A

when umbilical cord is clamped - exposed to cooler temperatures .’. vessels get constricted.
blood no longer flowing into the umbilical vein or ductus venosus so it closes over 3-10 days.
so placental circulation ceases

23
Q

how do lungs change after birth

A

as baby starts to breathe air, remaining fluid is pushed out and fills with air.
o2 -> pulmonary arterioles dilate and resistance in pulmonary circulation falls .’. increase in bf in pulmonary circulation

24
Q

what happens to foramen ovale after birth

A

lower resistance and pressure in pulmonary circulation (and RA/RV) .’. more blood flow .’. more blood return to LA .’. LA pressure increases.
.’. RA and LA pressure equalise .’. foramen ovale =pushed against interatrial septum .’.closes shunt

25
Q

what happens to ductus arteriosus after birth

A

fall in pulm. artery resistance &pressure = blood flow both ways (up aorta and up aorta) in ductus arteriosus
rise in o2 and fall in PG -> ductus arteriosus to close. once closed it is called ligamentum arteriosum

26
Q

how does umbilical artery of fetus change after birth

A

umbilical artery that comes off the internal iliac will have very little blood flowing into it as it constricts due to lo1w prostaglandins and higher oxygen tensions.
Eventually it will close off

27
Q

why may the transition to extrauterine life not be permanent

A

pulm. arterioles are v reactive and may end up reconstricting due to certain stimuli:
- hypoxia. hypercarbia, acidosis, cold
.’. rise in pulmonary venous pressure .’. right to left shunting

28
Q

what is patent ductus arteriosus

A

where ductus arteriosus fails to close after birth .’. deoxygenated blood that has just entered aorta from LV flows back into pulmonary artery and goes to lungs.
asymptomatic early on but a continuous machinery murmur can be heard.
if uncorrected can lead to congestive heart failure.

29
Q

symptoms of heart failure

A

Fast breathing, Increased work of breathing, Sweating during feeding, Poor feeding, Poor growth, Rapid pulse, Bounding pulse

30
Q

treatment of patent ductus arteriosus

A

indomethacin, Ibuprofen, (NSAID) inhibits production of prostaglandins and therefore encourages the duct to close.
surgery may be used to ligate the vessel.

31
Q

examples of atrial septal defect

A

Ostium primum, Ostium secundum defect, Sinus venosus defect, Common atrium, Patent foramen ovale

32
Q

why are neonates at increased risk of heat loss

A

high surface area to body mass ratio.

lack thermal insulation - lower % body fat, less subcutaneous fat

33
Q

mechanism for maintaining heat in neonates

A

thermogenesis - (babies cannot shiver .’. rely on non shivering thermogenesis through brown fat)
brown fat has high levels of mitochondria. proton movement down their gradient (from intermitochondrial space to matrix) is coupled to heat production.

34
Q

what is evaporation of heat

A

Heat loss through wet skin

35
Q

what is convection of heat

A

Heat loss caused by cooler air circulating around/over warm skin, esp. when exposed

36
Q

what is the conduction of heat

A

Heat loss through direct contact with a cold surface

37
Q

what is radiation of heat

A

Heat loss caused by heat radiating towards a cooler surface e.g. towards a window

38
Q

what is thermal stress

A

the energy needed to maintain a normal body temp
the colder the temperature the greater the thermal stress (bc body metabolism needs to increase in order to warm the body)

39
Q

how does body fluid compartment change before and after birth

A

before birth - most of the volume of water is extracellular. less intracellular
nearing birth - ECFV decreases and ICFV increases
by 6 months - ICFV is higher than ECFV

40
Q

how is fluid lost

A

from: respiratory tract, kidneys, stool, skin

41
Q

how much water is lost from resp tract affect fluid

A

depends on temperature, humidity of inspired gas, resp rate, tidal volume, amount of dead space will influence fluid loss