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Obstetric IAC > Foetal Circulation > Flashcards

Foetal Circulation Flashcards

1
Q

Where does gas exchange occur in the fetus?

A

The placenta recieves deoxygenated blood from the umbilical arteries and returns oxygenated blood to the fetus via the umbilical vein.

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2
Q

What kind of circulation is the fetal one?

A

Shunt-dependent circulation

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3
Q

How is cardiac output in the fetus defined?

A

In terms of combined ventricular output.

This is because stroke volume of the fetal LV is not equal to the SV or the RV.

The RV receives about 65% of the venous return and LV about 35%. Also only 45% of the CVO is directed to the placental circulation with only 8% entering the pulmonary circulation.

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4
Q

How is oxygen delivery maintained in the fetus despite low oxygen partial pressures?

A

The presence of fetal Hb and a high combined ventricular output

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5
Q

What does transition from fetal to neonatal life involve?

A

Closure of circulatory shunts and acute changes in pulmonary and systemic vascular resistance

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6
Q

What is the partial pressure of O2 in the umbilical vein?

A

4.7 kPa

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7
Q

What is the sats of blood delivered to the fetus?

A

80%

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8
Q

What does the eustachian valve do in fetal circulation?

A

It’s a tissue flap at the junction of the IVC and RA. It directs more highly oxygenated blood, streaming along the dorsal aspect of the IVC, across the foramen ovale and into the left atrium.

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9
Q

What is the O2 saturation in the left atrium of the fetus?

A

65%

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10
Q

Where is the majority of the LV blood in the fetus delivered?

A

To the brain and coronary circulation to ensure the blood with the highest possible O2 concentration is delivered to these vital structures

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11
Q

What saturation does desaturated blood from the SVC and coronary sinus have in the fetus?

A

SvO2 25-40%

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12
Q

Why does only 12% of the RV output in fetuses reach the pulmonary circulation?

A

Because of high pulmonary vascular resistance (PVR) - the remaining 88% crosses the ductus arteriosus into the descending aorta.

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13
Q

What is the pO2 of the blood supplying the lower half of the fetus?

A

2.7 kPa

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14
Q

Why does the fetal circulation have a high PVR?

A
  • fetal pulmonary arterioles have a high muscle mass and resting tone
  • fetal lungs are collapsed and there’s low resting O2 tension
  • ductus arteriosus contains muscle that’s sensitive to O2 tension and vasoactive substances
    • DA patency in utero is maintained by low O2 tension and vasodilating effect of prostaglandin E2
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15
Q

What is the peripheral circulation of the fetus under the influence of?

A

Tonic adrenergic influence - predominately vasoconstriction

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16
Q

Where is oxygenated blood from the mother delivered to the placenta from?

A

The uterine artery

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17
Q

Why is gas exchange in the placenta less efficient than the lung?

A

Because of the larger diffusion distance and the permeability of the blood-blood barrier is also lower in the placenta.

The inefficiency of this is offset by the large surface area of the placenta compared to the size of the fetus.

18
Q

How does fetal haemoglobin differ to adult?

A
  • the fetus has a high Hb level (16g/dL at term)
  • high percentage of fetal Hb - lower content of 2,3 DPG which shifts the O2 dissociation curve to the left
    • this favours O2 uptake in the placenta
19
Q

What is the Bohr effect and how does it affect the fetus?

A

As the level of CO2 in tissues rises, the O2 affinity of Hb decreases.

CO2 excreted by the fetus is removed by the placenta, which has a relatively high PCO2 in the maternal intervillous sinuses - assists unloading of O2.

The fall in PCO2 on the fetal side leads to better O2 loading (double Bohr effect).

20
Q

What is the PO2, SO2 and O2 content of the uterine artery?

A

PO2 = 13.3 kPa

SO2 = 98%

O2 content = 16 ml/dL

21
Q

What is the uterine blood flow?

A

600 ml/min

22
Q

What is the PO2, SO2 and O2 content in the uterine vein?

A

PO2 - 5.3 kPa

SO2 - 75%

O2 content - 19.5 ml/dL

23
Q

What is umbilical blood flow?

A

300ml/min

24
Q

What is the PO2, SO2 and O2 content of the umbilical artery?

A

PO2 - 2.4 kPa

SO2 - 45%

O2 content - 10.3 ml/dL

25
Q

What is the PO2, SO2, oxygen content of the umbilical vein?

A

PO2 - 4.7 kPa

SO2 - 80%

O2 content - 16 ml/DL

26
Q

How much does uterine blood flow increase by in pregnancy?

A

20 x

27
Q

What % of fetal Hb does the fetus have?

A

75%

28
Q

What does HbF do in the neonate?

A

It impairs O2 extraction at the tissue level.

The p50 of HbF is around 3.6 kPa compared to 4.8 kPa in adult blood.

So when PO2 is 5.3 kPa it approximates to normal neonatal venous value, the O2 content of fetal blood is much higher than adult, so this causes the impairment.

29
Q

What cardiopulmonary adaptations must be made as the fetus transitions to post-natal life?

A

Gas exchange must be transferred from placenta to lungs.

Fetal circulatory shunts must close.

Left ventricular output must increase.

30
Q

At birth, what happens to PVR?

A
  • dramatic fall in PVR following expansion of lungs
  • 10 fold increase in pulmonary blood flow
  • better oxygenation of neonatal blood also reverses the pulmonary vasoconstriction caused by hypoxia, further reducing PVR
  • this leads to a massive rise in pulmonary venous return to the left atrium
  • the decrease in IVC flow results from a fall in venous return to the right atrium - pressure in LA and RA equalize
  • the foramen ovale is closed (mins to hours after birth)
31
Q

What happens at birth to the ductus arteriosus?

A

THe shunt becomes bidirectional and the increased PO2 in neonatal blood causes direct constriction of smooth muscle within the duct.

Also, levels of PGE2 (produced by the placenta), falls rapidly after birth leading to ductal constriction.

32
Q

How long does ductus arteriosus closure take?

A

By 96hrs.

33
Q

What factors are involved in the cessation of the placental circulation?

A
  • umbilical veins are reactive and constrict in response to longitudinal stretch and increased blood PO2 - external clamping of the cord augments this process
  • dramatic fall in flow through the ductus venosus and a significant fall in the venous return through the IVC (from placenta being removed)
  • DV closes passively 3-10 days after birth
34
Q

How does a persistent fetal circulation occur?

A
  • pulmonary arterioles will constrict in response to
    • hypoxia
    • hypercarbia
    • acidosis
    • cold
  • this leads to increased PVR, which favours right to left shunting through the DA and FO which have not yet anatomically closed
  • the neonate reverts back to it’s fetal pattern of circulation but with no placenta to provide oxygenation
    • worsening cycle of hypoxia and acidosis set in motion
35
Q

What does a patent ductus arteriosus cause?

A
  • left to right shunt
  • due to rise in SVR and fall in PVR
  • results in increased volume and workload on the LA and LV and eventually left heart failure
36
Q

What does a ventricular septal defect cause?

A

VSDs are one of the most common forms of congenital heart disease.

In neonates with large VSDs, as SVR rises and PVR falls, a significant left-to-right shunt through the VSD becomes apparent.

This shunt increases as PVR continues to fall in the 1st weeks of life, leads to congestive heart failure.

37
Q

What is tetralogy of fallot?

A
  • RV outflow obstruction, nearly always infundibular and/or valvular in location, often associated with a hypoplastic pulmonary artery
  • a large subaortic VSD associated with malalignment of the conal septum
  • after birth the effect of duct closure will depend on the severity of the pulmonary obstruction and right-to-left shunt - if severe, duct closure will lead to severe cyanosis
  • needs restablishment of ductal flow by prostaglandin infusion
38
Q

What is transposition of the great arteries?

A
  • the aorta arises from the RV and the pulmonary artery from the LV
  • after birth, since the pulmonary and systemic circulations are in parallel rather than series, survival depends on an ASD, VSD or PDA between the 2 circulations to get an arterial O2 saturation compatible with life
  • infants born with this will be cyanosed, acidotic and have cardiovascular collapse
  • immediate management with prostaglandin PGE1 infusion and creation of an ASD by balloon atrial septostomy (under echo guidance in PICU)
39
Q

In the fetal circulation, are the left and right stroke volumes the same?

A

No - cardiac output is defined in terms of combined ventricular output (CVO).

40
Q
A

Obstetric IAC (9 decks)

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