Foetal Circulation Flashcards

1
Q

In the foetus, what is cardiac output defined as?

A

The right and left ventricles have different stroke volumes and CO is described in terms of combined ventricular output (CVO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where does deoxygenated blood arrive at the placenta via?

A

The two umbilical arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What % of the output of the right ventricle enters the pulmonary circulation in the foetus?

A

12% - because the rest is diverted to the ductus arteriosus into the descending aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where does highly oxygenated blood go in the foetus?

A

It enters the inferior vena cava via the ductus venosus and is directed into the left atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the P50 for HbF?

A

3.6 kPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the Hb concentration in a fetus at term?

A

High, up to 16 g/dl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Does fetal blood have a higher or lower concentration of 2,3-DPG?

A

Lower - shifts the O2 dissociation curve to the left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why is having a HbF at birth a disadvantage?

A

It impairs O2 extraction at the tissue level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What factors are associated with a persistent fetal circulation?

A

Hypoxia, hypercarbia and acidosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What factors increase pulmonary vascular resistance in the neonate?

A

Hypoxia, acidosis, hypercarbia and cold will all increase PVR and make persistent fetal circulation more likely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does a neonate with transposition of the great arteries have?

A

The pulmonary and systemic circulations are arranged in parallel. The neonate is dependant on the presence of one or more mixing points (i.e. ASD, VSD or PDA). Duct closure can lead to severe cyanosis and circulatory collapse. Medical management can include a prostaglandin infusion in order to re-establish ductal patency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In a neonate with transposition of the great arteries - what does creation of an atrial septal defect do?

A

Creation of an ASD allows better mixing at an atrial level and may stabilize the neonate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When should surgery be performed on neonates with transposition of the great arteries?

A

The aim is to stabilize the neonate and then wait for a short period (usually about 14 days) prior to definitive surgical correction. This delay allows time for end organ recovery and also for the PVR to fall, thus improving outcome from surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

The partial pressure of oxygen (PO2) in the umbilical vein is around 4.7 kPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the saturation of foetal Hb?

A

80–90% saturated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the eustachian valve?

A

It is a tissue flap at the junction of the IVC and the right atrium (RA). It directs the more highly oxygenated blood, streaming along the dorsal aspect of the IVC, across the foramen ovale (FO) and into the left atrium (LA).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the saturation of blood in the LA of the fetus?

A

In the LA, the oxygen saturation of fetal blood is 65%.

18
Q

How is it ensured that blood with the highest possible oxygen concentration is delivered to these the brain and heart of the fetus?

A

The majority of the LV blood (65% saturated) is ejected via the aorta and delivered to the brain and coronary circulation

19
Q

What is the PO2 of fetal blood in the lower half of the body?

A

The lower half of the body is thus supplied with relatively desaturated blood (PO2 2.7 kPa).

20
Q

What % of the venous return do the LV and RV receive in the fetus?

A

The RV receives about 65% of the venous return and the LV about 35%.

21
Q

What controls the peripheral circulation of the fetus?

A

The peripheral circulation of the fetus appears to be under a tonic adrenergic influence (predominantly vasoconstriction), probably mediated by circulating catecholamines eg norepinephrine

22
Q

Why does the fetus have a high PVR?

A

The fetal pulmonary arterioles have a high muscle mass and resting tone. The fetal lungs are collapsed and there is a low resting oxygen tension. The DA also contains muscle that is sensitive to oxygen tension and vasoactive substances

23
Q

What maintains ductus arteriosus patency in the fetus?

A

DA patency in utero is maintained by the low oxygen tension and the vasodilating effect of prostaglandin E2 (PGE2)

24
Q

How is O2 delivery maintained in the fetus despite low partial pressures of O2?

A

High CVO, high haemoglobin concentrations and the presence of HbF

25
Q

What cardiopulmonary adaptations must be made in the newborn?

A
  • Gas exchange must be transferred from the placenta to the lungs
  • the fetal circulatory shunts must close
  • the left ventricular output must increase
26
Q

What happens in the neonate when the placental circulation is removed?

A
  • dramatic fall in flow through the ductus venosus
  • significant fall in venous return through the IVC which results in fall in venous return to the RA
  • ductus venosus closes passively 3-10 days after birth
  • dramatic fall in PVR
  • an 8-10 fold increase in pulmonary blood flow which leads to a massive rise in pulmonary venous return to the LA
    • THEREFORE PRESSURES IN LA AND RA EQUALIZE and the foramen ovale(/atrial shunt) is closed within minutes to hours of birth
27
Q

When does the DA close in newborns?

A

In 96hrs via the increased PO2 in neonatal blood producing direct constriction of smooth muscle within the duct and reduced concentrations of PGE2 - constriction.

28
Q

What is the CVO in the fetus?

A

400-500 ml/kg/min

29
Q

What is the CO in the neonate?

A

300-400 ml/kg/min (this is a single ventricular output)

30
Q

What is the neonatal cardiac index?

A

4 litres/min/m2 at 1hr age

31
Q

What can increase it’s cardiac output in response to filling volume more - the fetus or the neonate?

A

The neonate can significantly increase it’s cardiac output with volume loading

32
Q

What accounts for the gradual decrease in cardiac output over the first few months of life in the neonate?

A

HbF is replaced by adult Hb - resulting in better O2 delivery to tissues. So cardiac output declines

33
Q

What is a persistent fetal circulation?

A

It’s when the neonate revers back to fetal-type circulation (pathological)

34
Q

How does persistent fetal circulation happen?

A
  • Pulmonary arterioles are very reactive in the neonate
  • this can lead to constriction to hypoxia/hypercarbia/acidosis/cold
  • this leads to increase in PVR which can favour right to left shunting through the FO and DA which have not yet fully closed
  • this leads to fetal circulation without the placenta to provide O2 - leads to worsening hypoxia and acidosis
35
Q

What will happen if the neonate continues to have a patent ductus arteriosus?

A

Left to right shunt - the opposite direction to that in the fetus because the SVR has risen and the PVR has fallen

This results in increased volume and workload with respect to the LA and LV, and eventually left heart failure

36
Q

What will a ventricular septal defect do in the neonate?

A

Well tolerated in fetus as LV and RV pressures equal

After birth the SVR rises, PVR falls and a left to right shunt will occur. As PVR continues to fall in the first weeks of life the shunt increases leading to congestive heart failure.

37
Q

What is tetralogy of fallot?

A
  • RV outflow obstruction, often associated with a hypoplastic pulmonary artery
  • large subaortic VSD associated with malalignment of the conal septum
  • when the DA closes after birth, if the pulmonary obstruction is severe, the neonatal circulation is “duct-dependent” and duct closure leads to severe cyanosis
  • ductal flow can be re-established by a prostaglandin infusion
38
Q

What is transposition of the great arteries?

A
  • results from abnormal rotation and septation of the arterial truncus during embryogenesis
    • the aorta arises from the RV and the pulmonary artery from the LV
  • at birth, survival depends on the presence of one or two mixing points (ASD, VSD or PDA) to achieve an arterial O2 consistent with life
39
Q

What is the immediate management of neonates with TGA?

A
  • prostaglandin infusions to re-establish ductal patency
  • creation of an ASD by means of a balloon atrial septostomy to allow a larger degree of mixing at the atrial level (usually performed under echocardiographic guidance)
    • will need surgery at later date
40
Q
A