The fetal circulation differs from adult circulation in several key ways that allow for gas exchange via the placenta rather than the lungs. In the fetus, about 45% of the combined ventricular output is directed to the placental circulation, with only 8% going to the pulmonary circulation. At birth, closure of the ductus arteriosus and foramen ovale is facilitated by the onset of lung ventilation and increased pulmonary blood flow. Persistence of fetal shunts can lead to conditions like patent ductus arteriosus, patent foramen ovale, or persistent pulmonary hypertension of the newborn.

1. Fetal Circulation & Changes
occurring at birth
Moderator:Dr.Anil Rawat

2. The Fetal Circulation…
• differs from adult circulation in several
ways
• differences are attributable to the
fundamental difference in the site of gas
exchange – the placenta as compared to
lungs in adults

3. Concepts
• CVO
• Fetal Hemoglobin

4. The concept of CVO
• In the adult circulation, circulatory system is in
series and there are no shunts,
• the stroke volume of the RV should equal that of
the LV and cardiac output can be defined in terms
of the volume of blood ejected by one ventricle in
1 min.
• In the fetus, as a result of intracardiac/extracardiac
shunting, the stroke volume of the fetal LV is not
equal to the stroke volume of the RV.

5. • The RV receives about 65% of the venous return and
the LV about 35%. the situation is much more
complex and cardiac output must be defined in
different terms
• The cardiac output of the fetus can only be spoken of
in terms of the total output of both ventricles—the
combined ventricular output (CVO).
• 45% of the CVO is directed to the placental circulation
with only 8% of CVO entering the pulmonary
circulation.

6. Circulation at Materno Placental Level
• placenta is anchored to the wall of the
mother's uterus.
• chorion acts as a barrier between the maternal
and fetal circulation

7. • Maternal blood is
delivered to the
intervillous space of the
chorionic plate,
• bathes the chorionic villi
that carry umbilical
capillary beds, allowing
fetal/maternal gas
exchange
• the deoxygenated blood
returns via open ended
venules

8. • the admixture of oxygenated and
deoxygenated blood, produces a po2 lower
than usual
• fetal hemoglobin in order to compensate for
the relatively lower oxygen tension of the
maternal blood supplying the chorion, must
be able to bind oxygen with greater affinity

9. Feta Hb and Oxygen delivery in the fetus
• Oxygen delivery is related to CVO
and the oxygen content of blood.
• Oxygen content of blood is
determined by quantity of
haemoglobin and its oxygen
saturation.
• The fetus has a high Hb
concentration ,a high percentage
of haemoglobin F (HbF), having
lower content of 2,3-DPG, thus
shifting the oxygen dissociation
curve to the left.

10. • High CVO,high haemoglobin concentrations
and the presence of HbF help to maintain
oxygen delivery in the fetus despite the
relatively low partial pressures of oxygen.

12. Course Of Flow

13. Course Of Flow
• 50% of the umbilical venous blood is distributed to the
left and right lobes of the liver,
• the other half bypasses the liver through the ductus
venosus
• Portal venous blood is almost completely distributed to
the right lobe of the liver;only 5–10% passes through
the ductus venosus,none enters the left lobe of the liver.

14. • the left lobe of the
liver receives
exclusively well-
oxygenated umbilical
venous blood
• the right lobe
receives umbilical
venous blood and
most of portal venous
blood

15. • The ductus venosus
and left hepatic vein
enter the inferior vena
cava through a single
orifice
• blood from these veins
is well oxygenated and
streams in the
posterior and left
portion of the inferior
vena cava in the
direction of the
foramen ovale to enter
the left atrium

16. • The poorly oxygenated
blood from the right
hepatic vein joins blood
returning from the
distal inferior vena cava
• these stream along the
anterior and right
portions of the inferior
vena cava towards the
tricuspid valve to enter
the right ventricle.

17. • The inferior vena cava just
below the diaphragm
receives blood from four
sources, all with different
oxygen saturations,
– umbilical vein
– distal inferior vena cava
– left and right hepatic veins
• The blood flowing from
these four veins does not
mix completely but shows
differential streaming.

18. • Blood returning to the heart through the
superior vena cava has a PO2 of 12–15
mmHg and an oxygen saturation of 20–30%.
• It is deflected by the tubercle of Lower in
the right atrium in the direction of the
tricuspid valve, and ~95% enters the right
ventricle, whereas only ≤5% of superior
vena caval blood passes across the foramen
ovale into the left atrium.

19. • The preferential
streaming of the venous
blood results in blood of
higher oxygen saturation
in the left atrium than in
the right ventricle and
pulmonary artery
• The blood entering the
left atrium through the
foramen ovale is joined
by pulmonary venous
blood.

20. • In the fetus,there is no gas exchange in the lung,
the oxygen saturation of pulmonary venous
blood (~50%) is slightly lower than pulmonary
artery
• pulmonary blood flow is low in the fetus and is
considerably less than the volume of blood
traversing the foramen ovale
• oxygen saturation of mixed blood in the left
atrium and left ventricle(65–70%) is only
moderately lower than that of ductus venosus
(80–90%).

21. Distribution Of Flow
• The placenta receives the
largest amount of
combined right and left
ventricular output (55%)
and has the lowest
vascular resistance in the
fetus
• The blood is oxygenated
in the placenta, the
oxygen saturation in the
IVC (70%) is higher than
that in the SVC (40%)

22.  The highest partial pressure of oxygen (Po2) is
found in the umbilical vein (32 mm Hg).
 SVC drains the upper part of the body, including
the brain (15% of combined ventricular output),
IVC drains the lower part of the body and the
placenta (70% of combined ventricular output).

23. • the right ventricle ejects ~65% of combined
ventricular output
– This is twice of volume ejected by the left ventricle.
• since pulmonary vascular resistance is high in the
fetus,only ~12% of blood ejected into the
pulmonary trunk is distributed to the lungs
• remaining 88% of blood ejected by the right
ventricle passes through the ductus arteriosus to
the descending aorta.

24. • The left ventricle is filled by blood returning
to the left atrium from the pulmonary veins
and through the foramen ovale
• of the 35% of combined ventricular output ejected
by the left ventricle,~22% is distributed to the
forelimbs, heart, head, and brain
• only ~10% of CVO crosses the aortic isthmus to the
descending aorta to join the blood traversing the
ductus arteriosus from the pulmonary trunk.

25. • The descending aortic flow is ~67% of CVO
• Umbilical placental circulation receives ~40% of
CVO
• lower trunk, hind limbs, and abdominal organs
receive ~27% of CVO
• low flow explains why the aortic isthmus is the
narrowest part of the aorta in the term infant and
why lesions that alter ascending aortic flow in
utero affect the diameter of the aortic isthmus
and transverse aortic arch.

27. Regulation of the circulation in the
fetus
• In the adult, the systemic and pulmonary
circulations are separate.
• The preload and afterload of the right and left
ventricles are different, and their stroke
volumes could differ.
• The Frank–Starling mechanism adjusts the
outputs of the two ventricles so that over a
short period the ventricles eject similar
volumes.

28. • reduction in venous return to right atrium
decreases filling pressure and end-diastolic
volume of RV, resulting in a decrease in stroke
volume.
• Pulmonary blood flow and venous return to the
LA and LV are also reduced and the stroke volume
decreases.
• An increase in systemic arterial pressure
decreases LV stroke volume; the end-diastolic
volume increases so that, with the next beat,
greater force is generated to increase the stroke
volume.

29. • In fetus, the foramen ovale tends to equalize right
and left atrial pressures throughout the cardiac
cycle
• The ductus arteriosus provides a large
communication between the aorta and the
pulmonary artery, resulting in almost identical
pressures in the two vessels.

30. • Due to similar atrial /aortic/pulmonary arterial
pressures, differences in stroke volumes of the left
and right ventricles are the result of differences in
afterload
• The aortic isthmus, which is narrower than the
ascending and descending aorta, functionally
separates the upper and lower body circulations

31. Changes Occurring at Birth

32. • Conversion of the fetal to the adult
circulation requires
–eliminating the umbilical–placental
circulation
–Increase of pulmonary blood flow to a
level necessary for adequate gas
exchange
–separation of the left and right sides of
the heart by closure of fetal channels.

33. • The major events occurring at the time of birth
include
• separation of the placental circulation and
establishment of rhythmic ventilation
• Ventilation comprises two components:
– physical expansion of the lungs with gas
– elimination of fluid in the alveoli and increase in
alveolar oxygen concentration associated with
breathing air.

34. Changes ln patterns of blood flow
• changes in circulation at the time of birth
occur almost simultaneously.
• the changes in the circulation after birth can
be accounted for largely by the onset of
rhythmic ventilation with air
• removal of the placental circulation
abolishes umbilical venous return

35. • The elimination of umbilical venous blood
flow reduces inferior vena caval return
• facilitates closure of the foramen ovale and
causes a small decrease in right atrial
pressure.

36. • Even without eliminating the placental circulation,
ventilation increases pulmonary flow and results in
foramen ovale closure
• though the ductus arteriosus does not close
completely immediately after birth, flow from the
pulmonary trunk to the aorta is almost completely
eliminated.
• Hepatic blood flow is reduced within the first few
hours after birth but increases after the portal
blood flow is increased in association with feeding.

37. Changes in pulmonary circulation
• During fetal life, pulmonary blood flow is low due
to the high pulmonary vascular resistance.
• related to both morphologic and functional
features of pulmonary vessels.
• Small pulmonary arteries have a thick medial layer
composed predominantly of smooth muscle cells
• These vessels are extremely reactive; they constrict
markedly with hypoxia and dilate with an increase in PO2
• Endothelial factors, such as endothelium-derived relaxing
factor and NO play an important role in regulating
pulmonary vascular resistance.

38. • The reduction in pulmonary vascular resistance
after birth is associated with rhythmic ventilation
and oxygenation
• A rise in PO2 is thought to increase endothelial
release of nitric oxide,a potent vasodilator
• vasoactive agents, such as endothelin, bradykinin
& angiotensin also have a role

39. • Following the immediate fall in pulmonary
vascular resistance following birth, morphologic
changes in the pulmonary vessels result in a
permanent fall in pulmonary vascular resistance.
– most striking change is a decrease in the thickness of
the smooth muscle layer in the small arteries.
– results in a gradual further decrease in pulmonary
vascular resistance and pulmonary arterial pressure
within 2–3 weeks after birth

40. Closure of the ductus arteriosus
• normally widely patent in the fetus,constricts
after birth
 Functional closure of the DA occurs within 10 to
15 hours after birth by constriction of the medial
smooth muscle in the ductus.
 Anatomic closure is completed by 2 to 3 weeks of
age by permanent changes in the endothelium
and subintimal layers of the ductus.

41. • current concept is that two factors are largely
responsible for maintaining ductus patency
inutero –
– low oxygen tension of pulmonary arterial blood
– effect of circulating prostaglandin(prostaglandin E2),
which relaxes ductus arteriosus smooth muscle.

42. • Constriction of the ductus arteriosus occurs with
increase in arterial PO2 associated with
ventilation
• a decrease in plasma prostaglandin E2
concentrations is an important mechanism
• oxygen-sensitive potassium channels have been
demonstrated to play an important role in the
contraction of ductus arteriosus smooth muscle in
response to increased oxygen levels
• permanent closure of the ductus is achieved by
fibrosis.

44. Clinical Significance
• Persistence of any of the fetal
shunts/physiology may lead to
– Persistent Ductus Arteriosus
– Patent Foramen Ovale/ASD
– PPHN

45. Persistent Ductus Arteriosus
• Occurs in 5-10% of all
CHD
• Persistent patency of
ductus arteriosus
between left PA and
descending aorta
• Ductus is usually cone
shaped with small
orifice to pulmonary
artery

46.  The responsiveness of the ductal smooth muscle to
oxygen is related to the gestational age of the
newborn;
 the ductal tissue of a premature infant responds less
intensely to oxygen than that of a full-term infant.
 This decreased responsiveness of the immature
ductus to oxygen is due to its decreased sensitivity to
oxygen-induced contraction; it is not the result of a
lack of smooth muscle development, as the immature
ductus constricts well in response to acetylcholine.
 It may also be due to persistently high levels of PGE2
in preterm infants.

48. • Patients are usually asymptomatic when ductus is
small
• Large shunt PDA may cause CHF and consequently
recurrent pneumonia
• Pulmonary vascular obstructive disease may
develop if large PDA with Pulmonary hypertension
is left untreated

49. PFO/ASD
• Failure of functional closure of foramen ovale
causes formation of a small LR shunt
• Common in newborn (75%)
• ASD occurs as isolated anomaly with female
preponderance

50. • Of 3 types
– Secundum defect (most
common,located in middle
portion of atrial septum)
– Primum defect(located in the
anteroinferior atrial septum)
– Sinus venosus defect(located
in the posterosuperior atrial
septum)

51. • Are usually asymptomatic
• Spontaneous closure occurs in 40% patients in
first 4 years of life
• If large defect is untreated, CHF and Pulmonary
HTN may develop in 2nd or 3rd decade of life

52. PPHN
• 1 in 1500 live births
• Characterized by persistence of pulmonary
hypertension which causes varying degree of
cyanosis from a RL shunt through PFO or PDA
• Causes
– Pulmonary vasoconstriction in presence of normally
developed pulmonary vascular bed
– Hypertrophy of pulmonary vascular smooth mucle
– Developmentally abnormal pulmonary arterioles with
decreased cross sectional area of pulmonary vasular
bed

53. • Symptoms begin 6-12 hours after birth
–Cyanosis
–Retractions
–Grunting
–A gradient of 10% or more in oxygen
saturation between preductal/postductal
ABG s/o ductus arteriosus RL shunt
–Cardiomegaly on CxR

54. Thank You