foetal circulation

2. The fetal circulation is the circulatory system of
a human fetus, often encompassing the entire
fetoplacental circulation which includes
the umbilical cord and the blood vessels within
the placenta that carry fetal blood.

4. -Begins to develop toward the end of the
third week.
-Heart starts to beat at the beginning of the
fourth week.
- The critical period of heart development is
from 20 day to 50 day after fertilization.
- Many critical events occur during cardiac
development, and any deviation from this
normal pattern can cause congenital heart
defects, if development of heart
doesn't occur properly.

6. Foetal circulation consequently differs from the
adult one predominantly due to the presence
of 3 major vascular shunts:
Ductus venosus: between the umbilical vein
and IVC
Foramen ovale: between the right and left
atrium
Ductus arteriosus: between the pulmonary
artery and descending aorta

7. 4 unique FETAL CVS structures : FOUR SHUNTS

8. Umbilical Cord
2umbilical arteries:
return non-oxygenated blood, waste product,
CO2 to placenta
1umbilical vein:
brings oxygenated blood and nutrients to the
fetus

9. Pair of umbilical
arteries carry
deoxygenated blood
& wastes to
placenta.
Umbilical vein carries
oxygenated blood
and nutrients from
the placenta.

10. organ that connects the developing
fetus to the uterine wall to allow
nutrient uptake, waste elimination,
and gas exchange via the mother's
blood s
two components: the fetal placenta,
or (Chorion frondosum), which
develops from the fetus; and the
maternal placenta, or (Decidua
basalis), which develops from the
maternal uterine tissue

11. Facilitates gas and
nutrient exchange
between maternal and
fetal blood.
The blood itself does
not mix.

12. The core concept behind foetal circulation is that
foetal hemoglobin has a higher affinity for oxygen
than does adult hemoglobin, which allows a diffusion
of oxygen from the mother's circulatory system to the
foetus.
The circulatory system of the mother is not directly
connected to that of the fetus, so the placenta
functions as the respiratory center for the fetus as
well as a site of filtration for plasma nutrients and
wastes.
Water, glucose, amino acids, vitamins, and inorganic
salts freely diffuse across the placenta along with
oxygen.
The umbilical arteries carry blood to the placenta,
and the blood permeates the sponge-like material
there. Oxygen then diffuses from the placenta to the
chorionic villus, an alveolus-like structure, where it is
then carried to the umbilical vein.

13. Diagram of a section through the human placenta, showing the
way the fetal villi project into the maternal sinuses.

14. Placenta
Umbilical Vein
Umbilical Arteries
Liver
Ductus Venosus
Inferior Venacava
Right Atrium
Foramen Ovale
Right Lung
Arch of Aoarta
Ductus Arteriosus
Left Atrium
Left Ventricle
Right Ventricle
Portal Vein

15. COURSE OF FETAL CIRCULATION:
1.Placenta:
Has the lowest vascular resistance in the fetus.
Receives the largest amount of combined (Rt + Lt)
Ventricular Output (55%)

16. 2. Superior Vena Cava:
Drains the upper part of the body,including the brain (15% of
combined ventricular output).
Most of SVC blood goes to the Right Ventricle.

17. 3. Inferior Vena Cava:
Drains lower part of body and
placenta (70% of combined
ventricular output)
Part of IVC blood with high O2
goes into LA via Foramen Ovale.
Remaining IVC blood enter RV
and Pulmonary artery.
Since blood is oxygenated
in the placenta, Oxygen
saturation in IVC
(PO2 = 26-28%) is higher
than that in SVC (12-14%).

18. COURSE OF FETAL CIRCULATION:
Most of SVC blood (less oxygenated blood) goes into RV.
Most of IVC blood (high O2 concentration) is directed by the Crista
Dividens to the LA through Foramen ovale.
Rest of IVC blood enters RV & pulmonary artery.
Less oxygenated blood in Pulmonary artery flows through Ductus
Arteriosus to descending aorta and then to placenta for oxygenation.

19. COURSE OF FETAL CIRCULATION:
The Result is:
Brain and coronary circulation receive blood with higher
concentration (PO2 = 28 mm Hg) than the lower part of the
body (PO2 = 24 mm Hg)

20. FETAL CIRCULATION: The pathway:
Placenta  Oxygenated blood  Umbilical vein
Hepatic circulation Bypasses liver & joins IVC
via ductus venosus
Partially mixes with poorly oxygenated
IVC
blood derived from lower part of fetal
body

21. FETAL CIRCULATION:
Combined lower body blood plus umbilical venous blood
flow (PO2 of ≈26–28 mm Hg) passes through IVC to the
Right atrium and is preferentially directed across the
foramen ovale to the left atrium.
The blood then flows into the left ventricle and is ejected
into the ascending aorta.
Fetal SVC blood, which is considerably less oxygenated
(PO2 of 12–14 mm Hg), enters the Right atrium and
preferentially traverses the tricuspid valve, rather than
the foramen ovale, and flows primarily to the right
ventricle.

22. FETAL CIRCULATION:
From the right ventricle  Pulmonary artery.
Because the pulmonary arterial circulation is
vasoconstricted, only about 10% of right ventricular
outflow enters the lungs.
The rest 90% blood (which has a PO2 of ≈18–22 mm Hg)
bypasses the lungs and flows through the ductus
arteriosus into the descending aorta to perfuse the lower
part of the fetal body.
It the returns to the placenta via the two umbilical
arteries.

23. Thus, upper part of fetal body (including coronary & cerebral arteries
and those to upper extremities) is perfused exclusively from the Left
ventricle with blood that has a slightly higher PO2 , than the blood
perfusing the lower part of the fetal body, which is derived mostly
from the Right ventricle.
Only a small volume of blood from the ascending aorta (10% of fetal
cardiac output) flows across the aortic isthmus to the descending
aorta.

24. Thus, upper part of fetal body (including coronary & cerebral arteries
and those to upper extremities) is perfused exclusively from the Left
ventricle with blood that has a slightly higher PO2 , than the blood
perfusing the lower part of the fetal body, which is derived mostly
from the Right ventricle.
Only a small volume of blood from the ascending aorta (10% of fetal
cardiac output) flows across the aortic isthmus to the descending
aorta.

25. LA  LV  Aorta  Ductus arteriosus
Foramen ovale RV
SVC  upper
body
IVC
50% through 50% to
ductus venosus Portal circulation
Umbilical Vein
Oxy.blood
PLACENTA

26. Aorta
Deoxygenated blood
Descending aorta
Abdominal aorta
Common iliac artery
Umbilical arteries
PLACENTA
Oxygenation
Umbilical Vein

28. FETAL CIRCULATION:
The total fetal cardiac output—the combined output of
both the left and right ventricles—is ≈ 350 mL/kg/min.
Descending aortic blood flow :
-65%  returns to placenta;
-Remaining 35%  perfuses the fetal organs &
tissues.
Right ventricular output is about 1.3 times the left
ventricular flow.
Thus, during fetal life the right ventricle
-is pumping against systemic blood pressure
-is performing greater volume of work than LV.

29. During fetal life
350ml per kg per min
Cardiac Output
Following birth
500ml per min
Heart Rate 120-140per min

30. It is the fetal heart and not the mother's heart that
builds up the fetal blood pressure to drive its blood
through the fetal circulation.
Intracardiac pressure remains identical between the
right and left ventricles of the human fetus.
The blood pressure in the fetal aorta is
approximately 30 mmHg at 20 weeks of gestation,
and increases to ca 45 mmHg at 40 weeks of
gestation.The fetal pulse pressure is ca 20 mmHg at
20 weeks of gestation, increasing to ca 30 mmHg at
40 weeks of gestation.
The blood pressure decreases when passing through
the placenta. In the arteria umbilicalis, it is ca 50
mmHg. It falls to 30 mmHg in the capillaries in the
villi. Subsequently, the pressure is 20 mm Hg in the
umbilical vein, returning to the heart

31. Pulmonary circulation is reduced in the human
fetus because the baby gets its oxygen from
its mother and does not breath on its own.

33. The change from fetal to postnatal circulation
happens very quickly.
Changes are initiated by baby’s first breath.

34. TRANSITIONAL CIRCULATION:
At birth
Mechanical expansion of lungs Increase in arterial
PO2
Rapid DECREASE in pulmonary vascular
resistance
Removal of the low-resistance placental
circulation

35. TRANSITIONAL CIRCULATION:
Right ventricle output now flows entirely into the
pulmonary circulation.
Pulmonary vascular resistance becomes lower
than systemic vascular resistance,
Shunt through ductus arteriosus reverses &
becomes left to right.

36. TRANSITIONAL CIRCULATION:
High arterial PO2 (In several days)
Constriction of ductus arteriosus
It closes, becoming the ligamentum arteriosum.

37. TRANSITIONAL CIRCULATION:
Increased volume of pulmonary blood flow
returning to left atrium
Increases left atrial volume and pressure
Closure of foramen ovale (functionally)
(Although the foramen may remain probe patent)
Becomes Fossa Ovalis

38. Removal of the placenta from the circulation
Also results in closure of the ductus venosus.
The left ventricle is now coupled to the high-resistance
systemic circulation  its wall thickness and mass
begin to increase.
In contrast, the right ventricle is now coupled to the low-
resistance pulmonary circulation  its wall thickness
and mass decrease slightly.

39. Foetal circulation: The left ventricle in the fetus pumped
blood only to the upper part of the body and brain
After birth, LV must deliver the entire systemic cardiac
output (≈450 mL/kg/min). (almost 200% increase in
output)
This marked increase in left ventricular performance is
achieved through a combination of hormonal and
metabolic signals, including an INCREASE IN :
-The level of circulating catecholamines and
-The myocardial receptors (β-adrenergic)
(through which catecholamines have their effect)

40. When congenital structural cardiac defects are
superimposed on these dramatic physiologic changes,
they often impede this smooth transition and markedly
increase the burden on the newborn myocardium.
In addition, because the ductus arteriosus and foramen
ovale do not close completely at birth, they may remain
patent in certain congenital cardiac lesions.

41. Patency of these fetal pathways may either :
Provide a lifesaving pathway for blood to bypass a
congenital defect
(eg: -Patent ductus in Pulmonary atresia or COA.
-Foramen ovale in Transposition of the great vessels)
or
Present an additional stress to the circulation
(eg: -Patent ductus arteriosus in a premature infant,
-RtLt shunt in infants with pulmonary
hypertension)
Therapeutic agents may either :
Maintain fetal pathways open - PGE1
Promote their closure - Indomethacin

42. Umbilical arteries → Umbilical ligaments
Umbilical vein → Ligamentum teres
Shunt Functional
closure
Anatomical
closure
Remnant
Ductus
arteriosus
10 – 96 hrs
after birth
2 – 3 wks
after birth
Ligamentum
arteriosum
Formamen
ovale
Within several
mins after birth
One year
after birth
Fossa ovalis
Ductus
venosus
Within several
mins after birth
3 – 7 days
after birth
Ligamentum
venosum

44. Neonatal Circulation:
Adaptation to extrauterine life: Some of these changes
are instantaneous with the 1st breath, whereas others
develop over a period of hours or days.
Gas exchange: Transferred from the placenta to the
lungs.
Systemic blood pressure: After an initial slight fall in
systemic BP, progressive rise occurs with increasing age.
Heart rate: Elimination of Placental circulation
Increase in systemic vascular resistance
Baroreceptor response  Slowing of HR

45. Neonatal Circulation:
Decrease in PVR (pulmonary vascular resistance):
With the onset of ventilation, pulmonary vascular
resistance is markedly decreased, as a consequence of
both
active (PO2 related) and passive (mechanical related)
pulmonary vasodilation.
In a normal neonate, closure of the ductus arteriosus and
the fall in pulmonary vascular resistance result in a
decrease in pulmonary arterial and right ventricular
pressures.

46. Neonatal Circulation:
Decrease in PVR:
The major decline in pulmonary resistance from the high
fetal levels to the low “adult” levels in the human infant at
sea level usually occurs within the 1st 2–3 days but may
be prolonged for 7 days or more.
Over the 1st several weeks of life, pulmonary vascular
resistance decreases even further, secondary to
remodeling of the pulmonary vasculature, including
thinning of the vascular smooth muscle and recruitment
of new vessels.

47. Neonatal Circulation:
Decrease in pulmonary vascular resistance influences the
timing of clinical appearance of many congenital heart
lesions that are dependent on the relative systemic and
pulmonary vascular resistance.
Eg: Left-to-right shunt through VSD may be minimal in 1st
wk after birth when pulmonary vascular resistance is still
high.
As pulmonary resistance decreases in the next 1-2
weeks, the volume of the left-to-right shunt through an
unrestrictive ventricular septal defect increases and
eventually leads to symptoms of heart failure.

48. FETAL
NEWBORN
Gas exchange Placenta Lungs
RV,LV circuit Parallel Series
Pulmonary circulation Vasoconstricted Dilated
Fetal myocardium
Contractility,Compliance Less Good
Dominant ventricle Right Left
Change in Structure Umbilical vein Ligamentum teres
Umbilical artery Medial umb ligament
Ductus venosus Ligamentum
venosum
Ductus arteriosus Ligamentum

49. Differences between neonatal circulation and that of older
infants:
(1) Right-to-left or left-to-right shunting may persist
across patent foramen ovale;
(2) In the presence of cardiopulmonary disease,
continued patency of ductus arteriosus may allow left-to-
right, right-to-left, or bidirectional shunting;
(3) The neonatal pulmonary vasculature constricts more
vigorously in response to hypoxemia, hypercapnia, and
acidosis;
(4) The wall thickness and muscle mass of the neonatal
left and right ventricles are almost equal;

50. Differences between neonatal circulation and that of older
infants: contd…
(5) Newborn infants at rest have relatively high oxygen
consumption, which is associated with relatively high
cardiac output.
(6) Newborn cardiac output (about 350 mL/kg/min) falls in
the 1st 2 mo of life to about 150 mL/kg/min and then more
gradually to normal adult C.O of about 75 mL/kg/min.
(7) High percentage of fetal hemoglobin present in the
newborn may interfere with delivery of oxygen to tissues
in neonate, so increased cardiac output is needed for
adequate delivery of oxygen

51. CLOSURE of:
Foramen ovale :
Functional Closure: 3rd month of life.
Anatomical closure of septum primum & septum
secundum by 1 year of age.
Ductus arteriosus :
Functional Closure: By 10–15 hr in a normal neonate.
Anatomic closure: May take several weeks.

52. CLOSURE OF DUCTUS ARTERIOSUS:
In a full-term neonate, oxygen is the most important
factor controlling ductal closure.
When the PO2 of the blood passing through the ductus
reaches about 50 mm Hg, the ductal wall constricts.
The effects of oxygen on ductal smooth muscle may be
direct or mediated by its effects on prostaglandin
synthesis.
Gestational age also appears to play an important role;
The ductus of a premature infant is less responsive to
oxygen, even though its musculature is developed.

54. Patent ductus arteriosus:
Failure of a child's DA to close after birth
generation of a left-to-right shunt as blood flows form
hogh pressure aorta to low pressure pulmonary artery.
If left uncorrected, patency leads to pulmonary
hypertension and possibly congenital heart disease
and cardiac arrythmia
Prostaglandins are responsible for maintaining the
ductus arteriosus by dilatation of the vascular smooth
muscles.
Closure may be induced with NSAIDs because these
drugs inhibit prostaglandin

55. Patent foramen ovale:
is an incomplete closure of the atrial septum that
results in the creation of a flap or a valve-like opening
in the atrial septal wall
is present in everyone before birth but seals in about
80% of people.
With each heartbeat, blood can flow in either direction
directly between the right and left atrium.
When blood moves directly from the right atrium to the
left atrium, this blood bypasses the filtering system of
the lungs

56. Patent (open) ductus arteriosus and patent
foramen ovale each characterize about 8% of
congenital heart defects.
Both cause a mixing of oxygen-rich and oxygen-
poor blood; blood reaching tissues not fully
oxygenated. Can cause cyanosis
Surgical correction now available, ideally
completed around age two.
Many of these defects go undetected until child is
at least school age.