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.

-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.

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

4 unique FETAL CVS structures : FOUR SHUNTS

Umbilical Cord

2 umbilical arteries:

return non-oxygenated blood, waste product,

CO2 to placenta

1 umbilical vein:

brings oxygenated blood and nutrients to the

fetus

Pair of umbilical

arteries carry

deoxygenated blood

& wastes to

placenta.

Umbilical vein carries

oxygenated blood

and nutrients from

the placenta.

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

Facilitates gas and

nutrient exchange

between maternal and

fetal blood.

The blood itself does

not mix.

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.

Diagram of a section through the human placenta, showing the

way the fetal villi project into the maternal sinuses.

Placenta

Umbilical Vein

Umbilical Arteries

Liver

Ductus VenosusInferior VenacavaRight AtriumForamen Ovale

Right LungArch of Aoarta

Ductus Arteriosus

Left Atrium

Left Ventricle

Right Ventricle

Portal Vein

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%)

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.

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%).

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.

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)

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

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.

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.

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.

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.

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

Aorta

Deoxygenated blood

Descending aorta

Abdominal aorta

Common iliac artery

Umbilical arteries

PLACENTA

Oxygenation

Umbilical Vein

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.

During fetal life

350ml per kg per min

Cardiac Output

Following birth

500ml per min

Heart Rate 120-140per min

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

Pulmonary circulation is reduced in the human

fetus because the baby gets its oxygen from

its mother and does not breath on its own.

The change from fetal to postnatal circulation

happens very quickly.

Changes are initiated by baby’s first breath.

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

INCREASE in systemic vascular resistance.

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.

TRANSITIONAL CIRCULATION:

High arterial PO2 (In several days)

Constriction of ductus arteriosus

It closes, becoming the ligamentum arteriosum.

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

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.

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)

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.

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,

-RtLt shunt in infants with pulmonary

hypertension)

Therapeutic agents may either :

Maintain fetal pathways open - PGE1

Promote their closure - Indomethacin

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

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

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.

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.

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.

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 Ligamentumvenosum

Ductus arteriosus Ligamentumarteriosum

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;

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

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.

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.

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

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

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.