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Fetal circulation

Dr Shreetal Rajan Nair

Fetal circulation

Fetal circulation :

Physiological and morphological aspects

Post natal and transitional circulation:

Changes at birth and thereafter

Pathophysiological considerations in CHDs

All our present day knowledge about fetal circulation is based on continuing research of more than 40 years.

Most of the work has been done in fetal lambs whose circulation closely resembles to that of human fetal circulation.

Fetal circulation

Fetal circulation

Central circulation

Arteries

Veins

Shunts

Peripheral components

Various regional vascular beds

Salient features

Presence of shunts

Parallel arrangement of two main arterial systems and their respective ventricles.

Preferential streaming of blood

High impedance and low flow of pulmonary circulation.

Low impedance and high flow of placental circulation.

Placenta is the site of gas exchange

Shunts in the fetal circulation

The fetal circulation is characterised by four shunts.

first, within the placenta

second, across the ductus venosus

third, through the foramen ovale

fourth, across the ductus arteriosus

The Placenta

Facilitates gas and nutrient exchange between maternal and fetal blood.

The blood itself does not mix.

Umbilical Circulation

Pair of umbilical arteries carry deoxygenated blood & wastes to placenta.

Umbilical vein carries oxygenated blood and nutrients from the placenta.

Arrangement of blood vessels in placenta

Oxygen exchange function

Higher hemoglobin level in fetus as compared to mother facilitates oxygen uptake by the fetus in the placenta.

Oxygen dissociation curve of fetal red cells is shifted to left as compared to adult red cells.

HbF has less affinity towards organic phosphates like 2,3 DPG and ATP.


These phosphates that are present in red cells compete with oxygen for binding to hemoglobin.

Affinity of reduced hemoglobin to 2,3 DPG is higher than that of oxyhemoglobin and this facilitates oxygen delivery at tissue site.


As CO2 crosses placenta from fetus to mother, it creates a local acidosis.

In the face of decreasing pH, mothers hemoglobin shows less affinity towards Hb and oxygen release is enhanced[Bohr effect]

This supports diffusion of more oxygen across the diffusion membrane to fetus.

Umbilical vein to portal circulation

Some blood from the umbilical vein enters the portal circulation allowing the liver to process nutrients.

The majority of the blood enters the ductus venosus, a shunt which bypasses the liver and puts blood into the hepatic veins.

Foramen ovale

Blood is shunted from right atrium to left atrium, skipping the lungs.

Is a valve with two flaps that prevent back-flow.

Foramen ovale

Ductus arteriosus

The blood pumped from the right ventricle enters the pulmonary trunk.

Most of this blood is shunted into the aortic arch through the ductus arteriosus.

Fetal circulation physiology

Most of the unsaturated blood reaches the right ventricle and this blood is channelled via the ductus arteriosus and descending aorta to the placenta for oxygenation

Most of the saturated blood reaches the left ventricle which is driven into the ascending aorta to the heart and brain

Ref : Moss and Adams textbook of congenital heart diseases

Ref : Moss and Adams textbook of congenital heart diseases

21

How this is achieved?

By the appropriate mixing of the venous blood returning to the heart

And its preferential streaming

Central venous circulation

5 sources:

upper body - SVC

myocardium coronary sinus

the lungs pulmonary veins

the lower body - IVC

placenta umbilical vein ductus venosus

IVC

Least saturated blood

From upper body via SVC

From myocardium via coronary sinus

This blood is directed to the RV via the tricuspid valve

Venous return from lungs

Not well saturated

Preferential flow to RV is not possible because of the normal drainage of pulmonary veins to LA

But pulmonary blood flow only 8% of combined ventricular output

So no appreciable effect on oxygen delivery

Inferior venacaval return

Lower body

Placenta

How this blood is preferentially directed to the RV

SVC blood is directed away from the foramen ovale and through the tricuspid valve due to the leftward and superior course of the eustachian valve

The location of the coronary sinus caudad to the foramen causes venous blood from the myocardium to flow through the tricuspid valve to the RV

How preferential flow occurs

Lower body flow except that from the liver ascends the distal IVC and this stream of relatively desaturated blood enters the lateral margin of the right atrium and directed to the RV via TV

Umbilical venous return to the LV

Venous flow from the liver from right lobe to the RV and the left lobe to the LV via foramen ovale

Venous return to heart

Umbilical vein gives branches to left lobe of liver and then divides into DV and arcuate vein.

Arcuate vein joins the portal vein and then gives of branches to right lobe of liver.

Left hepatic vein joins the DV at its entry to IVC and Right hepatic vein joins the IVC directly.


Right lobe of liver receives poorly oxygenated portal venous blood and left lobe receives well oxygenated umbilical venous blood.

Both lobes receive small contribution of blood from hepatic artery.

Saturation of RHV is lower than that of LHV.


Posterior and left stream of IVC blood carries oxygenated blood while anterior and right stream carries poorly oxygenated blood.

Preferential streaming of DV and LHV blood across the foramen ovale and abdominal IVC and RHV blood across the TV.


Eustachian valve helps to direct the IVC blood to cross the foramen ovale.

The lower margin of septum secundum [crista dividens] helps to direct the left posterior stream to preferentially across the foramen ovale.

SVC blood is directed aross the TV.

THE PRENATAL PULMONARY CIRCULATION

Physiologic regulation of pulmonary vascular resistance

Pulmonary vascular resistance in the fetal lung is initially high

The most prominent factor associated with high fetal pulmonary vascular resistance is the normally low blood O2 tension (pulmonary arterial blood pO2 = 17 to 20 torr).

PVR in FETUS is high

In the fetus and newborn, all small pulmonary arteries have a thicker medial smooth muscle layer in relation to diameter than similar arteries in adults.

This increased muscularity is partly responsible for the increased vasoreactivity and pulmonary vascular resistance in the fetus, particularly near term.

PULMONARY CIRCULATION

Experiments show fetal PBF increases dramatically in response to increase in maternal PO2.

This response is evident only in latter part of gestation.

Doppler studies indicate similar changes in humans as well.

Modulation of pulmonary vascular tone

Oxygen modulates the production of both prostacyclin and endothelium-derived nitric oxide (EDNO); two potent vasoactive substances that may in part underlie the responses of the developing pulmonary circulation to changes in oxygenation

Vasoconstrictors in the pulmonary circulation of the fetus, such as alpha agonists, thromboxane, and the leukotrienes are other mediators of increased pulmonary vascular tone

Combined ventricular output

The combined ventricular output

The term 'combined ventricular output(CVO)' has been applied to the output of the two ventricles, and it also represents total venous return to the fetal heart.

The right ventricle ejects about 55-65%, and the left only 35-45% of CVO.

Adapted from Hursts THE HEART

Hursts THE HEART

43

Cardiac output and its distribution

CVO is 450 ml/kg/wt

UV flow is 200 ml/mt/kg [45% of CVO]

Of this,110 ml/mt [24%] passes through DV and 90 ml/mt[21%] passes through hepatic circulation


Portal venous flow forms 7% and of CVO and abdominal IVC blood forms 30% of CVO.

Total venous return to heart from IVC is 315 ml/mt and represents 70% of CVO.

Of this 115 ml/mt [25% of CVO] passes through FO and and 200 ml/mt [44%] passes through TV.


Venous return to heart from SVC is 90 ml/mt/ and represents 21% of CVO most of this passes through tricuspid valve.

RV ejects about 300 ml/mt or about 55% of CVO.

About 35 ml/mt [8% of CVO] enters the pulmonary circulation


About 265 ml/mt [60%]passes through ductus arteriosus.

LV ejects 150 ml/kg [ 45% ].

Of this,90 ml/mt [20%] distributed to head and upper half and 45 ml/mt [10%]passes through isthmus.

3% of CVO enters coronary circulation.

Cardiac output in human fetus

Fetus increases the cardiac output by increasing the heart rate as it is incapable of increasing the stroke volume

Myocardium is underdeveloped

Fluid content is more

Myocardium surrounded by fluid filled lung

BLOOD OXYGEN SATURATIONS


Blood oxygen saturations

The highest partial pressure of oxygen (Po2) is found in the umbilical vein (32 mm Hg)

The brain and coronary circulation receive blood with higher oxygen saturation (Po2 of 28 mm Hg) when compared to the saturation in the blood supply to the lower body (Po2 of 24%)

The atrial and ventricular pressures

The wide communication at the atrial level (foramen ovale) allows for near equalization of atrial and ventricular end-diastolic pressures.

Similarly, at the great vessel level, the nonrestrictive ductus arteriosus allows equalization of systolic pressures in the aorta and the pulmonary artery and, in the absence of aortic or pulmonic stenosis, at the ventricular level


Rudolph congenital heart diseases

55

What happens at birth?

The change from fetal to postnatal circulation happens very quickly.

Changes are initiated by babys first breath.

Post natal circulation

The changes in the central circulation at birth are primarily caused by external events rather than by primary changes in the circulation itself

What are the changes?

rapid and large decrease in pulmonary vascular resistance

disruption of the umbilical-placental circulation

Abruptly at birth, the ductus arteriosus changes from a right-to-left conduit of blood to the descending aorta, to a left-to-right conduit of blood to the lungs

POST NATAL PULMONARY CIRCULATION

PULMONARY CIRCULATION

Breathing at birth is associated with a marked fall in PVR and rise in PBF.

PA pressure does not fall as rapidly and remain elevated till the ductus is widely patent.

Once the ductus is closed, PA pressure can vary independent of systemic pressure.

The transitional circulation

In humans by 24 hours of age, mean pulmonary arterial blood pressure may be only half systemic.

After the initial rapid decrease in pulmonary vascular resistance and pulmonary arterial blood pressure, there is a slow, progressive decrease, with adult levels reached after 2 to 6 weeks.

This is due to vascular remodeling, muscular involution, and rheologic changes.

In the first 4 to 6 weeks after birth, there is progressive involution of the circumferential medial smooth muscle with overall reduction in medial muscular thickness of the walls of the small pulmonary arteries

CLOSURE OF THE SHUNTS

Ductus arteriosus closure

Postnatal closure of the ductus arteriosus is effected in two phases. Immediately after birth, contraction and cellular migration of the medial smooth muscle in the wall of the ductus arteriosus produce shortening, increased wall thickness, and protrusion into the lumen of the thickened intima (intimal cushions or mounds), resulting in functional closure .

This commonly occurs within 12 hours after birth in full-term human infants

The second stage usually is completed by 2 to 3 weeks in human infants, produced by infolding of the endothelium, disruption and fragmentation of the internal elastic lamina, proliferation of the subintimal layers, and hemorrhage and necrosis in the subintimal region.

The mounds enlarge progressively, and there is connective tissue formation and replacement of muscle fibers with fibrosis and permanent sealing of the lumen to produce the ligamentum arteriosum

Closure of the ductus arteriosus

The increased level of oxygen probably causes vasoconstriction of the ductal musculature, but there are strong suggestions that a reduction in circulating prostaglandins of the E series plays a role

Oxygen, prostaglandin E2 (PGE2) levels, and maturity of the newborn are important factors in closure of the ductus.

Acetylcholine and bradykinin also constrict the ductus.

Closure of the umbilical vein and ductus venosus

As the placental circulation stops at birth the flow to the umbilical vein and hence the ductus venosus stops

It closes by a process of fibrous obliteration of the lumen almost similar to the process involved in the closure of the ductus arteriosus

It completely obliterates by the seventh postnatal day

Closure of the foramen ovale

Closure of the foramen ovale at birth is entirely passive, secondary to alterations in the relative return of blood to the right and left atria

At birth combined ventricular output returning from the lung changes from 8% prenatally to >50%

Left atrial pressure thus exceeds right, and the redundant flap of tissue of the foramen ovale that previously bowed into the left atrium is now pressed against the septum

Fate of the shunts

Foramen ovaleCloses shortly after birth, fuses completely in first year.Ductus arteriosusCloses soon after birth, becomes ligamentum arteriosum in about 3 months.Ductus venosusLigamentum venosumUmbilical arteriesMedial umbilical ligamentsUmbilical vein Ligamentum teres

Blood circulation in various regional vascular beds

Post natal changes in various circulatory beds

Skin blood flow is high in utero as the vessels are dilated because the skin is exposed to warm amniotic fluid.

Cutaneous vasoconstriction occurs post natally as evaporation from skin starts.

Cutaneous flow falls and the vascular resistance increases.


Coronary Blood flow decreases dramatically as the oxygen content increases.

Cerebral circulation also behaves in the same fashion as coronary circulation.


Hepatic blood flow falls rapidly post natally with reduction in umbilical venous return and then increases as the GI flow is re established.

Hepatic blood flow progressively increases after birth and by 7 days after birth reaches a level of 250 ml/minute /100 g by which time there is no flow through ductus venosus.

Changes in Cardiac output

Oxygen consumption increases from 6-8 ml/mt/kg body weight pre natally to 15 20 ml/mt/kg post natally

Changes in Cardiac outputMechanisms

Neonate has to increase the metabolism to increase the body temperature as it is exposed to external temperature.

Improved diastolic function due to removal of compression by maternal organs and uterus causes increased cardiac filling and hence the cardiac output.

Changes in Cardiac outputMechanisms

Perinatal increase in thyroid hormones is the principal mechanism for increase in cardiac output.

Improvement in myocardial growth and maturation brought about by cortisol may also play important role.

Changes in hemoglobin and tissue oxygen delivery

Human new born has a high hemoglobin level (about 16g/dl) so that the oxygen carrying capacity is quiet high and the total amount of oxygen transported to tissues is quiet high.

Since the Hb F levels are still high facilitation at tissue site is not as great as in adults.

Over the first 8-10 weeks after the birth,Hb concentration falls to 10-11 g/dl. This is accompanied by loss of Hb F and almost 100% is adult type.

Fetal circulation in pathological conditions


Development of a structural abnormality will modify the fetal circulation.

This will affect the development of other components and can lead to other defects.

The impact of a defect will depend on its severity and time of gestation at which it occurs.


Cardiovascular malformations may:

cause hydrops fetalis by increasing venous pressure

change the volume or direction of blood flow

cause obstruction to blood flow

alter the oxygen saturation of blood delivered to various organs.


Many of the defects, though it modifies the circulation, will not significantly affect fetal perfusion and hence the growth and development.

This is because of the presence of shunts and mixing of blood.

Fetus tolerates the obstructive lesions very much.

Fetal circulation is jeopardized by regurgitant lesions and myocardial disease.

Pulmonary edema in a fetus

Increased fluid accumulation in the lung of the fetus is manifested as pulmonary lymphangiectasia.

This occurs only in those conditions in which pulmonary venous pressure can be raised to high levels, such as total pulmonary venous drainage with obstruction and aortic or mitral atresia with a small or closed foramen ovale.

PDA

O2

PGE2,PGE1 and PGI2 concentration

Pulmonary vascular resistance

Surfactant replacement therapy

Ability of fetal myocardium to handle cardiac output

Septal defects

They in general do not modify the fetal circulation significantly.

VSD may have a transient left to right shunt in systole.

In OP ASD, due to close proximity of defect with TV, more than normal amount of SVC blood may enter the LA.

Septal defects

In atrioventricular septal defects, the obligatory flow from LV to RA will result in decrease in LV output and an increase in RV output.

This will reduce the flow across the isthmus and can predispose to coarctation.

It is the degree of severity of AV valve lesion and regurgitation which will determine the outcome.

PATENT FORAMEN OVALE

ASSOCIATIONS

Cryptogenic stroke

decompression sickness (arterial gas embolism from the venous side)

migraine headaches.

Platypnea-orthodeoxia syndrome (dyspnea and arterial desaturation in the upright position, which improves on lying down)

LVOT Obstruction

Severe obstruction developing early result in a small LV with an increased mass.

RV is able to compensate fully if LVOTO develops slowly.

LVOT Obstruction

SVC flow courses normally.

Majority of IVC blood flow crosses TV to RV.

Flow across the ductus increases.

PBF has higher than normal saturation.

A retrograde flow in arch and ascending aorta indicates severe obstruction

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Aortic arch abnormalities

Most of the alteration in the circulation are due to co existing intra cardiac defects.

Common features are, reduced flow in to ascending aorta, increased flow in to the pulmonary trunk and greater proportion of CVO carried across ductus to descending aorta.

The decreased volume loading of LV may possibly interfere with its development.

Mitral and aortic atresia

All blood must pass through RV and ductus has to provide for both AA and DA blood flow.

Complete mixing of blood occurs in RA and saturation in PA,AA and DA are all same.

If the foramen ovale is sufficiently large and ductus accomodates whole of systemic blood flow, there will be no significant interference with intrauterine development and survival.

Left to right flow through foramen ovale seen.

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Mitral and aortic atresia

If the foramen ovale is restrictive, severe pulmonary venous hypertension develops.

If the ductus does not enlarge to accommodate the whole of systemic blood flow increased blood flow to lungs and pulmonary hypertension develops.

Both these can lead to increased development of smooth muscle in the pulmonary vasculature.

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RVOTO with intact IVS

In pulmonary atresia, all systemic venous blood is carried to left side through foramen ovale and all blood supply to DA is provided through isthmus.

Larger than normal foramen ovale, left sided chambers,AA and aortic isthmus.


If severe RVOTO develops early in gestation,the flow through the ductus is reversed and carries only 8 to 10 % of cardiac output.

The ductus will be narrower and will make an acute inferior angle with aorta.

The ductus will remain patent for longer than normal duration


If the fetus develops significant TR,RV pressure remains low and myocardial sinusoids and coronary fistulae do not develop.

If TR does not develop,significant RV systolic pressure develops and if occurs early in gestation, intramyocardial sinusoids and coronary fistulae develop.

TAPVC

Usually does not affect the development of fetus.

If whole of PV return drains to RA,LV will be totally free of PV blood and hence will be of higher saturation.

Left atrium and left ventricle will be relatively small in TAPVC.

TOF and related disorders

Does not appear to affect fetal circulation adversely.

The volume and direction of flow across the PA and ductus are dependent on the severity of obstruction.

Total flow through the ductus will be reduced considerably if there is severe RVOTO

TOF and related disorders

This can markedly reduce the diameter of fetal ductus and also reduce the development of smooth muscle in its wall.

If blood flows from aorta to PA in fetal life,the orientation of ductus changes and it forms an acute inferior angle with aorta.

AA and the isthmus carries large than normal amount of blood and they tend to be larger.

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TOF with absent PV

Ductus is frequently either atretic or not developed.

RV would be subjected to both volume and pressure overload and this can develop in utero.

Significant pulmonary regurgitation can seriously affect perfusion of pulmonary vessels and cause abnormal development of intrapulmonary vessels.

TGA

Compatible with fetal survival and normal intrauterine development.

Does not affect the pattern of venous return.

Blood with higher oxygen saturation will go to lungs. This will reduce the PVR and hence increase in PBF.

TGA

This will reduce the blood flow across the ductus and increases the flow across the isthmus.

Blood with lower oxygen saturation perfuses coronary and cerebral circulation.

Hence cerebral and coronary blood flow are increased considerably.

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TGA with VSD

Bidirectional shunting occur depending on after load of each ventricle.

The difference in saturation between AA and DA will be lesser.

TGA with VSD and PS

Almost complete admixture of SVC and IVC streams in RV.

AA and DA will have similar oxygen saturations.

Blood flow in the ductus will be from aorta to PA.

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Truncus arteriosus

Various degree of mixing occurs just above the semilunar valve.

Degree of mixing depends on morphology.

In type 1,there is differential streaming of blood and in others there will be complete mixing.

Ductus is usually small or absent and increased flow traverses through isthmus and it is large.

Ebsteins anomaly

Severe TR can manifest as in utero cardiac failure especially if foramen ovale is restrictive.

Marked enlargement of RA and atrialised RV can cause septal displacement and compromise LV output.

Functional pulmonary atresia can result and ductal flow may be reversed.

Ebsteins anomaly

Marked enlargement of right atrium can cause pulmonary hypoplasia

Severe TR alters the preferential drainage of venacaval blood and causes complete mixing of blood in right atrium.

Tricuspid atresia

All of the venous return traverses foramen ovale and it is considerably larger than normal .

Complete admixture of blood in the left atrium

It is compatible with normal intrauterine development and survival.

Tricuspid atresia

If IVS is intact, whole PBF is from aorta through ductus and ductal flow is lesser than normal.

75% of combined VO traverses the isthmus and it tends to be larger.

In the presence of VSD, the flow pattern is decided by the size of the defect and presence of pulmonary stenosis.

Some clinical pearls

Umbilical vein catherisation

Umbilical vein catheterization may be a life-saving procedure in neonates who require vascular access and resuscitation.

Indications

To gain vascular access during emergency resuscitation,central venous access in neonate,exchange transfusions

Contraindications

Omphalitis,peritonitis,NEC

Some clinical pearls

The fact that the right lobe of the liver receives blood of considerably lower oxygen saturation probably explains the frequent presence of a larger number of hemopoietic cells in the right as compared with the left lobe of the liver

REFERENCES

1.BRAUNWALDS HEART DISEASES

2.HURSTS THE HEART

3.RUDOLPHS CHD

4.MYUNG PARKS PEDIATRIC CARDIOLOGY

5. Distribution and regulation of blood flow in the fetal and neonatal lamb;A M RUDOLPH;

Circ Res. 1985;57:811-821

6.Preferential streaming of ductus venosus blood to the brain and heart in fetal lambs;Edelstone DI, Rudolph AM; 1979 Dec;237(6):H724-9; Am J Physiol.

7. The ductus venosus;Kiserud T; Semin Perinatol. 2001 Feb;25(1):11-20.

8. Assessment of Flow Events at the Ductus VenosusInferior Vena Cava Junction and at the Foramen Ovale in Fetal Sheep by Use of Multimodal Ultrasound Klaus G. Schmidt,MD; Norman H. Silverman,MD; Abraham M. Rudolph,MD; Circulation. 1996; 93: 826-833

Thank you

Flow Chart of Fetal Circulation

Flow Chart of Fetal Circulation

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