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As Overview of Fetal
Circulation
Rima Bader MD ,PhD, FASE, FACC
Professor of Pediatrics, Consultany Pediatric &Perinatal cardiology
King Abdul Aziz University College of medicine
Jeddah, Saudi Arabia
Flow Chart of Fetal Circulation
Fetal Circulation
 By the third month of development, all major
blood vessels are present and functioning.
 Fetus must have blood flow to placenta.
 Resistance to blood flow is high in lungs.
Umbilical Circulation
 Pair of umbilical
arteries carry
deoxygenated blood
& wastes to
placenta.
 Umbilical vein
carries oxygenated
blood and nutrients
from the placenta.
Overview of the Fetal circulation
 Blood is oxygenated in the placenta
 Oxygenated blood returns to the fetus via the
umbilical vein
 Umbilical vein courses into the hilum of the
liver and joins the portal vein
 Umbilical venous blood is directed in part
through the ductus venosus which joins the IVC
 O2 rich ductus venosus blood is preferentially
directed into the left atrium and left heart
through the foramen ovale
 Venous return of the left heart is comprised of
both ductus venosus and pulmonary venous
blood
 less oxygenated blood of the liver (largely right
lobe) and the SVC is directed into the right
atrium and right heart
 The left and right hearts function in parallel
rather than in series
 . The left ventricle ejects largely to the coronary
arteries and upper body with an arterial PaO2 (in fetal
lambs) of 25-28mmHg.
 The right ventricle ejects largely to the lungs, the
lower body and the umbilical artery via the ductus
arteriosus with an arterial PaO2 of 20-23mmHg (in
fetal lambs)
 With a high pulmonary vascular resistance, less
than 20% of the cardiac output goes through the
fetal lungs with an increase in the third
trimester
 The combined cardiac output of the fetal heart
is 450cc/kg/min with mild RV dominance
through the second and third trimesters in
contrast to the 800cc/kg/min of the combined
output that occurs in the in series circulation
The Placenta
 Facilitates gas and
nutrient exchange
between maternal and
fetal blood.
 The blood itself does
not mix.
The placenta
 Comprised of maternal (utero-placental) and fetal
(feto-placental) components
 Provides nutrients, respiratory gas and metabolic
exchange between the mother and fetus
 Placental development begins at implantation with
attachment and invasion of trophoblast cells into
the uterine mucosa (6-7 days post conception)
 Complete fetoplacental circulation is established
around the start of the 5th week post conception
 Uteroplacental flow increases during gestation
in 3 phases as a result of vasodilation:
 first of which may occur within days or weeks of
pregnancy,
 second with development of intravillous spaces,
 third during rapid fetal growth after 30 weeks and
this corresponds with a change in uterine blood flow
from <1% of the maternal cardiac output to 16-25%
near term.
 Fetoplacental blood flow also exponentially
increases throughout gestation which is likely the
consequence of both vasodilation and vascular
growth and may be an index of fetal growth.
 Placental blood volume is approximately 30% of
the combined fetal cardiac output in this same
period.
 Clinically, umbilical artery Doppler flow studies
have demonstrated
 evidence of a gestational-age dependent fall in
placental resistance with essentially no forward
diastolic flow in the late first trimester
 to increasing flow velocities in diastole through
the second and third trimesters
The fetal shunts
1. Ductus venosus
 Provides access for much of the highly oxygenated
blood from the umbilical vein to the fetal inferior vena
cava
 This streams preferentially into the left atrium as a
consequence of the IVC’s central position and
relationship with the foramen ovale, septum primum and
septum secundum.
Ductus Venosus
.
 In its absence (also known as agenesis of the ductus
venosus)
 the umbilical vein may connect with the portal
venous system, another systemic vein such as the
inferior vena cava or the right atrium itself. .
 Observations of changes in ductus venosus patterns in the
context of evolving fetal heart failure with
 gradual reduction in forward velocities during atrial systole
in the ductus venosus
 with ultimate development of a wave reversal that occurs

before the development of umbilical venous notching
 This could also suggest a protective mechanism that
prevents modestly elevated central venous pressures from
significantly influencing the critical umbilical venous
return
Lets go!
2- Foramen ovale
 Blood is shunted from
right atrium to left
atrium, skipping the
lungs.
 More than one-third of
blood takes this route.
 Is a valve with two
flaps that prevent backflow.
Foramen ovale ( cont’d)
 a communication between the left and right atrium
with a flap-valve (septum primum)
 that allows the oxygen rich blood of streaming
through the ductus venosus from the umbilical vein to
enter into the left atrium
 . Septum primum serves to prevent blood flow from
moving from the left atrium to the right atrium
 In humans Doppler studies suggest the proportion of
combined cardiac output that crosses the foramen
goes from 34% at 20 weeks to 18% at term.
3- Ductus Arteriousus
 The blood pumped
from the right ventricle
enters the pulmonary
trunk.
 Most of this blood is
shunted into the aortic
arch through the ductus
arteriousus.
3- Ductus Arteriosus
 The ductus arteriosus is a vessel that permits the
majority of the right ventricular output to be ejected
into the descending aorta. Early in gestation its size is
very similar to that of the aortic arch
 Later in gestation, however, likely in preparation for
postnatal closure, intimal cushions form within its
lumen as a result of vascular smooth muscle cell
proliferation and migration into the subendothelium.
The formation of intimal cushions could correspond
with the very high velocities observed in the ductus
arteriosus of late third trimester human fetuses
 Circulating PGE2 probably controls the patency of the
ductus arteriosus in utero
4- Aortic Isthmus
 While not a true fetal shunt,
 The aortic isthmus acts somewhat as a
watershed between the aortic arch and ductus
arteriosus-descending aorta
 which reflects differences in vascular
impedance between the cerebral vascular bed
and the lower body and placenta
The Fetal Myocardium
 A- Developmental changes in
structure/growth:
 knowledge of the developmental changes that occur
in the fetal heart are important in understanding the
fetal circulation
 Fetal myocardial growth–in the fetus particularly
early in gestation, is largely through cardiac
myocyte and nonmyocyte proliferation
 Rapid myocardial growth and general somatic
occurs in fetal life, particularly in the first half of
gestation after embryogenesis
B-Developmental Changes in Myocardial
Function
 Systolic function

echocardiographic parameters of systolic performance
are not so different in the fetus versus the postnatal heart
normal dP/dt max 1500-3000mmHg/s

LV and RV shortening fraction is 30-34% and does not
change with age
LV ejection fraction is 60-65% in the fetus and postnatally




cardiac output changes from 450ml/kg/min in utero to
800ml/kg/min for the combined ventricular output.
In utero the RV output is approximately 1.2-1.4 that of the
LV
 Diastolic function
 Changes with gestational age and
postnatallysingle muscle strip preparations suggest
greater passive tension of the fetal myocardium
 Ventricular Doppler filling patterns
demonstrate increasing e wave (early ventricular
diastole) with gestation and no change in the a
wave velocity (during atrial systole) which
suggests changes in the ability of the ventricles to
relax with gestation
 Isvolumic relaxation time does not significantly
change between the second and third trimesters
 Preload
 Fetal myocardium does follow Frank-Starling rules as
is most simply demonstrated by the increased
ventricular output following a premature beat
 Left ventricular (LV) preload is determined by





inferior vena cava flow,
pulmonary venous return,
size of the foramen ovale,
right heart filling pressures, in the right atrium,
the diastolic or filling function of the left ventricle
 Right ventricular (RV) preload is determined by the




superior and inferior vena caval flow
left heart filling pressure
foramen ovale size
and right ventricular diastolic function
 Afterload
 left ventricular afterload is largely from the upper body

right ventricular afterload is largely determined by the
vascular bed of the lower body (including the placenta) and
patency of the ductus arteriosus
 afterload has a significant impact on cardiac output
 the low vascular impedance of a normal placenta results in a
large proportion of the combined ventricular output to go
through the umbilical circulation
 at midgestation 50% of the total fetal blood volume is
contained within the placenta, however this decreases to
about 33% by term
 Heart rate





normal fetal heart rates range
110-150bpm at less than 10 weeks,
from 150-180bpm at 10-16 weeks
120-160bpm from 20 weeks to term
over the normal range of heart rates, the human fetus
does not significantly change the cardiac output but
rather changes stroke volume to maintain a stable
cardiac output
What happens at birth?
 The change from fetal to postnatal circulation
happens very quickly.
 Changes are initiated by baby’s first breath.
Foramen ovale
Ductus venosus
Closes shortly after birth,
fuses completely in first
year.
Closes soon after birth,
becomes ligamentum
arteriousum in about 3
months.
Ligamentum venosum
Umbilical arteries
Medial umbilical ligaments
Umbilical vein
Ligamentum teres
Ductus arteriousus
Problem with persistence of fetal
circulation
 Patent (open) ductus arteriosus and patent
foramen ovale each characterize about 8% of
congenital heart defects.
 Both cause a mixing of oxygen-rich and oxygenpoor blood; blood reaching tissues not fully
oxygenated. Can cause cyanosis.
 Transcatheter closure or surgical correction now
available, ideally completed around age two.
 Many of these defects go undetected until child is
at least school age.
Take home message
1. Fetal left and right hearts function in parallel
2.
rather than in series and this is a result of the
unique fetal shunts and placental circulation
As a consequence of the fetal circulation and
streaming of blood, the left heart in utero sees
more highly oxygenated blood
 which goes to the fetal myocardium and brain
3. Normal fetal heart rates range from 110150bpm at less than 10 weeks, from 150180bpm at 10-16 weeks and 120-160bpm
from 20 weeks to term
4. There are key developmental differences
between the fetal, neonatal and adult
myocardium that result in differences in
diastolic and systolic function
 The fetal myocardium does follow Frank-Starling

rules as is most simply demonstrated by the
increased ventricular output following a premature
beat
The fetal response to stress includes increase in the
mean arterial pressure, decrease in the fetal heart
rate, late in the course decrease in the combined
cardiac output and redistribution of the cardiac
output to critical organs: the brain, heart, adrenal
glands.
Thank you!