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By: Nicole Stevens
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To have an understanding of the anatomy and
physiology of fetal circulation
To identify the 3 fetal shunts
To have an understanding of newborn
transition and conversion of fetal to neonatal
circulation
Identify impediments to this transition
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Includes:
 Placenta
 Umbilical Vein (X1)
 Ductus Venosus
 Foramen Ovale
 Ductus Arteriosus
 Umbilical Arteries (X2)
Human fetal circulation works differently to extrauterine
circulation, and there are 3 key differences:
The presence of a placenta in the “circuit”
Blood flowing through the foramen ovale between the
right atrium and the left atrium
Blood bypassing through the ductus arteriosus from the
pulmonary artery to the aorta
There are also many other embryonic circulatory vessels;
these are slowly obliterated postnatally and remain in the
adult only as fibrous remants
ROLES OF THE PLACENTA:
 Secretes endocrine hormones which increase through
the pregnancy, causing progressive changes in
maternal metabolism; this creates an increase in the
maternal glucose and amino acids available to the
foetus
 The placenta facilitates the exchange of oxygen and
carbon dioxide between the mother and fetus. The
presence of fetal Hb in the fetal blood supply ensures
the movement of oxygen from mother to fetus
because the fetal Hb has a higher affinity to oxygen
than adult Hb.
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The placenta is responsible for
the provision of nutrients such
as water, glucose, vitamins
and electrolytes.
The placenta also manages
waste disposal of products
such as urea, uric acid and
bilirubin
These substances diffuse
between maternal and fetal
blood through the placental
membrane.
Adequate blood flow
throughout the pregnancy to
the placenta is vital to
maintain healthy growth and
development of the fetus
ROLES OF THE PLACENTA cont..:
 The maternal and fetal circulations are not joined,
instead, the respiratory gases, carbohydrates, lipids,
vitamins, minerals and amino acids diffuse across the
placental membrane
 The placenta is a low resistant component of fetal
circulation
 The fetal heart generates the force to pump blood
through the umbilical arteries (2) to the placenta
 Blood returns from the placenta to the fetus via the
umbilical vein
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Transports O2 rich
blood & nutrients
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Enters ductus venosus
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80% saturated with O2
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Approximately 45% of blood
from the umbilical vein enters
the portal circulation allowing
the liver to process nutrients.
Approximately 55% of the
blood passes thru the Ductus
Venosus, a shunt which
bypasses the liver.
The ductus venosus travels a
short distance and joins the
Inferior Vena Cava.
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From the inferior vena cava
the blood flows into the
right atrium and is shunted
directly into the left atrium
through an opening called
the foramen ovale.
Foramen
Ovale
R ►L shunt
There is a valve with two
flaps that prevents backflow.
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The fetus has high
pulmonary vascular
resistance due to partially
collapsed alveoli
There is decreased blood
flow to lungs
It is a relatively hypoxic
environment
The pulmonary vessels are
relatively constricted
Pulmonary
Vascular
Constriction
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DUCTUS ARTERIOSUS:
 Connects the pulmonary trunk to the descending
aorta
 Allows bypassing of the non-functioning lungs
 Returns blood to the placenta for oxygenation
Systemic circulation returning to the heart goes into
the right atrium then the right ventricle, this is
pumped into the pulmonary artery; blood wants to
travel on the path of least resistence, there is high
resistence in the lungs of the fetus and low resistence
in systemic circulation, the blood will prefer to flow
across the ductus arteriosus into the aorta, rather than
down the right and left pulmonary arteries to the
lungs.
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Return deoxygenated
blood from Descending
Aorta to placenta
The blood is then reoxygenated in the
placenta
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FETAL
CIRCULATION
THE PATH: (may help to track it on your heart
drawings)
 Deoxygenated fetal blood is carried to the placenta by
the two umbilical arteries; these arise from the
internal iliac arteries
 Gas exchange occurs in the placenta
 Oxygenated blood travels from the placenta via the
umbilical vein and enters the IVC
 About 50% of this passes through the liver and the
rest bypasses the liver via the ductus venosus; the
IVC also drains blood returning from the lower part
of the body
THE PATH cont..
 On reaching the heart at the right atrium the blood is
divided into 2 streams (of unequal sizes); the larger
stream is shunted to the left atrium through the FO,
the smaller stream joins the flow of blood returning
from the SVC (returning from the myocardium and
upper body)
 The blood that goes through the FO ends up in the
left ventricle and is ejected into the aorta
 The blood that goes into the right ventricle is
pumped into the pulmonary artery but most will go
across the DA and end up in the aorta as well
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Most of the relatively O2 rich blood that comes up
the ascending aorta from the left ventricle will end up
at the head and upper extremeties (the vessels
feeding these areas come off the aorta prior to the DA
union point)
The patency of the DA is maintained by the relatively
low O2 tension and the vasodilating effects of
prostaglandin E2 (maternal hormone coming through
the placenta)
The newborn, must make five major
adjustments at birth.
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1) World of air
2) Circulation
3) Wastes
4) Body temperature
5) Response to infection
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Fetal
 Low pressure system
 Lungs non-functional
 Right to left shunting
in the heart
 High pulmonary
resistance
 Low systemic
resistance
Neonate
 High pressure system
 Lungs functional
 Left to right blood flow
in the heart
 Low pulmonary
resistance
 High systemic
resistance
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At birth, the circulation of fetal blood through the
placenta ceases; the umbilical vessels are obliterated
when the cord is clamped externally
There is a reduction in blood flow through the IVC
and the ductus venosus (this will close within 3 – 10
days)
There is a dramatic fall in PVR with lung expansion
(opening up of pulmonary vessels)
A reduction in hypoxic pulmonary vasoconstriction and stimulation of pulmonary stretch
receptors contribute to this process
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At birth the first breaths are the catalyst for
the transition to neonatal circulation
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Lungs inflate with oxygen with an increased
atmospheric pressure
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Lungs now become a low-pressure system as
pulmonary vessels dilate with rise in oxygen level
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Alveolar fluid is displaced
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At birth, the circulation of fetal blood through the
placenta ceases; the umbilical vessels are obliterated
when the cord is clamped externally
There is a reduction in blood flow through the IVC and
the ductus venosus (this will close within 3 – 10 days)
There is a dramatic fall in PVR with lung expansion
(opening up of pulmonary vessels)
A reduction in hypoxic pulmonary vasoconstriction and stimulation of pulmonary stretch
receptors contribute to this process
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The rise in pulmonary blood flow leads to an increase
in blood returning to the left atrium; the left atrial
pressure therefore exceeds the right atrial pressure; this
reversal of pressure causes the flap of the FO to be
pushed closed (the initial closure occurs within
minutes, anatomical closure takes several days
The ductus arteriosus constricts due to the high partial
pressure of oxygen (the failure of this to occur will be
discussed in the presentation on PDA)
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Highly oxygenated arterial blood in the Ductus
Arteriosus causes it to constrict.
Cessation of circulating PGE2 from maternal
circulation. And increased metabolism of circulating
prostaglandins by the lungs
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Bradykinin – released on lung inflation
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Within 10-15 hours the DA constricts and will
eventually become the Ligamentum Arteriosus
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Increased blood flow
of oxygenated blood
returning from the
lungs
Increases the pressure
to the left side of the
heart forces blood
against the Septum
Primum causing the
Foramen Ovale to
close and become
Fossa Ovalis
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NEONATAL
CIRCULATION
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Lungs inflate  decrease in pulmonary vascular
resistance and increase in pulmonary vascular flow
Blood O2 levels rise  further decrease in
pulmonary vascular resistance and ductus arterious
constricts
Increased pressure in LEFT atrium and decreased
pressure in RIGHT atrium  formamen ovale closes
Umbilical cord is clamped  ductus venosus closes
 increased systemic vascular resistance
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What happens to these special structures after
birth?
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Umbilical arteries atrophy
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Umbilical vein becomes part of the fibrous support
ligament for the liver
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The foramen ovale, ductus arteriosus, ductus
venosus atrophy and become fibrous ligaments
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Foramen ovale
Closes shortly after birth, fuses
completely in first year.
Ductus arteriousus
Closes soon after birth, becomes
ligamentum arteriousum in about 3
months.
Ductus venosus
Ligamentum venosum
Umbilical arteries
Medial umbilical ligaments
Umbilical vein
Ligamentum teres
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The Five H’s
Hypothermia
 Hypoxia
 Hypoglycaemia
 Hypotension
 Hypercarbia
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Blood flow to all organs is reduced
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Lack of adequate organ perfusion
& tissue oxygenation
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Brain damage
& multisystem organ damage
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DEATH
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Inter-uterine distress: abnormal presentations,
maternal haemorrhage/seizures, ascending infection,
cord prolapse
Congenital cardiac abnormalities: HLHS, coarction of
the aorta, TGA, TOF
Pulmonary abnormalities: hypoplastic lungs,
congenital pneumonia, decreased surfactant
production (prematurity/diabetic mother)
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Insufficient ventilation and/or airway blockage
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Excessive blood loss or poor cardiac contractility
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Sustained constriction of pulmonary arterioles
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BEWARE THE UNDIAGNOSED CARDIAC
ABNORMALITY – IF THEY ARE DUCT
DEPENDENT DISORDERS THESE BABIES WILL
DETERIORATE AS THE DUCT CLOSES
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In some circumstances a neonates circulation may
revert back to be fetal-like; this state is known as
persistent foetal circulation (PFC)
A neonates pulmonary arterioles remain very reactive
and will constrict in response to: hypoxia,
hypercarbia, acidosis and cold; this can lead to an
increase in PVR, which favours right to left shunting
through the FO and ductus arteriosus
The result of this is the neonate reverting to PFC,
with one major difference – there is no placenta to
provide oxygenation; a vicious cycle of worsening
hypoxia and acidosis is then set in motion.
The management of this requires treatment of the
underlying causes:
 Such as, escalating respiratory support to provide
better ventilation (and reduce hypercarbia)
 Use of nitric oxide if there is pulmonary
hypertension, to aid in dilating the pulmonary
vessels (nitric is inhaled through the ventilation
circuit)
 Management of infection with antibiotics
 Management of thermoregulation
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American Academy of Pediatrics
 Textbook of Neonatal Resuscitation 4th Ed (2000)
 NRP Slide Presentation Kit
Askin,D.F. (2001) Complications in the Transition from Fetal to Neonatal Life JOGNN
Vol33(3) 318-327
Blackburn,S. (2006) Placental Fetal and Transitional Circulation Revisited. Perinatal
Neonatal Nursing Vol20 (4) 290-294
Witt C. (1997) Cardiac Embryology. Neonatal Network Vol16(1) 43-49
Merenstein, G.B & Gardner, S.L, (2002), Handbook of Neonatal Intensive Care ,
5th Ed, Mosby, St. Louis.
www.echocharity.org.uk
http://www.nhlbi.nih.gov/health/dci/Diseases/pda/pda_heartworks.html
http://user.gru.net/clawrence/vccl/chpt1/fetcirc.HTM
http://www.cayugacc.edu/people/facultypages/greer/biol204/heart4/heart4.html
http://www.indiana.edu/~anat550/cvanim/fetcirc/fetcirc.html
http://www.embryology.ch/anglais/pcardio/umstellung01.html
http://mcb.berkeley.edu/courses/mcb135e/fetal.html
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http://www.indiana.edu/~anat550/cvanim/f
etcirc/fetcirc.html
http://www.embryology.ch/anglais/pcardio/
umstellung01.html
http://www.youtube.com/watch?v=T79sMqvN
3BE
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