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Fetal Circulation
Thanks to SMARAK RANJAN ROUT ,DM CARDIOLOGY ,SGPGI
Fetal circulation
UMBILICAL VEIN
Hepatic Circulation
IVCLEFT LOBE RIGHT LOBE
PORTAL VEIN
RA
LA
LHV
DUCTUS VENOSUS
RHV
Contents
• Embryology of heart
• Anatomy fetal circulation
• Physiology of fetal circulation
• Transition from fetal to infant circulation
• Compared fetal to infant circulation
• Impact of fetal circulation on various congenital heart during
intrauterine life and during transition
FETAL CIRCULATION
• The term usually encompasses the entire fetoplacental circulation,
which includes the umbilical cord and the blood vessels within the
placenta that carry fetal blood
Embryology
of heart
Foetus heart starts beating on 18th to 22nd day
– Formed by the overlapping
edge of the septum secundum
against the ruptured upper
portion of the septum
primum.
– Acts like a flap valve for
preferential blood flow from
the right atrium to the left
atrium.
Foramen Ovale
• Blood column in IVC inlet (to RA)
• hits the interatrial ridge, the crista
dividens
left arm Right arm
fills the ‘windsock’ TV
Foramen Ovale RV
LA
• Foramen Ovale
– Connects the left branch of the
pulmonary trunk to arch of
aorta(beyond the origin of left
subclavian artery)
– It protects the lungs from circulatory
overloading.
– Less oxygenated blood in Pulmonary
artery flows through Ductus
Arteriosus to descending aorta and
then to placenta foroxygenation
Ductus Arteriosus
Vena-caval Circulation
Superior Vena Cava
• Drains the upper part of the
body,including the brain (15% of
combined ventricular output).
• Most (95%)of SVC blood goes
to the Right Ventricle.
•SVC SpO2- 40%
Inferior Vena Cava
• Drains lower part of body and
placenta (70% of combined
ventricular output)
• Most of IVC blood is directed to
the LA through Foramen ovale.
• IVC SpO2 -Inlet- 70%
Distal- 35%
Fetal Pulmonary Circulation
• Fetal lung does not serve gas exchange function.
• MPA continues as Ductus and RPA and LPA arise as branches.
• PVR is high and PBF is low (10 % of CCO). This helps to reduce workload
of fetal heart.
Causes – - Thick muscular layer
• decreased NO synthetase ,Adrenomedullin
• increased endothelin 1 ,Leukotriens
• mechanical – fluid filled alveoli
• PVR – In early gestation-> extremely high : small number of small arteries
In last half of gestation-> decreases progressively : growth of new
arteries and an overall increase in cross section.
Mean PAP - increases progressively with gestation and at term is about
50 mm Hg, exceeds mean aortic blood pressure.
Coronary
,Cerebral,
Supex
Infex And Viscera
SVC
SpO2 80–90%
Fetal Blood volume• The blood volume - fetus: 10-12% of BW
Adult: 7-8% of BW
• The main reason for this difference is the large pool of blood contained within
the placenta; a volume that reduces as gestation progresses.
• Compared with adults, the fetus is capable of much faster regulation and
restoration of the blood volume due to high diffusion rates between fetal
compartments.
• Placental Blood flow regulation:
 Endothelin and prostanoids  vasoconstriction
 Nitric oxide  vasodilation.
 No neural vascular regulation, and
 Catecholamines - Little effect.
20
5 4.5
55
25
6
0
10
20
30
40
50
60
SBP DBP UVP
MID GESTATION TERM GESTATION
Fetal Blood Pressure
Johnson P, Maxwell DJ, Tynan MJ, Allan LD. Intracardiac
pressures in the human fetus. Heart 2000;84:59e63.
Fetal Cardiac performance
• The myocardium grows by cell division until birth, and growth beyond birth
is due to cell enlargement.
• The density of myofibrils increases particularly in early pregnancy and the
contractility continues to improve during the second half of pregnancy.
• Fetal and neonatal myocardial cells
• are smaller in diameter
• contain relatively more non-contractile mass (primarily mitocondria,
nuclei & surface membrane).
• force of generation , extent and velocity of shortening arelow
• stiffness and water content of ventricular myocardium are high
Fetal Cardiac Output
• The cardiac output of the fetus is expressed in terms of the total output of
both ventricles—the combined Cardiac output (CCO).( Because of Parallel
circulation)
• Right ventricular output is about 1.3 times the left ventricular flow.
• During fetal life the right ventricle
• -is pumping against systemic blood pressure
• -is performing greater volume of work than LV.
• The fetal and neonatal heart has limited ability to increase CO in presence
of increased preload or afterload.
• CO determinants-
-HR ( Most important determinant)
-SV- Frank starling mechanism, Adrenergic drive
Changes in blood flow to various organs during
the latter half of gestation.
Maternal Physiology during Pregnancy & Fetal & Early Neonatal Physiology: Current
Diagnosis & Treatment: Obstetrics & Gynecology, 11e
|
Physiology of Foetal Hb
• Approximately 80% of foetal
haemoglobin is Hb F.
Oxygen Uptake Facilitated by
-Low P50 of Hb F
- Lower content of 2,3-DPG of
Hb F.
Oxygen Delivery Maintained by
-High CCO, high haemoglobin
concentrations , and more O2
content (despite the relatively
low partial pressures of oxygen.
-Lower Foetal pH (normal values
7.25-7.35) than in adults.
Response of fetal circulation to stress• Acute hypoxic insult
Autonomic
Responses
Activates a chemoreflex mediated by the carotid
bodies - vagal effect - reduced heart rate and a
sympathetic vasoconstriction
Endocrine
Responses
• Early-
adrenaline and noradrenaline, RAAS
• maintaining vasoconstriction (a-
adrenergic),
• increasing heart rate (b-adrenergic)and
• reducing blood volume with
renin release and increased
angiotensin II concentration
Delayed-
• Increased concentrations of adrenocorticotrophic
hormone, cortisol, atrial natriuretic peptide,
neuropeptide Y and adrenomedullin
Watershed Areas in Fetal Circulation
• Isthmus aortae –
• As a watershed between the aortic arch and the ductus arteriosus
• Retrograde flow ( DA to Ascending aorta) in LV obstructive lesions
• An Indicator of placental compromise
• Left portal vein-
• As a watershed between umbilical vein and main portal vein
• Retrograde flow (Main portal vein to Umbilical vein) in compromised placental venous
return.
• An Indicator of placental compromise
• Foramen Ovale-
• Between RA and LA
• Normally Left arm ( wind sock effect) and Right arm.
• In cases with increased venous return (e.g. arterio-venous malformation), an increased
volume of blood is diverted to the right side
Overview of fetal circulatory dynamics
Parallel arrangement of two main arterial systems and their respective
ventricles.
Presence of shunts. (in the venous system, heart & arterial system.)
High impedance and low flow of pulmonary circulation.
Low impedance and high flow of placental circulation.
Mixing of venous return and preferential streaming.
Most oxygenated blood from the umbilical vein perfuses the brain and heart
preferentially by shunting across Ductus Venosus & Foramen Ovale.
Lesser oxygenated blood perfuses the lower body by shunting across the
DuctusArteriosus.
Remnants of the fetal circulation can be found in the adult
Fetal vs. Infant Circulation
• Fetal
• Low pressure system
• Right to left shunting
• Lungs non-functional
• Increased pulmonary resistance
• Decreased systemic resistance
• Infant
• High pressure system
• Left to right blood flow
• Lungs functional
• Decreased pulmonary resistance
• Increased systemic resistance
Anatomy of fetal circulation
• Blood from the placenta is carried to the fetus by the umbilical vein. In
humans, less than a third of this enters the fetal ductus venosus and is
carried to the inferior vena cava, while the rest enters the liver proper from
the inferior border of the liver. The branch of the umbilical vein that
supplies the right lobe of the liver first joins with the portal vein. The blood
then moves to the right atrium of the heart. In the fetus, there is an
opening between the right and left atrium (the foramen ovale), and most
of the blood flows through this hole directly into the left atrium from the
right atrium, thus bypassing pulmonary circulation. The continuation of this
blood flow is into the left ventricle, and from there it is pumped through
the aorta into the body. Some of the blood moves from the aorta through
the internal iliac arteries to the umbilical arteries, and re-enters the
placenta, where carbon dioxide and other waste products from the fetus
are taken up and enter the maternal circulation
• Some of the blood entering the right atrium does not pass directly to
the left atrium through the foramen ovale, but enters the right
ventricle and is pumped into the pulmonary artery. In the fetus, there
is a special connection between the pulmonary artery and the aorta,
called the ductus arteriosus, which directs most of this blood away
from the lungs (which are not being used for respiration at this point
as the fetus is suspended in amniotic fluid).
Placenta
• 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 uterine 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.
Circulation at Materno Placental Level
umbilical
arteries
umbilical Veins-
chorionic villi
intervillous space
Maternal venules Maternal Arterioles
Circulation at Materno Placental Level
umbilical
arteries
umbilical
Veins
chorionic villi
intervillous space
Maternal
venules
Maternal
Arterioles
Fetal hemoglobin (HbF)
the developing fetus also employs a different type of oxygen transport
molecule in its hemoglobin from that when it is born and breathing its
own oxygen. Fetal hemoglobin enhances the fetus' ability to draw
oxygen from the placenta. Its oxygen-hemoglobin dissociation curve is
shifted to the left, meaning that it is able to absorb oxygen at lower
concentrations than adult hemoglobin. This enables fetal hemoglobin
to absorb oxygen from adult hemoglobin in the placenta, where the
oxygen pressure is lower than at the lungs. Until around six months'
old, the human infant's hemoglobin molecule is made up of two alpha
and two gamma chains (2α2γ). The gamma chains are gradually
replaced by beta chains until the molecule becomes hemoglobin A with
its two alpha and two beta chains (2α2β)
Blood pressure
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 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 umbilical, it is 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.
Flow
• The blood flow through the umbilical cord is approximately 35 mL/min at
20 weeks, and 240 mL/min at 40 weeks of gestation. Adapted to the weight
of the fetus, this corresponds to 115 mL/min/kg at 20 weeks and 64
mL/min/kg at 40 weeks. It corresponds to 17% of the combined cardiac
output of the fetus at 10 weeks, and 33% at 20 weeks of gestation.
• Endothelin and prostanoids cause vasoconstriction in placental arteries,
while nitric oxide causes vasodilation. On the other hand, there is no neural
vascular regulation, and catecholamines have only little effect.
SpO2 80–90%
SVC
(65% )
(57% )
(8% )
(35%)
INFEX AND VISCERA
37%
(10%)
20%
CORONARY,CEREBRAL,
SUPEX
25%
(15% )
(70% )
The change from fetal to
postnatal circulation happens
very quickly.
Changes are initiated by baby’s first breath.
The first breath:
Pulmonary alveoli open up:
– pressure in pulmonary tissues decrease.
– Blood from right heart rushes to fill the alveolar capillaries.
– Pressure in right side of heart ↓.
– Pressure in the left side of the heart ↑ (as more blood is returned
from pulmonary tissue via pulmonary veins to the LA).
Conversion of the fetal to the adult circulation
requires
–Increase of pulmonary blood flow to a level necessary
for adequate gas exchange
-Eliminating the umbilical–placental circulation
–separation of the left and right sides of the heart by
closure of fetal channels.
Perinatal circulatory transition
↑ Pulmonary Blood Flow
↑Oxygenation
Removal of the low-resistance
placental circulation
Increase in systemic vascular
resistance.
Mechanical expansion of
lungs
Increase in arterial PO2
Rapid Decrease In Pulmonary
Vascular Resistance
Ductus
Arteriosus
Constriction
↑ Lt.AtrialFlow
↓Foramen Ovale
Shunt
F.O. Closure
Umbilical arteries → Umbilical ligaments
Umbilical vein → Ligamentum teres
Shunt Functional
closure
Anatomical
closure
Ductus
arteriosus
10 – 96 hrs
after birth
2 – 3 wks
after birth
Formamen
ovale
Within several
mins after birth
One year
after birth
Ductus
venosus
Within several
mins after birth
3 – 7 days
after birth
Foramen Ovale Closure
– After birth, the foramen ovale closes by apposition of the left and right atrial flaps bordering
the opening.
– Decreased flow from placenta & IVC to hold open foramen and;
– Increased pulmonary blood flow & pulmonary venous return to left heart causing pressure in
the LA > RA.
– Premature closure of the foramen in utero may cause hypoplasia of the left side of the heart
because only a minimal amount of blood would reach the left atrium.
Ductus Arteriosus Closure
• Factors favouring :
 O2- most important factor , At PO2- 50 mm Hg, By Direct effect (O2 Sensitive K channel
inhibition=> Voltage sensitive Ca Channels activation)/ Indirect effect- on decreasing PG E2 &
prostacyclin secretion.
prostaglandin antagonists- highest in third trimester and is enhanced by glucocorticoids and fetal
stress.
Increased Bradykinin and Decreased NO.
Contd…
• Immediately after birth: (Functional closure)
• contraction and cellular migration of the medial smooth muscle in
the wall of DA
• functional closure within 12 hours after birth in full-termhuman infants.
• The second stage : (Anatomical closure)
• completed by 2 to 3 weeks in human infants
• produced by infolding of the endothelium,
• disruption and fragmentation of the internal elasticlamina
• proliferation of the subintimal layers
• hemorrhage and necrosis in the subintimal region.
Contd..
In PRETREM: ( Delayed Closure)
 The responsiveness of the ductal smooth muscle to oxygen is related to the gestational age
of the newborn.
- decreased sensitivity to oxygen-induced contraction ( Not due to lack of smooth muscle
development)
- persistently high levels of PGE2
-Low PaO2 in preterm neonate ( due to immature lung)
- Deficient in K+ channels.
Ductus venosus Closure
• The shunt obliterates within 1-3 weeks of birth in term infants
• Takes longer time in :
• premature births
• persistent pulmonary hypertension
• various forms of cardiac malformations.
• As in DA, PGE1 may keep it open , thromboxane may close it .
• In contrast to the DA where increased oxygen tension triggers the closure, no O2
trigger for DV.
Changes in Pulmonay Circulation
• With initiation of pulmonary ventilation:
• pulmonary vascular resistance decreases rapidly
• pulmonary blood flow increased by eightfold to tenfold.
• mean pulmonary arterial blood pressure is half systemic by 24 hours of age.
• Morphologic changes (vascular remodeling, muscular involution, and rheologic
changes) in the pulmonary vessels result in a permanent fall in pulmonary vascular
resistance.
– most striking change is a decrease in the thickness of the smooth muscle layer in the
small arteries.
– Adult levels of PVR and PAP reached by 2-6 weeks.
Contd..
Contd..
Regulation of PVR-
• state of oxygenation
• the production of vasoactive substances:
– oxygen modulates the production of
both prostacyclin and endothelium-
derived nitric oxide (EDNO).
– Direct potassium channel activation
– Physical expansion
– Changes in alveolar surface tension
Post natal changes in various circulatory
beds
Coronary Blood flow Decreases dramatically as the oxygen content increases.
Cerebral circulation -DO-
Cutaneous blood flow Decreases(<= Cutaneous vasoconstriction )
Hepatic blood flow Falls rapidly f/b a surge ( on day 7,250 ml/minute /100 g )
Changes in Cardiac output
• The left ventricle in the fetus pumped blood mostly 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)
Contd..
• Improved diastolic function
due to removal of compression
by maternal organs and uterus
causes increased cardiac filling
and hence the cardiac output.
• 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
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
Umbilical artery
Ductus venosus
Ductus arteriosus
Foramen ovale
Ligamentum teres
Medial umb ligament
Ligamentum venosum
Ligamentum arteriosum
Fossa ovalis
Adaptation to extrauterine life
• At birth, when the infant breathes for the first time, there is a
decrease in the resistance in the pulmonary vasculature, which
causes the pressure in the left atrium to increase relative to the
pressure in the right atrium. This leads to the closure of the foramen
ovale, which is then referred to as the fossa ovalis. Additionally, the
increase in the concentration of oxygen in the blood leads to a
decrease in prostaglandins, causing closure of the ductus arteriosus.
These closures prevent blood from bypassing pulmonary circulation,
and therefore allow the neonate's blood to become oxygenated in the
newly operational lungs.
CHD compatible with fetal circulation
• VSD
• Atrial septal defect (ASD)
• Pulmonary stenosis (PS)
Heart diseases not compatible to fetal life
• Myocarditis
• Congestive heart failure
CHD those are fatal during transition
• TGA
• COA/IAA
• AS
• HLHS
• Mitral atresia
• PA
• obstructed TAPVR
Thanking you
Adjustment is life
There is no escape
Whether drink alcohol or
Take strong Nescafe

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Fetal circulation

  • 1. Fetal Circulation Thanks to SMARAK RANJAN ROUT ,DM CARDIOLOGY ,SGPGI
  • 3. UMBILICAL VEIN Hepatic Circulation IVCLEFT LOBE RIGHT LOBE PORTAL VEIN RA LA LHV DUCTUS VENOSUS RHV
  • 4. Contents • Embryology of heart • Anatomy fetal circulation • Physiology of fetal circulation • Transition from fetal to infant circulation • Compared fetal to infant circulation • Impact of fetal circulation on various congenital heart during intrauterine life and during transition
  • 5. FETAL CIRCULATION • The term usually encompasses the entire fetoplacental circulation, which includes the umbilical cord and the blood vessels within the placenta that carry fetal blood
  • 7. Foetus heart starts beating on 18th to 22nd day
  • 8. – Formed by the overlapping edge of the septum secundum against the ruptured upper portion of the septum primum. – Acts like a flap valve for preferential blood flow from the right atrium to the left atrium. Foramen Ovale
  • 9. • Blood column in IVC inlet (to RA) • hits the interatrial ridge, the crista dividens left arm Right arm fills the ‘windsock’ TV Foramen Ovale RV LA • Foramen Ovale
  • 10. – Connects the left branch of the pulmonary trunk to arch of aorta(beyond the origin of left subclavian artery) – It protects the lungs from circulatory overloading. – Less oxygenated blood in Pulmonary artery flows through Ductus Arteriosus to descending aorta and then to placenta foroxygenation Ductus Arteriosus
  • 11. Vena-caval Circulation Superior Vena Cava • Drains the upper part of the body,including the brain (15% of combined ventricular output). • Most (95%)of SVC blood goes to the Right Ventricle. •SVC SpO2- 40% Inferior Vena Cava • Drains lower part of body and placenta (70% of combined ventricular output) • Most of IVC blood is directed to the LA through Foramen ovale. • IVC SpO2 -Inlet- 70% Distal- 35%
  • 12. Fetal Pulmonary Circulation • Fetal lung does not serve gas exchange function. • MPA continues as Ductus and RPA and LPA arise as branches. • PVR is high and PBF is low (10 % of CCO). This helps to reduce workload of fetal heart. Causes – - Thick muscular layer • decreased NO synthetase ,Adrenomedullin • increased endothelin 1 ,Leukotriens • mechanical – fluid filled alveoli • PVR – In early gestation-> extremely high : small number of small arteries In last half of gestation-> decreases progressively : growth of new arteries and an overall increase in cross section. Mean PAP - increases progressively with gestation and at term is about 50 mm Hg, exceeds mean aortic blood pressure.
  • 15. Fetal Blood volume• The blood volume - fetus: 10-12% of BW Adult: 7-8% of BW • The main reason for this difference is the large pool of blood contained within the placenta; a volume that reduces as gestation progresses. • Compared with adults, the fetus is capable of much faster regulation and restoration of the blood volume due to high diffusion rates between fetal compartments. • Placental Blood flow regulation:  Endothelin and prostanoids  vasoconstriction  Nitric oxide  vasodilation.  No neural vascular regulation, and  Catecholamines - Little effect.
  • 16. 20 5 4.5 55 25 6 0 10 20 30 40 50 60 SBP DBP UVP MID GESTATION TERM GESTATION Fetal Blood Pressure Johnson P, Maxwell DJ, Tynan MJ, Allan LD. Intracardiac pressures in the human fetus. Heart 2000;84:59e63.
  • 17. Fetal Cardiac performance • The myocardium grows by cell division until birth, and growth beyond birth is due to cell enlargement. • The density of myofibrils increases particularly in early pregnancy and the contractility continues to improve during the second half of pregnancy. • Fetal and neonatal myocardial cells • are smaller in diameter • contain relatively more non-contractile mass (primarily mitocondria, nuclei & surface membrane). • force of generation , extent and velocity of shortening arelow • stiffness and water content of ventricular myocardium are high
  • 18. Fetal Cardiac Output • The cardiac output of the fetus is expressed in terms of the total output of both ventricles—the combined Cardiac output (CCO).( Because of Parallel circulation) • Right ventricular output is about 1.3 times the left ventricular flow. • During fetal life the right ventricle • -is pumping against systemic blood pressure • -is performing greater volume of work than LV. • The fetal and neonatal heart has limited ability to increase CO in presence of increased preload or afterload. • CO determinants- -HR ( Most important determinant) -SV- Frank starling mechanism, Adrenergic drive
  • 19. Changes in blood flow to various organs during the latter half of gestation. Maternal Physiology during Pregnancy & Fetal & Early Neonatal Physiology: Current Diagnosis & Treatment: Obstetrics & Gynecology, 11e |
  • 20. Physiology of Foetal Hb • Approximately 80% of foetal haemoglobin is Hb F. Oxygen Uptake Facilitated by -Low P50 of Hb F - Lower content of 2,3-DPG of Hb F. Oxygen Delivery Maintained by -High CCO, high haemoglobin concentrations , and more O2 content (despite the relatively low partial pressures of oxygen. -Lower Foetal pH (normal values 7.25-7.35) than in adults.
  • 21. Response of fetal circulation to stress• Acute hypoxic insult Autonomic Responses Activates a chemoreflex mediated by the carotid bodies - vagal effect - reduced heart rate and a sympathetic vasoconstriction Endocrine Responses • Early- adrenaline and noradrenaline, RAAS • maintaining vasoconstriction (a- adrenergic), • increasing heart rate (b-adrenergic)and • reducing blood volume with renin release and increased angiotensin II concentration Delayed- • Increased concentrations of adrenocorticotrophic hormone, cortisol, atrial natriuretic peptide, neuropeptide Y and adrenomedullin
  • 22. Watershed Areas in Fetal Circulation • Isthmus aortae – • As a watershed between the aortic arch and the ductus arteriosus • Retrograde flow ( DA to Ascending aorta) in LV obstructive lesions • An Indicator of placental compromise • Left portal vein- • As a watershed between umbilical vein and main portal vein • Retrograde flow (Main portal vein to Umbilical vein) in compromised placental venous return. • An Indicator of placental compromise • Foramen Ovale- • Between RA and LA • Normally Left arm ( wind sock effect) and Right arm. • In cases with increased venous return (e.g. arterio-venous malformation), an increased volume of blood is diverted to the right side
  • 23. Overview of fetal circulatory dynamics Parallel arrangement of two main arterial systems and their respective ventricles. Presence of shunts. (in the venous system, heart & arterial system.) High impedance and low flow of pulmonary circulation. Low impedance and high flow of placental circulation. Mixing of venous return and preferential streaming. Most oxygenated blood from the umbilical vein perfuses the brain and heart preferentially by shunting across Ductus Venosus & Foramen Ovale. Lesser oxygenated blood perfuses the lower body by shunting across the DuctusArteriosus.
  • 24. Remnants of the fetal circulation can be found in the adult
  • 25. Fetal vs. Infant Circulation • Fetal • Low pressure system • Right to left shunting • Lungs non-functional • Increased pulmonary resistance • Decreased systemic resistance • Infant • High pressure system • Left to right blood flow • Lungs functional • Decreased pulmonary resistance • Increased systemic resistance
  • 26. Anatomy of fetal circulation
  • 27. • Blood from the placenta is carried to the fetus by the umbilical vein. In humans, less than a third of this enters the fetal ductus venosus and is carried to the inferior vena cava, while the rest enters the liver proper from the inferior border of the liver. The branch of the umbilical vein that supplies the right lobe of the liver first joins with the portal vein. The blood then moves to the right atrium of the heart. In the fetus, there is an opening between the right and left atrium (the foramen ovale), and most of the blood flows through this hole directly into the left atrium from the right atrium, thus bypassing pulmonary circulation. The continuation of this blood flow is into the left ventricle, and from there it is pumped through the aorta into the body. Some of the blood moves from the aorta through the internal iliac arteries to the umbilical arteries, and re-enters the placenta, where carbon dioxide and other waste products from the fetus are taken up and enter the maternal circulation
  • 28. • Some of the blood entering the right atrium does not pass directly to the left atrium through the foramen ovale, but enters the right ventricle and is pumped into the pulmonary artery. In the fetus, there is a special connection between the pulmonary artery and the aorta, called the ductus arteriosus, which directs most of this blood away from the lungs (which are not being used for respiration at this point as the fetus is suspended in amniotic fluid).
  • 29. Placenta • 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 uterine 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.
  • 30. Circulation at Materno Placental Level umbilical arteries umbilical Veins- chorionic villi intervillous space Maternal venules Maternal Arterioles
  • 31. Circulation at Materno Placental Level umbilical arteries umbilical Veins chorionic villi intervillous space Maternal venules Maternal Arterioles
  • 32. Fetal hemoglobin (HbF) the developing fetus also employs a different type of oxygen transport molecule in its hemoglobin from that when it is born and breathing its own oxygen. Fetal hemoglobin enhances the fetus' ability to draw oxygen from the placenta. Its oxygen-hemoglobin dissociation curve is shifted to the left, meaning that it is able to absorb oxygen at lower concentrations than adult hemoglobin. This enables fetal hemoglobin to absorb oxygen from adult hemoglobin in the placenta, where the oxygen pressure is lower than at the lungs. Until around six months' old, the human infant's hemoglobin molecule is made up of two alpha and two gamma chains (2α2γ). The gamma chains are gradually replaced by beta chains until the molecule becomes hemoglobin A with its two alpha and two beta chains (2α2β)
  • 33. Blood pressure 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 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 umbilical, it is 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.
  • 34. Flow • The blood flow through the umbilical cord is approximately 35 mL/min at 20 weeks, and 240 mL/min at 40 weeks of gestation. Adapted to the weight of the fetus, this corresponds to 115 mL/min/kg at 20 weeks and 64 mL/min/kg at 40 weeks. It corresponds to 17% of the combined cardiac output of the fetus at 10 weeks, and 33% at 20 weeks of gestation. • Endothelin and prostanoids cause vasoconstriction in placental arteries, while nitric oxide causes vasodilation. On the other hand, there is no neural vascular regulation, and catecholamines have only little effect.
  • 35. SpO2 80–90% SVC (65% ) (57% ) (8% ) (35%) INFEX AND VISCERA 37% (10%) 20% CORONARY,CEREBRAL, SUPEX 25% (15% ) (70% )
  • 36. The change from fetal to postnatal circulation happens very quickly. Changes are initiated by baby’s first breath.
  • 37. The first breath: Pulmonary alveoli open up: – pressure in pulmonary tissues decrease. – Blood from right heart rushes to fill the alveolar capillaries. – Pressure in right side of heart ↓. – Pressure in the left side of the heart ↑ (as more blood is returned from pulmonary tissue via pulmonary veins to the LA).
  • 38. Conversion of the fetal to the adult circulation requires –Increase of pulmonary blood flow to a level necessary for adequate gas exchange -Eliminating the umbilical–placental circulation –separation of the left and right sides of the heart by closure of fetal channels.
  • 39. Perinatal circulatory transition ↑ Pulmonary Blood Flow ↑Oxygenation Removal of the low-resistance placental circulation Increase in systemic vascular resistance. Mechanical expansion of lungs Increase in arterial PO2 Rapid Decrease In Pulmonary Vascular Resistance Ductus Arteriosus Constriction ↑ Lt.AtrialFlow ↓Foramen Ovale Shunt F.O. Closure
  • 40. Umbilical arteries → Umbilical ligaments Umbilical vein → Ligamentum teres Shunt Functional closure Anatomical closure Ductus arteriosus 10 – 96 hrs after birth 2 – 3 wks after birth Formamen ovale Within several mins after birth One year after birth Ductus venosus Within several mins after birth 3 – 7 days after birth
  • 41. Foramen Ovale Closure – After birth, the foramen ovale closes by apposition of the left and right atrial flaps bordering the opening. – Decreased flow from placenta & IVC to hold open foramen and; – Increased pulmonary blood flow & pulmonary venous return to left heart causing pressure in the LA > RA. – Premature closure of the foramen in utero may cause hypoplasia of the left side of the heart because only a minimal amount of blood would reach the left atrium.
  • 42. Ductus Arteriosus Closure • Factors favouring :  O2- most important factor , At PO2- 50 mm Hg, By Direct effect (O2 Sensitive K channel inhibition=> Voltage sensitive Ca Channels activation)/ Indirect effect- on decreasing PG E2 & prostacyclin secretion. prostaglandin antagonists- highest in third trimester and is enhanced by glucocorticoids and fetal stress. Increased Bradykinin and Decreased NO.
  • 43. Contd… • Immediately after birth: (Functional closure) • contraction and cellular migration of the medial smooth muscle in the wall of DA • functional closure within 12 hours after birth in full-termhuman infants. • The second stage : (Anatomical closure) • completed by 2 to 3 weeks in human infants • produced by infolding of the endothelium, • disruption and fragmentation of the internal elasticlamina • proliferation of the subintimal layers • hemorrhage and necrosis in the subintimal region.
  • 44. Contd.. In PRETREM: ( Delayed Closure)  The responsiveness of the ductal smooth muscle to oxygen is related to the gestational age of the newborn. - decreased sensitivity to oxygen-induced contraction ( Not due to lack of smooth muscle development) - persistently high levels of PGE2 -Low PaO2 in preterm neonate ( due to immature lung) - Deficient in K+ channels.
  • 45. Ductus venosus Closure • The shunt obliterates within 1-3 weeks of birth in term infants • Takes longer time in : • premature births • persistent pulmonary hypertension • various forms of cardiac malformations. • As in DA, PGE1 may keep it open , thromboxane may close it . • In contrast to the DA where increased oxygen tension triggers the closure, no O2 trigger for DV.
  • 46. Changes in Pulmonay Circulation • With initiation of pulmonary ventilation: • pulmonary vascular resistance decreases rapidly • pulmonary blood flow increased by eightfold to tenfold. • mean pulmonary arterial blood pressure is half systemic by 24 hours of age. • Morphologic changes (vascular remodeling, muscular involution, and rheologic changes) in the pulmonary vessels result in a permanent fall in pulmonary vascular resistance. – most striking change is a decrease in the thickness of the smooth muscle layer in the small arteries. – Adult levels of PVR and PAP reached by 2-6 weeks.
  • 48. Contd.. Regulation of PVR- • state of oxygenation • the production of vasoactive substances: – oxygen modulates the production of both prostacyclin and endothelium- derived nitric oxide (EDNO). – Direct potassium channel activation – Physical expansion – Changes in alveolar surface tension
  • 49. Post natal changes in various circulatory beds Coronary Blood flow Decreases dramatically as the oxygen content increases. Cerebral circulation -DO- Cutaneous blood flow Decreases(<= Cutaneous vasoconstriction ) Hepatic blood flow Falls rapidly f/b a surge ( on day 7,250 ml/minute /100 g )
  • 50. Changes in Cardiac output • The left ventricle in the fetus pumped blood mostly 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)
  • 51. Contd.. • Improved diastolic function due to removal of compression by maternal organs and uterus causes increased cardiac filling and hence the cardiac output. • 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
  • 52. 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 Umbilical artery Ductus venosus Ductus arteriosus Foramen ovale Ligamentum teres Medial umb ligament Ligamentum venosum Ligamentum arteriosum Fossa ovalis
  • 53. Adaptation to extrauterine life • At birth, when the infant breathes for the first time, there is a decrease in the resistance in the pulmonary vasculature, which causes the pressure in the left atrium to increase relative to the pressure in the right atrium. This leads to the closure of the foramen ovale, which is then referred to as the fossa ovalis. Additionally, the increase in the concentration of oxygen in the blood leads to a decrease in prostaglandins, causing closure of the ductus arteriosus. These closures prevent blood from bypassing pulmonary circulation, and therefore allow the neonate's blood to become oxygenated in the newly operational lungs.
  • 54. CHD compatible with fetal circulation • VSD • Atrial septal defect (ASD) • Pulmonary stenosis (PS)
  • 55. Heart diseases not compatible to fetal life • Myocarditis • Congestive heart failure
  • 56. CHD those are fatal during transition • TGA • COA/IAA • AS • HLHS • Mitral atresia • PA • obstructed TAPVR
  • 57. Thanking you Adjustment is life There is no escape Whether drink alcohol or Take strong Nescafe