This document discusses fetal circulation and changes at birth. It begins with an overview of fetal circulation, including the three shunts of the ductus arteriosus, ductus venosus and foramen ovale that allow oxygenated blood to bypass the lungs and perfuse other organs. At birth, lung aeration causes pulmonary vascular resistance to decrease while systemic vascular resistance increases, closing the shunts. The document then reviews specific anatomical changes and defects such as patent ductus arteriosus and tetralogy of Fallot.

1. Anatomy of Foetal Circulation
Dr Leena Tayshete (Jr Reg)
Dr Anil K Sharma (Moderator)
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2. Objectives
• Review of Fetal Circulation
• Changes at Birth
• Postnatal circulation
• Defects
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6. – Begins to develop toward the end of 3rd wk
– Heart starts to beat at the beginning of 4th wk
– Critical period of heart development- day 20 to
day 50 aft fertilization.
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9. ‘Shunt-Dependent’ Circulation
• PaO2 in the umbilical vein around 4.7 kPa &
foetal blood saturation 80–90%.
• 50–60% of this placental venous flow bypasses
the hepatic circulation via the ductus venosus
(DV) to enter the inferior vena cava (IVC).
• Venous blood, which is returning from the lower
portions of the body SVO2 of around 25–40%.
• Eustachian valve -flap tends to direct the more
highly oxygenated blood, streaming along the
dorsal aspect of the IVC, across the foramen ovale
(FO).
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10. • In LA, O2 saturation of foetal blood is 65%.
Majority of the LV blood is delivered to the brain
and coronary circulation.
• Desaturated blood(SO2 25–40%),from SVC &
coronary sinus, in addition to the IVC’s anteriorly
streamed flow (comprised mainly of venous
return from lower body and hepatic circulation)
 directed across tricuspid valve.
• Due to high pulmonary vascular resistance (PVR)
about 12% of the RV output  pulmonary
circulation; remaining 88% crossing the ductus
arteriosus (DA)descending aorta
• Lower half of the body supplied with relatively
desaturated blood (PaO2 2.7 kPa).
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12. • Three shunts in foetal circulation
– Ductus arteriosus
� protects lungs against circulatory overload
� allows the right ventricle to strengthen
� hi pulmonary vascular resistance, low
pulmonary blood flow
� carries mostly medium oxygen saturated
blood.
– Ductus venosus
� connecting the umbilical vein to IVC
� blood flow regulated via sphincter
� carries mostly highly oxygenated blood.
– Foramen ovale
� shunts highly oxygenated blood from RA  LA.
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13. Foetal circulation is characterized by
• High PVR (fluid filled lungs and a hypoxic
environment).
• Low systemic vascular resistance (SVR) (large
surface area of low resistance utero-placental
bed).
• 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 Ductus Arteriosus.
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15. Physiology of Foetal Hb
• Umbilical vein PaO2 30-35 mmHg.
• Approximately 80% of foetal haemoglobin is Hb F
• Hb F (P50 19mmHg) is left shifted in comparison
to Hb A (P50 26mmHg), which improves oxygen
uptake at the placenta.
• Foetal pH (normal values 7.25-7.35) is lower than
in adults. Low foetal pH improves oxygen
unloading at tissue level.
• Foetal Hb is high compared to adult levels (raises
oxygen carrying capacity).
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17. • CaO2 (ml O2/dl blood) = (SaO2 x Hgb x 1.34) +
(PaO2 x 0.003)
• Umbilical vein PaO2 30-35 mmHg. Foetal Hb
70%-80% saturated at this PaO2 in
(comparison adult Hb SaO2 50-60%).
• CaO2 for foetus - Hb 18 grams/dl & SaO2 75%
in the umbilical vein yields: CaO2 = 0.75 x 18 x
1.34 = 18.1 ml O2/ dl blood
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19. • Foetal Hb conc. - 16 g dl/1 at term, with high % of
haemoglobin F (HbF), which has a lower content of 2,3-
DPG (shifting the oxygen dissociation curve to the left)
 favours oxygen uptake in placenta.
• After birth, presence of HbF becomes a disadvantage.
• The P50 fetal blood-3.6 kPa compared with adult
blood-4.8 kPa.
• When PO2 is 5.3 kPa (approximates to normal neonatal
venous value), the oxygen content of fetal blood is
much higher than that of adult blood. Thus, in the
neonate, HbF impairs oxygen extraction at tissue level.
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20. Combined ventricular output (CVO)
• SV of foetal LV ≠SV of RV.
• The RV receives about 65% of the venous return
and the LV about 35%.
• In the shunt dependent circulation of the foetus,
the situation is much more complex.
• The cardiac output of the foetus determined as
combined ventricular output (CVO)₂.
• About 45% of the CVO is directed to the placental
circulation with only 8- 12% of CVO entering the
pulmonary circulation.
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21. Review of changes at birth
• Overview-
– As soon as the baby is born
– Increasing uptake of oxygen by lungs (first and
subsequent breaths)  vasoconstriction of ductus
venosus and ductus arteriosus.
– The sphincter in ductus venosus constricts 
blood entering liver diverts to the hepatic
sinusoids).
� Occlusion of placental circulation  BP fall in
the IVC & RA.
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23. • Aeration of the lungs at birth
1. ↓ in PVR due to lung expansion.
2. ↑ in pulmonary blood flow (thus raising LA
pr > IVC pr)
3. progressive thinning of walls of the
pulmonary arteries (due to stretching).
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24. Factors affecting Pulmonary
Vasculature
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25. 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).
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26. • Resulting circulatory changes:
– blood pressure is now high in the aorta and systemic circulation
is well established
• Control of circulation is a reflex function regulated:
– Peripheral baroreceptors in aortic arch & carotid sinus.
– Central baroreceptors in cardiovascular center of medulla (close
proximity to chemoreceptors that regulate respiration).
• Respiratory and circulatory reflexes are usually strong in the
healthy full-term newborn, but efficiency in controlling
cardiovascular function is susceptible to environmental
factors.
• Parasympathetic > sympathetic activity.
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27. • Foramen ovale- Closes at birth
– 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.
• Other changes in the heart-
– The RV wall is thicker than LV wall in foetus and
newborn infants. By the end of the first month the
left ventricular wall is thicker than the right.
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28. Ductus Arteriosus-
– DA constricts at birth, often a small shunt from the
aorta to the left pulmonary artery for a few days in a
healthy, full-term infant.
– In premature infants and in those with persistent
hypoxia the DA may remain open longer.
– Oxygen, most important factor in controlling closure of
DA in full-term infants.
– Closure of DA appears to be mediated by bradykinin.
– PO2 of blood passing through DA reaches about 50
mm Hg, the wall of the DA constricts. (May be
mediated directly or by Oxygen effect on decreasing
PG E2 & prostacyclin secretion.
– Implication- Coarctation of aorta requires PGE2
infusion to reopen the DA for blood flow.
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29. • Umbilical Arteries constrict at birth
– To prevent loss of infant’s blood.
– Umbilical cord is not tied for 30-60s; transferring
blood from placenta to infant.
• The closure of the foetal vessels and foramen
ovale is initially a functional change; later
anatomic closure (from proliferation of
endothelial and fibrous tissues).
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30. UMBILICAL CORD CLAMPING
EXPOSURE TO ROOM AIR
TRANSITIONAL CIRCULATION
↓↓PVR
↑ SVR
↑ PULMONARY
BLOOD FLOW
↑ OXYGENATION
RESPONDS TO CHANGES IN PaO2, PaCO2, pH & CIRCULATING FACTORS
SVR – systemic vascular resistance PVR – pulmonary vascular resistance
↑ SVR ↓PVR
MECHANICAL INFLATION OF LUNGS
(↑ alveolar O2 tension,↑PaO2,↓PaCO2)
EDRF & PGs
↑ LT. ATRIAL FLOW
↓FORAMEN OVALE
SHUNT
F.O. CLOSURE
DUCTUS
ARTERIOSUS
CONSTRICTION

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FETAL CIRCULATION VIII: Conversion to post-natal*
Pulmonary
veinsVena cava Right
ATRIUM
Pulmonary
arteries
Right
VENTRICLE
Left
VENTRICLE
Aorta
LUNGS
SYSTEMIC
CAPILLARIES
HEART
Umbilical
arteries
Ductus arteriosus
IVC
OLef t
ATRIUM
Closure of Foramen ovale
DUCTUS VENOSUS
means that blood expelled from the
right ventricle has to go to the lungs
Closure of
Closure of
Stops use of umbilical
vessels, & converts all
vena cava blood to
deoxygenated
Forces venous blood (now all deoxygenated) into
the right ventricle for expulsion to the lungs
Closure of
Stops use of
umbilical vessels

32. Adult Derivatives of Fetal Vascular
Structures
Fetal Structure Adult Structure
Foramen Ovale Fossa Ovalis
Umbilical Vein (intra-abdominal part) Ligamentum Teres
Ductus Venosus Ligamentum Venosum
Umbilical Arteries and Abdominal
Ligaments
Medial Umbilical Ligaments,
Superior Vesicular Artery (supplies
bladder)
Ductus Arteriosum Ligamentum Arteriosum
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33. Persistent Foetal Circulation
• Neonate to revert back to foetal type
circulation, pathophysiological state- PFC.
• Causes- Hypothermia, hypercarbia, acidosis,
hypoxia and sepsis.
• One major difference—NO PLACENTA for
oxygenation vicious cycle of worsening
hypoxia and acidosis.
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34. Patent Ductus Arteriosus
• Female: Male, 2-3:1.
• Aortic blood shunted into Pulmonary Artery(shunt in
opposite direction to that in foetus). The magnitude
of the shunt increases as PVR continues to fall.
• Increased volume and workload left heart failure.
• Associated with maternal rubella infection during
early pregnancy.
• Premature infants usually have a PDA due to hypoxia
and immaturity.
• Surgical closure of PDA is achieved by ligation and
division of the DA.
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35. Patent Foramen Ovale
• Most common form of an ASDs
• Small isolated patent foramen ovale (no
hemodynamic significance); but if other defects
present (e.g. pulmonary stenosis or atresia),
blood is shunted through the foramen ovale into
LV  cyanosis.
• Probe patent foramen ovale, in up to 25% of
people (superior part of the floor of the fossa
ovalis). Though not clinically significant, may be
forced open because of other cardiac defects.
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36. Ventricular Septal Defects
• Ventricular septal defects (VSD) are one of the
most common forms of CHD.
• Well-tolerated in the fetus, as LV and RV
pressures are equal.
• After birth, circulatory effects are dependent on
size of the defect and balance between PVR &
SVR.
• In neonates with large VSD, as SVR rises and PVR
falls, L  R shunt through VSD develops. As PVR
continues to fall during the first weeks of life, this
shunt increases  CCF.
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37. Tetralogy of Fallot
• TOF, one of the most common congenital heart malformations.
• Most important features-
1. RV outflow obstruction, with hypoplastic pulmonary artery;
2. large subaortic VSD with malalignment of conal septum.
• In foetus, depending on severity of the obstruction to pulmonary
blood flow, the aorta will carry percentage of CVO. If obstruction
to pulmonary blood flow is very severe, blood flow to the lungs
will be supplied via the DA from descending aorta (i.e. the reverse
of normal).
• After birth- If pulmonary obstruction is severe, the neonatal
circulation is ‘duct-dependent’ and duct closure  severe
cyanosis.
• Re-establishment of ductal flow- prostaglandin infusion.
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38. Transposition of Great Arteries
• Abnormal rotation & septation of the arterial truncus during
embryogenesis.
• The aorta arises from the RV and the pulmonary artery from the LV
(pulmonary and systemic circulations are arranged in parallel ).
• The FO and DA develop as normal(no major circulatory
consequences of this lesion in utero).
• After birth, survival depends on presence of ASD, VSD or PDA
between the two circulations.
• Newborns with TGA & intact ventricular septum (IVS) who have
small PFO or ASD will be severely cyanosed after closure of the DA.
• Immediate management- establishing ductal patency (PGE1
infusion) and, if necessary, balloon atrial septostomy.
• Complete surgical repair- electively later.
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39. Anaesthetic Agents
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40. Propofol
• For induction/ procedural sedation.
• In healthy children without CHD, decrease in blood pressure of 30%
due to decreases in SVR (15%) and heart rate (10-20%).
• Children with CHD - primary effect is drop in BP through decrease in
SVR. Systemic cardiac output increased without a change in heart
rate or PVR.
• In children without shunt there was a small decrease in Pa02
(decreased respiratory drive), but no increase in PVR.
• In children with shunts the decrease in SVR  L-to-R shunting
decreased and R-to-L shunting increased.
• Used with caution as the sole agent in R-to-L shunts and in those
for whom a decrease in systemic afterload is dangerous (aortic
stenosis, hypertrophic cardiomyopathy, severe ventricular
dysfunction).
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41. Ketamine
• Anesthesia, analgesia, cardiovascular stability and lack of respiratory
depression with maintenance of airway reflexes.
• Drawbacks- prolonged action, emergence and dissociative anesthetic
state.
• Anesthetic dose 50-75 mcg/kg/min, analgesic dose 5-10 mcg/kg/min.
• In children with CHD, ketamine (50-75 mcg/kg/min) maintenance of the
relationship between SVR and PVR. Systemic blood pressure increased
through an increase in cardiac output with little change in heart rate.
• Increased inotropy- beneficial for children with significant ventricular
dysfunction.
• Sympathomimetic increased PVR??? In the setting of normocarbia with
supplemental oxygen , PVR is not increased.
• Combined with 0.5 minimal alveolar concentration (MAC) sevoflurane in
spontaneously breathing children with severe PHTN, ketamine did not
raise PVR.
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42. Etomidate
• Few studies.
• Bolus dosing of 0.3 mg/kg well tolerated-
maintenance of systemic BP & preservation of
balance between SVR and PVR.
• Drawbacks- Transient adrenal suppression,
pain on injection, vomitting.
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43. Volatile Agents
• Halothane- equivalent MAC to isoflurane and sevoflurane,
greater myocardial depression and suppression of
baroreceptor mediated increase in heart rate.
• The Qp:Qs ratio is unchanged with halothane, sevoflurane
or isoflurane if ventilation is controlled even with high Fi02.
• Isoflurane- CO was maintained even at 1.5 MAC (decrease
in SVR and increase in HR counters reduced inotropy).
• Sevoflurane- similar, but overall decrease in CO (lack of
compensatory increase in HR with reduced inotropy).
• Children with significant ventricular dysfunction may not
hemodynamically tolerate MAC levels of volatile
anesthesia.
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44. Fentanyl/ Midazolam
• Limited to sick children who will remain intubated
at the end of procedure.
• The ratio of Qp:Qs is unchanged in controlled
ventilation.
• Fentanyl 25 mcg/kg maintains SVR, PVR and
systemic blood pressure. Caution- Avoid
bradycardia.
• The general tone of the sympathetic nervous
system influences BP.
• Sympatholytic- combination of synthetic opioids
with volatile anesthetics, midazolam or propofol.
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45. Dexmedetomidine
• Selective α-2 agonist.
• Analgesic and sedative with minimal respiratory
depression. Similar to natural sleep state.
• Decreased sympathetic outflowrelative bradycardia
and stable blood pressure.
• Side effects detrimental to children with CHD -
hypertension (peripheral α-2 agonist effect),
bradycardia and hypotension.
• Poorly tolerated in heart rate dependent neonates and
infants.
• Lack of respiratory depression  ICU sedation in
children at risk for OSA such as Down syndrome.
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