1. Fetal and Neonatal Circulation
Dr. Carol Brenner Ph.D
Gentleman’s Review
Daniel Martingano OMS I

2. 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.

3. Fetal Circulation The First Heart beat 4th week
Heart rate beats/min
Prior to delivery beats/min

4. Fetal Circulation The fetal circulatory system is adapted to:
Maximize : gas and nutrient exchange between the mother
and the fetus
Provide : a higher supply of oxygen to developing organs with
high metabolic demand
Bypasses the organs with low metabolic demand
High metabolic demand: Heart, Brain, Upper body
Low metabolic demand: Liver, Lungs, Lower body

5. Four Shunts in Fetal Circulation
The main features of the fetal circulation are:
Non functioning lungs
Course of the blood from the placenta to the heart
Four shunts permitting the blood to bypass the liver and lungs:
Placenta
Ductus Venosus
Foramen Ovale
Ductus Arterios 3 4 2 1

6. The Placenta
Facilitates gas and nutrient exchange between maternal and fetal blood.
The blood itself does not mix.

7. First Shunt - Placenta It replaces 4 separate organs
Lungs, GI system, Liver, and Kidneys
Participates in gas exhange, nutrition, fluid regulation, waste removal, fluid excretion and ion regulation
The Fetal Heart pumps blood primarily though the placenta (40%)
Placenta recieves most of the combined cardiac output

8. Umbilical Cord Umbilical arteries Umbilical vein
transport deoxygented blood away from the fetus
Umbilical vein
transport oxygenated blood towards the fetus

9. 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.

10. Second Shunt – Ductus Venosus
In the fetus, the ductus venosus shunts approximately half of the blood flow of the umbilical vein directly to the inferior vena cava
Thus, it allows oxygenated blood from the placenta to bypass the liver.
Plays a critical role in preferentially shunting oxygenated blood to the fetal brain.

11. Second Shunt – Ductus Venosus
The second shunt bypasses the liver which is nonfunctional.
Oxygenated blood from the umbilical vein enters the Inferior vena cava bypassing the liver
Inferior vena cava drains the lower body (deoxygenated)
IVC deoxygenated blood mixes with the Ductus Venosus oxygenated blood

12. Third Shunt – Foramen Ovale
The third major shunt is the blood entering the right atrium and then crossing the foramen ovale to enter the left atrium.
The oval hole in the septum which divides the right and the left atria
Shunts highly oxygenated blood from right atrium to left atrium
Right to Left shunt:
 O2 from the IVC is send in to the left ventricle (foramen ovale) and in to the aorta

13. Fourth Shunt – Ductus Arteriosus
The fourth shunt directs the blood from the pulmonary artery to the aorta through the ductus arteriosus.
Collapsed Right to Left Shunt
lungs- Vascular resistance
Aorta- Vascular resistance
Blood: Pulmonary artery  Aorta
Aorta:
Proximally to the DA, the oxygenated blood is shuttled in to the upper parts of the fetus (Aorta)
Distally to the DA blood is mixed and transported to the systemic circulation
Aorta  Umbilical arteries  Placenta  Maternal circulation

14. The Four Shunts of Fetal Circulation
Placenta
Ductus Vensosus
Ductus Arteriosus
Foramen Ovale

15. Fetal Hemoglobin Fetal Hb can carry 20-30% more O2 than the adult Hb
Fetal hemoglobin 2  and 2 
The γ chains of the fetal hemoglobin
the higher affinity for the oxygen than its adult form. (shift to the left)
High Hb concentration (Hct 40-60%)
High cardiac output

16. Transition to Neonatal Circulation
The infants lungs begin to function
The lungs inflate which tends to draw blood from the right ventricle
Oxygenated blood from the lung passes through the pulmonary veins to the left atrium
Results in closure of the foramen ovale effectively separating the two atria
This also increases blood flow to the lungs as blood entering the right atrium can no longer bypass the right ventricle

17. Transition to Neonatal Circulation
The mechanisms that trigger the shift from the fetal to the adult circulation are:
Newborn breathing
 pulmonary resistance
Removal of the placenta
systemic vascular resistance

18. Transition to Neonatal Circulation
The placental circulation ceases
Umbilical vessels are no longer needed. They become obliterated
Occlusion of the placental circulation causes fall of blood pressure in the inferior vena cava and right atrium
The shunts stop to function
Within a day or two of birth, the ductus arteriosus closes off, preventing blood from the aorta from entering the pulmonary artery
The ductus venosus closes off so that all blood entering the liver passes through the hepatic sinusoids.

19. Adult Derivatives of Vascular Structures
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

20. Closure of the Ductus Venosus
Cessation of blood flow due to the clipping and cutting of the umbilical vein (pressure rises)
Blood backs up from the portal vein
1-3 hrs after the birth- the strong contraction of DV smooth muscle
The closure of the DV causes an increase in the portal vein pressure-increased perfusion of liver

21. Closure of the Ductus Arteriosus
 pulmonary pressure + systemic pressure
Change of flow-from the aorta in to the pulmonary system
reversal of the flow
Increased O2/  prostanglandin E2 levels cause the progressive closure and formation of the fibrous tissue
4-6 days; forms ligamentum arteriosum
The role of prostaglandin E2 (keeps the duct open)
The usage of PE2 blocker drug Indometacin (closes the duct)

22. Persistence of Fetal Circulation
Patent ductus arteriosus and patent foramen ovale each characterize about 8% of congenital heart defects.
Both cause a mixing of oxygen-rich and oxygen-poor blood
Blood reaching tissues is not fully oxygenated and can cause cyanosis.
Many of these defects go undetected until child is at least school age.

23. Patent Ductus Arteriosus
Left to right shunt
Failure of ductus arteriosus to close
Leads to increased aortic pressure
Decreased blood flow through the PDA in to the pulmonary circulation
No problems in early life – no cyanosis
As patient grows
aortic pressure increases
cyanosis dude to increased diameter of PDA

24. Patent Ductus Arteriosus
Cyanosis usually occurs late in life
Prolonged left to right shunting -> pulmonary hypertensions -> right-sided heart pressures that exceed the left -> reversal of blood flow through the shunt
This shunting of unoxygenated blood to the systemic circulation is called Eisenmenger syndrome (irreversible pulmonary vascular sclerosis)
Eisenmenger syndrome indicates that the defect is non-operable

25. Patent Ductus Arteriosus
½ to 2/3 of blood from the aorta passes through the pulmonary system (recirculation)
Cyanosis occurs latter in life as heart and/or lungs fail
Diminished cardiac and respiratory reserve
Diminished physical activity (fainting)
The life span: years (MCCD: pulmonary edema and CHF)
Treatment : Indometacin
Heart surgery-historical
Watch for prematures !!!
Machinery murmur (S2 diminished)

26. Tetralogy of Fallot Blue Baby- EARLY CYANOSIS Group of anomalies:
Stenosis of pulmonary artery (bypass lungs)
Right ventricle enlargement
Aorta-originates from the right ventricle riding on the septum
Blood from the Right ventricle passes trough the ventricular septal defect in to the L Ventricle and in to the overriding aorta

27. Tetraology of Fallot Treatment:
Surgical: Dilate the pulmonary stenosis
Close the septal defect
Reconstruct the aorta
The life Expectancy:
2-3 (without the surgery)
50 years (after the surgery)
The cause of congenital heart defects:
Infectious: German Measles (Deafness, PDA , Blindness)
Genetics: Some populations are more prone to develop defects