Transcript Fetal and Neonatal Circulation

Fetal and Neonatal
Circulation
Dr. Carol Brenner Ph.D
Gentleman’s Review
Daniel Martingano OMS I
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.
Fetal Circulation
• The First Heart beat
– Heart rate
– Prior to delivery
4th week
65 beats/min
140 beats/min
Fetal Circulation
The fetal circulatory system is adapted to:
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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
Four Shunts in Fetal Circulation
The main features of the fetal
circulation are:
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Non functioning lungs
Course of the blood from the
placenta to the heart
Four shunts permitting the blood
to bypass the liver and lungs:
1.
2.
3.
4.
4
Placenta
Ductus Venosus
Foramen Ovale
Ductus Arterios
2
1
The Placenta
• Facilitates gas and
nutrient exchange
between maternal and
fetal blood.
• The blood itself does not
mix.
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
Umbilical Cord
• Umbilical arteries
– transport deoxygented blood
away from the fetus
• Umbilical vein
– transport oxygenated blood
towards the fetus
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.
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.
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
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
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
The Four Shunts of
Fetal Circulation
1. Placenta
2. Ductus Vensosus
3. Ductus Arteriosus
4. Foramen Ovale
Fetal Hemoglobin
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Fetal Hb can carry 20-30% more O2
than the adult Hb
Fetal hemoglobin 2  and 2 
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The γ chains of the fetal
hemoglobin
the higher affinity for the oxygen
than its adult form. (shift to the left)
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High Hb concentration (Hct 4060%)
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High cardiac output
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
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
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.
Adult Derivatives of Vascular
Structures
Foramen ovale
Closes shortly after birth, fuses
completely in first year.
Ductus arteriousus
Ductus venosus
Closes soon after birth, becomes
ligamentum arteriousum in about 3
months.
Ligamentum venosum
Umbilical arteries
Medial umbilical ligaments
Umbilical vein
Ligamentum teres
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
Closure of the Ductus Arteriosus
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 pulmonary pressure + systemic pressure
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Change of flow-from the aorta in to the pulmonary system
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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
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The role of prostaglandin E2 (keeps the duct open)
– The usage of PE2 blocker drug Indometacin (closes the duct)
Persistence of Fetal Circulation
• Patent ductus arteriosus and
patent foramen ovale each
characterize about 8% of
congenital heart defects.
• Both cause a mixing of oxygenrich 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.
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
Patent Ductus Arteriosus
• Cyanosis usually occurs late in life
• Prolonged left to right shunting -> pulmonary hypertensions -> rightsided 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
Patent Ductus Arteriosus
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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: 20-40 years (MCCD: pulmonary edema and CHF)
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Treatment : Indometacin
Heart surgery-historical
Watch for prematures !!!
Machinery murmur (S2 diminished)
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Tetralogy of Fallot
• Blue Baby- EARLY CYANOSIS
• Group of anomalies:
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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
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