Fetal Circulation

Overview

Diagram 1 - Fetal Circulation (color-coded by oxygen saturation)

Diagram 2 - Blood Flow as % of Combined Cardiac Output (CCO)

Diagram 3 - O₂ Saturation and PO₂ at Each Checkpoint

Step-by-Step Blood Flow

1. Placenta → Umbilical Vein

• Oxygenated, nutrient-rich blood leaves the placenta via the single umbilical vein
• O₂ saturation ~80-85%, PO₂ ~30 mmHg (highest in the fetal circuit)
• This is the only vessel in fetal life that carries oxygenated blood with a venous name

2. Umbilical Vein → Liver / Ductus Venosus (Shunt 1)

• On reaching the liver, blood splits:
  • ~50% enters the ductus venosus - a direct channel from umbilical vein to inferior vena cava (IVC), bypassing the liver sinusoids
  • ~50% flows into the portal system and liver sinusoids, then drains via hepatic veins into the IVC
• A physiologic sphincter near the umbilical vein regulates this split - it prevents cardiac overloading during uterine contractions by diverting more blood to the liver

3. IVC → Right Atrium

• Blood in the IVC is now a mixture of:
  • Well-oxygenated blood from ductus venosus + hepatic veins
  • Poorly oxygenated blood from lower limbs, pelvis, kidneys
  • Net O₂ saturation in IVC ~70%, PO₂ ~27 mmHg
• Blood enters the right atrium

4. Right Atrium → Foramen Ovale → Left Atrium (Shunt 2)

• The crista dividens (lower edge of the septum secundum) acts as a flow divider:
  • The larger stream (well-oxygenated IVC blood) is directed by the valve of the inferior vena cava through the foramen ovale directly into the left atrium
  • The smaller stream (poorly oxygenated IVC blood) stays in the right atrium and mixes with SVC blood returning from the head and upper limbs
• In the left atrium, blood mixes with the small volume of pulmonary venous return (~7% CCO from the lungs) - O₂ saturation ~65%, PO₂ ~25 mmHg

5. Left Atrium → Left Ventricle → Ascending Aorta

• Blood passes through the left ventricle and is pumped into the ascending aorta
• The first branches off the ascending aorta are the coronary arteries and the carotid arteries
• This means the heart muscle and brain receive the best-oxygenated blood available in fetal life - a critical preferential arrangement

6. Right Atrium → Right Ventricle → Pulmonary Trunk

• The poorly oxygenated stream (from SVC + small IVC portion) passes from right atrium → right ventricle → pulmonary trunk
• The right ventricle handles ~66% of the combined cardiac output (CCO); the left ventricle handles ~34%
• Pulmonary vascular resistance is very high in fetal life (due to hypoxic vasoconstriction), so only ~7-10% of this blood goes to the lungs

7. Pulmonary Trunk → Ductus Arteriosus → Descending Aorta (Shunt 3)

• ~90% of pulmonary trunk blood bypasses the lungs via the ductus arteriosus - a wide channel connecting the pulmonary trunk directly to the descending aorta
• This blood (O₂ saturation ~55-60%) enters the descending aorta and mixes with the smaller amount of blood coming from the ascending aorta

8. Descending Aorta → Body + Umbilical Arteries

• Blood in the descending aorta (~60% O₂ saturation, PO₂ ~23 mmHg) distributes to:
  • Viscera and lower body (~35%)
  • Two umbilical arteries (~65%) - which return deoxygenated blood back to the placenta (O₂ saturation ~58% in umbilical arteries)
• The umbilical arteries are branches of the internal iliac arteries

Sites of Oxygen Dilution (Langman's Five Mixing Points)

The Three Shunts - Summary Table

Why the Fetus Tolerates Low PO₂

1. Fetal hemoglobin (HbF) - has higher O₂ affinity than adult HbA (curve shifted left), allowing adequate saturation at lower PO₂
2. Elevated hematocrit - increases total O₂-carrying capacity
3. High cardiac output - maintains O₂ delivery despite lower saturation
4. Preferential streaming - the best-oxygenated blood is selectively directed to the coronary arteries and brain

Circulatory Changes at Birth

1. Clamping of the umbilical cord - removes the low-resistance placental circulation, doubling total peripheral resistance and raising aortic pressure
2. First breath / lung expansion - pulmonary vascular resistance falls >5-fold due to: mechanical expansion, rising alveolar PO₂, falling PCO₂, and release of prostacyclin (PGI₂)

Consequences:

• Pulmonary blood flow increases 4-fold → more blood returns via pulmonary veins → left atrial pressure rises above right atrial pressure → septum primum is pressed against septum secundum (functional closure)
• Anatomical closure (fusion) occurs over weeks to months
• Adult remnant: fossa ovalis

• Rising PO₂ causes smooth muscle contraction (hours)
• Falling prostaglandin E₂ levels (prostaglandins kept it open in utero)
• Functional closure: 10-15 hours after birth; anatomical closure: 2-3 weeks
• Adult remnant: ligamentum arteriosum

• Loss of umbilical venous flow, smooth muscle constriction over days
• Adult remnant: ligamentum venosum

• Umbilical vein → ligamentum teres hepatis (round ligament of liver)
• Umbilical arteries → medial umbilical ligaments (proximal portions persist as superior vesical arteries)

Neonatal Circulation (Post-Birth)

Key Clinical Points

• Persistent fetal circulation (Persistent Pulmonary Hypertension of the Newborn, PPHN): If pulmonary vascular resistance fails to fall after birth, right-to-left shunting continues through a patent ductus arteriosus and/or foramen ovale, causing cyanosis
• Patent ductus arteriosus (PDA): Failure of ductus arteriosus to close; common in premature infants; treated with indomethacin (inhibits prostaglandin synthesis) or surgical ligation
• Patent foramen ovale (PFO): Present in ~25% of adults as a probe-patent remnant; usually asymptomatic but may permit paradoxical embolism
• Indomethacin/prostaglandins in CHD: PGE₁ is used therapeutically to keep the ductus arteriosus open in duct-dependent congenital heart defects (e.g., pulmonary atresia, transposition)