NEW Written to fill a gap — the three shunts, the saturations, and what closes when at birth.
Fetal circulation
Three shunts, two circulations in parallel, and the transition at birth — with what reverses it.
The circuit
The two things that make it work
PVR is HIGH and SVR is LOW. The fluid-filled, hypoxic lung has a high resistance, while the placenta is a huge low-resistance bed. So blood takes the path of least resistance — right to left, away from the lungs and towards the placenta.
Streaming, not mixing. The crista dividens (the lower edge of the septum secundum) and the eustachian valve direct the well-oxygenated ductus venosus stream from the IVC preferentially across the foramen ovale to the left atrium, while poorly oxygenated SVC blood is directed to the right ventricle. This is why the brain and heart get the best blood available.
Saturations
Site
SaO₂
Why
Umbilical vein
~80%
The highest in the fetus — freshly oxygenated at the placenta
IVC
~67%
Umbilical venous blood diluted by systemic venous return
Ascending aorta
~65%
Supplies brain and coronaries — the best-oxygenated systemic blood
Descending aorta
~58%
Diluted by the ductus arteriosus stream from the right ventricle
Umbilical arteries
~58%
The lowest — returning to the placenta
Note the naming trap: the umbilical VEIN carries oxygenated blood to the fetus; the umbilical ARTERIES carry deoxygenated blood away. There is one vein and two arteries — a single umbilical artery is associated with congenital anomalies.
The fetus never exceeds about 80% saturation — it copes because HbF has a P50 of about 2.5 kPa (left-shifted, binds 2,3-DPG poorly), fetal haemoglobin concentration is high (~180 g/L), and combined cardiac output is high.
Output distribution
The ventricles work in parallel, not in series — so we speak of combined ventricular output, about 450 ml/kg/min.
The RIGHT ventricle is dominant, ejecting about two-thirds of the combined output. Most of it crosses the ductus arteriosus.
Only about 10–15% of combined output reaches the lungs.
About 40% of combined output goes to the placenta — the fetus's largest single "organ" by blood flow.
The fetal myocardium has fewer contractile elements and less compliance, so output is largely rate dependent — bradycardia is poorly tolerated at birth and beyond.
The cord is clamped → the low-resistance placenta is removed → SVR rises.
Increased pulmonary venous return raises left atrial pressure above right atrial pressure → the flap of the foramen ovale is pushed shut.
Flow through the ductus arteriosus reverses (now left to right) before it closes.
Structure
Closure
Becomes
Foramen ovale
Functional: immediate (LA pressure > RA) Anatomical: 3 months – 1 year
Fossa ovalis ~25% stay probe patent for life
Ductus arteriosus
Functional: 10–24 h (up to 48 h) Anatomical: 2–3 weeks
Ligamentum arteriosum
Ductus venosus
Functional: on cord clamping Anatomical: 1–2 weeks
Ligamentum venosum
Umbilical vein
On cord clamping
Ligamentum teres (round ligament of liver)
Umbilical arteries
On cord clamping
Medial umbilical ligaments proximal parts stay open as the superior vesical arteries
What closes the ductus arteriosus
A rise in PaO₂ is the main stimulus — it constricts ductal smooth muscle directly.
A fall in circulating prostaglandin E₂ — the placenta was its source, and the lung now clears it.
So the two drugs follow logically: indometacin or ibuprofen (prostaglandin synthesis inhibitors) CLOSE a patent duct; prostaglandin E₁ (alprostadil)KEEPS IT OPEN.
Prematurity is the major risk for a patent ductus arteriosus — the immature duct is less responsive to oxygen and more sensitive to prostaglandin.
When it matters clinically
Duct-dependent lesions
Some lesions rely entirely on the duct staying open, and the baby collapses when it closes at 1–2 days of age — often after discharge.
Duct-dependent pulmonary circulation: pulmonary atresia, critical pulmonary stenosis, severe tetralogy — presents with cyanosis.
Duct-dependent systemic circulation: hypoplastic left heart, critical aortic stenosis, coarctation, interrupted arch — presents with shock, absent femoral pulses and acidosis.
Treatment: prostaglandin E₁ infusion to reopen and maintain the duct. Side effects are apnoea (be ready to intubate), hypotension, pyrexia and jitteriness.
Do not give high-flow oxygen reflexively in a suspected duct-dependent lesion — oxygen closes the duct and drops PVR, worsening the systemic steal.
PVR fails to fall, or rises again, so the circulation reverts to right-to-left shunting across the foramen ovale and duct.
Precipitated by the four Hs and an A: Hypoxia · Hypercapnia · Hypothermia · Hypoglycaemia · Acidosis — plus sepsis, meconium aspiration, diaphragmatic hernia and polycythaemia.
The clue: a pre-ductal to post-ductal saturation difference of more than 10% — right hand higher than either foot.
Management: reverse the precipitants. Warm, oxygenate, correct acidosis and glucose, treat sepsis, gentle ventilation. Then inhaled nitric oxide (a selective pulmonary vasodilator), sildenafil, and ECMO in refractory cases.
This is why neonatal anaesthesia obsesses about warmth, oxygenation and avoiding acidosis — the fetal circulation is only just switched off and can switch back on.
Other anaesthetic consequences
A right-to-left shunt SLOWS inhalational induction (agent bypasses the lung) and SPEEDS intravenous induction. A left-to-right shunt has little effect on either.
Meticulous de-airing of every line. With a patent foramen ovale a venous air bubble can cross to the systemic circulation — a paradoxical embolus to the brain or coronaries.
Pre-ductal monitoring means the right hand — it reflects blood reaching the brain, before ductal mixing.
Delayed cord clamping (about 1 minute) raises neonatal haemoglobin and iron stores and improves transitional circulation, and is now standard in the uncompromised newborn.