Appearance
7.9 — The Fetal Circulation and the First Breath
A fetus lives underwater for nine months without breathing. Its lungs are collapsed, full of fluid, and receive almost no blood — sending blood to them would be pointless, because there is no air in them. Oxygen comes from the placenta instead, delivered through the umbilical vein.
Then, in the space of a few minutes after birth, the entire circulation reconfigures. Three shunts close, the lungs open, and pressures reverse. It is the most dramatic physiological change any human undergoes, and understanding it explains a set of newborn emergencies and a common adult finding.
The problem the fetus has to solve
Oxygen comes from the placenta, not the lungs. So blood must be routed to the placenta and away from the lungs.
And the fetal liver is not yet doing much of its adult job, so most of the oxygenated blood arriving from the placenta should bypass it too, to avoid losing oxygen unnecessarily.
Three shunts solve this, and each one is a temporary channel that must close after birth.
1. Ductus venosus — connects the umbilical vein directly to the inferior vena cava, bypassing the liver. About half the incoming oxygenated blood takes this route.
2. Foramen ovale — the flap valve between the two atria (Chapter 4.5). Blood passes from right atrium to left atrium, bypassing the lungs entirely.
3. Ductus arteriosus — connects the pulmonary artery to the aorta. Blood that did reach the pulmonary artery is diverted to the aorta rather than going to the lungs. Around 90 percent of right ventricular output takes this route.
The result is that only about 10 to 15 percent of the fetal cardiac output goes to the lungs, just enough to nourish the developing tissue.
Why the shunts flow the way they do
In the fetus, pressure on the right side of the heart is higher than on the left. This is the reverse of the adult arrangement, and it is the reason the shunts work in the direction they do.
The lungs are collapsed and their blood vessels are constricted, partly by the low oxygen levels — the hypoxic pulmonary vasoconstriction of Chapter 7.5, which in the fetus applies to the entire lung. So pulmonary vascular resistance is very high, and right-sided pressure is correspondingly high.
Meanwhile the placenta is a large, low-resistance circuit connected to the systemic side, so systemic vascular resistance is low.
Right pressure high, left pressure low: blood therefore flows right to left through both the foramen ovale and the ductus arteriosus. No valve or mechanism directs it; it simply follows the pressure gradient.
The blood is also cleverly streamed. The inferior vena cava, carrying the best-oxygenated blood, enters the right atrium aimed at the foramen ovale, so the most oxygenated blood is preferentially directed to the left heart, the aorta, and therefore the heart and brain. Blood from the superior vena cava, returning from the head with low oxygen, is aimed at the tricuspid valve and goes to the right ventricle and out through the ductus to the lower body.
So the fetal brain gets the best blood available, and the lower body gets the worst. This is why the ductus arteriosus joins the aorta after the arteries to the head and arms have branched off.
Fetal oxygen levels are low by adult standards. The most oxygenated fetal blood is only about 80 percent saturated, and blood reaching the lower body around 60 percent.
Two adaptations compensate. Fetal haemoglobin (HbF) has two gamma chains instead of beta, and it binds oxygen more tightly than adult haemoglobin — so it pulls oxygen across the placenta from the mother's blood (Chapter 8.4). And the fetal haemoglobin concentration is high, around 170 to 180 g/L.
HbF is switched off around 3 to 6 months after birth, which is why beta-thalassaemia and sickle cell disease do not present at birth (Chapter 2.8) — and why reactivating fetal haemoglobin is the strategy behind hydroxyurea and the CRISPR therapy for those diseases.
The first breath
The transition is triggered by the first breath and by clamping the cord, and everything follows from those two events.
1. The lungs inflate. The first breath requires a large negative pressure — around 40 to 60 cmH₂O, several times a normal adult breath — to overcome the surface tension of fluid-filled airways. Fluid in the lungs is cleared by absorption into the circulation and lymphatics, a process that begins during labour, driven by hormonal changes.
This is one reason babies born by elective caesarean without labour more often have transient breathing difficulty — the labour-driven fluid clearance has not happened.
2. Pulmonary vascular resistance falls dramatically. Oxygen reaching the lung tissue reverses the hypoxic vasoconstriction, and the mechanical expansion opens the vessels. Pulmonary blood flow increases roughly eight to tenfold within minutes.
3. The cord is clamped. The placenta — a large low-resistance circuit — is removed from the systemic circulation, so systemic vascular resistance rises sharply.
4. The pressures reverse. Right-sided pressure has fallen and left-sided pressure has risen. This is the reversal that closes the shunts.
How each shunt closes
The foramen ovale closes mechanically and immediately. With left atrial pressure now exceeding right, the flap is pressed against the septum and held shut. Functional closure occurs within minutes.
Anatomical fusion takes months, and in about 25 percent of adults it never fully fuses — a patent foramen ovale (PFO). It is usually harmless, since the flap stays pressed shut.
But it can matter. Straining, coughing or lifting momentarily raises right atrial pressure and can push the flap open, allowing a small right-to-left shunt. If a clot from a leg vein passes through, it reaches the arterial circulation directly instead of being filtered by the lungs — a paradoxical embolism — and can cause a stroke. This is why a PFO is looked for in young people with an otherwise unexplained stroke, and closure devices are used in selected cases.
PFO is also implicated in decompression sickness in divers, allowing nitrogen bubbles to cross to the arterial side.
The ductus arteriosus closes chemically, and the chemistry is the treatment.
It is held open during fetal life by prostaglandin E2, produced by the placenta and by the ductus itself, and by low oxygen. After birth, the placenta is gone and the oxygen level rises sharply — and rising oxygen constricts the ductus. Functional closure occurs within 12 to 24 hours, anatomical closure over 2 to 3 weeks, leaving a fibrous remnant.
Both halves of that mechanism are used clinically, in opposite directions.
To close a patent ductus in a premature infant, where it often fails to close and causes heart failure: give indometacin or ibuprofen, which block prostaglandin production (Chapter 22.5).
To keep a ductus open, in a baby with a duct-dependent congenital heart defect such as transposition of the great arteries (Chapter 4.5): give prostaglandin E1 by infusion. In these babies the duct is the only connection keeping them alive, and this infusion is what buys time to get them to surgery. It is one of the clearest examples of a drug used as a bridge to an operation, and knowing to start it is the single most important intervention in a blue newborn.
The ductus venosus closes within days as flow through the umbilical vein stops, leaving a fibrous remnant.
The umbilical vessels close by muscular constriction, leaving the medial umbilical ligaments and the round ligament of the liver.
And cord clamping timing matters. Delayed cord clamping — waiting 1 to 3 minutes — allows an extra 80 to 100 ml of blood to transfer from placenta to baby, raising iron stores and reducing anaemia in infancy, particularly in preterm infants. It is now recommended routinely where the baby does not need immediate resuscitation, having previously been standard practice to clamp immediately.
When the transition fails
Persistent pulmonary hypertension of the newborn (PPHN). Pulmonary vascular resistance fails to fall, so right-sided pressure stays high and the shunts continue to flow right to left. The baby remains blue despite breathing.
A characteristic sign follows directly from the anatomy: oxygen saturation is higher in the right hand than in the feet. The right arm is supplied before the ductus joins the aorta, so it receives well-oxygenated blood; the lower body receives blood shunted through the ductus. Measuring pre-ductal and post-ductal saturations simultaneously is a bedside test that identifies the problem in seconds.
Treatment includes oxygen, ventilation, and inhaled nitric oxide, which dilates the pulmonary vessels selectively — inhaled, so it acts where it is delivered and is inactivated before reaching the systemic circulation (Chapter 1.8).
Patent ductus arteriosus in prematurity. In preterm infants the ductus frequently stays open, because the constricting response to oxygen is immature. Once pulmonary resistance falls, flow reverses and blood shunts left to right, flooding the lungs and stealing from the systemic circulation. It causes a characteristic continuous "machinery" murmur, and it contributes to lung disease and gut injury in premature babies.
Newborn pulse oximetry screening is now routine in many countries: measuring oxygen saturation in the right hand and a foot at 24 hours detects a substantial proportion of critical congenital heart defects that would otherwise be missed on examination, before the baby collapses at home.
What Part 8 does next
The transition at birth turns the lungs from an unused organ into the one that keeps you alive minute to minute. Part 8 covers the respiratory system: the airway, the lungs, the mechanics of breathing, how gases actually move and are carried, what controls your breathing rate — and why it is carbon dioxide rather than oxygen that your brain is monitoring.