We know that fetal physiology is drastically different to the physiology we see in babies after birth. One such difference is the fetal heart and the fetal circulation. In utero, the fetus does not need to rely on its lungs for oxygen. Therefore, there are a number of adaptations the system makes to compensate.
In this article, we will look at those differences, and how they change perinatally.
Comparison to Adults
The adult heart consists of 4 chambers, each with inflow and outflow. Its objective is to take deoxygenated blood from the body, transport it to the lungs for oxygenation, and then take this oxygenated blood to the tissues. For more information on this, you can look at the physiology and anatomy of the heart.
A fetus is surrounded by amniotic fluid and will use the placenta as its source of oxygen and nutrients. While the lungs are developing, they are not functional and provide no oxygenation. There are also high energy demands of developing tissue, in particular the brain. As a result, the fetal circulation must direct blood away from non-functional organs and ensure that growing tissues receive their oxygen requirements.
Fetal Heart structure
Due to these differences, the fetal heart has a number of different structures to direct blood flow:
- The umbilical vein delivers oxygenated blood from the placenta to the fetus, providing oxygen and nutrients.
- The umbilical arteries are used to transport deoxygenated blood away from the fetal tissue and back towards the placenta for re-oxygenation.
- The ductus venosus allows blood from the placenta to bypass the highly demanding, but relatively inactive liver.
- The ductus arteriosus is the fusion of the primitive pulmonary artery to the aorta, therefore allowing blood to pass straight from the right ventricle into the aorta and bypass the inactive lungs.
- The foramen ovale creates a shunt between the right atrium and the left atrium so oxygenated blood from the placenta can move to the left atrium. This allows for the oxygenated blood to pass through the left ventricle and into the ascending aorta, oxygenating the brain.
Oxygenation in utero
The highest partial pressure of oxygen in the feto-placental circulation is approximately 4kPa. This is compared to 13kPa in an adult. However, the fetus is able to maintain adequate oxygen delivery to tissues through the use of the shunts above, assisted by a relative polycythaemia and the properties of fetal haemoglobin.
How is fetal haemoglobin different?
Fetal haemoglobin has a different quaternary structure to adult haemoglobin. Adult haemoglobin (HbA) is formed of 2 alpha subunits and 2 beta subunits. However, fetal haemoglobin contains different subunits, namely 2 alpha subunits and 2 gamma subunits.
This change in three dimensional structure of the protein means that fetal haemoglobin can bind more readily to oxygen from maternal circulation. This allows for adequate oxygenation of tissues.
Fetal Heart to Neonatal Heart
The fetal heart undergoes changes during birth to allow the newborn to effectively oxygenate itself with newly open lungs. This occurs in a series of steps:
- The first breath causes a rise in the partial pressure of oxygen
- An increase in partial pressure of oxygen causes pulmonary vasodilation
- Pulmonary vasodilation leads to a drop in right heart pressure.
- Simultaneously, placental circulation ceases, causing left heart pressure to rise.
- These factors combine to cause the foramen ovale to shut.
- The pulmonary and systemic circulations become separate, and the whole output of the right ventricle passes through the pulmonary circulation.
- The final step in the sequence is the closure of the ductus arteriosus, occurring 2 to 3 days after birth.
- The structural remnants of the fetal circulatory structures are referred to as the fossa ovalis (foramen ovale), the ligamentum arteriosum (ductus arteriosus) and the ligamentum venosum (ductus venosus).
Clinical relevance: Congenital Abnormalities
Patent Ductus Arteriosus
If the ductus arteriosus remains open beyond 3 months of life in preterm infants and after 1 year of life in full-term infants, it is a persistent patent ductus arteriosus (PDA). 5 – 10% of congenital heart defects in term infants are PDAs, but they are far more common in preterm neonates. Prostaglandin-E2 is responsible for keeping PDAs open.
Risk factors for persistent PDA include trisomy 21, Holt-Oram Syndrome, exposure to sodium valproate in-utero and asphyxia during birth. Rubella infections during pregnancy can also predispose to PDAs.
We recognise a PDA by a continuous, machinery murmur over the upper left sternal border. Generally, they are asymptomatic, but large shunts can lead to recurrent lower respiratory tract infection, feeding difficulties, failure to thrive and even heart failure.
We identify these via echocardiograms, and can give indomethacin in preterm infants, or use surgical methods to close in term, symptomatic infants.
Patent Foramen Ovale
In up to 20% of healthy adults, the foramen ovale will not completely close. We refer to this as a patent foramen ovale. Large, or slightly displaced “holes” in the septum are called atrial septal defects. While these may be asymptomatic, they can cause tachypnoea, poor weight gain and recurrent chest infections in children and adults.
They can be detected by widely split second heart sounds alongside a soft systolic ejection murmur at the upper left sternal border. If necessary, surgical closure can take place.