Fetal Circulation And Transition To Neonatal Circulation

Major Differences in Fetal Versus Adult Circulation

Site of Oxygenation 

In a fetus, oxygenation takes place in the placenta; in adults or children who have just given birth, oxygenation takes place in the lungs.

Systemic and Pulmonary Pressures

As opposed to adults, who have low pulmonary pressure and high systemic pressure, fetuses have low pulmonary systemic pressure and high pulmonary vascular resistance. 

Parallel Circuit Versus Series Circuit

The circulatory system is organized in series in adults, whereas it is arranged in parallel in fetuses.

Shunts

In order to guarantee the fetus's optimal growth, there are four shunts, according to Park's paediatric cardiology, sixth edition. The placenta is the site of foetal oxygenation. The structure that joins the inferior vena cava to the umbilical vein is called the Ductus venosus. 

Ductus arteriosus is an arterial vessel that joins the aorta and pulmonary artery; Foramen ovale is the conduit between the left and right atriums.  The four variations between fetal and adult circulation are as follows. 

Placenta

The placenta, often referred to as the exchange efficiency, has a lower oxygen efficiency than the postnatal lungs. The placenta is the site of oxygenation in a fetus. Thus, according to Nelson's 21st edition, the partial pressure of oxygen in the umbilical vein is only about 30-35 ml of mercury; according to Park's 6th edition, the placenta has the lowest vascular resistance in the fetus. The organ's total production from the left and right ventricles was greatest. An umbilical cord is a conduit that emerges from the placenta. It transports both the umbilical artery and vein.

All normal children have one umbilical vein (UV) and two umbilical arteries (UA) according to the configuration of an umbilical cord.
Because umbilical arteries have a muscular wall and typically carry blood that is deoxygenated, they are aberrant. The umbilical vein, on the other hand, is a single, thin-walled conduit that typically transports oxygenated blood within the fetus.

The tissue that holds them together is known as Wharton's jelly tissue, and the amnion covers the umbilical cord. The anterior division of the internal iliac artery branches off into both umbilical arteries and veins. The umbilical veins originate from the placenta and merge into the ductus venosus, with a portion of the veins continuing as part of the hepatic circulation. 

Fetal Circulation

This is the appearance of fetal circulation, which is the location of the fetal placenta. The placenta produces oxygen, which is then carried via the umbilical vein. The umbilical vein will therefore have the highest oxygen saturation level. It splits into two zones as it reaches the near liver. Hepatic blood flow is supplied by one zone. 50% is thus sent to the hepatic system. A ductus venosus that connects to the inferior vena cava carries 50% of the blood. Saturation will slightly decrease as deoxygenated blood from the inferior vena cava mixes with oxygenated blood from the umbilical vein. 

This mixed blood enters the right atrium and splits into two sections when it opens up. A third of this blood flows straight through the foramen ovale from the right atrium to the left because of the eustachian valve and the crista dividends. The right atrium and the right ventricle will be crossed by the remaining two thirds. This whole blood will combine at the same moment the superior vena cava opens into the right atrium.

Compared to the IVC, the right ventricle's saturation is usually lower. The fetus will now experience systole, causing both ventricles to contract.

Blood is sent into the pulmonary artery by the right ventricle, but because to excessive pulmonary vascular resistance, blood cannot flow from the pulmonary artery to the lungs. This will reroute into the descending aorta via the ductus arteriosus. Blood flows from the left ventricle during contraction into the ascending aorta, which then passes through the subclavian arteries to the head, neck, and upper limbs. 

A portion of the blood will travel through the descending aorta and combine with blood from the ductus arteriosus. 35% of the blood is used by the tissues after it enters the descending aorta, with the remaining 65% returning to the placenta. The internal iliac artery sends two umbilical arteries to the placenta and the circuit will be completed.

Also Read: Arrhythmias in Children : NEET SS Pediatrics

Course of Fetal Circulation

An umbilical vein that carries oxygenated blood from the placenta splits, with 50% of the blood entering the ductus venosus and the other 50% going into the hepatic circulation.

This ductus venosus opens into the right atrium and then the inferior vena cava. Half of this blood travels to the right ventricle once it opens into the right atrium, and the remaining half crosses the foramen ovale to enter the left atrium.

The left ventricle will receive this blood and use it to pump blood into the aorta when it contracts. Following contraction, blood arrives at the right ventricle simultaneously. Only 5–15% of this blood makes it to the lungs, while the remaining 85% is returned to the aorta via the ductus arteriosus.

Blood is also delivered straight into the right ventricle from the right atrium by the superior vena cava. The blood will return to the placenta through umbilical arteries that emerge as it reaches the aorta.

Rapid Fire MCQ Points and Facts

Q. What is the saturation content of various fetal structures?

Ans. Umbilical vein (80% saturation content) > IVC (70% saturation content) > LV (65% saturation content) > RV (60% saturation content) > UA (below 50% saturation content).

Q. What is the PO2 content in major fetal structures?

Ans. In the umbilical vein, the PO2 content is 30 to 35 mm Hg, IVC has 26 to 28 mm Hg, SVC has 12 to 14 mm Hg, LV, and ascending aorta has 26 to 28 mm Hg, and finally, the descending aorta has 24 mm Hg.

Q. Which structure diverts IVC blood from reaching RA into LA via foramen ovale?

Ans. Eustachian Valve and Crista dividends.

Q. What is the fate of UV blood?

Ans. 50% goes into the liver, and 50% goes into IVC via ductus venosus.

Q. What is the fate of descending Aorta blood?

Ans. 65% returns to the placenta, and 35% perfuses the fetal organs and tissues and is returned back through the inferior vena cava.

Q. What are the ventricular dimensions in fetus?

Ans. Since RV output is 1.3 times LV output in a fetus and handles more blood, the RV wall is thicker than LV in the fetal and first few days of post-natal life.

Q. What percentage of the total ventricular output is handled in fetus by the two ventricles individually?

Ans. RV handles 55%, whereas the left ventricle handles 45%.

MCQ Concept

Q. Why does fetal distress produce a fall in cardiac output?

Ans.The following formula gives cardiac output:

 CO = Heart Rate × Stroke Volume

In adult patients, bradycardia causes a proportionate increase in stroke volume, which maintains cardiac output.Bradycardia in the fetus and the first few days of life is caused by fetal discomfort or hypoxia. Nevertheless, in these patients, the fetal heart's low compliance prevents the stroke volume from increasing, which tends to lower cardiac output and cause the patient to appear to be in a shock-like state.

Changes In Circulation After Birth

 As the lungs enlarge, they become the location of gas exchange.  As a result, the pulmonary vascular resistance is decreased. It results in an increase in pulmonary blood flow. Increased systemic vascular resistance is the result of placenta removal. The umbilical vein's blood supply has stopped. 

Closure of Shunt Vessels- Ductus Venosus

The structure in question joins the umbilical vein to the inferior vena cava. The umbilical vein normally splits into two sections: 

The portal vein on the left.  The umbilical vein's continuation, the ductus venosus. The inferior vena cava, a bigger vessel, connects with the ductus venosus. Of the oxygenated blood, 50% enters the inferior vena cava by the ductus venous and 50% travels via the left portal vein, which is the liver. The primary portal vein is connected to this vein. Venous closure results from the cessation of blood flow in the umbilical vein.
There are two kinds of closures. Functional closure: takes place a few hours after delivery. On day seven of life, true or anatomic closure takes place. 

Foramen Ovale 

A shift in the pressure gradient between the right and left atriums causes the foramen ovale to close. It is located between the left and right atriums.  After birth, increased blood flow via the pulmonary veins causes the left atrium pressure to rise while the right atrium pressure fails as a result of the closure of the ductus venosus. 

Septum primum and septum secundum are pushed against one another whenever there is a decrease in the pressure in the right atrium and an increase in the pressure in the left atrium. The foramen ovale is closed by this compression. There is disagreement over when functional closure occurs. Three months following the postnatal age, true or anatomic closure takes place. 

Closure of Shunt Vessels

Ductus Arteriosus-Physiological: D/t spasm of smooth muscles in funica media. Within few hr of birth (Nelson” within 10-15 hr).

The ductus arteriosus is fixed, located distal to the origin of the left subclavian artery, and it is a true channel that joins the aorta with the pulmonary artery.  Two factors keep it open in utero:  High maternal prostaglandin levels; low oxygen tension. 

Also Read: Aneuploidies Including Turner And Klinefelter Syndrome

Clinical Question

Q. Which is the most important prostaglandin in keeping the ductus arteriosus open in utero?

Ans. PGE2.

Four elements or triggers encourage its closure in the post-birth period:
An increase in oxygen tension, the most crucial component.
A sharp decline in prostaglandin levels. A rise in the amounts of acetylcholine. A rise in the amounts of bradykinin. 
Nelson 21st edition states that physiological closure happens within 10-15 hours of delivery due to the spasm of smooth muscle in the tunica media, which typically happens within two hours of birth. Changes in the endothelium and intimal cell proliferation and fibrosis result in anatomical or definitive closure. Between day 10 and day 21 of postnatal life, anatomical closure occurs.

Facts To Know About Ductus Arteriosus - Park's 6th Edition 

Aspirin consumption by the mother during pregnancy has the potential to narrow the ductus arteriosus in utero, which might result in persistent pulmonary hypertension of the newborn (PPHN). The ductus arteriosus can only reopen in the presence of hypoxia and acidosis prior to anatomic closure. As in the case of asphyxia, high altitude, or the administration of prostaglandin E1 infusion (Alprostadil).

Preterm infants have reduced ductus arteriosus smooth muscle reactivity to oxygen; oxygen dilates pulmonary arterioles but constricts the ductus arteriosus. 

Pulmonary Vascular Resistance (PVR)

There are three primary causes of elevated PVR in utero: Because of pulmonary vasoconstriction, there is relative hypoxia during pregnancy.
The walls of the small pulmonary veins have more smooth muscle, which keeps them closed.  A non-expandable lung.  After birth, the PVR decreases.

Assume that intrauterine pressure is elevated. The pulmonary vascular resistance will rapidly decrease within two minutes of delivery in the event of an unexpected birth. It will then turn static. Six to eight weeks after birth, there will be another fall, which will result in a sluggish, continuous descent.  There is a sharp initial decline in PVR at birth for two reasons: 

The lungs' mechanical expansion. Sudden dilation of the pulmonary vessels. The second decline happens as a result of remodeling of the pulmonary arteries and happens between 6 and 8 weeks. There is a tendency for the smooth muscle to become thinner during pulmonary vascular remodeling. The youngster will experience the gradual, uninterrupted descent for up to two years of age. It happens as a result of an increase in alveolar units and the recruitment of additional vessels.

What are the Implications?

Large VSD prevents the rapid fall in pulmonary vascular resistance, which makes the left-to-right shunt negligible. Large VSD causes the left atrial pressure to be directly transmitted to the pulmonary artery via a large septal defect. As a result, infants with large amounts of VSD develop CCF only after 6–8 weeks of age due to the delayed fall in PVR.
Nevertheless, after the 6- to 8-week age is reached, there will be vascular remodeling. When the left to right shunt starts, the pulmonary vascular resistance decreases, which causes congestive heart failure.

.As living at high altitudes, infants with high VSD do not acquire CCF; however, as they descend toward sea level, CCF manifests. If the patient resides at a high altitude, hypoxia will occur in a large VSD, which will cause the pulmonary arterioles to remain constricted over time. Therefore, there is no CCF since there is less left-to-right shunt and pulmonary vascular resistance does not decrease significantly. The patient has a reduction in hypoxia and a subsequent decrease in pulmonary vascular resistance upon reaching sea level, which leads to an improvement in the left-to-right shunt.

Preterm infants with severe HMD and a left-to-right shunt do not develop CCF; nevertheless, ironically, CCF may manifest as HMD improves. In cases of severe HMD, hypoxia will cause a prolonged rise in PVR, which will reduce the left-to-right shunt and eliminate the need for a CCF.
As the patient or HMD gets better, pulmonary vascular resistance declines and oxygen concentration rises, which causes CCF.

Park's 6th Edition

Conditions that prevent pulmonary arterioles from maturing normally in the womb - Elevation or hypoxia. Acidosis or Acidemia. Elevated pulmonary arterial pressure as a result of a large PDA or VSD. Elevated left atrial or pulmonary vein pressure.

Q. Preterm babies have a higher risk of PDA. Why?

Ans. There are majorly two reasons:

• The ductal smooth muscle in preterm babies does not show a constrictor response to oxygen.
• These babies have relatively higher PGE2 levels due to decreased lung degradation.

Q. Why do preterm babies have early onset CCF in PDA?

Ans. Compared to full-term newborns, the pulmonary vascular smooth muscle is not as developed. As a result, the L-R shunt begins early and PVR falls extremely quickly.
Preterm infants without respiratory illnesses rapidly reduce in pulmonary vascular resistance, resulting in early CCF in PDA, however preterm newborns with HMD will develop hypoxia and have late CCF in PDA.

Nelson's 21st Edition Says

 During the first two months of life, the newborn's 350 mL/kg/min cardiac output decreases to about 150 mL/kg/min, and then more gradually to the typical adult cardiac output of 75 mL/kg/min.  With aging, cardiac output in mL/kg/min decreases. 

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