Fetal Circulation

1. Introduction

• The circulation of blood from the placenta to and through the fetus and back to the placenta is known as fetal circulation.
• It is a parallel circuit, unlike adult circulation, which is a serial circuit.
• Both the right and left ventricles pump blood in parallel to the systemic and placental circuits, rather than one after the other.
• Postnatal circulation shifts to a serial design: the right side pumps blood exclusively to the lungs, while the left side pumps blood to the body.

The Three Fetal Shunts

• The fetus has three shunts that bypass the non-functioning lungs and largely bypass the liver:

2. Fetal  Circulation

• Fetal pulmonary circulation is a high-resistance circuit because the lungs are collapsed and not yet functioning for gas exchange.
• The placenta acts as the fetal organ of gas exchange. Normally, there are two umbilical arteries and one umbilical vein.
• Oxygenated blood from the placenta returns to the fetus via the umbilical vein and enters the portal venous system.
• The ductus venosus connects the left portal vein to the hepatic venous circulation near its junction with the inferior vena cava (IVC).
• Fetal IVC blood is a combination of blood from the lower fetal body, umbilical venous blood, and hepatic venous blood.
• The stream of blood from the ductus venosus has a higher velocity in the IVC than blood returning from the lower body and hepatic veins.
• This higher-velocity stream facilitates preferential delivery of relatively oxygen-rich blood across the foramen ovale into the left atrium.
• IVC blood enters the right atrium and, because of the orientation of the Eustachian valve, Chiari network, and foramen ovale, a large proportion is directed toward the left atrium. During atrial systole, some IVC blood crosses the tricuspid valve into the right ventricle.
• The overwhelming majority of superior vena cava (SVC) blood crosses the tricuspid valve and enters the right ventricle.
• Approximately 10–15% of right ventricular output passes through the pulmonary circulation and reaches the left atrium; most of the remainder is shunted through the ductus arteriosus to the descending aorta.
• As a result, about two-thirds of total fetal cardiac output is provided by the right ventricle (approximately 330 mL/kg/min), with the remaining one-third (approximately 170 mL/kg/min) provided by the left ventricle.
• The dynamics of fetal shunting result in preferential delivery of the most highly oxygenated blood to the coronary and cerebral circulations.

3. Transition at Birth

• At birth, removal of the placenta and initiation of alveolar ventilation have immediate effects that establish serial circulation.
• The new arrangement is: right ventricle → pulmonary artery → lungs, and left ventricle → aorta → systemic circulation.
• For adult-type serial circulation to be maintained, the fetal shunting channels must close.

4. Closure of the Ductus Arteriosus

• In the fetus, patency of the ductus arteriosus is maintained by high levels of prostaglandins, particularly PGE1 and PGI2.
• An increase in PaO₂ and a decrease in prostaglandin levels contribute to functional closure within the first day of life.
• Oxygen is a dose-dependent ductal constrictor that acts in part by increasing oxidative phosphorylation within smooth-muscle cells.
• Permanent anatomical closure of the ductus usually occurs by 2–3 weeks of life in a normal full-term neonate.
• Some neonates with congenital cardiac lesions depend on ductal patency for survival. Because functional closure is reversible, PGE₁ (alprostadil) infusion, approximately 0.01–0.05 µg/kg/min, may be used to stabilize neonates with ductal-dependent heart lesions.
• Preterm neonates are at increased risk of delayed ductal closure. Possible mechanisms include decreased degradation of PGE₁, increased production of PGE₁, or diminished sensitivity to the ductal constricting effects of oxygen.
• Prostaglandin inhibitors such as indomethacin (approximately 0.1–0.3 mg/kg PO or IV) have been used to promote ductal closure.

5. Closure of the Foramen Ovale

• In utero, right atrial pressure is higher than left atrial pressure.
• After birth, clamping of the umbilical cord causes cessation of umbilical venous flow and a significant decrease in venous return to the right heart, leading to a decrease in right atrial pressure.
• At the same time, ventilation causes a marked increase in pulmonary arterial and pulmonary venous blood flow, resulting in an increase in left atrial pressure.
• The elevation of left atrial pressure relative to right atrial pressure causes the flap-like valve of the foramen ovale to functionally close.
• Functional closure usually progresses to anatomical closure.

6. Closure of the Ductus Venosus

• The umbilical vessels constrict strongly after mechanical stimulation, and the high oxygen tension after birth facilitates this process.
• The resulting decrease in umbilical venous blood flow causes passive closure of the ductus venosus.
• The ductus venosus does not appear to be as sensitive as the ductus arteriosus to PaO₂, PaCO₂, or pH.
• It is functionally closed by about 1 week of life and anatomically closed by about 3 months.

7. Pulmonary Vascular Changes

• The fetus has low pulmonary blood flow because of high pulmonary vascular resistance (PVR).
• The minimal blood flow reaching the pulmonary vascular bed has a very low PaO₂, which may cause hypoxic pulmonary vasoconstriction and contribute to elevated pulmonary resistance.
• At birth, initiation of breathing leads to expansion of the lungs, which increases pulmonary oxygenation and results in a dramatic reduction in pulmonary vascular resistance.

8. Fetal Structures and Their Corresponding Adult Structures

9. Anesthesia Considerations

9.1 Reversion to Fetal Circulation

• Hypoxia, hypercarbia, acidosis, hypothermia, or excessive stimulation can cause pulmonary vascular resistance to rise again postnatally.
• This can reopen or increase right-to-left shunting through the foramen ovale and/or ductus arteriosus, worsening hypoxemia.
• Avoid hypoxia, hypercarbia, acidosis, and hypothermia intraoperatively in neonates.

9.2 Duct-Dependent Congenital Heart Disease

• Duct-dependent pulmonary flow (e.g., pulmonary atresia or tricuspid atresia) requires PDA patency to maintain pulmonary blood flow. PGE₁ infusion is used; avoid unnecessarily high FiO₂ when appropriate to the clinical situation.
• Duct-dependent systemic flow (e.g., hypoplastic left heart syndrome or interrupted aortic arch) requires PDA patency to maintain systemic and lower-body perfusion.
• Side effects of PGE₁ include apnea, fever, flushing, and hypotension; airway and ventilation equipment should be readily available.

9.3 Patent Ductus Arteriosus / Patent Foramen Ovale

• Failure of closure can leave residual shunts and may permit paradoxical air or thrombus embolism, which is particularly relevant when placing IV lines or obtaining central access.
• Avoid introducing air bubbles in neonates and in adults with a known patent foramen ovale (PFO).

10. References

1. Nasr VG, DiNardo JA. The pediatric cardiac anesthesia handbook. 2nd ed. Chapter 1, Cardiovascular development.
2. Andropoulos DB. Anesthesia for congenital heart disease. 4th ed.