Fetal Circulation
Fetal circulation varies from neonatal circulation simply because the lungs are not active in a fetus. A fetus relies on the placenta for gas exchange. The lungs are full of amniotic fluid and are mostly collapsed. Once the baby is born and begins to cry and breath, the lungs are expanded and the amniotic fluid is expelled. Since the pulmonary circulation is unable to provide oxygenation, there are three important shunts throughout the fetal circulation that allows for oxygenated blood returning from the placenta to supply oxygen to metabolically active organs, like the brain. These shunts are the ductus venosus (DV), foremen ovale (FO), and ductus arteriosus (DA).
The umbilical vein carries blood with a partial pressure of O2 of around 30-35 mmHg. In the liver, the umbilical vein has two branches: one to the portal vein and the other becoming the DV. The DV then connects to the inferior vena cava (IVC). The IVC carries this oxygenated blood to the right atrium (RA). Between the RA and the left atrium (LA), we encounter the second right to left shunt - the FO. The FO is an intraatrial septum hole created by the overlapping flaps of the septum primum (inferior/leftward) and the septum secundum (superior/rightward). Oxygenated blood crosses through the FO entering the left sided circulation. This then exits the LV into the aorta and supplies the coronaries, head vessels, and upper torso. The deoxygenated blood from the superior vena cava (SVC) and the coronary sinus tends to flow through the tricuspid valve into the right ventricle (RV) and into pulmonary circulation. Since the lungs are collapsed, the pulmonary vascular resistance (PVR) is extremely high compared to the systemic vascular resistance (SVR). The pulmonary artery is where we find our third and last right to left shunt - the DA. About 90% of the pulmonary circulation will shunt through the DA and travel to the descending aorta and to the internal iliac arteries before entering the umbilical veins and returning to the placenta to pick up more oxygen.
Fetal circulation is thought to have two parallel circuits (right and left) with the right side providing deoxygenated blood to the midsection and lower extremities (65% of cardiac output) and the left sided circulation providing oxygenated blood to vital organs such as the heart and brain (35% of CO). 2/3 of aortic flow goes to the placenta because the SVR within the placental blood vessels is relatively low. Placental blood flow is largely influenced by maternal blood pressure.
The transition from fetal to neonatal circulation essentially takes two parallel circuits and puts them in series as the right to left shunts slowly start to disappear and the neonate relies on its own lungs for oxygenation. There are two abrupt changes that occur at birth. First, there is stark increase in SVR once the placenta is removed from circulation. Secondly, inflation of the lungs and release of endogenous nitric oxide decreased PVR. The DA starts to close as the direction of flow switches (now L to R), increase in pO2, drop in prostaglandin E and an increase in bradykinin. This functionally happens in the first 24 to 48 hours and ultimately closes within 4 to 8 weeks of life. The FO closes due to a pressure difference between the LA and the RA with the LA being greater than the RA. The two flaps of the FO seal on each and close the hole. And the DV begins to close and the flow through it is ultimately eliminated when the placenta is removed from circulation. This occurs functional between 3 to 7 days of life and it is completely gone by 1 to 3 weeks.
If persistent fetal circulation (PFC) were to occur, it most commonly happens because of hypoxia and/or hypercarbia. However, it can also be caused by parenchymal lung disease or congenital heart disease. Once diagnosed, nitric oxide or a vasodilating prostaglandin should be administered to decrease PVR, attenuate or eliminate the PFC, and correct the right to left shunt.
Neonatal cardiovascular physiology is different than that of an infants due to the fetal myocytes. They are structurally different - smaller, more immature, fewer contractile proteins, and less complaint. They are generally thought to have stiff ventricles. This makes the heart very dependent on heart rate since it cannot modulate its contractility force. Typically, neonates have a heart rate greater that 140 bpm
