Abstract
This chapter, provides an overview of the transitional circulation from fetal to neonatal life. The authors describe the physiology of fetal circulation, fetal hemoglobin as well as the changes occurring with transition at birth. Persistent fetal circulation in the setting of a vein of Galen malformation is presented with the relevant anesthetic considerations reviewed.
A 38-week-old, 3.67 kg boy born to a G15P4 mother had the prenatal diagnosis of a large vein of Galen malformation. The child was found to have high output cardiac failure on a fetal echocardiogram (hydrops faetalis), which required maternal digoxin therapy during pregnancy. Due to significant hydrocephalus, the child was delivered via cesarean section, with Apgar scores of 2 and 7.
The neonatologist intubated the child at birth due to poor respiratory effort, and placed arterial and venous umbilical catheters. The child now requires assisted ventilation with an FiO2 of 0.50. The chest X-ray reveals cardiomegaly and poorly aerated lungs. The transthoracic echocardiogram reveals a large patent ductus arteriosus and a patent foramen ovale, both with right to left shunting, as well as moderate tricuspid regurgitation with estimated suprasystemic right ventricular systolic pressures, moderately depressed right ventricular function, and normal left ventricular systolic function.
Vital signs include: UAC: 69/30, HR 120, SpO2 92% (FiO2: 0.50)
Describe the Pathway of Normal Fetal Circulation
Oxygenated blood leaves the placenta from one umbilical vein. Most of the oxygenated blood bypasses the hepatic circulation via the ductus venosus and enters the inferior vena cava (IVC). At this juncture, oxygenated blood from the ductus venosus mixes with deoxygenated blood from the lower extremities. Blood from the IVC enters the right atrium, a majority of which is directed by the Eustachian valve across the foramen ovale, through the left atrium and into the left ventricle. Here, the left ventricle pumps blood across the aortic valve to supply the coronary vessels and aortic arch, supplying blood to the upper and lower body.
The superior vena cava (SVC) directs deoxygenated blood from the upper body to the right atrium. As opposed to IVC blood, the majority of SVC blood crosses the tricuspid valve and enters the right ventricle. From the right ventricle, the blood enters the pulmonary arteries, and, due to high pulmonary vascular resistance (PVR), the blood crosses the ductus arteriosus to the distal aortic arch. At this point, this blood mixes with blood from the left ventricle as it travels down the descending thoracic aorta towards the internal iliac arteries and back to the placenta. An umbilical artery originates from each of the internal iliac arteries to deliver fetal blood to, and oxygenate, the placenta (Figure 58.1).
Figure 58.1 Schematic representation of fetal circulation.
What Are the Important Physiological Differences between Fetal and Adult Circulations?
Fetal circulation is characterized by a high PVR state due to fluid filled lungs and a hypoxic environment. In addition, systemic vascular resistance (SVR) is low due to the large surface area and low resistance of the utero-placental interface. There is shunting across the:
Liver via the ductus venosus (oxygenated blood)
Right heart across the foramen ovale (oxygenated blood)
Lungs and upper body across the ductus arteriosus (deoxygenated blood)
The physiologic shunts allow for the more oxygenated blood from the umbilical vein to preferentially perfuse the brain and heart and the less oxygenated blood from the SVC to perfuse the lower body. Taken as a whole, the placenta, rather than the lungs, provides oxygenated blood for systemic oxygen delivery, and as such pulmonary blood flow is diminutive (8–10 fold) compared to that of postnatal life. Shunts carry fully oxygenated blood (ductus venosus) to the heart and blood with mixed oxygenation (foramen ovale and ductus arteriosus) to the body and ultimately back to the placenta via the iliac vessels for oxygenation.
How Is the Fetal Oxygen Carrying Capacity Regulated?
For oxygen transport to occur in the fetal hypoxic environment (normal umbilical vein PaO2 is 30–35 mmHg), the majority (80%) of hemoglobin (Hgb) is Hgb F, whereas Hgb A accounts for 90% of adult hemoglobin. The different protein structure of fetal hemoglobin confers its greater affinity for oxygen, represented as the PaO2 at which the hemoglobin molecules are 50% saturated, or the P50 value. Hgb F has a P50 of approximately 19 mmHg whereas Hgb A has a P50 of approximately 26 mmHg (Figure 58.2). This improves fetal oxygen uptake at the placenta. In addition, normal fetal pH (7.25–7.35) is lower compared to adults (7.35–7.45). This acidosis also shifts the oxygen-hemoglobin dissociation curve to the right, facilitating the unloading of oxygen at the fetal tissue level (Figure 58.2).
