Fetal and Neonatal Oxygen Transport

Fetal and Neonatal Oxygen Transport

The Fetus Depends on the Placenta for the Exchange of Gas, Nutrients, and Metabolic Byproducts

From conception until birth, the embryo and fetus depend on the mother for a supply of oxygen and nutrients and for removal of carbon dioxide and other metabolic byproducts. The embryo exchanges these substances by diffusion through the uterine fluids. As the conceptus increases in size, the specialized exchange organ, known as the placenta, becomes essential. The placenta brings maternal and fetal blood into close apposition over a large surface area that is provided by a network of capillaries.

The gross appearance of the placenta of different species varies widely. In horses and pigs the placenta is diffuse and covers most of the uterine epithelium. In ruminants the placenta has rows of discrete circular-to-oval cotyledons that are attached to approximately 100 highly vascularized caruncles in the uterine epithelium. In dogs the placenta is zonary, forming a circular band around the allantochorion of the puppy. Table 51-1 lists types of placentation for different species.

In addition to differing in the amount of uterine surface to which they are attached, placentas also differ in the number of layers of cells that separate the maternal and fetal blood (see Table 51-1). In horses, pigs, sheep, and cows the fetal chorion is applied to the maternal uterine epithelium (epitheliochorial placentation), whereas in cats and dogs the chorion is applied to the endothelium of maternal vessels (endotheliochorial placentation); in rodents and most primates the chorion invades the uterine mucosa and erodes the maternal capillaries, so it becomes bathed by maternal blood (hemochorial placentation).

The Efficiency of Gas Exchange at the Placenta Depends on the Species-Variable Arrangement of Fetal and Maternal Blood Vessels

The exchange of gases and other substances across the placenta is determined by several factors, including the amount of surface apposition between fetal and maternal tissues and the number of layers of cells separating fetal and maternal blood. However, a major factor determining exchange is the arrangement of fetal and maternal blood vessels within the small, interdigitating villi of the placenta (Figure 51-1). Countercurrent flow of maternal and fetal blood provides the most efficient exchange and allows equilibration of fetal and maternal arterial gas tensions. Concurrent flow of fetal and maternal blood allows fetal vessels to equilibrate with the maternal venous gas tensions. In crosscurrent and pool types of equilibrators, fetal capillaries loop down to maternal vessels or into a pool of maternal blood. No simple model easily describes these types of exchangers. It is likely that several different arrangements of vessels are found in the placentas of all species, but some seem to have more of the characteristics of countercurrent exchangers, and others have those of venous equilibrators.

Figure 51-2 shows the arrangement of vessels in the microcotyledon of the horse, a species in which fetal and maternal blood flow is primarily countercurrent. The cotyledonary placenta of sheep functions as a venous equilibrator, whereas the hemochorial placenta of the rabbit seems to be a countercurrent exchanger.

Placental gas exchange has been best studied in the sheep (Figure 51-3). Maternal blood enters the uterus through the uterine artery with an oxygen tension (PO2) of 80 mm Hg and leaves through the uterine vein with a PO2 of 50 mm Hg. Some of the blood entering the uterus supplies the myometrium and endometrium, but most participates in gas exchange in the cotyledon. Fetal arterial blood reaches the placenta through the umbilical artery and enters the cotyledon with a PO2 of 24 mm Hg. Placental gas exchange occurs, and the blood leaving the placenta in the umbilical veins has a PO2 of only 32 mm Hg. This is because the sheep placenta is a venous equilibrator, so the maximal possible PO2 would be 50 mm Hg. However, this maximum is not reached because venous blood, which has provided nutrient blood flow to the chorion, dilutes the better-oxygenated blood draining from the cotyledon. The countercurrent exchanger of the horse is apparently more efficient because umbilical venous PO2 averages 48 mm Hg.

The amount of placenta available for exchange partly determines the ultimate size of the fetus. If uterine caruncles are surgically removed from sheep so that there are fewer sites for formation of fetal cotyledons, the full-term weight of lambs is reduced. The diffuse placenta of the horse apparently can support only one full-size fetus. One foal in a set of twins usually dies in utero or is very small. It is rare for horse twins to survive to term and be of equal size.

The Fetal Circulation Mixes Oxygenated and Deoxygenated Blood at Several Points, So the Fetus Exists in a State of Hypoxemia

In the adult the cardiac output of the right and left ventricles is separate and perfuses the pulmonary and systemic circulations, respectively. In the fetus the output of the two sides of the heart mixes at several points, so it is convenient to use the term cardiac output to refer to the combined output of the right and left ventricles. The combined cardiac output averages 500 mL/min/kg in fetal sheep; the output of the right ventricle exceeds that of the left (Figure 51-4). Because the right and left ventricles of the fetus pump into a common circulation, the two are of equal size and wall thickness.

The placenta, which has a low vascular resistance, receives 45% of the cardiac output through the umbilical arteries. The umbilical veins drain the placenta toward the liver. In species such as the sheep, most of the umbilical venous blood passes through the liver via a low-resistance channel known as the ductus venosus; in other species, such as the pig and horse, the ductus venosus disappears early in gestation, and umbilical venous blood flows through the liver capillaries. Within the liver, the oxygenated blood from the placenta is mixed with a small amount of more poorly oxygenated blood draining the liver sinusoids. The hepatic venous blood enters the posterior vena cava, where it mixes with poorly oxygenated blood, draining the hind end of the fetus, so the blood returning to the right atrium has a PO2 of 25 mm Hg.

A low-resistance pathway, the foramen ovale, connects the right and left atria, and a structure known as the crista dividens directs the better-oxygenated blood from the posterior vena cava through the foramen ovale to the left atrium. The poorly oxygenated blood returning to the right atrium in the cranial vena cava is directed into the right atrium and right ventricle. Most of the output of the right ventricle does not go through the lungs, however, because fetal lungs have a high vascular resistance. Another low-resistance channel, the ductus arteriosus, connects the pulmonary artery with the aorta and allows blood to bypass the lungs. It is important to note that the arrangement of the fetal circulation allows the better-oxygenated blood to enter the left ventricle, from which it reaches the brachycephalic vessels and the front of the animal. The less well oxygenated blood from the ductus arteriosus enters the aorta downstream from the brachycephalic vessels. The tissues of the hind end of the animal and the placenta receive blood with a PO2 of approximately 22 mm Hg.

Flow of blood from the right atrium to the left atrium through the foramen ovale and from the pulmonary artery to the aorta through the ductus arteriosus requires that the pressure in the right side of the fetal circulation be greater than that in the left side. This pressure difference occurs because the left side of the circulation provides most of its output to the low-resistance placenta, whereas the right side of the fetal circulation is opposed by the high-resistance pulmonary circulation. At term, systemic arterial pressure in the lamb is about 42 mm Hg.

The fetal circulation is not a passive system and is capable of considerable regulation, particularly as the fetus matures. Fetal hypoxia can stimulate vasodilation in the heart and brain and vasoconstriction in the gut, kidneys, and skeletal tissues. The fetal pulmonary circulation constricts vigorously when the fetus is hypoxic. This constriction diverts more blood through the ductus arteriosus to the systemic tissues.

< div class='tao-gold-member'>

Stay updated, free articles. Join our Telegram channel

Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Fetal and Neonatal Oxygen Transport

Full access? Get Clinical Tree

Get Clinical Tree app for offline access