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Fetal and neonatal physiology

21.1 Introduction

The fetus is totally dependent upon the placenta for gas exchange, nutrition, and waste disposal while it remains within the uterus of its mother. It is adapted in a number of important ways to life within a fluid-filled bag. This chapter will consider some of the more important aspects of the physiology of the fetus itself, as well as the physiological changes that take place at, or soon after, birth to enable the baby to make a successful transition from its uterine existence to a semi-independent air-breathing life. While the changes occurring around the time of birth within the cardiovascular and pulmonary systems are of paramount importance to the survival of the infant, it is also important to remember that a number of other organs are func­tioning throughout fetal life and that these, too, must adapt at birth to the different requirements of extrauterine life. Of these, the adrenal glands, kidneys, thermoregulatory tissues, and gastrointestinal tract will be considered briefly. The chapter will

end with a simple account of the differentiation of the male and female fetal sexual organs.

^ 21.2 The fetal circulation is arranged to make the best use of a poor oxygen supply

The fetal circulation differs from that of the adult in a number of important ways. The pattern of circulation is adapted for placental rather than pulmonary gas exchange and organs that are virtually nonfunctional, such as the lungs, gut, and liver, are largely bypassed.

The fetal heattbeat is detectable at 4—5 weeks of gestation and by the eleventh week the cardiovascular system is fully developed, in miniature. Figure 21.1 shows a simplified plan of the organization of the fully developed fetal cardiovascular system. It illustrates the three important shunts that different­iate the fetal from the adult circulations. These are:

Fig. 21.1 The organization of the fetal cardiovascular sysrem. Note that the structure of the heart has been distorted to show the operation of the crista dividens. The dashed arrow indicates the direct flow of blood from the inferior vena cava through the foramen ovale to the left atrium.


21 Fetal and neonatal physiology

  1. The foramen ovale, which is a gap formed by incomplete
    fusion of the septum between the left and right atria. As
    shown in Figs 21.1 and 21.2, the foramen ovale provides a
    direct path for blood to pass between the inferior vena cava
    and the left atrium.

  2. The ductus arteriosus, which forms a direct link between the
    pulmonary artery and the aorta.

  3. The ductus venosus, which links the umbilical vein with the
    inferior vena cava.

These shunts, which normally close at birth, enable the two sides of the fetal heart to work in parallel, with mixing of the right ventricular and left ventricular outputs. This arrangement differs from that of the adult in which the pulmonary and systemic circulations are perfused entirely separately (see section 21.3).

In order to understand the way the parallel organization of the fetal circulation operates, it will be helpful to refer to Fig. 21.1 while considering the route taken by the blood as it flows round the fetal cardiovascular system.

Venous return to the right side of the heart consists of deoxy-genated blood carried by the superior vena cava together with oxygenated blood from the placenta carried by the inferior vena cava. About 80 per cent of the blood in the umbilical veins bypasses the somewhat immature fetal liver and passes directly to the inferior vena cava via the ductus venosus, while the remaining 20 per cent travels to the liver via the portal vein. Oxygenated blood in the umbilical vein is therefore mixed with the deoxygenated blood returning from the lower parts of the body in the inferior vena cava. If this blood were also to be mixed with the deoxygenated blood traveling in the superior vena cava from the upper parts of the body, as it is in the adult, oxygen saturation of the blood from the placenta would be reduced still further. In the fetus complete mixing of inferior

Fig. 21.2 Detailed drawing to show the pattern of blood flow in the right atrium. Note how the crista dividens diverts the flow of oxygenated blood in the inferior vena cava through the foramen ovale to the left atrium.

and superior vena caval blood in the hearr is avoided as a result of the anatomical position and mode of operation of the crista dividens and the foramen ovale, which allow most of the blood from the inferior vena cava to pass directly to the left side of the heart instead of to the right as it would in the adult. This is shown in Figs 21.1 and 21.2. The remainder continues upwards to enter the right atrium. No blood from the superior vena cava normally passes the crista dividens (the upper part of the incomplete septum dividing the two sides of the heart). Instead, all of it enters the right atrium.

Blood from the left ventricle is pumped into the ascending aorta from which the carotid arteries supplying the brain branch off (Fig. 21.1). Blood from the right ventricle enters the pul­monary artery. There is, however, a direct link between the pul­monary artery and the descending aorta—the ductus arteriosus— so when blood reaches the point at which the ductus arteriosus branches off from the pulmonary artery, it may take one of two routes. It may travel to the fetal lungs in the pulmonary arteries, or it may bypass the lungs and travel directly to the descending aorta in the ductus. In practice, only around 20 per cent of the blood from the right ventricle perfuses the lungs because of the high vascular resistance of the pulmonary circulation (see below). The rest flows through the ductus arteriosus.

An important consequence of this arrangement of the fetal circulation is that the blood in the ascending aorta has a higher oxygen content than that in the descending aorta because of the operation of the foramen ovale. This means that the blood supplying the brain is comparatively well oxygenated.

Control of the fetal circulation

By the eleventh week of gestation, when the fetal cardiovascular system has been laid down, the fetal heart is beating at around 160 beats per minute (b.p.m.), a very high rate when compared with the average resting heart rare of the adult, which is about 70 b.p.m. The high rate is due to an absence of autonomic control of the heart at this stage of embryonic development— remember that, in the adult, the resting heart rate is influenced predominantly by the tonic vagal (parasympathetic) activity. Later, during the third trimester (the final 3 months) of gesta­tion, the autonomic nervous system becomes functional and the parasympathetic innervation of the heart is established. At this stage the fetal heart rate slows to around 140 b.p.m. This gradual development of the autonomic control of the cardio­vascular system is also evident in the changes in blood pressure that occur during fetal life. Pressure is comparatively low— around 9/6 kPa (c. 70/45 mmHg) in the early months of gestation when there is very little peripheral vascular tone and therefore a low total peripheral resistance. Blood pressure gradually rises as autonomic activity becomes established and vascular tone is increased. At the same time, aortic and carotid baroreceptors begin to function. This increase in blood pressure and drop in heart rate continues after

^ 21.2 The fetal circulation


delivery until, by the age of about 7 years, values similar to those of the adult are achieved.

The fetus depends upon the placenta for

gas exchange as its lungs are collapsed

and the alveoli filled with fluid

The role of the placenta in the transport of oxygen and carbon dioxide between the maternal and fetal blood was described in some detail in Chapter 20 (Sections 20.4 and 20.5). As far as gas exchange is concerned, the fetal lungs are nonfunctional and the alveoli are almost collapsed and filled with fluid. This fluid is secreted by type I alveolar cells (epithelial cells which overlie the pulmonary capillaries) and its composition differs from that of the amniotic fluid. It first appears around mid-gestation. By full term the lungs contain a total of about 40 ml of this fluid. Because the alveoli are collapsed, their capillaries are tortuous and offer a high resistance to blood flow. Consequently, the lungs are relatively poorly perfused.

Breathing movements develop before birth

Although the fetal lungs do not participate in gas exchange, ventilatory movements are seen during gestation. Ultrasound scans have revealed that fetal breathing movements begin at around 10 weeks of gestation. They remain shallow and irregular up until around week 34 of gestation, after which they start to display a more rhythmical pattern, with periods of activity interspersed with periods when movements are absent. Occasionally, gasping movements are seen, especially if the fetus experiences hypercapnia—for example as a result of pla­cental insufficiency or compression of the umbilical cord. This response suggests that chemoreceptors (see Chapter 16) are functional during the latter part of gestation. It is now believed that fetal breathing movements are important in the preparation of the respiratory system for its postnatal function of gas exchange.

Fetal blood has a higher affinity for oxygen than adult blood

The partial pressure of oxygen in the blood traveling from the placenta to the fetus in the umbilical veins is around 5 kPa (35— 40 mmHg), much lower than that of normal adult arterial blood (see Fig. 20.7). Moreover, PaO2 in the fetus is only about 2.5 kPa (c. 20 mmHg; see Fig. 21.3) as the umbilical blood is mixed with blood returning from the lower part of the body before reaching the left heart. Such a low value for PaO2 would be expected to result in a very low value for blood oxygen satura-

tion and content in the fetus. In fact, even at this low PaO2, the arterial blood in the fetus is about 60 per cent saturated, com­pared with 98 per cent or so in the adult arteries, and the oxygen content of the arterial blood is about 16 ml dl_1. Two important factors are responsible for this state of affairs:

  1. Fetal blood has a higher hemoglobin concentration than
    adult blood (around 20 g dH compared with around
    15gdH). This increases the oxygen-carrying capacity of
    fetal blood.

  2. Fetal hemoglobin (HbF), which has a different structure
    to that of the adult, has a higher affinity for oxygen than
    adult hemoglobin. The oxygen dissociation curve for fetal
    blood is shifted to the left in relation to that of the adult
    (Fig. 21.3). As a result of this, even at the low Po2 values
    experienced by the fetus, fetal blood has a relatively high
    oxygen saturation and total oxygen content. Further­
    more, the portion of the curve over which the fetus nor­
    mally operates is very steep. Consequently, even though
    there is a relatively small difference between arterial and
    systemic venous blood Po2, there is a large difference in
    oxygen saturation, and oxygen is offloaded readily to the

There are species variations in the magnitude of the fetal—adult difference in hemoglobin oxygen affinity. Most of the research in this area has been done using sheep, in which the dif­ference is rather large. In humans, the differences are thought to be smaller, although still significant.

Fig. 21.3 The oxygen dissociation curves for adult and fetal sheep hemoglobin. Note that the dissociation curve for the fetus is displaced to the left, indicating a higher degree of saturation of fetal hemoglobin for a given partial pressure of oxygen. The approximate values for the partial pressure and percentage saturation in the ascending aorta of the fetus and in the umbilical artery and vein of the sheep are indicated. The difference in O2 carriage in the human adult and fetal blood is believed to be slightly smaller.

^ 478

21 Fetal and neonatal physiology


l.The fetus is dependent on the placenta for gas exchange, waste disposal, and nutrition.

  1. The fetal circulation is arranged so that the two sides of the heart
    work essentially in parallel and the three fetal shunts permit the
    blood to bypass those organs with little or no function.

  2. The fetal heart rate is high and the blood pressure low.

  3. The fetal lungs are fluid filled and virtually collapsed. The pulmonary
    vascular resistance is elevated and so pulmonary blood flow is only
    20 per cent of the right ventricular output; the other 80 per cent
    passes through the ductus arteriosus.

5. Despite its low Pao2, fetal blood carries about l6mlO2 dl~'. This
capacity is the result of a high hemoglobin concentration and the
high affinity of fetal hemoglobin for oxygen.

21.3 Respiratory and cardiovascular changes at birth

The changes that occur at birth can be summarized as follows:

  1. The initiation of the first breath.

  2. The expansion of the lungs followed by a reduction in the
    pulmonary vascular resistance that results in a striking rise
    in pulmonary blood flow.

  3. The ductus arteriosus gradually closes so that all the
    right ventricular output eventually passes through the
    pulmonary circulation.

  4. The increase in pulmonary blood flow into the left atrium
    leads to the closure of the foramen ovale.

  5. The ductus venosus closes so that all the blood in the
    portal vein passes through the liver.

The changes in the pattern of the circulation following birth are summarized in Fig. 21 A.

The first breath is probably triggered by cooling and hypercapnia

Once the infant has been delivered, it is cut off from the placenta which has acted as its site of gas exchange for the previous 9 months. If the cord is not clamped surgically in the delivery room, the umbilical vessels quickly shut down of their own accord. So, despite the fact that both the fetus and neonate are able to tolerate degrees of hypercapnia and hypoxia that would be likely to kill an adult, the infant has to start breathing independently if is to survive for more than about 10 minutes. What mechanisms are responsible for triggering its first breath?

  • First, the infant experiences a drop in ambient temperature
    following delivery.

  • Secondly, there is an increase in Pco2 following delivery.
    During labor and delivery, particularly if this has been long
    and difficult, the placental blood supply may be partially or

Fig. 21.4 Schematic diagram to show how the pattern of the circulation changes following birth.

wholly occluded for short periods of time. Certainly, once the baby has been born the placental blood supply will be lost. Consequently, the baby will experience a considerable degree of hypercapnia. Indeed measurements of the Pco2 of scalp blood sampled during and just after delivery have revealed a marked increase which may well provide the neonate with an important stimulus to gasp for air. This reflex is known to be functional in the fetus, whose breathing movements become more pronounced during asphyxia (see above).

• Finally, once it has been born, the neonate is subjected to a barrage of sensory information from which it had been insulated while in the womb. It is known that tactile and painful stimuli can stimulate breathing movements even in the fetus.

It is not known which, if any, of these factors is responsible for the initiation of ventilation following delivery—perhaps a combination of both physical and chemical stimuli is required.

^ 21.3 Respiratory and cardiovascular changes at birth


Lung inflation is facilitated by surfactant

The lungs have remained collapsed and fluid filled throughout embryonic life. In order to inflate its lungs for the first time, the newborn baby must overcome the enormous surface tension forces at the gas—liquid interface of the alveoli. Around week 20 of gestation, type II epithelial cells start to appear in the devel­oping alveoli, and 8-10 weeks later, under the control of fetal Cortisol, these cells start to secrete phospholipid surfactants, the most important of which are lecithin and sphingomyelin. Surfactant molecules are responsible for reducing the surface tension forces that oppose lung inflation. This reduction makes it possible for the newly born infant to inflate its lungs. Nevertheless, a considerable ventilatory effort is still required in order to expand the lungs for the first time.

It can be seen from Fig. 21.5 that an enormous negative pressure must be generated to make the initial inspiration poss­ible. The figure illustrates the pressure/volume relationships for the neonatal lung operating during the first and subsequent breaths. It also shows that a large positive pressure must be gen­erated for expiration because lung compliance is still rather low. A great mechanical effort is demanded from the baby. The diaphragm contracts strongly and the ribs and sternum, which at this stage are very flexible, become slightly concave during the initial breaths. After the first breath, the volume of the lungs does not return to zero after expiration but a little air remains in the lungs to form the beginnings of the residual volume which remains throughout life. Subsequent breaths are achieved with much smaller pressure changes and consequently require much less mechanical effort, indicating that lung compliance has increased (see Chapter 16 for more detail of the mechanics of breathing).

Once the fetal shunts are closed after delivery and the lungs are expanded, the pulmonary vascular resistance is decreased and the pulmonary blood flow is greatly increased (Section 21.4). As

a result, the fluid that filled the alveoli during fetal life is reab­sorbed quickly into the pulmonary capillary blood which has a higher osmotic pressure than the alveolar fluid.

What happens if surfactant is inadequate?

The presence of sufficient quantities of surfactant is crucial to the initiation of ventilation following delivery and, even then, the first breath requires a considerable mechanical effort on the part of the baby (Fig. 21.5). Imagine, therefore, the problems faced by babies born prematurely, i.e. before adequate surfactant secretion has been established. If a baby is born before weeks 28-30 of gesta­tion, it will almost certainly have difficulty overcoming the surface tension forces opposing ventilation, and is very likely to show res­piratory distress. If such infants are to have a chance of survival, they must be ventilated artificially until their lungs are sufficiently well developed to permit independent respiration.

How does neonatal respiration differ from that of the adult?

Once the first few—rather difficult—breaths have been accom­plished, respiration settles down into the 'neonatal' pattern, a somewhat erratic rhythm with certain characteristics that differ significantly from those of a more mature child or adult. There are, understandably, considerable difficulties associated with the study of lung function in very small babies but some informa­tion has been obtained, much of which is contained in Table 21.1. The ventilatory rate of a newborn infant (i.e. less than about 1 month old) is rather high and extremely variable. Neonatal breathing often resembles the fetal pattern of respira­tory movements, with episodes of shallow breathing or even apnea interspersed with periods of normal respiration. Periods of apnea are most often seen during sleep and prolonged sleep apnea is believed to be a major cause of sudden infant death syndrome (SIDS, or 'cot death').

Fig. 21.5 The lung pressure—volume relationships during the first, second, and third breaths, together with that for breathing about 40 min after the first breath. Note that the residual volume (R.V.) is established with the first brearh and that the compliance increases with subsequent breaths (i.e. the pressure change required for a given change in volume falls after the first breath).


21 Fetal and neonatal physiology

Table 21.1 Comparison of respiratory variables of the neonate and the adult





Body weight (kg)



Ventilation rate (breaths min-1)



Minute volume (ml)

c. 500

c. 6500

Tidal volume (ml)



Vital capacity (ml)



Surface area for gas exchange in lungs (m2)



Lung compliance (liters kPa-1) (ml cmHp-1)

0.051 5

1.7 165

Bronchiole diameter (mm)



Oxygen diffusion capacity (mis-1 kPa",) (ml min^ mmHg"1)



6 25

Energy expended in breathing as % of total O2 consumption



  1. After delivery, the baby is cut off from its placental blood supply and
    must begin to use its lungs. Physical factors such as temperature
    changes may stimulate breathing, but a likely trigger for the first
    breath is hypercapnia following cord compression during delivery.

  2. To inflate its lungs for the first time, the baby must overcome the
    enormous surface tension forces at the gas—liquid interface in the
    alveoli. Surfactant plays a vital role in reducing these forces but a
    massive effort is still required by the baby to generate the intratho­
    racic pressures needed to open the lungs.

  3. Babies born before adequate levels of surfactant have been produced
    (around week 28) are at risk of showing respiratory distress.

  4. Neonatal respiration differs in certain respects from that of the adult.
    Ventilatory rate is higher but more erratic, airway resistance is
    higher, and the work of breathing greater in the neonate.

  5. The ventilatory response to hypercapnia is well developed in both the
    fetus and neonate, with central medullary chemoreceptor activity
    present from about mid-gestation. In the fetus the peripheral
    chemoreceptors have a very low level of activity but start to respond
    to reductions in oxygen tension following delivery.

As a consequence of its high rate of ventilation, the infant's minute volume is relatively high in relation to its body weight. As Table 21.1 shows, neonates have a rather low lung com­pliance, which indicates high airway resistance when compared with that of an adult. A number of factors contribute to this resistance. First, during the early weeks of its life a baby tends to breathe mostly through its nose. Secondly, the bronchioles are very narrow, and, thirdly, lung compliance is itself still rather low. These characteristics mean that the energy expenditure of breathing in the neonate is high.

Regulation of ventilation in the neonate

Regulation of ventilation during the first weeks of life represents a transitional stage somewhere between that of the fetus and that of the adult. Central medullary chemoreceptor activity seems to be present from about the time of the onset of fetal breathing movements. The evidence for this is that fetal hypercapnia seems to initiate 'gasping' movements (see Section 21.2). The periph­eral chemoreceptors appear to be desensitized or switched off in the fetus, probably because the partial pressure of oxygen in the fetal blood is always low. They show slight tonic activity in the full-term fetus at the normal PaO2 of 2.5 kPa (c. 20-23 mmHg). After birth, however, the hypoxic sensitivity gradually changes to that of the adult by a mechanism that is still unclear. This means that, in the neonate, the same tonic activity is now present ar much higher levels of PaO2 and a reduction in the PaO2 below that level causes the expected stimulation of the chemoreceptors. The ventilatory response to hypercapnia is very marked in the newborn baby—the addition of only 2 per cent CO2 to the inspired air produces an increase in the minute volume of around 80 per cent.

^ 21.4 Following delivery the fetal circulation must adapt to pulmonary gas exchange

The anatomical arrangemenr of the fetal circulation differs from that of an adult in a number of ways (see Fig. 21.4). In essence, rhe rwo sides of the circulation work in parallel, with the three fetal shunts permitting blood to bypass those organs with little or no function. Such an arrangement is well adapted to gas exchange via the placenta, but would be quite inappropriate once the baby has begun to breathe for itself. Following delivery, the placental blood supply is lost and the lungs become the sole source of oxygen. As the infant takes its first breaths of air the fetal circulation must start to adapt to the adult pattern so that blood no longer bypasses the pulmonary circulation. To achieve this it is essential that the three fetal shunts close.

Probably the most important step in the initiation of shunt closure is rhe increase in pulmonary perfusion that accompanies the establishment of ventilation. During fetal life only about 20 per cent of the cardiac ourpur enters rhe pulmonary circulation because resistance to blood flow through the vessels is high in the collapsed lungs. After the first breath pulmonary blood flow is dramatically increased. Two key factors are involved:

  1. Inflation of the alveoli reduces the tortuosity of the
    pulmonary capillaries, thereby reducing their resistance to
    blood flow.

  2. As a result of breathing air there is a considerable increase
    in the partial pressure of oxygen in the blood perfusing the
    lungs. In response to this rise, there is vasodilatation of the
    pulmonary vessels and a corresponding fall in resistance.
    Both of these changes cause a large increase in the amount
    of blood circulating in the pulmonary vessels.

21.4 Adaptions to pulmonary gas exchange


At the same time, the fetus is separated from its placental blood supply. Following delivery, the umbilical cord is normally clamped, but even if this is not done, the umbilical vessels appear to shut down spontaneously as a result of vasoconstriction in response to the raised systemic Po2. (Note that this is the opposite teaction to that of the pulmonary arterioles, which dilate in response to a raised Po2; see also Chapter 16.)

How do the changes in the pattern of

blood flow following delivery bring about

closure of the fetal shunts?

Consider first the foramen ovale, i.e. the shunt between the left and fight atria. During fetal life, right atrial pressure is similar to, or just exceeds, left atrial pressure because of the telatively high pulmonary resistance and the relatively low systemic resist­ance. After bitth and the onset of independent breathing, increased pulmonary perfusion results in an increase in venous feturn to the left atrium. At the same time loss of the umbilical blood supply reduces the venous teturn in the inferior vena cava to the fight atrium. Consequently, left atrial pressure rises above right atrial pressure. The foramen ovale consists of two unfused septa. When fight atrial pressure exceeds left atrial pressure, the septa part and the shunt is open. Once the pressures are reversed

Fig. 21.6 The changes in the pressures of the right and left atria that lead to closure of the foramen ovale. While the lungs are nonfunctional with respect to gas exchange the pressure in the right atrium is greater than that in the left and blood passes through the foramen ovale. Following the first breath, the pressure in the left atrium becomes greater than that in the right and this leads to the closure of the foramen ovale.

the septa will be forced against each other and the shunt will be closed. At first, closufe is purely physiological, but within a few days the septa fuse permanently and closure is anatomically com­plete. Figure 21.6 shows how the pressure changes bring about the closure of the foramen ovale.

Consider next the closufe of the ductus arteriosus, the fetal shunt between the aorta and the pulmonary artefy. This is an extremely wide channel, almost as large in diametef as the aorta itself (see Fig. 21.1), and the mechanisms by which closure is effected are not established beyond doubt. The ductus receives little or no innervation, so the most likely cause of closure follow­ing delivery and the onset of breathing is constriction in response to bloodborne factors. In rather the same way as the umbilical vessels, the smooth muscle of the ductus arteriosus is thought to constrict in response to the substantial rise in Po2 seen after the first breaths. Permanent closure of the shunt occufs within 10 days or so as a result of fibrosis within the lumen of the vessel.

The third shunt is the ductus venosus, the channel that bypasses the liver and Carries about 80 per cent of the blood in the umbilical veins directly to the inferior vena cava during fetal life. Once again, the exact mechanisms of closure are poorly understood, but it is believed to occur as a result of constriction of the umbilical vessels following delivery.

In essence, the parallel arrangement of the two sides of the heart, characteristic of the fetus, is converted to a serial arrange­ment soon after birth and the commencement of pulmonary gas exchange (see Fig. 21.4). At rhe same time, the relative work-loads of the two sides of the heart are altered. Because the resist­ance to flow in the vascular bed of the lung is only about 12 per cent of that of the systemic circulation, the wofkload of the right side of the heart is considerably less than that of the left. As a consequence of this, there is an accelerated growth of the more heavily loaded left ventricle, which eventually develops a mass of muscle about three times that of the right.

Occasionally, the fetal shunts fail to close

While there have been no reports of the ductus venosus failing to close during the first days of life, persistent fetal connections in the form of a patent foramen ovale or ductus arteriosus are seen. Indeed, each accounts for probably about 15-20 pef cent of congenital heart defects. During very early neonatal life it is not unusual to see intermittent flow through the fetal shunts but, if they remain open for a prolonged period after birth, circulatory function is impaired and surgical intervention will be required to correct the defect. For example, if the foramen ovale remains patent, the volume of blood ejected by the tight ventricle is often increased and there is likely to be persistent admixture of oxygenated and deoxygenated blood (the blue baby syndrome). Where the ductus arteriosus remains open, 50 per cent of more of the left ventricular stroke volume can be diverted into the pulmonary circulation, resulting in pulmonary hypertension and heart failure. This condition can be treated surgically by tying the ductus arteriosus.


21 Fetal and neonatal physiology


  1. After delivery, the circulation of the infant must adapt to pulmonary
    gas exchange.

  2. The parallel arrangement of the two sides of the heart seen during
    fetal life converts to a serial arrangement as a result of closure of the
    three fetal shunts.

  3. Closure of the shunts depends upon ventilation itself. As the lungs
    expand, pulmonary perfusion increases, while at the same time the
    umbilical vessels close. This causes left atrial pressure to rise above
    right atrial pressure with subsequent closure of the septa which form
    the foramen ovale. The ductus venosus and the ductus arteriosus are
    thought to close as a tesult of vasoconstriction in response to a rise in
    arterial Po,.

^ 21.5 The fetal adrenal glands and kidneys

The fetal adrenal gland secretes large quantities of Cortisol during development

The adrenal glands are vital endocrine organs in the adult. They consist of two distinct regions, the cortex, which synthesizes and secretes a variety of steroids (see Chapter 12), and the medulla, which produces the catecholamines epinephrine and norepineph­rine. During fetal life, the adrenal glands appear to be, if anything, more important, as they play a key role in the devel­opment of many of the fetal organ systems and are important in the initiation of parturition (see Section 20.7).

In relation to the overall body size of the fetus, the fetal adrenal gland is much bigger than that of the adult. Further­more, it is organized in a different way. Unlike the adult gland, which consists of a medulla and a zoned cortex, the fetal adrenal gland is divided into three areas with differing characteristics. These are: a small region of medullary tissue derived from embryonic neural crest cells; a small, zoned cortex—the so-called definitive cortex—-which resembles that of the adult; and a third, very large region, the fetal zone. The relative sizes of these areas are shown in Fig. 21.7.

The functions of the different regions of the fetal adrenal gland are not fully established, but the medullary tissue is

capable of secreting catecholamines. This occurs particularly in response to hypoxic stress, and, immediately after delivery, to cold stress. The fetal zone seems to be very important in pro­ducing the precursors required for the placental synthesis of estrogens (see Section 20.6) and its large size probably reflects the enormous output of these steroids during gestation. The 'definitive cortex' seems to carry out little in the way of steroid synthesis itself during fetal life but it does perform one very important task—it converts progesterone to Cortisol, especially during the last 3 months of pregnancy.

Fetal Cortisol has several crucial functions:

  1. It is linked with the production of surfactant by type II
    alveolat cells.

  2. It accelerates functional differentiation of the liver
    and induces the enzymes that are involved in glycogen

  3. It plays an important role in the triggering of parturition.
    After delivery, the fetal zone of the adrenal gland regresses

rapidly while the definitive zoned cortex grows quickly to estab­lish the adult organizational pattetn.

Renal function and fluid balance in the fetus and neonate

Although the placenta is the major organ of homeostasis and excretion of metabolic waste products duting gestation, the fetal kidneys do play a role in the regulation of fluid balance and the control of fetal arterial blood pressure. In addition, amniotic fluid volume is regulated chiefly by the formation of fetal urine. The human fetus begins to produce urine at about 8 weeks' gestation. Its volume increases progressively throughout gestation and is roughly equivalent to the volume of amniotic fluid swallowed by the fetus (around 28 ml h~' in late gestation). Fetal urine is usually hypotonic with respect to the plasma. Indeed, the ability of the kidney to concentrate the urine is not fully developed until after birth, when the organ matures; the loops of Henle increase in length, and sensitivity of the tubules to ADH increases.

In the adult, virtually all the filtered sodium is reabsorbed by the renal tubules. In the fetus, sodium reabsorption is com-

Fig. 21.7 Schematic diagram showing the changes in the adrenal gland during development. Note the tegtession of the fetal zone following birth.

^ 21.6 Temperature regulation in the newborn infant
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