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Fetal and
Neonatal
Physiology
NEWBORN-first 24 hrs of life
NEONATE-from birth to under four weeks(<28 days)
TERM NEONATE-between 37 to < 42 gestational week
PRETERM NEONATE-<37 gestational week
POST TERM NEONATE-> or egual to 42 gestational week
LOW BIRTH WEIGHT(LBW)<2500 GRAM
VERY LOW BIRTH WEIGHT(VLBW)<150O GRAM
EXTREMELY LOW BIRTH WEIGHT(ELBW)< 1000 GRAM
Irrespective of birth weight
Birth weight dependent
Placenta
 The placenta (also known as afterbirth) is an organ that
connects the developing fetus to the uterus.
 The placenta functions as a fetomaternal organ with two
components: the fetal placenta (Chorion frondosum), which
develops from the same blastocyst that forms the fetus, and
the maternal placenta (Decidua basalis), which develops from
the maternal uterine tissue.
Placental function
 Nutrition:
The perfusion of the intervillous spaces of the placenta with
maternal blood allows the transfer of nutrients and oxygen from the
mother to the fetus.
 Excretion
Waste products excreted from the fetus such as urea, uric acid,
and creatinine are transferred to the maternal blood
by diffusion across the placenta.
 Immunity
IgG antibodies can pass through the human placenta, thereby
providing protection to the fetus in utero.
Placental function
 Endocrine function
• The first hormone released by the placenta is called the human
chorionic gonadotropin hormone.
• promotes the maintenance of the corpus luteum during the
beginning of pregnancy. This allows the corpus luteum
to secrete the hormone progesterone which enriches
the uterus with a thick lining of blood vessels and capillaries so
that it can sustain the growing fetus.
• Progesterone
• Estrogen
• Human placental lactogen – promote fetal growth and
development
Why mother’s
immune cell do
not attack the
fetus? The placenta uses several mechanisms:
•It secretes Neurokinin B
containing phosphocholine molecules.
•There is presence of small lymphocytic
suppressor cells in the fetus that inhibit
maternal cytotoxic T cells by inhibiting the
response to interleukin.
Fetal Circulation
Yolk sac and placenta
Endothelium of fetal blood vessel
Fetal Circulation
 Umbilical vein carries oxygenated blood and
nutrients from the placenta to the fetus.
 Pair of umbilical arteries carry deoxygenated
blood & wastes to placenta.
Umblical vein
Liver
Portal vein
Ductus venosus
Inferior vena
cava
Right Atrium
Left Atrium
Foramen Ovale
Left
Ventricle
Oxygenated blood from mother
Placenta
Descending
Aorta
Deoxygenated blood
Superior vena
cava
Right
Ventricle
Pulmonary
artery
Lung
Ductus ateriosus
Ascending
Aorta
Supplies
head n neck
Umblical
artery
Supplies
lower body
Changes in fetal circulation after birth
Decreased Pulmonary and Increased Systemic Vascular
Resistances at Birth:
 Loss of the tremendous blood flow through the
placenta, which approximately doubles the systemic
vascular resistance at birth.
 The pulmonary vascular resistance greatly decreases
as a result of expansion of the lungs.
Closing of Shunts
Shunt Functional
closure
Anatomical
closure
Remnant
Ductus
arteriosus
10 – 96 hrs after
birth
2 – 3 wks after
birth
Ligamentum
arteriosum
Formamen
ovale
Within several
mins after birth
One year after
birth
Fossa ovalis
Ductus
venosus
Within several
mins after birth
3 – 7 days
after birth
Ligamentum
venosum
Umbilical arteries → Umbilical ligaments
Umbilical vein → Ligamentum teres
 Closure of the Foramen Ovale
• Flow backward through the foramen ovale
• low right atrial pressure
• the high left atrial pressure
• Small valve that lies over the foramen ovale on the left side of the
atrial septum closes
 Closure of the Ductus Arteriosus
• increased systemic resistance elevates the aortic pressure while
the decreased pulmonary resistance reduces the pulmonary
arterial pressure after birth, blood begins to flow backward from
the aorta into the pulmonary artery through the ductus arteriosus.
• 1 to 8 days- functional closure of the ductus arteriosus
• 1 to 4 months- ductus arteriosus ordinarily becomes
anatomically occluded by growth of fibrous tissue into its
lumen
 Patent ductus arteriosusone- the ductus fails to close
 excessive ductus dilation caused by vasodilating
prostaglandins in the ductus wall.
 indomethacin- blocks synthesis of prostaglandins
Characteristics of new born
circulation
 B lood Volume .
- 300 ml
- if the infant is left attached to the placenta for a few minutes after birth
or if the umbilical cord is stripped to force blood out of its vessels into
the baby, an additional 75 milliliters of blood enters the infant, to make a
total of 375 milliliters.
 C a rdia c Out put
500 ml/min- is about twice as much in relation to body weight as in the
adult.
 Arterial Pressure.
The arterial pressure during the first day after birth averages about 70
/50 mm Hg and increases slowly during the next several months to
about 90/60.
Neonatal Jaundice and
Erythroblastosis Fetalis.
 In the fetus
 bilirubin can cross the placenta into the mother and
be excreted through the liver of the mother
 After birth
 the only means for ridding the neonate of bilirubin
is through the neonate’s own liver
 first week of life liver functions poorly- incapable of
conjugating significant quantities of bilirubin with
glucuronic acid for excretion into the bile the plasma
bilirubin concentration rises from a normal value of less
than 1 mg/dl to an average of 5 mg/dl during the first 3
days of life  liver becomes functional gradually falls
bilirubin back to normal
 Physiological hyperbilirubinemia
 mild jaundice (yellowness) of the infant’s skin and
especially of the sclerae of its eyes for a week or
 The most important abnormal cause of serious
neonatal jaundice is erythroblastosis fetalis.
 the baby inherits Rh-positive red blood cells from the
father, while the mother is Rh negative.
 The mother then becomes immunized against the Rh-
positive factor (a protein) in the fetus’s blood cells,
 Mothers antibodies destroy fetal red blood cells,
releasing extreme quantities of bilirubin into the
fetus’s plasma .
 Often causing fetal death because of a lack of
adequate red blood cells.
 The most obvious effect of birth on the baby - loss of the
placental connection with the mother - loss of Oxygen support
 One of the most important immediate adjustments required of the
infant is to begin breathing.
 child ordinarily begins to breathe within seconds and has a
normal respiratory rhythm within less than 1 minute after birth
Cause of Breathing at Birth.
 A slight asphyxiated state incident to the birth process
 sensory impulses that originate in the suddenly cooled
skin
Onset of breathing
Tolerability of hypoxia
 Adults – 4 minute
 Neonate – 10 minutes
 Permanent and serious brain impairment
often ensues if breathing is delayed more
10 minutes.
Expansion of Lung at birth
At birth
- Alveoli are collapsed due to surface tension of viscid
fluid present in them.
- 25 mm Hg of negative pressure required to open
them.
The first inspirations of the normal neonate are
extremely powerful; they are usually capable of creating
as much as 60 mm Hg negative pressure in the
intrapleural space.
Respiratory Distress Syndrome
 Caused When Surfactant Secretion Is Deficient.
 premature infants and infants born of mothers with
diabetes mellitus are mainly affected.
 A characteristic finding in respiratory distress
syndrome is failure of the respiratory epithelium to
secrete adequate quantities of surfactant.
 Surfactant – secreted by Type II alveolar epithelial
cells decreases the surface tension of the alveolar
fluid,.
 Secretion begins only in the last 1-3 month of
gestation.
Body temperature regulation
 The normal metabolic rate of the neonate in relation to body
weight is about twice that of the adult,
■ body surface area is large in relation to body mass, heat is readily
lost from the body body temperature of the neonate, particularly of
premature infants, falls easily
 Body temperature of even a normal infant often falls several
degrees during the first few hours after birth but returns to
normal in 7 to 10 hours.
 The premature infant’s temperature tends to
approach that of its surroundings.
 At normal room temperature, the infant’s temperature
may stabilize in the low 90s.
 Studies show that a body temperature maintained
below 96°F (35.5°C) is associated with a particularly
high incidence of death
 This explains the almost mandatory use of the
incubator when treating prematurity
■ The neonate inherits much immunity from the mother
because many protein antibodies diffuse from the
mother’s blood through the placenta into the fetus.
■ Baby’s own immunity system begins to form
antibodies and the gamma globulin
concentration returns essentially to normal by
the age of 12 to 20 months.
■ Despite the decrease in gamma globulins soon after
birth, the antibodies inherited from the mother protect
the infant for about 6 months against most major
childhood infectious diseases, including diphtheria,
measles, and polio.
■ Inherited antibodies against whooping cough are
normally insufficient to protect the neonate-
immunization
Immunity
Liver Function
■ Liver function in the neonate may be quite deficient, as
evidenced by the following effects:
1. The liver of the neonate conjugates bilirubin with glucuronic
acid poorly and therefore excretes bilirubin only slightly
during the first few days of life.
2. The liver of the neonate is deficient in forming plasma
proteins, so the plasma protein concentration falls during
the first weeks of life and the infant develops
hypoproteinemic edema.
3. The gluconeogenesis function of the liver is particularly
deficient. As a result, the blood glucose level of the unfed
neonate falls to about 30 to 40 mg/dl (about 40 percent of
normal) and the infant must depend mainly on its stored fats
for energy until sufficient feeding can occur.
4. The liver of the neonate usually also forms too little of the
blood factors needed for normal blood coagulation.
Need for Calcium and Vitamin
D
 The neonate is in a stage of rapid ossification of its
bones at birth, so a ready supply of calcium
throughout infancy is necessary.
 This is ordinarily supplied adequately by the usual diet
of milk.
– absorption of calcium by the gastrointestinal
tract is poor in the absence of vitamin D–deficient
infant can develop severe rickets
 This is particularly true in premature babies because
their gastrointestinal tracts absorb calcium even less
effectively than those of normal infants
Necessity for Iron in the Diet
 If the mother has had adequate amounts of iron in
her diet, the liver of the infant usually has stored
enough iron to keep forming blood cells for 4 to 6
months after birth.
 But if the mother has had insufficient iron in her
diet, severe anemia is likely to occur in the infant
after about 3 months of life.
 To prevent this possibility, early feeding of the infant
with egg yolk, which contains reasonably large
quantities of iron, or the administration of iron in some
other form is desirable by the second or third month of
life.

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  • 2. NEWBORN-first 24 hrs of life NEONATE-from birth to under four weeks(<28 days) TERM NEONATE-between 37 to < 42 gestational week PRETERM NEONATE-<37 gestational week POST TERM NEONATE-> or egual to 42 gestational week LOW BIRTH WEIGHT(LBW)<2500 GRAM VERY LOW BIRTH WEIGHT(VLBW)<150O GRAM EXTREMELY LOW BIRTH WEIGHT(ELBW)< 1000 GRAM Irrespective of birth weight Birth weight dependent
  • 3. Placenta  The placenta (also known as afterbirth) is an organ that connects the developing fetus to the uterus.  The placenta functions as a fetomaternal organ with two components: the fetal placenta (Chorion frondosum), which develops from the same blastocyst that forms the fetus, and the maternal placenta (Decidua basalis), which develops from the maternal uterine tissue.
  • 4.
  • 5. Placental function  Nutrition: The perfusion of the intervillous spaces of the placenta with maternal blood allows the transfer of nutrients and oxygen from the mother to the fetus.  Excretion Waste products excreted from the fetus such as urea, uric acid, and creatinine are transferred to the maternal blood by diffusion across the placenta.  Immunity IgG antibodies can pass through the human placenta, thereby providing protection to the fetus in utero.
  • 6. Placental function  Endocrine function • The first hormone released by the placenta is called the human chorionic gonadotropin hormone. • promotes the maintenance of the corpus luteum during the beginning of pregnancy. This allows the corpus luteum to secrete the hormone progesterone which enriches the uterus with a thick lining of blood vessels and capillaries so that it can sustain the growing fetus. • Progesterone • Estrogen • Human placental lactogen – promote fetal growth and development
  • 7. Why mother’s immune cell do not attack the fetus? The placenta uses several mechanisms: •It secretes Neurokinin B containing phosphocholine molecules. •There is presence of small lymphocytic suppressor cells in the fetus that inhibit maternal cytotoxic T cells by inhibiting the response to interleukin.
  • 8. Fetal Circulation Yolk sac and placenta Endothelium of fetal blood vessel
  • 9.
  • 10. Fetal Circulation  Umbilical vein carries oxygenated blood and nutrients from the placenta to the fetus.  Pair of umbilical arteries carry deoxygenated blood & wastes to placenta.
  • 11.
  • 12.
  • 13. Umblical vein Liver Portal vein Ductus venosus Inferior vena cava Right Atrium Left Atrium Foramen Ovale Left Ventricle Oxygenated blood from mother Placenta Descending Aorta Deoxygenated blood Superior vena cava Right Ventricle Pulmonary artery Lung Ductus ateriosus Ascending Aorta Supplies head n neck Umblical artery Supplies lower body
  • 14. Changes in fetal circulation after birth Decreased Pulmonary and Increased Systemic Vascular Resistances at Birth:  Loss of the tremendous blood flow through the placenta, which approximately doubles the systemic vascular resistance at birth.  The pulmonary vascular resistance greatly decreases as a result of expansion of the lungs.
  • 15. Closing of Shunts Shunt Functional closure Anatomical closure Remnant Ductus arteriosus 10 – 96 hrs after birth 2 – 3 wks after birth Ligamentum arteriosum Formamen ovale Within several mins after birth One year after birth Fossa ovalis Ductus venosus Within several mins after birth 3 – 7 days after birth Ligamentum venosum Umbilical arteries → Umbilical ligaments Umbilical vein → Ligamentum teres
  • 16.  Closure of the Foramen Ovale • Flow backward through the foramen ovale • low right atrial pressure • the high left atrial pressure • Small valve that lies over the foramen ovale on the left side of the atrial septum closes
  • 17.  Closure of the Ductus Arteriosus • increased systemic resistance elevates the aortic pressure while the decreased pulmonary resistance reduces the pulmonary arterial pressure after birth, blood begins to flow backward from the aorta into the pulmonary artery through the ductus arteriosus. • 1 to 8 days- functional closure of the ductus arteriosus • 1 to 4 months- ductus arteriosus ordinarily becomes anatomically occluded by growth of fibrous tissue into its lumen  Patent ductus arteriosusone- the ductus fails to close  excessive ductus dilation caused by vasodilating prostaglandins in the ductus wall.  indomethacin- blocks synthesis of prostaglandins
  • 18. Characteristics of new born circulation  B lood Volume . - 300 ml - if the infant is left attached to the placenta for a few minutes after birth or if the umbilical cord is stripped to force blood out of its vessels into the baby, an additional 75 milliliters of blood enters the infant, to make a total of 375 milliliters.  C a rdia c Out put 500 ml/min- is about twice as much in relation to body weight as in the adult.  Arterial Pressure. The arterial pressure during the first day after birth averages about 70 /50 mm Hg and increases slowly during the next several months to about 90/60.
  • 19. Neonatal Jaundice and Erythroblastosis Fetalis.  In the fetus  bilirubin can cross the placenta into the mother and be excreted through the liver of the mother  After birth  the only means for ridding the neonate of bilirubin is through the neonate’s own liver  first week of life liver functions poorly- incapable of conjugating significant quantities of bilirubin with glucuronic acid for excretion into the bile the plasma bilirubin concentration rises from a normal value of less than 1 mg/dl to an average of 5 mg/dl during the first 3 days of life  liver becomes functional gradually falls bilirubin back to normal  Physiological hyperbilirubinemia  mild jaundice (yellowness) of the infant’s skin and especially of the sclerae of its eyes for a week or
  • 20.  The most important abnormal cause of serious neonatal jaundice is erythroblastosis fetalis.  the baby inherits Rh-positive red blood cells from the father, while the mother is Rh negative.  The mother then becomes immunized against the Rh- positive factor (a protein) in the fetus’s blood cells,  Mothers antibodies destroy fetal red blood cells, releasing extreme quantities of bilirubin into the fetus’s plasma .  Often causing fetal death because of a lack of adequate red blood cells.
  • 21.  The most obvious effect of birth on the baby - loss of the placental connection with the mother - loss of Oxygen support  One of the most important immediate adjustments required of the infant is to begin breathing.  child ordinarily begins to breathe within seconds and has a normal respiratory rhythm within less than 1 minute after birth Cause of Breathing at Birth.  A slight asphyxiated state incident to the birth process  sensory impulses that originate in the suddenly cooled skin Onset of breathing
  • 22. Tolerability of hypoxia  Adults – 4 minute  Neonate – 10 minutes  Permanent and serious brain impairment often ensues if breathing is delayed more 10 minutes.
  • 23. Expansion of Lung at birth At birth - Alveoli are collapsed due to surface tension of viscid fluid present in them. - 25 mm Hg of negative pressure required to open them. The first inspirations of the normal neonate are extremely powerful; they are usually capable of creating as much as 60 mm Hg negative pressure in the intrapleural space.
  • 24. Respiratory Distress Syndrome  Caused When Surfactant Secretion Is Deficient.  premature infants and infants born of mothers with diabetes mellitus are mainly affected.  A characteristic finding in respiratory distress syndrome is failure of the respiratory epithelium to secrete adequate quantities of surfactant.  Surfactant – secreted by Type II alveolar epithelial cells decreases the surface tension of the alveolar fluid,.  Secretion begins only in the last 1-3 month of gestation.
  • 25. Body temperature regulation  The normal metabolic rate of the neonate in relation to body weight is about twice that of the adult, ■ body surface area is large in relation to body mass, heat is readily lost from the body body temperature of the neonate, particularly of premature infants, falls easily  Body temperature of even a normal infant often falls several degrees during the first few hours after birth but returns to normal in 7 to 10 hours.
  • 26.  The premature infant’s temperature tends to approach that of its surroundings.  At normal room temperature, the infant’s temperature may stabilize in the low 90s.  Studies show that a body temperature maintained below 96°F (35.5°C) is associated with a particularly high incidence of death  This explains the almost mandatory use of the incubator when treating prematurity
  • 27. ■ The neonate inherits much immunity from the mother because many protein antibodies diffuse from the mother’s blood through the placenta into the fetus. ■ Baby’s own immunity system begins to form antibodies and the gamma globulin concentration returns essentially to normal by the age of 12 to 20 months. ■ Despite the decrease in gamma globulins soon after birth, the antibodies inherited from the mother protect the infant for about 6 months against most major childhood infectious diseases, including diphtheria, measles, and polio. ■ Inherited antibodies against whooping cough are normally insufficient to protect the neonate- immunization Immunity
  • 28. Liver Function ■ Liver function in the neonate may be quite deficient, as evidenced by the following effects: 1. The liver of the neonate conjugates bilirubin with glucuronic acid poorly and therefore excretes bilirubin only slightly during the first few days of life. 2. The liver of the neonate is deficient in forming plasma proteins, so the plasma protein concentration falls during the first weeks of life and the infant develops hypoproteinemic edema. 3. The gluconeogenesis function of the liver is particularly deficient. As a result, the blood glucose level of the unfed neonate falls to about 30 to 40 mg/dl (about 40 percent of normal) and the infant must depend mainly on its stored fats for energy until sufficient feeding can occur. 4. The liver of the neonate usually also forms too little of the blood factors needed for normal blood coagulation.
  • 29. Need for Calcium and Vitamin D  The neonate is in a stage of rapid ossification of its bones at birth, so a ready supply of calcium throughout infancy is necessary.  This is ordinarily supplied adequately by the usual diet of milk. – absorption of calcium by the gastrointestinal tract is poor in the absence of vitamin D–deficient infant can develop severe rickets  This is particularly true in premature babies because their gastrointestinal tracts absorb calcium even less effectively than those of normal infants
  • 30. Necessity for Iron in the Diet  If the mother has had adequate amounts of iron in her diet, the liver of the infant usually has stored enough iron to keep forming blood cells for 4 to 6 months after birth.  But if the mother has had insufficient iron in her diet, severe anemia is likely to occur in the infant after about 3 months of life.  To prevent this possibility, early feeding of the infant with egg yolk, which contains reasonably large quantities of iron, or the administration of iron in some other form is desirable by the second or third month of life.