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The placenta becomes subdivided into a number of lobes by septa that grow into the
intervillous spaces from the maternal side. Each of such lobe of placenta is often called
a maternal cotyledon. If the placenta is viewed from the maternal side, the bases of
the septa are seen as grooves, while the cotyledons appear as convex areas bounded by
the grooves. Each lobe contains a number of anchoring villi and their branches. One such
villi and its branches constitute fetal cotyledon. The placenta then forms a compact
mass.

Structures
found in
the cut
section of
placenta
1. Amnion
2. Chorion
3. Chorio-
decidual
space
1.
Cotyledons
2. Decidua.

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Attachment
Placenta is attached mostly in the posterior wall high up of the uterus.

Dimensions at full term

 Weight: 500-600 gms.
 Diameter; 15-25cm.
 Thickness: 3 cm.

Functions
Mother Placenta Fetus

O2
1. 2’
CO2

Protein
Carbohydrate
Fat
2. Vitamin

Urea
Uric
Urea
acid
3. Antibodies >
4. Drugs
5. Infectious agents
6. Hormones
Hormones

Diagram: functions of placenta

Placenta transports some substances and synthesizes others. As a whole
placental functions can be listed as follows.
1. Exchange of respiratory gases. i.e. 02& C02 between fetus & mother.
2. Exchange of nutrients & metabolic waste products between fetus and
mother.
3. Transmission of maternal antibodies to the fetus.
4. Drug transfer from mother to fetus.
5. Transfer of infectious agents from mother to the fetus.
6. Synthesis of hormones- It synthesizes following hormones-
• Human chorionic gonadotropin (HCG). • Relaxin.
• Placental somatotropic hormone • Estrogen
• Estradiol. • Progesterone
7. Detoxify the toxic substances.

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8. Acts as a connecting media of the embryo (or fetus) to the mother.

Types
Placenta may be of following types
A.According to position:

Figure: Normal position of placenta

1. Placenta parietalis: When placenta lies on the

other walls of the uterus than the fundus.
2. Placenta praevia: When it is implanted in lower
uterine segment near internal os or in the os.

B. According to the shape:

1. Discoid: Disc shaped. It is the most common type.
2. Diffuse type: Spreading
3. Cotyled
4. onary: Seed leaf like.
5. Zonary: Girdle like.

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C. According to the number:

1. Bilobed with one umbilical cord.

2. Trilobed.
3. Placenta succenturiata- A small placenta is connected with main placenta by
blood vessels & membranes.

D. According to attachment of the umbilical cord

Figure: Normal attachment of umbillical cord

1. Battle dore placenta-When the umbilical cord is attached close to the margin
of placenta.
2. Vallamentous placenta- When the cord fails to reach the placenta and is
attached to the fetal mb. close to the periphery of the organ.
3. Furcuate placenta

Figure: Battle dore placenta

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Figure: Furcuate placenta

Figure: Vallamentous placenta

Placental barrier
(Placental membrane)
Definition-
The membrane, that separates the maternal & fetal blood in placentalcirculation
is called placental barrier.

Constituents
From maternal to fetal side, they are
1. Syncytotrophoblast
2. Cytotrophoblast.
3. Mesoderm (connective tissue in the core of villous)
4. Endothelium of fetal blood vessels.
Types
Several types of placental membranes have been recognized in different animals.
They are-
1. Epithelio-chorial (e.g. pig)
2 Endothelio- chorial (e g Dog)
3. Heamo- chorial (e.g. Human)
4. Hemo-endothelial (e g rabbit)
5. Endothelio-endothelial (e.g. Bovine)
[NB. Placenta can also be classified according to p. barrier]

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Figure: Different types of placental barrier

Placental circulation
1. Cotyledons receive their blood through 40 to 100 spiral arteries that pierce
the decidual plate and enter the intervillous spaces at more or less regular
intervals The lumen of the spiral artery is narrow, so blood pressure in the
intervillous space is high. This pressure forces the blood deep into the
intervillous spaces and bathes the numerous small villi of the villous tree in

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oxygenated blood. As the pressure decreases, blood flows back from the
chorionic plate toward the decidua, where it enters the endometrial veins.
Hence, blood from the intervillous lakes drains back into the maternal
circulation through the endometrial veins. Collectively, the intervillous spaces
of a mature placenta contain approximately 150 ml of blood, which is
replenished about 3 or 4 times per minute.
2. This blood moves along the chorionic villi, which have a surface area of 4 to 14
m2. However, placental exchange does not take place in all villi, only in those
whose fetal vessels are in intimate contact with the covering syncytial
membrane. In these villi, the syncytium often has a brush border consisting of
numerous microvilli which greatly increases the surface area and consequently
the exchange rate between maternal and fetal circulations.
3. The placental membrane separates maternal and fetal blood,. From the fourth
month on, however, the placental membrane thins, since the endothelial lining
of the vessels comes in intimate contact with the syncytial membrane, greatly
increasing the rate of exchange. The placental membrane is not a true
barrier, since many substances pass through it freely. Because the maternal
blood in the intervillous spaces is separated from the fetal blood by a
chorionic derivative, the human placenta is considered to be of the
hemochorial type.
a
Table: Substances That Cross or Do Not Cross the Placental Membrane
SUBSTANCES THAT CROSS THE PLACENTAL MEMBRANE
Beneficial Substances
Gases: Oxygen, carbon dioxide
Nutrients:Glucose, amino acids, free fatty acids, vitamins
Electrolytes: Water, sodium, potassium, chloride, calcium, phosphate
Fetal waste products: Carbon dioxide, urea, uric acid, bilirubin
Cells : fetal and maternal red blood cells
Proteins:Maternal serum proteins *

Harmful substances
Gases:Carbon monoxide
Viruses: Human immunodeficiency virus (HIV), cytomegalovirus, rubella ,coxsackievirus, variola,
varicella, measles, poliomyelitis.
Immunoglobulins: anti-Rh antibodies
Drugs: Thalidomide, cocaine, alcohol, caffeine, nicotine, warfarin, trinethadione,
Phenytoin, cancer chemo agents, anesthetics, sedatives, analgesics**.
Microorganisms: Treponema pallidum, Toxoplasma gondii

SUBSTANCES THAT DO NOT CROSS THE PLACENTAL MEMBRANE

Nutrients:Maternally derived cholesterol, triglycerides, phospholipids
Hormones:All protein hormones (including insulin)

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Immunoglobulins. IgM
Drugs : Succinylcholine. curare, heparin. drugs similar to amino acids (methyldopa)
Microorganisms : Bacteria
*Cross at a very low rate; most fetal serum proteins are synthesized de novo by thefetus
** in general. most drugs and their metabolites cross the placental membrane.

Placental Hormones
In addition to its role in transporting molecules between mother and fetus, the placenta
is a major endocine organ. It turns out that the placenta synthesizes a huge and diverse
number of hormones that have major influences on ovarian, uterine, mammary and fetal
physiology, not to mention other endocrine systems of the mother.

Steroid Hormones
Progesteron
Estrogens
Protein Hormones
Chorionic gonadotropins: The human hormone is called human chorionic gonadotropin or
simply hCG.
Placental lactogens
Relaxin

Twinning

Definition
Birth of two infants in a single pregnancy iscalled twinning

Types
1. Dizygotic- Twins which are developed from fertilization of two ova by two
sperms These twins may or may not be of same sex
2.Monozygotic-Twins which are developed from a single fertilized ovum.They
result from splitting of the zygote.
3. Conjoined- Twins in which fetuses are not entirely splittedfrom each other.

Differences between Monozygotic and Dizygotic twin

Monozygotic Dizygotic
1. Developed from single fertilized 1. Developed from fertilization of two
ovum (by splitting into division) ova fertilized by two separate
2. Sex is same sperms at the same time
3. There is similarity in physical, 2. Sex may or may not be same
physiological&mental characteristics. 3.Usually, there is not so similarity.
4.There may be separate or common Usually, there is separate placenta,

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placenta, amnion & chorion of the amnion & chorion
embryo (depending upon the time
of split of the zygote)

13. Congenital Malformations

(Syn.congenital anomalies, birth defects)

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Congenital malformations are anatomical abnormalities present at birth (L.
congenital born with). They may be macroscopic or microscopic, on the surface or
within the body. Teratology is the study of abnormal development and the causes
of congenital malformations (Gr. teratos, born with). [Ref. keith L Moore]

Types of congenital anomalies

There are several types of anomalies:
 Malformations
 occur during formation of structures e.g., during organogenesis.
 They may result in complete or partial absence of structure or in alterations
of its normal configuration.
 Malformations are caused by environmental and/or genetic factors acting
independently or in concert.
 Most malformations have their origin during the 3rd to 8th weeks of
gestation.
 Disruptions
 result in morphological alterations of structures after their formation and
 are due to destructive processes. Vascular accidents leading to bowel atresias
and defects produced by amniotic bands are examples of destructive factor
that produce disruptions.
 Deformations
 are due to mechanical force that mold a part of the fetus over a prolonged
period of time. Clubfeet due to compression in the amniotic cavity is an
example.
 Deformations often involve the musculoskeletal system and may be reversible
postnatally.
 Syndrome
 refers to a group of anomalies occurring together that have a specific
common etiology. This term indicate that a diagnosis has been made and that
the risk of recurrence is known.
 In contrast, association refers to the nonrandom appearance of two or more
anomalies that occur together more frequently than by chance alone
but for which the etiology has not been determined.
 Examples include CHARGE (colobomas, heart defects, retarded growth,
genital anomalies, and ear abnormalities) and VACTERL, (vertebral, and
cardiac, tracheoesophageal, renal and limb anomalies)
 Associations are important because although they do not constitute a
diagnosis, recognition of one or more of the component promotes the search
for others in the group. [Ref. Langman]

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Causes of malformations:
The causes fall under two major groups: genetical and environmental.

Genetical factors-
These are discussed in details in the chapter of genetics. A synopsis of the
disorders is mentioned here.

Disorders due to chromosomal abnormalities

1.Affecting autosomes: e.g.
 Patau’s syndrome - Trisomy 13
 Edwards syndrome -Trisomy 18
 Downs syndrome- Trisomy 21,
Translocation D/G; 21/22; 21/21
 Chronic Myeloid leukemia - Philadelphia Chromosome (22q-; 9q+)
2. Affecting sex chromosomes:
 Klinefelter’s syndrome- XXY; XXXY; XXYY: XXXXY
 Turner’s syndrome- 45, XO; XX/XO; XXqi
 Triple X syndrome- XXX

Disorders due to mutation of genes

1. Autosomal dominant traits  Phenylketonuria
 Achondroplasia b. Haemoglobinopathies
 Angioneurotic edema  Sickle-cell anemia
 Familial hypercholesterolemia  Thalassemia
 Huntington’s chorea X-linked recessive traits:
 Marfan’s syndrome  Hemophilia
 Osteogenesis imperfecta  Partial color blindness
2. Autosomal recessive traits  G-6-P dehydrogenase
a. Inborn errors of metabolism e.g. deficiency
 Albinism  Testicular feminization

Environmental Factors
Different environmental agents cause different congenital malformations. Here
are some examples of agents causing malformation.

 Infectious agents -HIV

-Rubella virus -Syphilis
-Cytomegalo virus  Physical agents
-Herpes simplex virus -X-rays
-Varicella virus -Hyperthermia

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 Chemical agents -Isotretinoin (Vii. A)
-Thalidomide -Organic mercury
-phenytoin  Nutritional
-Valproic acid -Maternal iodine deficiency
-Lithium - Hypervitaminosis
-Amphetamines -Seed corn or food grains
-Cocaine sprayed over by mercury
-Alcohol containing fungicide.

Principles of Teratology
Factors determining the capacity of an agent to produce birth defects have been
defined and set forth as the principles of teratology. They include the following:
1. Susceptibility to teratogenesis depends on the genotype of the conceptus and
the manner in which this genetic composition interacts with the environment.
The maternal genome is also important with respect to drug metabolism,
resistance to infection, and other biochemical and molecular processes that
affect the conceptus.
2. Susceptibility to teratogens varies with the developmental stage at the time
of exposure.
 The most sensitive period for inducing birth defects is the third to eighth
weeks of gestation, the period of embryogenesis.
 Each organ system may have one or more stages of susceptibility. For
example cleft palate can be induced at the blastocyst stage (day 6), during
gastrulation (day 14), at the early limb bud stage (fifth week), or when the
palatal shelves are forming (seventh week).
 Furthermore, while most abnormalities are produced during embryogenesis,
defects may also be induced before or after this period; no stage of
development is completely safe.
3. Manifestations of abnormal development depend on dose and duration of
exposure to a teratogen.
4. Teratogens act in specific ways (mechanisms) on developing cells and tissues
to initiate abnormal embryogenesis (pathogenesis).
5. Manifestations of abnormal development are death, malformation, growth
retardation, and functional disorders.[Langman]

14.Cardiovascular System
SAQ of first professional examination
1. Give the fates of the different parts of primitive heart tube.
2. Mention the process of cardiac loop formation.

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3. What are the developmental sources of different parts of right atrium right ventricle/left
ventricle?
4. How interatrial septum is developed?
5. Give the development of interventricular septum. (03M)
6. Describe the fetal circulation. (001, 96S)
7. What are the circulatory changes occur at birth?
8. Give the development & derivatives of aortic arches. (03], 04M)
9. Give the development of superior/Inferior vena cava. (00M)
10. Give the development of aorta/Arch of the aorta.
11. Give the development of coronary sinus.
12. Give the mechanism of closure of foramen ovale.
13. Give the fates of vitelline/umbilical artery.
14. Give the development of pericardium.
15. Right recurrent laryngeal nerve hooks around the right subclavian artery but left recurrent
laryngeal nerve hooks around the ligamentum arteriosum.
16. How circulation is maintained in post ductal aortic coarctation?

Introduction for grasping the chapter (Heart)

Whole of the cardiovascular system develops from the mesoderm. Cells from the
splanchnopleuric mesoderm layer proliferate to form angiogenic cell
cluster.These clusters form a straight primitive heart tube & two dorsal aortae.

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

Figure: showing a fully developed heart tube with two dorsal aortae.

 The heart tube later bends in purpose of giving the tube the shape and forms
of adult heart (Figure 14.3). Now, atria, ventricles etc. can be seen. Septa then
appear in the heart and divide the atria and ventricle into right and left.

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Very few organs or systems of the body develop from single germ layer.
They are
 CVS
 Skeletal system,

Heart

Primitive heart tube

How the heart tube is derived, has been indicated in 'introduction'. Here its
layers, parts & fate will be described.

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Layers of the heart tube

During formation of endocardial heart tube, mesoderm adjacent to it forms
epimyocardial mantle which later differentiates to form myocardium. As a whole
the layers are
 Endocardium
 Myocardium
 Epicardium [Langman]

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Figure: Layers of the heart tube (sagital section above, cross section below)

Beginning of heartbeat
[Blood vessels appear at about the 20th day of intrauterine life. Then heart tube begins
to form. The formation of the tube requires 3 days. Within these 3 days, when
myoepicardium is formed, heart beat begins.

120 days + 3 days = 23 days]

So heart beat begins between 20th to 23rd days of development i.e at the end of 3rd
week or beginning of the 4th. [Langman]

Parts of the heart tube & their fates

The primitive heart tube has the following parts from cranial to caudal direction:
(i) Truncus arteriosus
(ii) Bulbus cordis
(iii) Primitive ventricle
(iv) Primitive atrium
(v) Sinus venosus, [Ref inderbir Singh]

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Fig,: Main subdivision of heart tube and their fate.

SINUS VENOSUS
Parts
In the middle of 4th week (a 4mm. embryo) it consists of
(1) A transverse part &
(2) Two horns- right & left. Each horn receives 3 venous channels.
1. Vitelline vein
2. Umbilical vein
3. Common cardinal vein

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Figure: Fate of sinus venous

Fate
1.Left horn -
o Proximal part -Contributes to coronary sinus.
o Distal part - Forms oblique vein of Marshall.
2. Body and right horn (See fig 14 .6) - Incorporate into the right atrium to
form
o Posterior smooth part of it. [During its incorporation, right & left venous
valves are flanked. These valves cranially fuse to form septum spurium. This
septum spurium&lower halt of the left valve fuse with the developing atrial

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septum. The lower right valve gives rise to valve of interior vena cave and
valve of coronary sinus.]
o The Crista terminalis. (Langman)

ATRIUM
After absorption of the sinus venosus, the atrial chamber is partitioned to form
the right and left atria

ATRIOVENTRICULAR CANAL
It is a narrow canal in the primitive heart tube separating the primitive atrium &
ventricle. Later, it is divided by septum intermedium to contribute in both atria.
[I. Singh]

VENTRICLE
The bulbus cordis proper (conus) is absorbed into the ventricular chamber the
chamber thus formed is partitioned to give rise to the right and left ventricle.

TRUNCUS ARTERIOSUS
This is partitioned to form the ascending aorta and pulmonary trunk. We have
seen that the endothelial heart tube is derived from the splanchnopleuric
mesoderm related to the pericardial cavity. After formation of the head fold
this tube lies dorsal to the pericardial cavity. [Re. Inderbir, 5th Ed. Page-231]

Table: Fate of (or structures derived from) Primitive heart tube

Parts Adult structure

1. Truncus arteriosus (i) Aorta
(ii) Pulmonary Trunk
2. Bulbus cordis (i) Smooth part of right ventricle (Conus
arteriousus}
(ii) Smooth part of left ventricle (aortic vestibule)
3. Primitive ventricle (i) Trabeculated part of right ventricle
(ii) Trabeculated part of left ventricle
4. Primitive atrium (i) Trabeculated part of Right atrium
(ii) Trabeculated part of left atrium
5. Sinus venosus
 Right horn (i) Smooth part of right atrium ( Sinus Venarum)
 Left horn (i) Coronary Sinus
(ii) Oblique Vein of left atrium

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Development of the heart
Different parts of the adult heart are derived from the parts of the primitive
heart tube as follows -
1. Right atrium –

It develops from
i. Rt. half of Primitive atrium - It forms the trabeculated part and rt. auricle
ii. Sinus venous
o Right horn forms
 Smooth part of right atrium
 crista terminalis [Lang]
o Right venous valve forms
a. Valve of C Sinus
b. Valve of I v Cava

Figure: Coronal sections through the heart to show the development of the smooth-walled
portions of the right and left atrium
2. Left atrium- It develops from --
(i) Lt. half of Primary atrium - Forms ant. rough part &
left auricle.
(ii) Absorbed proximal parts Or Pulmonary veins - Form
posterior smooth part.
(iji) Lateral half of AV canal –Forms most ventral
part.
3. Right ventricle-- It develops from
(i) Rt. half of primitive ventricle- forms inflowing part
(ii) Proximal part of Bulbus cords -- Form outflowing part.

4. Left ventricle-It derives from -

(1) Lt half of Primitive ventricle - Forms inflowing part

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(ii) Proximal part of Bulb I us cords – Form outflowing part.
5. Others-
(a) Cardiac muscle - From myoepicardial mantle
(b) Endothelium - From endothelium of primitive tube.
(c) Pericardium
 Fibrous pericardium - From septum transversum
 Serous pericardium - From myoepicardial mantle (visceral layer)
- From somatopleuric mesoderm (parietal layer)
(d) Pericardial cavity - From cranial part of intra embryonic celom.
(e) Conducting system (Datta)
 SA node - Sinus venosus.
 AV node -- Sinus venosus & cells from AV canal
 Other conducting parts -Myoepicardial mantle
(f) AV valves -- From subendocardial proliferation.
 Cusps - From the proliferation of AV canal.
 Chorda tendinae- From the atrial extremities of the
subendocardial proliferation.
 Papillary muscle - From the ventricular extremities of that
proliferation.
(g) Semilunar valve --It is formed by the hollowing out of truncus swelling
[Ref. Langman and Datta]

Figure: Formation of AV valve

Septum formation - Internal subdivision of the heart

Process of Septum Formation
There are two processof septum formation. They are-
1 Approaching of actively growing masses towards each other until they fuse.
Some time, only one mass approaches

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2 Fusion of two expanding portions from the wall of the heart
[Ref. Langman]

FORMATION OF INTER ATRIAL SEPTUM

Figure: Formation of interatrial septum. The arrows in 'D' indicate the path of
blood through the foramen ovale.

There are three sources -- Septum primum, septum intermedium & septum
secundum. They contribute in forming the septa as follows –
1. Septum primum - It is a told of endocardium grows downwards from the
roof and dorsal wall of the primitive atrium towards the septum intermedium
of AV canal. The gap between the two septa is called ostiurn primum
(Foramen primum) Septum primum fuses with septum intermedium. Thus
ostium primum is closed. Then septum primum breaks down to give rise
ostiurnsecundum (Foramen secundum)
2. Septum intermedium- It developed by the fusion of ventral and dorsal
endocardial cushions of AV canal. It takes part in formation of the septum in
the manner mentioned above (point 1)
3. Septum secundum – It arises from the ventral wall of the right atrium just
right to the septum primurn. The ostiurn secundum is now called foramen)
ovale. Foramen ovale is closed and the atria are separated. Thus the
interatrial septum is formed (Ref. Langman 6th.)

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Q:How foramen ovale is closed?
Ans.: After birth [When lung circulation begins) pressure in the left atrial wall
increases and the upper end the septum primum is pressed against the septum
secundum. Thus foramen ovale is closed [Ref. Langman]

Explanatory SAQ: Foramen ovale starts to close after birth. Why? (J-05 new
curriculum)
Ans.: because –
1. Before birth right atria pressure is higher than left atrium and this drive blood
form right atrium to left atrium through foramen ovale by pushing the flap like
septum primum.
2. After birth, pressure rises in pulmonary vessel and pulmonary circulation starts.
3. This causes rising left atrial pressure after 1st. breathing.
4. Raise of left atrial pressure press the septum primum against septum secundum and
closes the foramen ovale.
If foramen ovale closes before birth right atrium and right ventricle become
hypertrophied.
5. So, due to physiological cause foramen ovale starts to close after birth).

Explanatory SAQ: Right side of heart is hypertrophied due to premature closure of

foramen oval. Why? (J-05, new curriculum)
Answer:
 Before birth foramen ovale act as a physiological shunt that flows blood form right
atrium to left atrium.
 The fetal right atrium contain a large volume of blood form following sources:
a) Superior vena cava.
b) Inferior vena cava- Which receives blood form-
- Lower limb and
- Placenta (through umbilical vein)
 Due to high pulmonary vascular pressure, blood can not enter into lungs (as
respiration does not start).
 If closure of foramen ovale occurs before birth, high volume of blood in right atrium
propel against high pressure.
 So blood flows form right atrium to right ventricle.
 Right ventricle then have to drive blood against high pressure in pulmonary artery.
 As a result right atrium and right ventricle have to work against pressure leading, to
increase thickness of right side of heart.
So, right side of the heart becomes hypertrophied due to premature closure of
foramen ovale.

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FORMATION OF INTERVENTICULAR SEPTUM

Figure: Two stages in the formation of the ventricular septum B and D

correspond to 'A' and `C` respectively.

1. A septum called the interventricular septum (or septuminferius.) - grows

upwards from the floor of the bulboventricular cavity and, divides the lower
dilated part of this cavity into right and left halves (Fig 14.8A) It meets the

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fused atrioventicular cushions (septum intermedium) and partially fuses with
them (Fig, i4,8C).
2. Two ridges - right arid left bulbar ridges - arise in the wall of the conical
upper part of the bulbo-ventricular cavity. They are continuous with the right
and left endocardial cushions that help to separate the aortic and pulmonary
openings. These ridges grow towards each other and fuse to form a bulbar
septum [Fig14. 8 A B] The bulbar septum grows downwards towards the
interventricular septum but does not quite reach it so that a gap is left
between two.
3. The gap between the upper edge of the interventricular septum, and the
lower edge of the bulbar septum is tilled by proliferation of tissue from the
atrioventicular cushions

Summary
1. Muscular part From septum inferius (muscular wall of the common ventricle)
2. Membranous part From
(a) Bulbar septum
(b) Proliferation of AV cushion
[Bulbar septum HI & Lt bulbar ridges appear in the upper part of bulboventricular cavity.
These ridges grow towards, each other & fuse to form bulbar septum]

Table: Timetable of heart development

Weeks Days Cardiac Events

1-2 0-20 No heart or great vessels
3 20 Cardiogenic plate
3 21 Endocardial tubes
4 22 Fusion of endocardial tubes
4 23 Single median cardiac tube, first contraction ( ineffective)
4 25 Cardiogenic loop
4 26 Single atrium
5 29 Bilobed atrium
5 30 Beginning of circulation
7 49 4-chambered heart, Absorption of pulmonary veins
Table courtesy of Dr. Ra-id Abdulla, Rush Chicago

Anomalies in Development of Heart & Septum

1. Anomalies in Position
a. Dextrocardia - Heart lies in the rt. side of the thorax
b. Ectopia cordis - Heart protrudes through a defect in ventral body wall

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Figure: Dextrocardia

Figure: Ectopia cordis

c. Situs inversus viscerum. - This is associated with general transposition of

the.- viscera due to reverse rotation, including rotation of the heart to the
rt.

Figure: Situs inversus viscerum

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2. Anomalies in Septa Formation

Interatrial septal defect
a. Patent foramen ovale
b. Persistence of foramen primum &secundum
c. Common atrium - Complete absence of atrial septa

Figure: Normal interatrial septum

Figure: Patent Foramen Ovale (arrow)

Interventricular septum
a. Prenatal closure of foramen ovale.
b. Persistent inter ventricular foramen
c. Cor triculare- Absence of interventricular Septum

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Figure: Absence of interatrial Septum

Figure: Absence of Interventricular septum

3. Common AV canal.

Figure: Persistent of Atrioventricular Canal

4. Defect in bulbus cordis & truncus arteriosus

(a) Fallot's Tetralogy-Compound anomalies of heart & great vessels. It is the
total combination of the following defects –
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Figure: Fallot’s tetralogy

i. Pulmonary stenosis
ii. Ventricular septal defect
iii. Overriding of aorta.
iv. Hypertrophy of the right ventricle (Ref. I Singh)
The basis, cause of defect is an unequal division of the conus due to an anterior
displacement of the trunco-conal cushion.
5. Failure of separation of aortic & pulmonary trunks

Explanatory SAQ: Why congenital heart disease is accompanied by neural

crest defect.

Answer:
 Neural crest is group of cell that arise form neuroectoderm.
 They contribute to the formation of conoturncal septum of heart & head and
neck.
 Because of their abnormalities in these cells produce both heart &
craniofacial defect by teratogenic agent or genetic cause.
 Common congenital heart diseases due to neural crest defect are artial&
ventricular septal defect, transposition of great vessel, tetralogy of fallot.

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Development of arteries

Introduction
When branchial arches are formed (see chapter 16), aortic arches are also
formed.
 These (aortic) arches arise from the primitive dorsal aortae. They give rise
to main arteries of thorax.
 Vitelline artery, which in embryo supplies yolk sac. gives to arteries of gut.
 Umbilical arteries, receiving blood from the placenta in embryonic life,
later give rise to internal iliac & sup. Vesical artery

Figure: Primitive vascular systems