2. In the 4th week of intrauterine life while the
primitive atrium is being divided into right
and left atria, a muscular septum projects
upwards from the midline of the floor of the
primitive ventricle.
This septum is called the ventricular or
interventricular septum
3. It is crescent shaped and extends upwards
towards the fused atrioventricular cushions
(septum intermedium).
The opening between the free edge of the
interventricular septum and the septum
intermedium is called the interventricular
foramen
4. The left and right ventricles communicate
with each other and with the cavity of the
bulbus cordis until about the end of the 7th
week of intrauterine life when the
interventricular foramen closes.
The interventricular septum divides the
primitive ventricle into left and right
ventricles
5.
6.
7.
8. Bulbus cordis
The bulbus cordis consists of three portions:
a proximal third, a middle third called the
conus cordis, and a distal third called the
truncus arteriosus.
In the 5th week of IUL a pair of endocardial
swellings appear in the distal end of the
truncus arteriosus. These swellings are called
the truncal ridges.
9. The left and right truncal ridges grow
towards each other in a spiral manner.
In the 8th week they fuse to form a
spiral or aorticopulmonary septum
which divides the truncus arteriosus
into ascending aorta and pulmonary
trunk.
12. Similar endocardial swellings appear in the
conus cordis and are called the conal or
bulbar ridges.
They grow towards each other and fuse to
form the bulbar septum.
The truncal and bulbar ridges are derived
mainly from neural crest mesenchyme
The conus cordis becomes incorporated into
the wall of the ventricle
13. The bulbar septum divides the conus cordis
into:
1. Anterolateral portion called the conus
arteriosus or infundibulum. This is the
outflow tract of the right ventricle
2. Posterolateral portion called the aortic
vestibule. This is the outflow tract of the
left ventricle.
14. The proximal third of the bulbus cordis
takes part in the formation of the
trabeculated portion of the right
ventricle
15. The bulbar septum grows downwards
towards the interventricular septum. The gap
between the interventricular septum and the
bulbar septum is the interventricular foramen.
The foramen is closed by the membranous
interventricular septum which is formed by
the proliferation and fusion of tissue from the
fused atrioventricular endocardial cushions
and the left and right bulbar ridges
16. The closure of the interventricular
foramen not only separates the right
and left ventricles but also ensures that
the RV communicates with the
pulmonary trunk and the LV with the
aorta
17. Cavities appear in the wall of the
ventricles and separate the muscles into
bundles.
Some of the bundles become trabeculae
carneae while others are transformed
into papillary muscles and chordae
tendinae.
18.
19. Pulmonary and aortic valves
The pulmonary and aortic valves are
derived from the endocardial swellings
or cushions that are formed in the wall
of the conus cordis close to its junction
with the truncus arteriosus .
Right and left endocardial swellings
appear in the wall of the conus cordis.
20. Soon after, two more swellings, anterior
and posterior endocardial swellings, also
appear in the wall of the cordis cordis.
The left and right endocardial swellings
approach each other, fuse and become
subdivided into two parts.
As a result of this subdivision aortic and
pulmonary openings have three swellings
each
21. These swellings become hollowed out
(excavated) on the distal surface to
form 3 semilunar valves.
The pulmonary valve is at first ventral
to the aortic valve.
Later as a result of rotation it lies
ventrolateral and to the left of the
aortic valve.
22. The aorta has one anterior and two
posterior aortic sinuses while the
pulmonary trunk has two anterior and one
posterior sinuses.
The right coronary artery arises from the
anterior aortic sinus while the left coronary
artery arises from the left posterior aortic
sinus
25. Atrioventricular valves
Endocardial swellings also appear at the
margins of the atrioventricular orifices.
They are invaded by mesenchymal tissue
and later become hollowed out on the
ventricular side.
Three cusps appear in the right
atrioventricular orifice while two appear in
the left atrioventricular orifice
26. The valve of the right atrioventricular orifice is
called tricuspid valve because it has three
cusps while that of the left has two cusps and
is called bicuspid valve. The latter is also called
the mitral valve because it looks like the a
bishop’s mitre.
The cusps enlarge and are attached to the
ventricular wall by muscle strands that will form
the papillary muscles and the chordae tendinae
27. During the IUL the thickness of the LV
is about the same as that of the RV.
By the 6th month of postnatal life it is
about three times the thickness of the
RV.
28. Formation of the conducting system of the heart
Initially a peacemaker lies in the caudal
part of the left heart tube.
In the 5th week of intrauterine life, it lies
in the right wall of the sinus venosus and
is called the sinuatrial node
When the sinus venosus is incorporated
into the atrium the sinuatrial node lies
near the opening of the superior vena
cava
29. The atrioventricular node and the
bundle of His are formed in the left wall
of the sinus venous and the
atrioventricular canal
When the sinus venosus is incorporated
into the right atrium, the
atrioventricular node lies near the
interatrial septum
30. CONGENITAL ANOMALIES
The aetiology or cause of congenital anomalies
is unknown in most of the cases.
Most of the anomalies are caused by multiple
factors
Some anomalies are simple and do not require
treatment while others are complex and may
require surgeries.
Some anomalies do not cause a significant
31. Common causes of heart anomalies
include:
A. Genetic factors e.g. Turner’s syndrome,
Down syndrome
B. Infections e.g. viral infections: TORCH
C. Drugs e.g. Ethanol, thalidomide etc.
32. 1. Acardia. This is congenital absence of
the heart. It may be seen in conjoint twins.
2. Anomalies of position
a) Ectopia cordis. The heart is exposed
partially or completely on the chest wall due
to defective development of the sternum
and the pericardium. The sternal halves are
widely separated from each other
33. b) Dextrocardia. The apex of the heart is
located on the right side of the chest instead
of the left. It is as a result of reversal of the
endocardial heart loop.
It may occur alone or may be associated with
other anomalies such as situs inversus in
which there is transposition of some or all of
the thoraco-abdominal viscera: the structures
that normally lie on the left side are on the
right side and vice versa.
34. 3. Anomalies of atrial septum:
Atrial septal defect. There are various
forms of atrial septal defect
a) Probe patency of foramen ovale.
At birth the foramen ovale usually
closes functionaly and later physically.
In 20-25% of adults the foramen does
not close physically after birth.
35. A narrow oblique cleft is left between
the right and left atria. A probe can be
passed from the right atrium to the left
atrium. This anomaly is usually
asymptomatic.
36.
37. b) Ostium primum defect: the
septum primum fails to fuse with the
atrioventricular endocardial cushions
and the ostium primum persists. The
defect is located in the most inferior
aspect of the atrial septum: at the level
of the tricuspid and mitral vlaves
38.
39. c) ostium or foramen secundum defect: It
is the most common type of atrial septal defect.
It is as result of by either excessive resorption
of septum primum, poor development of
septum secundum or enlarged foramen ovale
The opening between the LA and the RA is
large. Depending on the size of the opening,
oxygenated blood from the LA passes to the
RA. This leads to right sided heart failure as a
result of overloading of the right side of the
40. d) Common atrium: It is a rare form
of atrial septal defect. There is
complete absence of the atrial septum
as a result of non-development of the
septum primum and septum secundum.
It is a very serious condition and is
usually associated with other defects.
41. e) Premature closure of foramen
ovale. Closure of the foramen ovale
before birth results in hypertrophy of
the right side of the heart (RA and RV)
and atrophy of the LA and LV.
Death occurs within the uterus
42. 4. Anomalies of the atrioventricular
canal. Non fusion of the atrioventricular
endocardial cushions results in:
a) Persistent atrioventricular canal: there
is a single atrioventricular orifice
b) Atrial septal defect
c) Ventricular septal defect
43. 5. Ventricular septal defects.
Ventricular septal defects (VSD) are more
common in females than males.
In VSD, the defect may be in the membranous
or muscular part of the ventricular septum.
In membranous VSD the opening is in the
superior part of the ventricular septum, near the
aortic and tricuspid valves. It is more common
than the muscular VSD
44. The size of the defect varies. Blood
passes from the LV to the RV and leads
to enlargement of the RV.
Complete absence of the ventricular
septum gives rise to a three-chambered
heart called cor triloculare biatriatum
45. Anomalies of bulbus cordis
a) Tetralogy of Fallot. It is due to unequal
division of the conus cordis by the bulbar
septum. It is usually characterized by 4 defects
i) Stenosis of the pulmonary trunk: narrowing
of RV outflow tract)
ii) Large VSD
iii) Hypertrophy of the RV
iv) iii) Overriding aorta: the aorta overrides the
free edge of the ventricular septum and
48. b) Persistent or patent truncus
arteriosus. The aorticopulmonary
septum fails to develop and divide the
truncus arteriosus into aorta and
pulmonary trunk. There is only one
arterial trunk.
The pulmonary trunk originates from this
single trunk some distance above its origin
49. Persistent truncus arteriosus is always
accompanied by VSD.
In aorticopulmonary septal defect there is
an oval or round window between the
aorta and the pulmonary trunk. This
window is called the aortic window. Blood
from the aorta flows into the pulmonary
artery, and as a result too much blood
flows to the lungs and causes pulmonary
51. c) Transposition of the great arteries:
This is due to maldescent of aorticopulmonary
septum; the septum descends straight
downwards instead of in a spiral manner.
The aorta is anterior to the pulmonary artery
and originates from the RV while the
pulmonary trunk originates from the LV.
Transposition of the great arteries may be
associated with a defect in the membranous
part of the ventricular septum, etc.
54. 7. Defects of the aortic valve
a) Aortic atresia. There is complete
obstruction of the aorta or its valve
b) Aortic valvular stenosis. The
aortic valves are thickened and
deformed. The edges of the valves fuse
to form a dome with a narrow opening.
55. c) Subvalvular aortic stenosis
It is usually caused by a ring or band
of fibrous tissue just below the aortic
valve. It encircles the outflow tract of
the LV.
There is narrowing of the left ventricle
below the level of the aortic valve
56.
57. 8. Defects of pulmonary valve
a) Pulmonary atresia. The pulmonary
valve is not properly formed. The cusps
of the pulmonary valve are fused to form
a solid sheet of tissue. The pulmonary
artery does not have a lumen.
It may be due to unequal division of the
truncus arteriosus
58. b) Pulmonary valve stenosis. The cusps
of the pulmonary valve are fused together
to form a dome with a central perforation. If
the fusion is complete the pulmonary trunk
becomes atretic. The foramen ovale
becomes the only outlet of blood from the
RV
59. c) Infundibular pulmonary stenosis.
This occurs when the conus cordis is
underdeveloped. There is obstruction of the
outflow tract of the RV
60. 9. Defects of atrioventricular valves.
a) Tricuspid atresia. The right atrioventricular
valve is absent or poorly developed.
Tricuspid stenosis: there is narrowing of the
tricuspid valve opening.
b) Mitral atresia: The left atrioventricular valve
is absent or poorly developed.
Mitral stenosis: there is narrowing of the mitral
valve opening.
