Development of the Heart.pdf

PAEDIATRICS AND CHILD HEALTH
• NEONATOLOGY
• DEVELOPMENT OF THE HEART
Dr. Chongo Shapi (BSc.HB, MBChB, CUZ)
- Medical Doctor.
-
3/20/2022
Dr. Chongo Shapi, BSc.HB, MBChB, CUZ.
.
1

Development of the Heart
• The heart is initially a tube
• The heart tube has 4 parts arranged as follows from cranial to
caudal end:
1. Truncus arteriosus
2. Bulbus cordis (conus arteriosus, conus cordis)
3. Primitive ventricle
4. Primitive atrium
• The tube continues to elongate and bend on day 23
• The cephalic portion of the tube bends ventrally, caudally, and
to the right, and the atrial (caudal) portion shifts
dorsocranially and to the left
• Hence, normal cardiac looping is to the LEFT
• Cardiac looping to the RIGHT gives DEXTROCARDIA
• The cardiac looping is complete by day 28
3/20/2022 Dr. Chongo Shapi, BSc.HB, MBChB, CUZ. 2

• Truncus arteriosus = Roots + Proximal portion of
the Great Vessels (Aorta and Pulmonary arteries)
• Bulbus cordis + primitive ventricle = Common
Ventricle
• Primitive atrium = Common Atrium
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Formation of Cardiac Septa
Formation of septa by growth of opposite ridges and by
a single actively growing cell mass

Septum formation by merging of two expanding portions of the wall
of the heart.
Such a septum never completely separates two cavities

Partitioning of the Heart into 4 Chambers
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Endocardial cushions
• The masses, known as endocardial cushions,
develop in the atrioventricular and conotruncal
regions
• In these locations they assist in formation of:
a. Atrial and ventricular (membranous portion)
septa
b. Atrioventricular canals and valves, and
c. Aortic and pulmonary channels

• Because of their key location, abnormalities in
endocardial cushion formation contribute to many
cardiac malformations:
a. ASDs
b. VSDs
c. AVSDs
d. Defects involving the great vessels (i.e.,
transposition of the great vessels and tetralogy
of Fallot)
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• Cells populating the conotruncal cushions include
neural crest cells
• The crest cells also contribute extensively to
development of the head and neck
• Thus, abnormalities in the neural crest cells,
produced by teratogenic agents or genetic causes,
often produce both heart and craniofacial
defects in the same individual
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Septum Formation in Common Atrium
• The atrial septum begins as an ingrowth of the
septum primum from the dorsal wall of the common
atrial chamber toward the developing endocardial
cushion
• A gap, termed the ostium primum, initially separates
the two
• Continued growth and fusion of the septum with the
endocardial cushion ultimately obliterates the ostium
primum
• However, a second opening, ostium secundum, now
appears in the central area of the primary septum
(allowing continued flow of oxygenated blood from
the right to left atria, essential for fetal life)

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• As the ostium secundum enlarges, the septum
secundum makes its appearance adjacent to the
septum primum
• This septum secundum proliferates to form a
crescent-shaped structure overlapping a space
termed the foramen ovale
• The foramen ovale is closed on its left side by a
flap of tissue derived from the primary septum
• This flap acts as a one-way valve that allows
right-to-left blood flow during intrauterine life

• At the time of birth, falling pulmonary vascular
resistance and rising systemic arterial pressure
causes left atrial pressures to exceed those in the
right atrium; the result is a functional closure of
the foramen ovale
• In most individuals the foramen ovale is
permanently sealed by fusion of the primary and
secondary septa, although a minor degree of
patency persists in about 25% of the general
population
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Abnormalities in Septation of the Common Atrium
• Abnormalities in this sequence result in the development
of the various ASDs
• There are 3 types:
1. Ostium secundum ASD (90%): occurs when the septum
secundum does not enlarge sufficiently to cover the
ostium secundum
2. Ostium primum ASDs (5%): less common and these occur
if the septum primum and endocardial cushion fail to
fuse and are often associated with abnormalities in other
structures derived from the endocardial cushion (e.g.,
mitral and tricuspid valves)
3. Sinus venosus ASDs (5%): are located near the entrance
of the superior vena cava (SVC)
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Embryonic Origin of Other CHDs
• VSDs: defects in the membranous part of the
interventricular septum. Usually associated with
conotruncal abnormalities
• TOF: abnormalities of the conotruncal region
• Persistent truncus arteriosus:
- Failure of fusion of the conotruncal ridges and
failure to descend towards the ventricles
- Since the ridges also participate in formation of the
interventricular septum, truncus arteriosus is
ALWAYS accompanied by a VSD
- The undivided truncus overrides both ventricles and
receives blood from both sides

• Transposition of the Great Vessels:
- Failure of conotruncal septum to follow its normal spiral
course and runs straight down
- Hence, aorta is from the RV and pulmonary artery is from
the LV
- Usually accompanied by a PDA (L to R shunt, as blood
moves from thoracic aorta to pulmonary trunk)
- Is also sometimes associated with a VSD
• Tricuspid atresia: fusion of the tricuspid valves. Is always
associated with:
- Patency of the foramen ovale
- VSD
- RV under-development (hypoplasia)
- LV hypertrophy
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ASD, VSD, and PDA
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Coarctation of the Aorta (CoA)
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Persistent Truncus Arteriosus

THE END!
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Development of the Heart.pdf

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