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4.

Primitive atrium
EMBRYOLOGY 5. Sinus venosus
CARDIOVASCULAR SYSTEM

OUTLINE
I. Introduction
II. Development of the Primitive Heart tube
III. Development of Heart Septae
IV. Development of Atrial System
V. Development of Venous System

INTRODUCTION
 The entire CVS originates from the mesodermal
 germ layer
 3 germ layer: Endoderm, Mesoderm, Ectoderm
 Although initially paired, by the 22nd day of
development the two tubes form a single,
slightly bent heart tube consisting of an inner
endocardial tube and a surrounding myocardial
mantle
 The heart tube continues to elongate and bend
on 23rd day of development
 The cephalic portion of the tube bends
DEVELOPMENT OF HEART SEPTAE
ventrally, caudally and to the right (becomes
most part of the ventricle), and the atrial (caudal)  The primitive tube is a tube with a single lumen
portion shifts dorsocranially and the left (forms  This single lumen is partitioned into 4 definitive
most of the atrium) chambers by the formation of 4 septae:
 This bending, which may be due to cell shape  Aorticopulmonary (AP) (divides aorta and
changes, creates the cardiac loop (this pulmonary trunk)
distinguishes that why we have a ventricle,  Atrioventricular (AV) (divides atrium and
which has connections to aorta and pulmonary ventricle)
trunk while the atrium is connected to vena  Atrial (divides left and right atrium)
cavas)  Interventricular (IV) (divided left and right
 It is completed by the 28th day of development ventricle)
 The following markers and molecular signals  Many congenital heart defects can be traced
are involved in the formation of the heart: back to the abnormal formation of these septae
 NKS2.5 (transcription factor)
 BMPs 2 & 4 (bone morphogenic proteins) 1. Aorticopulmonary (AP) Septum
 Inhibitors of WNT genes  The AP septum divides the truncus arteriosus
 TBX5 (transcription factor) → contains into the aorta and pulmonary trunk
DNA-binding motif T-box which plays a role in  FORMATION: Neural crest cells migrate into the
septation truncal and bulbar ridges, which grow in a spiral
 fashion and fuse to form the AP septum
DEVELOPMENT OF PRIMITIVE HEART TUBE
 A pair of endocardial heart tubes (mesoderm in
origin) form within the cardiogenic region
 As lateral folding occurs, the endocardial heart
tubes fuse to form the primitive heart tube, which
develops into the endocardium
 Mesoderm surrounding the primitive heart tube
develops in to the myocardium and epicardium

The primitive heart tube forms 5 dilatations:


1. Partitioning of the truncus arteriosus and bulbus cordis,
(cranially to caudally)
involving neural crest cells migration
1. Truncus arteriosus
2. The AP septum develops in a spiral fashion
2. Bulbus cordis
3. Primitive ventricle
3. The spiral AP septum accounts for the adult gross - caused by abnormal neural crest cell
anatomic relationship between the aorta and pulmonary migration such that there is skewed
trunk (that’s why in adult it is in adult position) development of the AP septum
- This results in a condition classically
 CLINICAL CORRELATION: (problems in characterized by:
spiraling) 1. Pulmonary stenosis (small opening of
I. Persistent Truncus Arteriosus pulmonary trunk)
- caused by abnormal neural crest cells migration 2. Overriding of the aorta
such that there is only partial development of 3. IV septal defect
the AP septum 4. Right ventricular hypertrophy increase
- This results in a condition in which only one large pressure leads to histological
vessel leaves the heart, and it receives blood from changes increasing the size of the
both the right and left ventricles (no partition muscle. More pressure more force.
between the aorta and pulmonary trunk) More force cause hypertrophy.
- The resultant right-to-left shunting of blood leads to - The resultant right-to-left shunting of blood
cyanosis (Blood in the right ventricle contains leads to cyanosis
deoxygenated blood. So if there’s right to left
shunting, it will cause cyanosis)

II. D-Transposition of the Great Vessels (Complete)


2. Atrioventricular (AV) Septum
- caused by abnormal neural crest migration
 The AV septum divides the AV canal into the
such that there is nonspiral development of the AP
right AV canal and left AV canal
septum
 FORMATION: The dorsal and ventral AV
- This results in a condition in which the aorta
cushions fuse to form the AV septum
arises abnormally from the right ventricle
- The resultant right-to-left shunting of blood
leads to cyanosis
Aorta supplies blood to all body parts, it
receives deoxygenated blood which can cause
cyanosis

 CLINICAL CORRELATIONS:
I. Univentricular heart
- caused by an extremely skewed development
of the AV septum to the right
- This results in a condition in which one
ventricle receives both the tricuspid and mitral valve
III. Tetralogy of Fallot (mixing of blood)
II. Tricuspid Atresia
- caused by insufficient amount of AV cushion
tissue available for the formation of the
tricuspid valve
- This results in a condition in which there is
complete agenesis of the tricuspid valve so that
no communication exists between the right
atrium and right ventricle
- Characterized by:
1. Patent foramen ovale
2. IV septal defects
3. Overdeveloped left ventricle
4. Underdeveloped right ventricle
Infants with tricuspid atresia usually die in utero or when
delivered, they die immediately because there’s no - The foramen ovale is the opening between the
passageway of blood. upper and lower parts of the septum secundum
- During fetal life, blood is shunted from the right
atrium to the left atrium via the foramen ovale
- Closure of the foramen ovale normally occur
soon after birth and is facilitated by the increased
left atrial pressure that results from changes in
pulmonary circulation
 CLINICAL CORRELATIONS
- Heart defects involving the atrial septum are called
atrial septal defects (ASDs)
I. Foramen secundum defect
- caused by excessive resorption of the septum
primum, septum secundum or both
- This results in an opening between the right
3. Atrial Septum
and left atria (patent foramen ovale)
 The atrial septum divides the primitive atrium into
- If the ASD is small, clinical symptoms may be
the right and left atria
delayed as late as age 30
 FORMATION:
The heart have different pressures for the
- The septum primum grows toward the AV septum
blood to flow from the heart to the body and from the
- The foramen primum is located between the
body to the heart. Between the left atrium and the
edge of septum primum and AV septum; it is
right atrium the pressure is more on the left atrium.
obliterated when the septum primum fuses with the
That’s why even there’s a small whole there, the
AV septum
blood flow will be from the left to the right.
- The foramen secundum forms in the center of the
No shunting of deoxygenated blood throughout
septum primum
the body. Left-to-right shunting.
- The septum secundum forms to the right of the
- This is the most common clinically significant
septum primum and fuses (after birth) with septum
ASD
primum to form the atrial septum
Overlapping of the septum primum and septum
secundum will block the foramen secundum
 CLINICAL CORRELATION
I. Membranous ventricular septal defect (VSD)
- caused by incomplete fusion of the right bulbar
ridge, left bulbar ridge and AV cushions
- This results in a condition in which an opening
between the right and left ventricles allows
left-to-right shunting of blood through the IV
foramen
- Patients with left-to-right shunting complain of
excessive fatigue upon exertion
- Initially, a membranous VSD is associated with the
II. Premature closure of foramen ovale
left-to-right shunting of blood, increased pulmonary
- Closure of the foramen ovale during prenatal
blood flow and pulmonary hypertension
life
- Later, the pulmonary hypertension causes marked
- This results in hypertrophy of the right side
proliferation of the tunica intima and tunica media of
of the heart and underdevelopment of the left side
pulmonary muscular arteries and arterioles, thus
Atrial Septal Defect
narrowing the lumen
- Blood flows from the left atrium to the right
- Ultimately, pulmonary resistance becomes higher
atrium usually no sypmtoms
than systemic resistance and causes right-to-left
- This can increase blood flow to the right
shunting of blood and cyanosis
ventricle → histologic and anatomic changes
- At this stage, the condition is called the
Eisenmenger complex
4. Interventricular (IV) Septum
 The IV septum divides the primitive ventricle into the
right and left ventricles
 FORMATION:
- The muscular IV septum develops in the floor of
the ventricle; it grows towards the AV cushions
(important in the formation of the Atrioventricular
Septum) but stops short leaving the IV foramen
- The membranous IV septum forms by the fusion of
3 components:
1. Right bulbar ridge
2. Left bulbar ridge
3. AV cushions
- This fusion closes the IV foramen

At first only compalain for easy fatigability, weakness


upon exertion but later on because of
eisenmengerization blod now flows from the right to left 3. High risk of both cerebral hemorrhage
and causes cyanosis and bacterial endocarditis
- Collateral circulation around the constriction
DEVELOPMENT OF THE ARTERIAL SYSTEM involves the:
1. Internal thoracic artery
 FORMATION 2. Intercostal artery
- The atrial system develops from the aortic arches 3. Superior epigastric artery
(contributes to arteries in the head and neck region) 4. Inferior epigastric artery
and the dorsal aorta (contributes to the arteries in 5. External Iliac artery
the rest of the body) - Dilatation of the intercostal arteries causes
- The dorsal aorta sprouts posterolateral , lateral erosion of the lower border of the ribs (rib
and ventral branches (vitelline and umbilical notching), which can be seen on a radiograph
arteries) + rib notching if diagnosed with Coarctation of the
Aorta

II. Patent ductus arteriosus (PDA)


- Occurs when the ductus arteriosus, a connection
between the left pulmonary artery and the arch of
the aorta, fails to close
- Normally, the ductus arteriosus closes within a few
hours after birth via smooth muscle contraction to
form the ligamentum arteriosum
- PDA causes a left-to-right shunting of blood from
the aorta back into the pulmonary circulation
Development of the Atrial System - PDA is very common in premature infants and in
Embryonic Adult Structures infants born to mothers who contracted the rubella
Structures virus during the course of their pregnancy
Aortic Arches
1 *
2 * - Prostaglandin E, intrauterine asphyxia, and
3 Common carotid arteries neonatal asphyxia sustain the patency of the ductus
Internal carotid arteries (proximal part) arteriosus
4 Right Subclavian Artery (prosimal part)
Part of the aortic arch
- Prostaglandin inhibitors (ie indomethacin),
5 Regression in the human acetycholine, histamine and catecholamines
6 Pulmonary arteries (proximal part) promoted closure of the ductus arteriosus
Dustus arteriosus
Dorsal Aorta
Posterolateral Arteries to upper and lower extremity
branches Intercostal, lumbar and lateral sacral arteries
Renal, Suprarenal, and gonadal arteries
Lateral branches
Ventral branches Celiac, superios mesenteric and inferior
Vitelline arteries mesenteric
Umbilical arteries Part of internal iliac arteries, superior vesical
arteries
Medial Umbilical ligaments

Initially, there are 6 but only 4 will give rise to adult


arteries. 1 & 2 are usually obliterated.
*Vitelline supplies the digestive system, foregut, midgut,
and hindgut DEVELOPMENT OF THE VENOUS SYSTEM
 The venous system develops from the vitelline,
 CLINICAL CORRELATIONS
umbilical and cardinal veins that empty into the
I. Postductal coarctation of the Aorta
sinus venosus
- Occurs when the aorta is abnormally
 These veins undergo remodeling owing to a
constricted just distal to the ductus arteriosus and
redirection of venous blood from the left side of the
left subclavian artery
body to the right side in order to empty into the right
- This condition is clinically associated with:
atrium
1. Increased BP in the upper extremities
2. Lack of femoral pulse because of
constriction of blood flow
Development of Venous System
Embryonic Structure Adult Structure
Vitelline Veins
Right and left Hepatic veins and sinusoids, ductus
venosus, part of the IVC, portal vein,
superior mesenteric vein, inferior
mesenteric vein and splenic vein

Umbilical Veins Regresses early in development


Ligamentum teres

Cardinal Vein Internal Jugular veins, SVC, part of


the IVC, common iliac veins, renal
veins, gonadal veins, intercostal
veins, hemizygous vein, and azygos
vein

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Reference:
Dudek, R. (2014) BRS Embryology 6th ed. p. 37-49