What are hemangioblasts, from where do they arise, and what do they derive into?
Hemangioblasts are angiogenic cell clusters that arise from mesenchymal cells of the visceral (splachnic) mesoderm and differentiate into endothelial cells and blood cells.
Define Vasculogenesis and Angiogenesis, now.
Vasculogenesis - the coalescence of endothelial cells to form endothelium-lined vessels.
Angiogenesis - the sprouting of new vessels from existing vessels.
From where do myocardial cells (myoblasts) arise from?
What initial shape do these cells take and what occurs among them while they are in this shape?
Myocardial cells (myoblasts) arise from mesenchymal cells of the visceral (splanchnic) mesoderm.
Original islands of these myoblasts organize into a horseshoe-shaped primary heart field where the progression of vasculogenesis creates the crescent-shaped endocardial tube.
What physical action of the embryo creates the pericardial cavity? What other structure is created during this action and what holds this structure in place?
The lateral folding of the embryo creates the pericardial cavity.
During this lateral folding, the horse-shoe shaped endocardial tube fuses into a single heart tube with an inner endothelial lining and an outer myocardial layer.
This single heart tube is suspended from the posterior wall of the pericardial cavity by the dorsal mesocardium, which is a fold of visceral mesoderm.
Into what structure is the caudal end of the heart tube embedded and why is this developmentally significant?
The caudal end of the heart is embedded in the septum transversum, which is developmentally significant because mesothelial cells and fibroblasts derived from mesenchymal cells in the septum transversum migrate onto the heart tube to form the visceral and parietal layers of the serous pericardium.
What does the elongation of the heart tube cause?
Which part of this tube is the outflow portion, which is the inflow portion?
What forms the transverse pericardial sinus and what is its function?
The elongation of the heart tube causes the buldging tube to bend caudally.
The cranial part of the tube is the outflow part, while the caudal part is the inflow part.
The degradation of the dorsal mesocardium forms the transverse pericardial sinus which interconnects both sides of the pericardial cavity.
Describe the primitive formation of the chambers of the heart starting from the heart tube.
The singular heart tube forms dilatations (dilated vessels) along its craniocaudal axis beginning at the bulbus cordis (most superior segment of the tube), then the ventricle, then the atrium, then the sinus venosus. The primitive left and right ventricles remain connected by the interventricular foramen, and the primitive left and right atria also remain connected. The atria and ventricles are connected by the single atrioventricular canal.
What initiates septum formation in the atrioventricular canal?
What further event separates the single atrioventricular canal into right an dleft canals between the right and left atria and ventricles?
The development of mesenchyme-derived superior (posterior), inferior (anterior), right and left endocardial cushions is what initiates septum formation in the AV canal.
The separation of this singular AV canal into a right and left canal is a result of the fusion of the anterior and posterior endocardial cushions.
What forms the cusps of the tricuspid and mitral valves?
The cusps of the tri/bicuspid valves are formed by thinning of the fused anterior and posterior cushions and the non-fused right and left endocardial cushions.
What is tricuspid atresia and which cardiac shunts are always associated with it?
A tricuspid atresia is characterized by the absence or fusion of the tricuspid valves.
It is always associated with patency of the oval foramen, VSD, underdevelopment of the right ventricle, and hypertrophy of the left ventricle.
After blood flow hollows out the ventricular walls and ventricular surfaces of the valvular cusps, what structures remain?
What do these structures develop into?
Thin muscular cords retain attachment of the cusps to the ventricular walls. Cardiac myocyte derived papillary muscles develop at the attachment sites and after muscle tissue within the cords degenerates the remaining dense connective tissue forms the chordae tendineae.
How many portions does the bulbus cordis have and what does each portion develop into?
The bulbus cordis has three portions:
1) the proximal portion forms the trabeculated part (ridged with cardiac muscle) of the right ventricle.
2) the midportion (conus cordis) forms the smooth outflow tracts of both ventricles.
3) the distal portion forms the truncus arteriosus
What structure of the heart tube forms the trabeculated part of the left ventricle?
The primitive ventricle forms the tabeculated part of the left ventricle.
What does the truncus arteriosus come from and what does it subsequently form?
The truncus arteriosus comes from the distal portion of the bulbus cordis, and it forms the aortic sac and pulmonary trunk.
What forms on the walls of the conus cordis and proximal truncus arteriosus?
Neural crest cells migrate into the outflow tract and form left and right pairs of conal and truncal swellings or cushions on the walls of the conus cordis and proximal truncus arteriousus.
Describe the formation of the aorticopulmonary septum.
Then tell me why this septum exists.
While growing toward the aortic sac, ipsilateral conal and truncal cushions join to form left and right conotruncal ridges (purple strip and yellow strip respectively) that twist around each other and fuse to form the spiral aorticopulmonary septum.
The reason why this septum exists is to separate the left ventriular outflow tract and aortic sac from the right ventricular outflow tract and pulmonary trunk.
Wat causes Tetralogy of Fallot and what are the four characteristic cardiovascular alterations?
Tetralogy of Fallot is caused by an unequal division of the conus resulting from anterior displacement of the conotruncal septum.
The four cardiovascular alterations:
1) pulmonary infundibular stenosis (narrow right ventriular outflow region)
2) a large defect of the interventricular septum
3) an overriding aorta that arises directly above the septal defect
4) hypertophy of the right ventricular wall because of higher pressure on the right side.
Which septal malformation causes transposition of the great vessels and why is it the leading cause of death in neonates with cyanotic heart disease?
Transposition of the great vessels occurs when the conotruncal septum fails to follow its normal spiral course and runs straight down.
What are the main tributaries of the left and right sinus horns?
From where do these tributaries bring the blood they carry?
The umbilical, vitelline, and common cardinal veins are the main tributaries of the left and right sinus horns.
The umbilical vein brings blood from the placenta.
The vitelline vein brings blood from the temporary yolk sac.
The common cardinal vein brings blood from the body of the embryo.
After the development of a left to right venous shunt, which side of the sinus horn is favored for venous return? What do both the unfavored and favored sinus horns become?
The right sinus horn is favored after development of a left-to-right venous shunt.
The diminished left sinus horn forms the coronary sinus, while the expanded right sinus horn forms the sinus venarum which is the smooth portion of the the right atrial wall.
What forms the four veins of the left atrium?
One is an outgrowth of from the posterior wall of the left atrium.
The remaining three veins grow from the developing lungs into the left atrium to complete the formation of its smooth wall.
Septum primum, atrioventricular canal, ostium primum, ostium secundum, septum secumdum and foramen ovale...
how are all of these structures associated?
The septum primum initiates formation of the interatrial septum by growing toward the endocardial cushions within the atrioventricular canal, however atrial continuity is maintained by the ostium primum. The septum primum ultimately fuses with the endocardial cushions but apoptosis of fibroblasts and endothelial cells in the upper portion of the septum primum creates the ostium secundum. After creation of the ostium secundum, the subsequent formation of the septum secundum fails to competely close the ostium secundum thereby creating the foramen ovale.
What structure becomes the valve of the foramen ovale? what is responsible for transforming the foramen ovale into the fossa ovale?
The inferior part of the septum primum becomes the valve of the foramen ovale.
The increased left atrial pressure presses this valve against the septum secundum to transform the foramen ovale into the fossa ovale.
What are the two principal causes of the ostium secundum defect and why does shunting from the left atrium into the right atrium occur?
Two principle causes of the large opening between the left and right atria known as the ostium secundum defect:
1) excessive cell death and resorption of the septum primum
2) inadequate development of the septum secundum
Shunting from the left atrium into the right atrium occurs because of the higher pressure in the left atrium relative to the right atrium.
What forms the muscular portion of the interventricular septum?
The merger of the medial walls of the expanding ventricles forms the muscular portion of the interventricular septum.
What forms the membranous portion of the interventricular septum?
The fusion of the anterior endocardial cushion with the conal septum forms the membranous portion of the interventricular septum.
Why do about 80% of VSD resolve during childhood? How do the other 20% of VSD affect blood flow into the aorta and pulmonary trunk?
80% of VSDs occur in the muscular region of the interventricular septum.
In the remaining 20% of VSDs, the blood carried by the pulmonary artery may be 1.2 to 1.7 times as abundant as that carried by the aorta.
What is VSD with Eisenmenger syndrome?
VSD with Eisenmenger syndrome is when oxygenated blood from the left ventricle shunts through a VSD to the right ventricle and back into the pulmonary artery, causing pulmonary hypertension and systemic cyanosis.