Blood and blood vessels development:
Blood vessels formed in two ways:Vasculogenesis: (vessels arise from blood islands). The first blood island appears in mesoderm surrounding the wall of the yolk sac at the 3rd week and later in the lateral plate mesoderm. So the mesoderm cells, which form the blood islands, are induced by the VEGF to form hemangioblasts. Hemangioblasts at the center of the blood islands will form the hematopoietic stem cells (the precursor to all blood cells) while that at the periphery differentiates into angioblasts (the precursor to blood vessels).
Angiogenesis: sprouting of a new blood vessel from the existing one.
The first blood cells arise in the blood islands of the yolk sac are transitory. The definitive hematopoietic stem cells arise from the mesoderm surrounding the aorta in the region aorta-gonad-mesonephros (AGM). These cells will colonize the liver to be the major hematopoetic organ of the fetus. Later, stem cells from the liver will colonize the bone marrow, the definitive blood forming tissue.
Development of the cardiovascular system
The CVS appears in the middle of the 3rd week. Before this time, the embryo has its nutrition by diffusion. Later on blood and blood vessels develop (as mentioned previously) to assure the nutritional requirements of the embryo.
Cardiogenic progenitor cells lie in the epiblast lateral to the primitive streak. From there they migrate through the streak to form angiogenetic clusters that destined rostral to the buccopharyngeal membrane and neural folds, and reside in the splanchnic layer of the lateral plate mesoderm. The underlying pharyngeal endoderm will induce these cells to form the cardiac myoblasts. With time, the blood islands that appear in this mesoderm, to form blood cells and blood vessel, unite and form a horse-shoe shaped endothelial lined tube surrounded by myoblasts. This region is known as the cardiogenic field; the intraembryonic cavity over it developed later into the pericardial cavity.
The heart beating begins in the 4th week of development. In addition to the heart tube, two dorsal aortae are formed on the side of the midline as a derivative of the angiogenetic cell clusters. These aortae will gain connection with the cranial part of heart tube.
Formation and position of the endocadiac heart tube:
The cardiogenic field deviated ventrally and caudally by the passive effect of the cephalocaudal folding of the embryo in addition to the growth of the brain, thus the field become ventral and caudal to the buccopharyngeal membrane after 180 degree ventral deviation reaching the cervical region of the embryo and then the thoracic region. Also, the transverse folding of the embryo results in approximation of the lateral limbs of the U-shaped heart tube and then fusion of these limbs forming the single heart tube. This tube grows and is temporarily attached to the wall of the pericardial cavity by a dorsal mesocardium that disappears later on forming the transverse pericardial sinus. The endocardial heart tube is surrounded by a gelatinous cardiac jelly which is rich in hyaluronic acid; the jelly is secreted by the thickened myocardium. The mesothelium on the surface of septum transversum will migrate over the heart and form most of the epicardium. So the heart tube consists of three layers:1. The endocardium
2. The myocardium
3. The epicardium or visceral pericardium; which is responsible for formation of the coronary arteries.
Formation of the heart loop:
The heart tube has four parts from anterior to posterior:1. The bulbus cordis.
2. The ventricle.
3. The atrium.
4. The sinus venosus.
These four parts bend on day 23 and form the heart loop. The cephalic portion of the tube bends ventrally, caudally, and to the right: and the caudal (atrial) portion bends dorsocranially and to the left. It is completed on day 28. The bulboventricular part is located inside the pericardial cavity, the initially paired atrial and sinus parts are located inside the mesenchyme of the septum transversum, after bending the four parts of the heart loop become completely inside the pericardial cavity.
Derivatives of the heart tube:
1. Bulbus cordis:
Proximal third form the trabeculated part of the Rt ventricle,
Middle third (the conus cordis) forms the out flow of both ventricles,
Distal third (the truncus arteriosus) forms the root of the aorta and pulmonary arteries.
2. The ventricle:
it forms the trabeculated Lt ventricle, the sulcus between the bulbus cordis and the ventricle forms the primary interventricular foramen. The sulcus between the ventricle and the atrium forms the atrioventricular canal.
3.the atrium:
forms the common atrium, which the primordium of the trabeculated part of the Rt and Lt atria.
4.sinus venosus:
it consist of a transverse part and the Lt and Rt sinus horns, each horn has 3 tributaries; a. vitelline vein., b. umbilical vein., and c. common cardinal vein.
The fate of the Lt sinus horn:
After disappearance of the Lt umbilical and Lt vitelline and the Lt common cardinal veins, the Lt horn degenerate forming the coronary sinus and the oblique vein of the Lt atrium.The fate of the Rt sinus horn:
It forms the smooth part of the Rt atrium (the sinus venarum), the orifice of the Rt horn into the Rt atrium has 2 valves. These valves fused dorsocranially forming the septum spurium. The Lt valve and the septum spurium fused with the developing interatrial septum. The upper part of the Rt valve disappears, while the lower part of the Rt valve forms the valve of IVC and the valve of the coronary sinus.Septation of the heart:
Septation in the common atrium:In the 4th week, a sickle shaped septum primum projects from the roof of the common atrium. This septum grows toward the atrioventricular canal that has thickenings in its walls called the endocardial cushions. These cushions grow toward the septum primum to close the opening between them (the ostium primum). Just before closure of the ostium primum, perforations appear in the septum primum to form the ostium secondum that keeps the Rt to Lt flow of blood between the atria. Then after, the septum secondum is formed on the Rt side of the septum primum. This septum fuses with the left valve of Rt sinus horn and with the septum spurium. The development of the septum secondum stops resulting in an incomplete covering over the ostium secondum, the opening left is called the oval foramen. The floor of this foramen is the reminance of the septum primum that act as a valve for the oval foramen. After birth, the increased pressure inside the left atrium accompanied by beginning of the pulmonary circulation results in closure of the oval foramen.
Notes:
During cardiac septation, the bud of the pulmonary vein projects from the Lt atrium and grows toward the developing lungs. This bud incorporates into the Lt atrial wall forming the smooth part of the Lt atrium.
Anomalies of the interatrial Septation:
There are many types of defected atrial Septation with Rt to Lt shunt of blood:
1.ostium secondum defect: either by a large ostium secondum formation, or small septum secondum.
2.ostium primum defect: by abnormal endocardial cushions closing the ostium primum.
3.complete absence of the septum: common atrium is formed and is called triloculare biventriculare.
4.premature closure of the foramen ovale (before birth): leading to increased pressure and hypertrophy of the Rt atrium and ventricle, with atrophy of the left atrium and ventricle. It causes death shortly after birth.
Septation of the atrioventricular canal:
At early stages, the canal connects the common atrium and the Lt ventricle primordium only. Later on, the canal is enlarged on the Rt side to be connected with the Rt ventricle. After the 4th week, the four atrioventricular endocardial cushions develop at the canal as anterior, posterior, and 2 lateral cushions. These cushions fused with each other to from the Rt and Lt atrioventricular orifices. The mesenchymal proliferation developing around these orifices are hollowed by the blood flow forming the cusps of the mitral and tricuspid valves.Anomalies of atrioventricular Septation
1.persistent atrioventricular canal: by failure of fusion of the endocardial cushions that is associated with defected atrial and ventricular Septation.2.ostium primum defect.
3.tricuspid Artesia: associated with opened ovale foramen and defected ventricular septum, with hypertrophy of the Lt ventricle and atrophy of the Rt ventricle.
Ventricular Septation:
After the 4th week, the lateral walls of both ventricles grow on the outside and absorbed from the inside forming the Trabeculae carnea and papillary muscles. The medial walls of both ventricles fail to grow and thus become opposed and fused with each other forming the muscular interventricular septum. The opening between the upper free end of this septum and the endocardial cushions is closed by the membranous interventricular septum that is derived from the inferior cushion. The bulbus cordis is divided into: a. truncus arteriosus, b. conus cordis, and trabeculated part of the RT ventricle. So the conus and truncus swellings will contribute to the interventricular septum.Anomalies of the ventricular Septation:
1.defected muscular and membranous interventricular Septation.2.persistent atrioventricular canal.
3.tricuspid atresia.
4.tetralogy of fallote.
5.transposition of the great vessels.
Septation of the truncus arteriosus and conus cordis:
During the 5th week, two swellings develop in the trucus arteriosus as a Rt superior and Lt inferior swellings. Similar swellings appear in the conus cordis as Rt dorsal and Lt ventral swellings. These four swellings grow toward each other in a spiral way to separate the aorta from the pulmonary artery by a spiral septum that is connected with the septum derived from the conus swellings separating the out flow (smooth part) of the Lt and Rt ventricles. Tubercles of the semilunar valves develop inside the truncal swellings forming the semilunar valves.
Anomalies of the truncoconal septation:
1.tetralogy of Fallot: stenosis of the out flow of the Rt ventricle ( infundibular stenosis), is associated with defected interventricular septum, overriding of the aorta, and hypertrophy of the Rt ventricle. It is a cyanotic disease of the new born.2.persistent truncus arteriosus: by absence of the truncoconal swellings, associated with interventricular septal defect.
3.failure of spiral growth of the truncoconal swellings resulting in transposition of the great vessels, associated with defected interventricular septation and patent ductus arteriosus (PDA).
4.stenosis of the pulmonary valve with PDA.
5.stenosis of the aortic valve.
6.aortic valve atresia with PDA.
Anomalies of the cardiac position:
1.dextrocardia: the heart lies on the Rt side associated with or with out situs inversus (abnormal transposition of abdominal viscera).2.ectopia cordis: the heart lies on the surface of the chest.