(Transcribed from Dr. Kalliecharan’s lecture, 14 Mar 2000 by Brian Buschman)
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The heart begins to develop when the ectoderm induces the splancnic mesoderm to form into two angioblastic cords. The cords canalize and form two thin walled endothelial tubes. These tubes then fuse with each other from the top down and bulge into the pericardial cavity.
The heart is originally suspended from the dorsal wall by a mesentery, the dorsal mesocardium. It will degenerate to give the transverse pericardial sinus which is located in the middle of the pericardial cavity.
The mesoderm thickens around the endocardial tubes to form the myocardium.
The mesothelial cells of the sinus venosum form the epicardium.
The cardiac loop (the bulboventricular loop) forms because the bulbus cordis and ventricle grow faster then the rest of the tube. This results in the cephalic end moving left and slightly caudally but still pointing upwards. At the same time the atrial portion which first forms outside the pericardial cavity and then inside forms the common atrium. The common atria is now connected by the atrioventricular canal to the common ventricle.
The bulbus is a swelling near the outflow portion of the ventricle that can be divided into three parts:
1) The proximal part is what many books label as the bulbus cordis and forms the trabeculated part of the ventricle.
2) The middle section is the conus cordis (or conus arteriosus) is the outflow tract for the common ventricle and forms the smooth part of both ventricles.
3) The distal portion gives the truncus arteriosus which will give the roots of both the aorta and the pulmonary arteries.
Fetal circulation begins around the fourth week as peristalsis-like waves in the sinus venosus. Blood originally flows through the sinus venosus, into the common atria, through the atrioventricular canal, to the common ventricle, into the bulbus cordis, passing through the conus cordis, out the truncus arteriosus and into the aortic arches.
The sinus venosus is the original venous entrance into the heart. It collects from the common cardinal vein, umbilical vein and vitelline vein and empties into the common atrium. Early on the sinus venosus divides into two parts, the left and right horns which receive the left and right branches, respectively, of the above mentioned veins.
With development blood flow is shifted from the veins of the left horn in to the veins of the right horn. This causes the right horn to enlarge. Both continue to empty into the common atria (on the side that is soon to be the right atrium). The left horn ends up being much smaller then the right and persists as the coronary sinus and the oblique vein of the left atrium. The right becomes the superior and inferior vena cava. The right horn is incorporated into the atrium and forms the smooth part of the right atrium called the sinus venerium.
The valves of the left horn will become incorporated into the interatrial septum. The entrance to the right horn will give the valves of the IVC and of the coronary sinus. During the developmental process a process called the septum spurium grows towards the valves but then regresses.
The crista terminalis is the dividing line between what was originally atrium and what was originally sinus venosum (called sinus venerium in the developed heart).
The cardiac septa divide the right from the left and the atria and ventricles. All the septa form simultaneously.
The septum primum, a crescent shaped septum, grows across the atria and fuses with the endocardial cushions. A hole persists between the two called the foramen primum. It is closed as the septum primum completely fuses with the endocardial cushions. Before that happens another hole opens called the foramen secundum. They allow flow from the right atria to the left atria to bypass pulmonary circulation in the embryo. The septum secundum grows down over the foramen secundum but it does not seal it off but lasts as a flap to work as a valve until birth.
Within hours of birth the septum closes due to a pressure differential and within a few weeks will actually seal. It is now called the fossa ovale as can be seen in the adult heart. In about 20-25% of the population a part of the foramen ovale persists and come blood can still be shunted. This is called probe patency and in the majority of cases causes no clinical symptoms.
In the left atria one vein develops but branches into four pulmonary veins. One end of them will become incorporated into the heart and give the smooth part of the left atria.
Endocardial cushions fuse and by the fifth week the right and left atrioventricular canals are formed. They have valves made of connective tissue covered by endocardium making up the tricuspid and mitral (bicuspid) valves.
The ventricles divide when the medial wall expands to give the muscular interventricular septum but it does not fuse with the endocardial cushions. It leaves the crescent shaped interventricular foramen. Later the endocardial cushions will grow and become the muscular part of the ventricular septum.
(The conus cordis and bulbus cordis are two names for the same thing.)
In the fifth week swellings begin to appear in the truncus arteriosus and grow towards the aortic sac. As they grow they twist around each other and divide to give two unique arteries, the beginnings of the aorta and pulmonary arteries. They will join with the appropriate aortic arches to form the paths the blood follows. The conus cordis has dorsal and ventral swellings which result in the formation of the aortic and pulmonary valves.
The sinoatrial node is the primary pacemaker of the heart and comes from the sinus venosus. It was the only part of the conduction system discussed in this lecture. The rest were covered in anatomy and the histology lecture.
The aortic sac gives pairs of aortic arches which will develop into many of the large arteries. All the arches have both a right and left side so each arch will have a structure developing from the right and from the left sides. Arches I and II regress and arch V never develops. The other three form:
1) Arch III gives the common and proximal part of the internal carotid arteries.
2) Arch IV gives the aortic arch on the left and the beginning of the right subclavian vein. The rest of the of the right subclavian and the left subclavian develop from intersegmental arteries.
3) Arch VI gives the ductus arteriosus on the right and the pulmonary artery on the left.
In the fetal heart there is some blood that does not shunt through the foramen ovale but goes out through the pulmonary artery. The majority of this blood is then shunted to the aorta through a vessel called the ductus arteriosus. The ductus arteriosus should regress by birth and become the ligamentum arteriosus but as will be seen persists in some anomalies. This is the structure that the left recurrent nerve recurs around and why anatomists day it recurs around the ligamentum arteriosus rather then just saying the aortic arch.
The umbilical vein also regresses after birth and will persist in the adult as the ligamentum teres found running from the umbilicus to the liver and connecting with the ligamentum venosus. The ligamentum venosus is the remnant of the ductus venosus which was the fetal bypass around the liver between the umbilical vein and the IVC.
Anomalies in the heart can be found in about one in 125 births. Their etiology can be congenital or of environmental causes.
One type of abnormality is dextrocardia which is where the heart tube initially bends to the left instead of the right. This will cause everything to develop backwards and the backwards orientation can cause a degree of constriction on some vessels.
There are four types of atrial septal defects. Many are a result of a problem with probe patency and/or pulmonary atresia and the major clinical sign in either case is cyanosis (blue skin color due to lack of oxygen). All involve shunting of blood from the right to left and bypassing pulmonary circulation.
1) Secundum ASD involves an abnormal resorption of either the septum primum or septum secundum.
2) Endocardial Cushion ASD is where the septum primum fails to properly fuse with the endocardial cushion. This results in a patient foramen primum.
3) Sinus venosus ASD is a rare condition where there is an incomplete absorption of the sinus venosus into the right atria. It can also be caused by an abnormal development of septum secundum since it is septum secundum that fuses with the sinus venosus.
4) Common atrium is very rare and is found when there is a complete absence of the interatrial septum.
There are three main VSDs and they are the most common type of cardiac defect. They account for about 25% of congenital heart defects. Due to the greater pressure in the left ventricle then the right they almost always result in blood being shunted from the left back to the right ventricles.
1) Membrane VSD is when the membranous part of the interventricular septum fails to develop.
2) Muscular VSD is less common and is when the muscular part of the interventricular septum does not develop.
3) Common ventricle is a complete absence of the interventricular septum.
Tetralogy of Fallot is the anomaly resulting from an unequal division of the conus arteriosus. The aorta ends up with a larger share then it is supposed to so the pulmonary artery is left out. The resulting pulmonary stenosis results in a low blood oxygen level and can be first detected by cyanosis shortly after birth. More problems result because the unequal division causes the division of the conus to not line up with the interventricular septum and a hole between the left and right atria result. The right ventricle is hypertrophied as in any condition resulting in pulmonary stenosis as it needs to be stronger to pump blood through the smaller hole. There are four things associated with tetralogy of Fallot.
1) Pulmonary stenosis.
2) Overriding aorta.
3) Ventricular septal defect.
4) Hypertrophy of the right ventricle.
The aorta and pulmonary artery get switched so that the aorta comes off the right ventricle and the pulmonary artery off the left. This results in isolation of the systemic and pulmonary circulations and the baby will die very quickly if not detected and surgically corrected. Again the first sign will be cyanosis.
Atresia is the complete closure of a tube whereas stenosis is the narrowing of a tube. In cardiac development coarctation of the aorta can lead to one of two methods to maintain circulation. If the coarctation is before the ductus arteriosus then the ductus will remain patient after birth to shunt some blood from pulmonary circulation into the descending aorta. If it’s a postductal coarctation then the ductus will regress and collateral circulation is established by intercostal arteries as discussed in anatomy.
Pulmonary stenosis can occur at the pulmonary valve. The ductus arteriosus persists to shunt blood in the reverse direction, from the aorta to the pulmonary artery. Pulmonary stenosis is caused by a maternal infection with the rubella virus during pregnancy. It will also lead to right ventricle stenosis as it works harder to squeeze blood through the small hole.
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