Two lateral extensions of cardiac tissue become hollowed out to form a pair of endothelial tubes, which soon fuse to form the primitive cardiac tube. Paired veins from the trunk (the cardinal system), liver, yolk sac and placenta enter the heart tube from below and a series of arterial arches emerge from the upper end.
the sinus venosus the atrium the ventricle bulbus cordis arterial trunk
The fold of the loop is principally at the junction of bulbus cordis and ventricle. Note in panel C that the two end up side by side.
Formation of the Cardiac Loop 28 days Atrium grows dorsally to the left Ventricle & bulbus cordis grows ventrally & to the right
30 days At the end of the loop formation
normal d-loop l-loop
Dextrocardia : cardiac loop to the left. = Heart in the right thorax associated with situs inversus (transposition of the viscera) Ectopia cordis = Heart on the surface of chest caused by failure to close the midline
Formation of Ventricular Septum 1. Growth of Endocardial cushions
Septum Formation in A-V Canal
Secundum type defects are observed in 80% of cases. These are characterized by defects involving the foramen ovale and (usually) a defect in the septum primum. Sinus venosus defects are usually positioned near the entrance of the superior vena cava. These are generally associated with anomalous entry of the right superior pulmonary vein.
Ostium primum defects are very similar to defects caused by failure of endocardial cushion fusion. Rarely, complete agenesis of the septum occurs, giving a common atrium.
Type I defects are positioned in the infundibulum of the right ventricle, caudal to the pulmonary valve. These arise from defects in the formation of the bulbus cordis and truncus arteriosus. These are also referred to as supracristal, conal or infundibular VSD.
Type II defects occur in the membranous portion of the septum, and are the most commonly observed defects. These are also referred to as paramembranous VSD.membranous portion
Type III defects are found in close proximity to the tricuspid valve, within the inlet of the right ventricle. These are thought to arise from defects in the partitioning of the AV canal by the endocardial cushions. Also identified as atrioventricular canal defects or inlet defects.endocardial cushions
Type IV defects are present in the muscular portion of the interventricular septum. These can be single or multiple, showing extremely irregular borders (variable in many planes). Type IV defects are not easily visualized or repaired.
This structure does truly septate,but embryologically it is a simple coronal division in its embryonic straight position. The septation extends upwards from the valves to end just beyond the origin of the paired sixth aortic arches, where it seals off against the posterior truncal wall. As the sixth arch vessels are destined to be the branch pulmonary arteries, the posterior channel is now the main pulmonary artery. The anterior channel is the aorta.
RPA = right pulmonary artery LPA = left pulmonary artery APS = aortopulmonary (truncal) septum RVO = RV outflow LVO = LV outflow And so now you can compare the flow scheme on the left with the more lifelike image on the right
the truncal septum fails to fuse with the septal crest? - perimembraneous VSD the truncal septum is deviated to the PA side? - tetralogy of Fallot the truncal septum fails to develop? - truncus arteriosus the ventricular septum fails to reach the AV valve? - AV septal defects
the arterial trunk stays over the RV but does divide? - double outlet RV the aortic valve pushes up and right instead of the pulmonary? - transposition of the great vessels the ventricles fail to centralise over the AV valve - double inlet left ventricle (commonest form of single ventricle.