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Ventricular Septation & Outflow Tract Division

Notes
Key points:
Division of the outflow tract and ventricle occurs between weeks 5 and 9.
  • The outflow tract is divided by the aorticopulmonary septum.
    • This partition begins to form when second heart field and cardiac neural crest cells migrate to the elongating heart.
  • The primitive ventricle is divided by a septum comprised of muscular and membranous portions.
    • The muscular interventricular septum forms as the ventricle itself expands.
    • The membranous septum comprises the lower portion of the spiral aorticopulmonary septum and the ventricular side of the atrioventricular endocardial cushions.
Features of Week 5
Primitive ventricle with partial muscular ventricular septum
Bulbus cordis and truncus arteriosus (which comprise the outflow tract)
Arioventricular septum and canals connect atria and ventricle.
Right and left conotruncal ridges as they arise from the walls of the outflow tract and form a spiral configuration.
    • Their helical form reflects the flow of low oxygen and high oxygen blood through the heart.
    • Swellings grow towards each other, pinching the single lumen.
Features of Week 6
The muscular ventricular septum grows to meet the membranous contribution from the atrioventricular endocardial cushions
The conotruncal ridges fusing in a cranial-to-caudal direction, towards the ventricle, as blood spirals around them.
    • The interventricular foramen is narrowing, but not quite closed.
    • The fusing septum has divided a singular lumen into two.
Features of Week 7
Septum is fully fused and blood pathway is completely divided.
The interventricular septum now completely divides the primitive ventricle into left and right chambers.
  • It comprises a membranous portion, formed by the spiral septum and endocardial cushions, and, the muscular portion that arose from the ventricular tissue.
    • The interventricular foramen is completely closed; thus, the two sides of the heart are established, and blood flows unidirectionally through the heart.
Clinical Correlation:
Endocardial cushion defects can lead to incomplete or even absent septa. Blood shunting and mixing occurs in proportion to the size of the persistent opening, and can lead to heart failure.
  • **There is considerable intertextual variation in nomenclature of key structures.