Overview

Thickness≈8–12 mm (muscular part)

Commonest VSD sitePerimembranous

Muscular part. This makes up nearly all of the septum. It is as thick as the left ventricular free wall and moves with the left ventricle in systole.

Membranous part. This is a small, thin area high up and toward the back, just below the right and non-coronary cusps of the aortic valve. It develops from the endocardial cushions and conotruncal ridges, and it is the most common site of ventricular septal defects.

Surface markings. On the outside of the heart, the septum is marked by the anterior and posterior interventricular sulci. The anterior sulcus carries the LAD and the great cardiac vein. The posterior sulcus carries the posterior interventricular artery and the middle cardiac vein.

Septal activation. The septum is the first part of the ventricles to depolarise, from left to right. This produces the small septal q waves in leads I, aVL, V5 and V6, and the small r wave in V1.

Location: Between the right and left ventricles. It runs obliquely from the anterior to the posterior interventricular sulcus and is convex toward the right ventricle.

Parts & subdivisions

Muscular part
Thick lower part, containing the septal perforator arteries.
Membranous part
Thin fibrous upper part below the aortic valve, continuous with the fibrous skeleton.
Bundle of His and bundle branches
Run along the crest of the muscular septum and then down each side of it.

Anatomy

Arterial supply: Anterior two-thirds: septal perforator branches of the LAD. Posterior third: septal branches of the posterior interventricular artery.

Function

Separates the two ventricular circulations.
Contributes to the contraction of the left ventricle and, to a lesser extent, the right ventricle.
Carries the impulse to the ventricles through the bundle of His and bundle branches.

Clinical significance

Ventricular septal defect (VSD)

Apart from bicuspid aortic valve, VSD is the most common congenital heart defect, and most are perimembranous. It produces a harsh pansystolic murmur at the left lower sternal edge. Small, restrictive defects are often the loudest. Many small muscular defects close on their own. Large ones cause heart failure in infancy and, if left untreated, pulmonary vascular disease (Eisenmenger syndrome).

Post-infarction septal rupture

Rupture of the septum after a large myocardial infarction usually happens within the first week. It produces a new pansystolic murmur and cardiogenic shock.

Hypertrophic obstructive cardiomyopathy

In hypertrophic obstructive cardiomyopathy, the septum thickens much more than the rest of the wall and obstructs the left ventricular outflow tract. During systole the anterior mitral leaflet is pulled toward the septum (systolic anterior motion), which worsens the obstruction. The murmur gets louder with a Valsalva manoeuvre or on standing.

Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.