Ventricular septal defect

ISSN 2398-2993

Contributor(s) :

Introduction

The most common congenital cardiac defect in cattle.
Cause: congenital.
Signs: variable.
Diagnosis: auscultation of characteristic murmur/murmurs and visualization of lesion on echocardiography.
Treatment: none currently available; palliative if heart failure results.
Prognosis: dependent on position and size.

A defect in the ventricular septum of varying size .
Usually the defect is in the membranous portion of the ventricular septum beneath the aortic valve (perimembranous and subaortic).
Defects in the membranous portion are caused by lack of fusion of the atrioventricular endocardial cushion and the muscular ventricular septum.
Occasionally the defect occurs in the infundibular or outflow portion of the membranous septum with the result that shunted blood enters the RV close to the pulmonary valve (subpulmonic).
Defects in the muscular portion (rare) are caused by abnormal development of the bulbous cordis.
May occur alone or as part of a complex of malformations, e.g. Tetralogy of Fallot Tetralogy of Fallot.

Hemodynamic effect of a VSD depends on the size and amount of blood shunted through it.
Blood flows from the high pressure left ventricle to the low pressure right ventricle.
If a large proportion of the LV stroke volume is shunted this will → pulmonary over circulation and volume overload primarily of the LA.
Increased pulmonary and left atrial pressures can result in secondary right ventricular failure.
Flow across the defect depends both on the size of the defect and on the pressure differential between the LV and RV; an increase in RV pressure will → a decreased flow across the VSD.
A reverse shunt (Eisenmenger's syndrome) can theoretically occur if there is a very large defect and substantial increase in RV pressure.
Turbulence can lead to damage to the endocardium which in turn can predispose to bacterial endocarditis of the tricuspid valve.