Introduction

• Most common congenital heart defect in cat; 12-56% of feline congenital heart anomalies.
• Perimembranous isolated subaortic lesion communicating ventral to septal tricuspid valve leaflet most commonly identified. Muscular VSD uncommon.
• Tetralogy of Fallot is most common concurrent defect.
• Occasionally combined with atrial septal defect +/- atrioventricular valve defect producing common atrioventricular canal (endocardial cushion defect).
• Cause: congenital abnormality, resulting from anomalous formation of cardiac septa.
• Signs: vary from asymptomatic murmur to severe congestive heart failure.
• Diagnosis: auscultation, radiography, electrocardiography, ultrasonography.
• Treatment: medical management, surgery considered for severe cases.
• Prognosis: good with restrictive asymptomatic cases; poor with severe defects.
  Print off the owner factsheet Congenital heart disease - ventricular septal defect (VSD) Congenital heart disease - ventricular septal defect (VSD) to give to your client.

Pathogenesis

Etiology

• Embryological - maybe inherited - failure of closure of interventricular septum.

Pathophysiology

• Embryological failure of development of interventricular septum, leaving conduit between left ventricle and right ventricle   →   left ventricular pressure exceeds normal right ventricular pressure in systole   →   systolic left-to-right shunting occurs across the defect.
• Large defects in lower part of septum (less common)  →   volume overload of right ventricle, pulmonary circulation, left atrium and left ventricle.
• Defects higher in septum (more common)  →   discharge into the pulmonary artery   →   overloaded pulmonary circulation, left atrium and left ventricle.
• Majority of shunting occurs in systole when blood is leaving right heart out pulmonary artery   →   increased blood volume out pulmonary artery → volume overloaded pulmonary circulation +/- right ventricle   →   increased pulmonary venous return to left atrium (dilates) and left ventricle   →   dilation and eccentric hypertrophy, volume overloaded left heart   →   left-sided congestive heart failure.
• Magnitude of flow through VSD depends on size of defect and systemic and pulmonary vascular resistance.

• Small defects (restrictive VSDs) restrict right to left shunting and prevent transmission of left ventricular pressures to right ventricle, so pressure gradient between right and left ventricle remains high. 
• Higher pressure gradient between right and left ventricle with smaller defects mean smaller defects have louder murmurs; degree of murmur not related to severity of disease.
• Large defects are associated with loss of the pressure gradient between the left and right ventricles and shunt from left to right may even be laminar (so low grade murmur). Large defects may have diastolic bidirectional shunting, even with systolic left-to-right shunting, and subsequent cyanosis and polycythemia.
• The aortic valve may prolapse into the VSD, resulting in aortic regurgitation during diastole which can contribute to left ventricular overload.
• Large shunt with significant pulmonary overcirculation leading to pulmonary vascular changes then pulmonary hypertension which can cause pressure overloaded right ventricle. Right ventricular pressure increased so reduced left-to-right shunting or eventually right-to-left shunting (Eisenmenger's syndrome), which can lead to polycythemia and cyanosis. There is a significant risk in patients where pulmonary flow:systemic flow ratio (Qp:Qs) exceeds 2:1.

Timecourse

• From birth.
• Progression or development of symptoms/clinical signs depends on size of defect and volume of shunting and presence of concurrent defects.

Diagnosis

Treatment

Outcomes