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[[Image:VSD2.jpg|thumb|right|150px|<small><center><b>Ventricular septal defect</b>. Courtesy of A. Jefferies</center></small>]]  

[[Image:VSD2.jpg|thumb|right|150px|<small><center><b>Ventricular septal defect</b>. Courtesy of A. Jefferies</center></small>]]  

Ventricular septal defects (VSDs) are the most common congenital cardiac abnormality in large animals and the second most common congenital cardiac abnormality in cats. They less commonly occur in dogs.  

Ventricular septal defects (VSDs) are the most common congenital cardiac abnormality in large animals and the second most common congenital cardiac abnormality in cats (12-56% of congenital heart disease cases). They less commonly occur in dogs (6-12% of congenital heart disease cases).  

The lesion is usually in the '''membranous area''' of the interventricular septum, just below the aortic valve and the septal tricuspid leaflet.  

The lesion is usually in the '''membranous area''' of the interventricular septum, just below the aortic valve and the septal tricuspid leaflet.  

Ventricular Septal Defects can occur alone or in combination with other congenital malformations, such as [[Tetralogy of Fallot]]. Usually blood flows from the higher pressure left ventricle through the VSD to the lower pressure right ventricle during systole. Significant left-to-right shunting causes volume overload of the pulmonary circulation, increasing pulmonary venous return to the left atrium and consequently the left ventricle. This may result in volume overload of the left heart with consequent [[Heart Failure, Left-Sided|left-sided congestive heart failure]] and [[Pulmonary Hypertension|pulmonary hypertension]]. If chronic over-circulation of the pulmonary vasculature occurs, pulmonary hypertension may develop. Pulmonary hypertension causes increased right ventricular pressures and therefore right-to-left shunting during systole may occur; this is known as '''Eisenmenger's syndrome'''. Right-to-left shunting allows deoxygenated blood to enter the systemic circulation, resulting in arterial hypoxaemia and cyanosis.  

Ventricular Septal Defects can occur alone or in combination with other congenital malformations, such as [[Tetralogy of Fallot]]. Usually blood flows from the higher pressure left ventricle through the VSD to the lower pressure right ventricle during systole. Significant left-to-right shunting causes volume overload of the pulmonary circulation, increasing pulmonary venous return to the left atrium and consequently the left ventricle. This may result in volume overload of the left heart with consequent [[Heart Failure, Left-Sided|left-sided congestive heart failure]] and [[Pulmonary Hypertension|pulmonary hypertension]]. If chronic over-circulation of the pulmonary vasculature occurs, pulmonary hypertension may develop. Pulmonary hypertension causes increased right ventricular pressures and therefore right-to-left shunting during systole may occur; this is known as '''Eisenmenger's syndrome'''. Right-to-left shunting allows deoxygenated blood to enter the systemic circulation, resulting in arterial hypoxaemia and cyanosis.  

Small VSDs provide high resistance to flow, as high pressure gradients between the left and right ventricle are maintained. These are known as '''restrictive''' or '''resistive''' VSDs, and are usually of no haemodynamic consequence. Larger VSDs offer little resistance to the shunting of blood and are more likely to result in haemodynamic consequences.  

Small VSDs provide high resistance to flow, as high pressure gradients between the left and right ventricle are maintained. These are known as '''restrictive''' or '''resistive''' VSDs, and are usually of no haemodynamic consequence. Larger VSDs offer little resistance to the shunting of blood and are more likely to result in haemodynamic consequences. Very large, unrestrictive defects cause the pressures in both ventricles to equilibrate and the two ventricles behave as a common pumping chamber. Unless the pulmonary circulation is protected by a stenotic pulmonic valve, the development of pulmonary hypertension is unavoidable.

 

==Signalment==

==Signalment==

Predisposed breeds include the English Springer Spaniel, Cocker Spaniel, English Bulldog and West Highland White Terrier.

Predisposed breeds include the Lakeland Terrier, Cocker Spaniel, French Bulldog and West Highland White Terrier.

== History and Clinical Signs ==

== History and Clinical Signs ==

== Diagnosis ==

== Diagnosis ==

===Physical Examination===

===Physical Examination===

* '''Systolic''' murmur with point of maximum intensity on the '''right''' hemithorax (blood shunts to the right) The murmur can also be detected on the left side, either due to radiation of the primary murmur or the relative pulmonic stenosis caused by the increased blood flow across the pulmonic valve.  

* '''Systolic''' murmur with point of maximum intensity on the '''right''', cranial hemithorax (blood shunts to the right) The murmur can also be detected on the left side, either due to radiation of the primary murmur or the relative pulmonic stenosis caused by the increased blood flow across the pulmonic valve. There may also be a diastolic component to the murmur if aortic regurgitation is present, as a result of the aortic valve prolapsing into the VSD.

* Murmur grade is inversely proportional to the size of the defect, as smaller defects provide more resistance and therefore produce louder murmurs

* Murmur grade is inversely proportional to the size of the defect, as smaller defects provide more resistance and therefore produce louder murmurs

* Cyanosis may be present with right-to-left shunts

* Cyanosis may be present with right-to-left shunts

Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier.

Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier.