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Ventricular Septal Defects

By Sandra P. Tou, DVM, DACVIM, Assistant Clinical Professor of Cardiology, College of Veterinary Medicine, North Carolina State University

Ventricular septal defects are most commonly located in the perimembranous portion of the septum, high in the ventricular septum immediately beneath the right and noncoronary aortic valve cusps on the left and just below the cranioseptal tricuspid valve commissure on the right. They vary in size and hemodynamic significance. Doubly committed juxta-arterial septal defects (located beneath the aortic valve on the left and beneath the pulmonic valve on the right) and muscular septal defects (located at any site along the muscular septum) may also be seen. Ventricular septal defects may be seen with other congenital cardiac anomalies. This defect is heritable in miniature swine.

Ventricular septal defect, miniature pig

Paramembranous ventricular septal defect viewed from the left ventricle. The defect is seen high in the interventricular septum just below the aortic valve. Illustration by Dr. Gheorghe Constantinescu.

Pathophysiology:

Shunting of blood from the left ventricle into the right ventricle or right ventricular outflow tract occurs in most animals because of the pressure gradient between the two ventricles. The magnitude of the shunt depends on the size of the defect, the ratio of pulmonary to systemic vascular resistance, and the relative compliance of the two ventricles. Blood shunted into the right ventricle is recirculated through the pulmonary vessels and left cardiac chambers, which causes dilatation of these structures. The right ventricle may dilate as well, especially in animals with large ventricular septal defects (which are rare). Small defects limit the volume of shunted blood and minimize hemodynamic effects, whereas large defects usually result in severe circulatory derangements and clinical signs. Most ventricular septal defects are restrictive, in which the degree of shunting is small, allowing the left and right ventricles to maintain normal pressures and a normal pressure gradient. Significant shunting through the pulmonary arteries can induce vasoconstriction and pulmonary hypertension. As resistance rises, the shunt may reverse and result in right-to-left shunting of blood, cyanosis, and polycythemia. The reversal of shunt flow (right-to-left) through a septal defect as a consequence of pulmonary hypertension is referred to as Eisenmenger syndrome.

Clinical Findings and Treatment:

Clinical findings depend on the severity of the defect and the shunt direction. A small, restrictive defect usually causes minimal or no signs. Larger defects may result in left-side CHF. Cattle are prone to developing signs of right-side failure. The development of Eisenmenger syndrome is indicated by cyanosis, fatigue, and exercise intolerance. Most animals with a restrictive ventricular septal defect have a loud holosystolic murmur heard best over the right thorax that may be accompanied by a palpable thrill. This murmur is often absent or faint when a very large defect is present or when shunting is right to left. On occasion, aortic valvular insufficiency develops secondarily, because the defect may disrupt aortic valve apposition. In these cases, a concurrent diastolic murmur may be present, and the combination systolic/diastolic murmur (“to-and-fro” murmur) may be mistaken as that of a PDA. Thoracic radiographs can demonstrate generalized cardiomegaly with overcirculation of the pulmonary vessels. The defect can usually be visualized by echocardiography, although small defects may be missed. Doppler echocardiography can often confirm the presence of a shunt.

Therapy depends on use of the animal, severity of clinical signs, and direction of the shunt. Animals with small ventricular septal defects do not typically require therapy and have a good longterm prognosis if significant aortic insufficiency is not present. Animals with a moderate to severe ventricular septal defect and secondary volume overload to the left heart more commonly develop clinical signs, and treatment should be considered. Surgical closure of the defect requires cardiopulmonary bypass and is often limited by expense and availability. Percutaneous transcatheter closure can be considered for muscular septal defects and involves placement of an occluder or coil. Pulmonary artery banding to increase right ventricular outflow tract resistance, and thus decrease left-to-right shunting, can be considered. Medically, the use of drugs to reduce systemic vascular resistance (eg, vasodilators) may help to decrease the degree of left-to-right shunting. With right-to-left shunting, surgical closure of the defect is generally contraindicated. Phlebotomy to relieve the effects of polycythemia or use of hydroxyurea may be considered to relieve clinical signs; however, the prognosis is poor to guarded. Animals diagnosed with a ventricular septal defect should not be bred; the defect has been demonstrated to be heritable in at least one breed (English Springer Spaniels).

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