Case Studies In Small Animal

Cardiovascular Medicine

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Ventricular Septal Defect Section from "Small Animal Cardiovascular Medicine" On-Line

Text From "Small Animal Cardiovascular Medicine"

Ventricular Septal Defect

Ventricular septal defect (VSD) is a orifice in the interventricular septum that allows blood to flow from one ventricle to the other. It is the most common congenital cardiac abnormality identified in children. The prevalence is much lower in dogs and cats. Whereas a busy pediatric cardiologist encounters a patient with a VSD on a weekly basis, a busy veterinary cardiologist encounters such a patient once a month or less. The etiology of VSDs is usually unknown. In most cases, dogs or cats with this defect present with no family history of the disease. Recently, a family of English Springer spaniels has been reported in which the defect appears to be inherited as either an autosomal dominant trait with incomplete penetrance or as a polygenic trait.

Patients with small defects often have a loud heart murmur with no clinical or radiographic evidence of disease. The defect is often difficult to locate using two-dimensional echocardiography but can usually be identified using color flow Doppler echocardiography. On color flow Doppler echocardiography, flow is laminar in the left ventricle and then accelerates toward the defect. At the defect, velocity increases dramatically to produce a turbulent jet that extends into the right ventricular cavity and strikes the right ventricular free wall. Because the resistance to flow is high and because the systolic pressures in the left ventricle and the right ventricle are normal, the velocity of the jet measured with continuous wave Doppler is high. Normal left ventricular systolic pressure is 110-150 mmHg and normal right ventricular systolic pressure is 15-25 mmHg. Using the modified Bernoulli equation (4V2), one can quickly determine that jet velocity should be between 4.6 and 5.8 m/sec. Approximately 35% of small VSDs close spontaneously in children. Occasionally a small defect may close spontaneously in a dog, although this is rare in the authors’ experience. Spontaneous closure has been reported in two dogs. In one dog, the VSD was diagnosed at eight weeks of age. The murmur disappeared and the VSD was no longer evident on an angiocardiogram at 16 months of age. In the second dog, the VSD was diagnosed at eight weeks of age and the murmur and angiocardiographic evidence of a VSD were gone at 1 year of age.

Patients with moderate-size defects have a loud heart murmur. They may show no clinical signs or may develop mild to moderate left heart failure early in life. Right heart failure may become evident later in life. Cardiomegaly and pulmonary overcirculation may be identified on thoracic radiographs. The VSD may be identified on two-dimensional echocardiography, usually from a right-sided view. The defect can be seen immediately beneath the aortic valve on a long-axis view. On a short-axis view, the VSD may appear to be part of the aortic root. The location of the defect can be determined on the short-axis view, being at approximately 11:00 to 12:00(when the aortic root is viewed as a clock face) when the defect is a perimembranous inlet defect or a membranous defect and at 1:00 to 3:00 when it is a perimembranous outlet defect (Figures 12 and 13). The color flow jet may appear somewhat larger than with a small defect although this should not be used as a distinguishing characteristic. Jet velocity is decreased from that seen with a small defect but is not laminar. The left ventricular and left atrial cavities are enlarged and left ventricular wall thickness is normal. Myocardial failure (a large end-systolic diameter and decreased shortening fraction) may be present. The right ventricular and right atrial cavities may also be enlarged.

Large VSDs are rare in clinical veterinary practice. It is likely that most puppies and kittens with large VSDs die within the first weeks of life from left heart failure, when pulmonary vascular resistance decreases into the normal range. Patients that do survive may present in left heart failure or they may present with Eisenmenger’s complex and cyanosis (see below). Even in patients with left-to-right shunts, the heart murmur may be softer than with small and moderate-size defects as flow velocity is decreased. The cardiac silhouette is usually generally enlarged on thoracic radiographs and pulmonary overcirculation may be evident. Pulmonary edema may also be present. The large defect can be visualized and its location confirmed on two-dimensional echocardiography. The left ventricular and atrial cavities are enlarged. The right ventricular cavity may be enlarged due to diastolic flow through the VSD. The right ventricular wall thickness may be increased, secondary to the right ventricular systolic hypertension (pressure overload). Because of the massive amount of flow through the defect, flow velocity is still usually increased in patients with a left-to-right shunt. Consequently, turbulent flow through the defect can be demonstrated with color flow Doppler echocardiography. Peak systolic flow velocity, measured with continuous wave Doppler echocardiography, is decreased into the 1.0-2.5 m/sec range.

 

Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.