What is a Ventricular Septal Defect?
A ventricular septal defect (VSD) is the result of malformation of the intraventricular septum allowing an abnormal communication between the right and left ventricles. Normally during fetal development, several structures (trabecular muscular septum, inlet muscular septum, infundibular muscular septum and membranous septum from the endocardial cushions) fuse in specific fashion to form the intraventricular septum. Failure of any these structures to fuse can result in a VSD. The most common VSD is a perimembranous defect resulting from fusion failure of the membranous and muscular components. VSDs are classified based upon whether they are resistive or non-resistive. As the name implies, a resistive VSD is a smaller diameter VSD that provides resistance of blood flow. Due to normally higher systolic left ventricular pressures compared to right ventricular pressures, most resistive VSDs have blood flow from left-to-right. The amount of blood shunted depends on size of the VSD and the pressure gradient across the VSD. The shunted blood is quickly moved to the pulmonary arteries as blood flows during systole from the contracting left ventricle to the already contracting right ventricle. This shunting of blood results in volume overload to the left side of the heart due to pulmonary vascular overcirculation. Left ventricular eccentric hypertrophy results from the volume overload. Left-sided congestive heart failure can develop. Aortic insufficiency can also occur due to lack of aortic valve support from the position of the VSD. One can hear a systolic murmur from the VSD with a diastolic aortic insufficiency murmur at times (to-and-fro murmur). With non-resistive VSDs, a larger diameter defect allows blood to flow freely between the left and right ventricles. Direction of flow is determined by resistance to outflow into the pulmonary artery and the aorta from the right ventricle and left ventricle respectively. Normally systemic resistance is about five times that of pulmonary resistance so blood will shunt left-to-right through the large defect. An increase in pulmonary hypertension occurs due to massive pulmonary overcirculation. Both ventricles hypertrophy eccentrically secondary to volume overload and the right ventricle will concentrically hypertrophy due to pressure overload with time. Rarely, pulmonary hypertension can become severe due to pulmonary arterial vasoconstriction allowing right ventricular pressures to exceed left pressures, causing shunt reversal. VSD murmurs vary in intensity based on their size. Small to moderate resistive systolic murmurs may be louder than large non-resistive systolic murmurs.
Clinical signs of VSDs may include signs of left-sided heart failure. Clinical signs of left heart failure may be subtle such as increased respiratory rate at rest to mild decreases in activity or exercise intolerance. Other clinical signs may include coughing, not sleeping through the night, coughing more at night or decreased appetite. Signs may progress to coughing up pink-tinted foam to fulminate respiratory distress. Rarely, when large non-resistive VSDs reverse flow, cyanosis and weakness may be clinical signs seen.
Although small resistive VSDs often have loud murmurs, the consequences of this defect are small and this defect does not require treatment. Oppositely, moderate sized resistive VSDs can mild to severe consequences and outcome from this defect is difficult to predict. Some animals will have signs of congestive left heart failure early in life and will require treatment with standard drugs such as diuretics, angiotensin converting enzyme inhibitor. Potent arteriodilators are sometimes administered to reduce overall shunt flow by allowing a decrease in systemic blood pressure and more blood to flow out the left ventricle into the aorta. Other non medical treatment is surgically creating pulmonic stenosis or pulmonic banding in order to reduce shunt flow by increasing pulmonary vascular resistance. Surgery to correct the actual defect is rarely performed and interventional techniques to occlude the defect are being researched at this time. Patients with large non-resistive VSDs are managed medically as aforementioned for moderate sized resistive VSDs with early institution with an arteriodilator.
Animals with mild VSDs should be re-examined on an annual basis. Animals that are stable with moderate to large VSDs should be re-examined every 6-12 months.