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Septal Defects


Atrial Septal Defects

A communication between the atria may be the result of a patent foramen ovale or a true atrial septal defect. During fetal life, the foramen ovale, a flapped oval opening of the interatrial septum, allows shunting of blood from the right atrium to the left atrium, in order to bypass the nonfunctional lungs. This flapped oval opening develops between 2 septa: the septum primum and septum secundum, both of which make up the interatrial septum. At birth, the drop in right atrial pressure causes the foramen ovale to close and shunting to cease. Increased right atrial pressure may reopen the foramen ovale where the septa have not sealed and allow shunting to resume. This does not represent a true atrial septal defect because the septa have formed normally. A true atrial septal defect is a consistent opening of the interatrial septum, which allows blood to shunt from the atrium with the greater pressure. Septum secundum defects occur high in the interatrial septum, near the foramen ovale, and are the most common type. Septum primum defects are located lower in the interatrial septum, near the atrioventricular junction.

In most cases, blood shunts from the left atrium to the right atrium, causing a volume overload of the right-sided chambers. The magnitude of shunting depends on the size of the defect and the pressure gradient across the defect. Excessive blood flow through the right-sided chambers results in their dilation and hypertrophy. Pulmonary vasoconstriction may occur as a consequence of excessive pulmonary blood flow and may precipitate right-sided CHF. In situations in which right atrial pressure increases (eg, pulmonic stenosis) shunting from right to left across a patent foramen ovale or atrial septal defect may occur and cause cyanosis and, potentially, polycythemia.

Signs of right heart failure (eg, ascites, edema, cyanosis) may be present. An ejection-type systolic murmur is usually present over the pulmonic valve area, reflecting increased blood flow through the pulmonic valve. Blood flow through the defect itself does not produce a murmur. Prolonged ejection time of the right ventricle may result in a split second heart sound. Electrocardiography may reveal evidence of right ventricular or right atrial enlargement (right axis shift, deep S waves, tall P waves). Right bundle branch block and arrhythmias can also be noted. Radiographically, there are variable degrees of right ventricular enlargement and prominence to the pulmonary vessels indicating pulmonary overcirculation. Echocardiography is indicated in these animals and demonstrates varying degrees of right atrial and right ventricular dilatation as well as identifying the defect as a loss of echogenicity at the interatrial septum. The normal loss of echogenicity of the fossa ovale should not be interpreted as an atrial septal defect. Doppler evaluation confirms shunting through the defect and increased ejection velocities across the pulmonic valve. Surgical correction may be attempted but is associated with high expense and mortality. Animals with septum secundum defects can tolerate the defects well and many of these defects are noted as an incidental finding in older animals. Larger defects, such as noted with septum primum defects or endocardial cushion defects, are more likely to cause right-sided CHF; pulmonary hypertension can also occur as a result of pulmonary overcirculation. The prognosis is guarded to poor in these cases.

Ventricular Septal Defects

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. Defects of the muscular septum may also occur. Ventricular septal defects may occur with other congenital cardiac anomalies. This defect is heritable in miniature swine.

Fig. 3

Shunting of blood from the left ventricle into the right ventricle and right ventricular outflow tract occurs in most animals due to the higher pressures of the left ventricle. The magnitude of the shunt depends on the size of the defect and the pressure gradient between the 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 nonresistive ventricular septal defects or defects lower in the ventricular septum (which occur rarely). Small defects (highly resistive ventricular septal defects) limit the volume of shunted blood and minimize hemodynamic effects, whereas large defects usually result in severe circulatory derangements and clinical signs. Significant shunting through the pulmonary arteries can induce vasoconstriction of these vessels. As resistance rises, the shunt may reverse (ie, resistance to right ventricular outflow exceeds resistance to left ventricular outflow resulting in right-to-left shunting of blood), resulting in cyanosis and polycythemia. The shunting of blood from right to left through a septal defect as a consequence of pulmonary hypertension is referred to as Eisenmenger's complex.

Clinical findings depend on the severity of the defect and the shunt direction. A small defect usually causes minimal or no signs. Larger defects may result in acute left-sided CHF. Cattle are prone to developing signs of right-sided failure. The development of Eisenmenger's complex is indicated by cyanosis, fatigue, and exercise intolerance. Most affected animals have a loud systolic murmur that radiates widely with an accompanying left-sided thrill. This murmur is 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 a subaortic defect may disrupt aortic valve apposition. In these cases, a concurrent diastolic murmur is present, and the combination systolic/diastolic murmur (to-and-fro murmur) may be mistaken as that of a PDA. Chronic turbulence in the area of the defect can erode the endothelium and predispose affected animals to infective endocarditis. 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 or contrast studies will confirm the presence of a shunt.

Therapy depends on the 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 the prognosis is good. Animals with a moderate to severe ventricular septal defect more commonly develop clinical signs and treatment should be considered. Surgical closure of the defect; pulmonary artery banding to increase right ventricular outflow tract resistance and thus decrease left-to-right shunting; or use of therapy to reduce systemic vascular resistance (eg, a vasodilator such as hydralazine) may be considered in the treatment of animals with a large ventricular septal defect and 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 1 breed (English Springer Spaniels).

Last full review/revision April 2012 by Davin Borde, DVM, DACVIM

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