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 to bypass the nonfunctional lungs. This flapped oval opening develops between two septa that make up the interatrial septum: the septum primum and septum secundum. At birth, the drop in right atrial pressure and rise in left atrial pressure cause the foramen ovale to close and shunting to cease. Increased right atrial pressure may prevent closure of the foramen ovale and lead to persistent shunting through a patent foramen ovale. This does not represent a true atrial septal defect, because the septa have formed normally.
A true atrial septal defect is an opening or hole within 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 in the most apical portion of the interatrial septum, near the AV junction, and are often a component of AV septal (AV canal) defects. Sinus venosus defects are most often located at the junction of the right atrium and cranial vena cava.
Pathophysiology of Atrial Septal Defects in Animals
In most cases of atrial septal defect, 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, the ratio of pulmonary to systemic vascular resistance, and the relative compliance of the two ventricles. Excessive blood flow through the right-side chambers results in their dilation and hypertrophy. Pulmonary vasoconstriction and development of pulmonary hypertension may occur as a consequence of excessive pulmonary blood flow and may precipitate right-side CHF. In conditions associated with high right atrial pressure (eg, pulmonic stenosis), shunting may occur from right-to-left across a patent foramen ovale or atrial septal defect, potentially resulting in cyanosis and polycythemia.
Clinical Findings of Atrial Septal Defects in Animals
A systolic ejection murmur can usually be heard over the pulmonic valve area
With an atrial septal defect, signs of right heart failure (eg, ascites, jugular venous distention) may be present. A soft 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 due to the low velocity of shunt flow. Prolonged ejection time of the right ventricle may result in a split second heart sound (S2). 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 and demonstrates varying degrees of right atrial and right ventricular dilatation, as well as identification of the defect as a loss of echogenicity at the interatrial septum. The normal loss of echogenicity of the fossa ovale (artifactual drop out) should not be interpreted as an atrial septal defect. Doppler evaluation confirms shunting through the defect and increased ejection velocities across the pulmonic valve.
Treatment of Atrial Septal Defect in Animals
Surgery may be attempted but is expensive and has a high mortality risk.
Surgical correction for an atrial septal defect may be attempted but is associated with high expense and mortality. Animals with small or medium-sized 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-side CHF. The prognosis is guarded to poor in these cases, although many dogs show no clinical signs for years. For dogs with large defects and significant volume overload, surgical correction or interventional occlusion may be possible. Surgical closure of the defect requires cardiopulmonary bypass and is often limited by expense and availability. Transcatheter closure using a septal occluder has been reported for secundum and muscular defects.
Atrial septal defect (ASD) is an uncommon congenital heart defect caused by malformation of the interatrial septum, typically resulting in left-to-right shunting across the defect. The most common location is the septum secundum (secundum ASD).
ASD is commonly diagnosed incidentally during echocardiography for concurrent heart disease. Large ASD with significant shunting may lead to right heart overload, right heart failure, and acquired pulmonary hypertension.
Some types of ASD can be closed either surgically or by interventional occlusion.
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