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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. |
| Pathophysiology: |
| 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. |
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| Clinical Findings and Treatment: |
| 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. |
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