Ventricular septal defect and severe pulmonary hypertension: radiologic considerations in selection of patients for surgery.

Abstract

In recent years surgical closure of defects in the ventricular septum has become a beneficial and relatively safe procedure. This increase in the scope of cardiac surgery demands specificity not only in establishing an accurate anatomic diagnosis but also in evaluating the associated hemodynamic alterations. One must be able to predict whether surgical closure of the anatomic defect will result in improvement or deterioration of the cardiac status. There appears to be no unanimity of opinion among thoracic surgeons in regard to the criteria of operability for patients with ventricular septal defects and severe pulmonary hypertension. At the Mayo Clinic the decision as to operability has become increasingly dependent on the magnitude of the pulmonary artery flow, which is considered to be a reflection of the degree of resistance in the pulmonary vascular bed (3). It was the purpose of the study to be reported here to evaluate the role of conventional roentgen methods in estimating this flow in the presence of a ventricular septal defect. Funtional Pathology of Ventricular Septal Defect A defect may occur in either the muscular or the membranous portion of the ventricular septum, but is found more commonly in the membranous portion which forms the superior part of the septum. Of more significance than the location of the defect is its size. In small defects (maladie de Roger), the normal differential pressure between the right and left ventricles is maintained and the magnitude of the arteriovenous shunt through the defect is not clinically significant. If the defect is large, however, the differential pressure between the ventricles is not maintained and the resultant arteriovenous shunt may be 50 per cent or more of the left ventricular output. The consequent increase in the volume of blood and velocity of flow into the lesser circulation produces changes in the pulmonary vascular tree which may be recognized readily on the conventional postero-anterior roentgenogram of the thorax (2, 6, 7) (Figs. 1–4). These changes are usually manifested as an increase in the size of the main pulmonary artery and its branches, enlargement of both ventricles, and an associated hypoplastic aortic arch. Fluoroscopy shows vigorous pulsations of the central (hilar) branches of the pulmonary artery. Ventricular septal defect is more frequently associated with pulmonary arterial hypertension than are most other cardiac anomalies. The hypertension may be due to two factors (4): (a) It may be the result of the increase in volume and velocity of blood entering the pulmonary circulation in the presence of normal pulmonary vascular resistance. Since the pulmonary resistance is normally about a fifth of that in the systemic vascular bed, the arteriovenous shunt through any considerable defect is rather large and consequently the pulmonary artery flow is greatly increased.