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Congenital ventricular septal defects are lo­cated most commonly in the region of the mem­branous interventricular septum. There is a ten­dency as a child grows for the relative size of the defect to diminish, and sometimes spontaneous closure occurs. The hemodynamic consequences of a ventricular septal defect depend on the size of the defect and on the extent of pulmonary vas­cular resistance. A small defect causes little prob­lem, a moderate defect causes left-to-right shunt­ing with minimal elevation of pulmonary arterial pressure, and a large defect may result in equal­ization of systolic pressures in the two ventricles with the result that the shunt flow depends on the relative resistance in the pulmonary versus the systemic circulations. As pulmonary vascular re­sistance increases secondary to the increased pul­monary pressure and flow, the left-to-right shunt may gradually decrease and even become right-to-left (Eisenmenger’s complex). There is an in­creased incidence of aortic insufficiency in pa­tients with large ventricular septal defects, in some patients due to primary aortic valve abnor­mality and in others due to herniation of a valve leaflet through the septal defect.
Echocardiography reveals left ventricular vol­ume overload (hyperdynamic left ventricle). The defect usually cannot be directly visualized but may be indirectly visualized after a peripheral venous injection of echocardiographic contrast. Cardiac catheterization permits visualization and quantitation of the shunt and localizes it to the level of the ventricle. Associated defects are iden­tified. Pulmonary artery pressure and pulmonary vascular resistance are determined.
Patients with small ventricular septal defects should be watched for gradual closure. Larger de­fects should be corrected surgically unless the pulmonary vascular resistance has become mark­edly elevated, at which time operative risk is high and results are poor because pulmonary vascular resistance fails to decrease significantly postop­eratively.

• ELECTROPHYSIOLOGY
• NONPHARMACOLOQICAL MANAGEMENT OF HEART FAILURE
• ACYATJOTIC LESIONS
• ATRIAL SEPTAL DEFECT
• MANAGEMENT OF ACUTE PULMONARY EDEMA
• VENTRICULAR SEPTAL DEFECT
• MYOCARDIAL METABOLISM
• SYMPATHOMIMETIC AMINES
• PHYSIOLOGY OF THE PULMONARY CIRCULATION
• CONGENITAL HEART DISEASE
• MICROSCOPIC ANATOMY
• SHOCK
• CARDIAC DEVELOPMENT
• EVALUATION OF THE PATIENT WITH CARDIOVASCULAR DISEASE
• PHYSIOLOGY OF THE SYSTEMIC CIRCULATION
• PATENT DUCTUS ARTERIOSUS
• CIRCULATORY PHYSIOLOGY
• CARDIOVASCULAR RESPONSE TO EXERCISE
• GROSS ANATOMY
• HIGH-OUTPUT STATES
• PHYSIOLOGY OF THE CORONARY CIRCULATION