ABSTRACTLeft-to-right (L-R) shunting across a ventricular septal defect (VSD) often involves a direct VSD-pulmonary arterial component (jet) that surges from the VSD immediately into the pulmonary artery. We used the thermodilution technique in dogs with acute experimental VSD to quantify this component. In dogs with supracristal VSD (n = 7), the direct component represented 76 + 4% (mean ± SE) of the total L-R shunt on average, vs 39 ± 7% (p < .001) of the total in dogs with infracristal VSD and the same level of L-R shunting (n = 6). The direct component can be expected to impose additional hyperkinetic forces on the pulmonary artery since it is driven by the left ventricular pressure. Although not yet clinically proven, we speculate therefore that patients with supracristal VSD may be at greater risk of becoming jeopardized by late-onset pulmonary vascular obstructive disease. Since a part of the total shunt other than the direct component dropped into the right ventricle, the right ventricle bore only 24% of the total shunt in supracristal VSD, but 61% in infracristal VSD. We also found that the amount of direct component was decreased, and therefore another part must have increased, as the pulmonary vascular resistance was artificially raised. As a second speculation, therefore, we suggest that patients with supracristal VSD may have less enlargement of the right ventricle than those with infracristal VSD before pulmonary hypertension develops.