Failure of stroke volume augmentation during exercise and dobutamine stress is unrelated to load-independent indexes of right ventricular performanceafter the Mustard operation

Background-Impaired right ventricular function has been implicated as a cau se of reduced maximal exercise capacity after the Mustard operation for tra nsposition of the great arteries. Methods and Results-Fourteen asymptomatic survivors of the Mustard operatio n were studied. Each underwent conventional cardiac catheterization, and af ter satisfactory hemodynamics were confirmed, load-independent indexes of v entricular function were derived by conductance catheter during dobutamine infusion (0, 5, and 10 mug.kg(-1).min(-1)). Seven patients also underwent u pright exercise testing on a bicycle ergometer with analysis of respiratory gas exchange by continuous mass spectrometry. Accessible pulmonary blood f low was measured at each workload with an automated acetylene rebreathing t echnique. All patients exercised to a satisfactory end point (respiratory q uotient >1.1). Maximum oxygen consumption during exercise was impaired comp ared with predicted values (mean, 77%; P<0.02). Both exercise and dobutamin e infusion were associated with an increase in cardiac index and heart rate and a reduced stroke volume index response. This was despite significantly improved indexes of myocardial contraction tend-systolic pressure volume r elation, P<0.001), preload recruitable stroke work index (P<0.01), VA coupl ing (P<0.001), and isovolumic relaxation (P<0.001) during dobutamine infusi on. There were no changes observed in end-diastolic pressure-volume relatio ns, but there was failure to augment ventricular filling manifest by absenc e of change in dV/dt (P=NS). Conclusions-The stroke volume response to exercise stress is reduced in pat ients after the Mustard operation. A similar failure to augment stroke volu me occurs during dobutamine stress despite appropriate responses in lend-in dependent indexes of contraction and relaxation. This is due to failure to augment right ventricular filling rates during tachycardia, presumably as a result of impaired AV transport, consequent to the abnormal intra-atrial p athways.