Abstract

Patients who have had the Fontan procedure report poor exercise performance. Fontan subjects can tolerate a higher level of sub maximal activity than might be anticipated from VO2, suggesting a different mechanism of exercise limitation. Near-infrared spectroscopy (NIRS) provides a non-invasive, continuous method to monitor regional tissue oxygenation (rSO2) and thereby a window into regional oxygen supply-demand relationships. We hypothesized that Fontan patients would have altered rSO2 trends from normal population that might reflect the mechanisms of exercise limitation. All the patients without structural or acquired heart disease and Fontan patients were eligible for inclusion if they were ordered to undergo cardiopulmonary exercise testing (CPET). Four-site regional rSO2 were recorded continuously during exercise. The difference between the oxyhemoglobin saturation measured by pulse oximetry (SpO2) and NIRS (rSO2) was computed as the regional arterial-venous saturation difference (AVDO2). A total of 33 normal subjects and five Fontan subjects scheduled for CPET were recruited. None of the Fontan subjects had a fenestration of the conduit. In the cerebral circulation, the Fontan patients have a significantly higher initial slope of increasing AVDO2 compared with normals. After vAT, the AVDO2 slope is flat for Fontan patients (p = 0.02). There is also a substantially larger rebound of cerebral rSO2 than in normal subjects after QT (p < 0.0001). Reduced anaerobic exercise capacity in Fontan patients may be secondary to limitation of cerebral blood flow, secondary to low systemic venous compliance due to absence of a sub-pulmonary ventricle, and augmented hyperventilatory response during exercise.

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