Contributions of residual hypoxemia to exercise hyperventilation in Fontan patients

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It is unsettled whether increased exercise ventilation in Fontan subjects is due to increased pulmonary dead space or augmented ventilatory drive. Twenty-six Fontan patients underwent symptom-limited treadmill cardiopulmonary exercise testing. Two groups of age- and sex- matched subjects served as controls: the biventricularly repaired (Bi, n = 18), and the “true” control (C, n = 29) groups. Peak oxygen uptake (VO2peak) was not different among groups (41.0 +/– 8.4 ml/min/kg, 43.5 +/– 6.6 ml/min/kg, and 45.9 +/– 11.6 ml/min/kg for Fontan, Bi, and C groups, respectively, p = 0.16). Fontan subjects, however, showed steeper alveolar ventilation/carbon-dioxide (VA/VCO2) regression slope (35.5 +/– 5.3, 28.7 +/– 3.8, and 29.5 +/– 3.0 l/ml, for Fontan, Bi, and C groups, respectively, p<0.0001), and lower end-expiratory carbon-dioxide fraction (FetCO2VAT) at ventilatory threshold (VAT) (4.4 +/– 0.5%, 5.5 +/– 0.5%, and 5.5 +/– 0.4%, for Fontan, Bi, and C groups, respectively, p<0.001). The dead-space ventilation fraction at VAT was similar among groups (0.33 +/– 0.06, 0.33 +/– 0.04, 0.35 +/– 0.05 for Fontan, Bi, and C groups, respectively, p = 0.54). In Fontan subjects, arterial oxygen saturation at rest (SaO2rest) was correlated with VA/VCO2 regression slope (r = –0.41, p = 0.04) and with FetCO2VAT (p = –0.53, p<0.01). We conclude that Fontan patients show exercise hyperventilation due to augmented central and/or peripheral ventilatory drive, which is further augmented by residual hypoxemia.

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