Department of Lifelong Sports and Health Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan.
Department of Cardiology, Aichi Children's Health and Medical Center, Obu City, Japan.
Nagoya J Med Sci. 2020 May;82(2):281-289. doi: 10.18999/nagjms.82.2.281.
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 (V̇O) 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 (V̇A/V̇CO) 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 (FetCO) 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 (SaO) was correlated with V̇A/V̇CO regression slope (r = -0.41, p = 0.04) and with FetCO (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.
在 Fontan 患者中，增加的运动通气是由于肺死腔增加还是通气驱动增强尚不确定。26 名 Fontan 患者接受了症状限制跑步机心肺运动测试。两组年龄和性别匹配的受试者作为对照组：双心室修复（Bi，n = 18）和“真正”对照组（C，n = 29）。三组的峰值摄氧量（V̇O）无差异（Fontan、Bi 和 C 组分别为 41.0 ± 8.4 ml/min/kg、43.5 ± 6.6 ml/min/kg 和 45.9 ± 11.6 ml/min/kg，p = 0.16）。然而，Fontan 患者的肺泡通气/二氧化碳（V̇A/V̇CO）回归斜率更陡峭（Fontan、Bi 和 C 组分别为 35.5 ± 5.3、28.7 ± 3.8 和 29.5 ± 3.0 l/ml，p<0.0001），并且在通气阈值（VAT）时呼气末二氧化碳分数（FetCO）更低（Fontan、Bi 和 C 组分别为 4.4 ± 0.5%、5.5 ± 0.5% 和 5.5 ± 0.4%，p<0.001）。三组的 VAT 时死腔通气分数相似（Fontan、Bi 和 C 组分别为 0.33 ± 0.06、0.33 ± 0.04 和 0.35 ± 0.05，p = 0.54）。Fontan 患者静息时的动脉血氧饱和度（SaO）与 V̇A/V̇CO 回归斜率（r = -0.41，p = 0.04）和 FetCO 相关（p = -0.53，p<0.01）。我们得出结论，Fontan 患者的运动性过度通气是由于中枢和/或外周通气驱动增强所致，而残留低氧血症进一步增强了这种通气驱动。
