(988) - An Analysis of Mechanism of Hypoxia in Chronic Thromboembolic Pulmonary Hypertension

Abstract

In chronic thromboembolic pulmonary hypertension (CTEPH), residual hypoxia remains to be a limitation of physical activity, despite hemodynamic status improved. However, the precise mechanism of hypoxia and the medical contribution to the hypoxia have not been fully clarified. The purpose of our study was to clarify the determinants of hypoxia in CTEPH. We retrospectively analyzed patients with CTEPH who had measured hemodynamic status, respiratory function, and dead space ratio. Patients, who received medical intervention, were measured these parameters before and after treatment. We excluded chronic lung disease. In overall twenty-eight patients (19 female, 64±12 years), arterial oxygen saturation (SaO2) was 91.2±3.6% and dead space ratio (DSR) was 0.63±0.05. As far SaO2, %functional residual capacity (%FRC), mean pulmonary arterial pressure (mPAP) and DSR were significantly correlated (r= 0.53, 0.62, 0.44, p<0.05, respectively). Fifteen in 28 received medical intervention (7 patients were treated by balloon pulmonary angioplasty only, 2 by riociguat only, and 6 by combination of the two treatments). By improvement of mPAP (38.6±9.4 vs 25.2±2.8 mmHg, p<0.05), SaO2 and DSR were significantly improved (90.5±3.6 vs 93.9±1.9%, 0.64±0.5 vs 0.58±0.5, p<0.05, respectively). However %FRC was not improved. Furthermore, abnormality of SaO2 and DSR were persisting despite adequate hemodynamic improvement. Current therapy can improve hypoxia in CTEPH. It also improves DSR by correcting ventilation-perfusion imbalance. However, it is not enough to restore normal blood oxygenation level. It is possible that correcting %FRC is one of clue of the normalization of hypoxia in CTEPH.