Pulmonary hemodynamic and gas exchange effects of various oxygen concentrations in patients with severe pulmonary hypertension primarily affecting the pulmonary vasculature]

The aim of this study was to evaluate pulmonary hemodynamic and gas exchange response to oxygen inhalation in patients with severe pulmonary hypertension primarily affecting the pulmonary vasculature. This study included 7 patients with primary pulmonary hypertension (PPH), 11 with pulmonary hypertension related to collagen vascular diseases (CoPH), and 18 with chronic thromboembolic pulmonary hypertension (CTEPH). All patients had mean pulmonary arterial pressure (PPAm) of greater than 25 mm Hg. We divided the patients into two groups: a PPH + CoPH group comprising the 7 PPH and 11 CoPH patients, and the CTEPH group. We measured cardiopulmonary variables after 10 min inhalation of various oxygen concentrations (FiO2 0.24, 0.28, 0.4, 1.0). In the PPH + CoPH group, PPAm significantly decreased after the inhalation of oxygen concentrations of 40% or more. This was associated with a significant reduction in pulmonary arteriolar resistance (PAR), and suggested active pulmonary vasodilation was caused by oxygen inhalation. In the CTEPH group, on the other hand, PPAm significantly decreased after the inhalation of oxygen concentrations of 28% or more, apparently in association with a significant fall of cardiac output. However, PAR was unchanged regardless of the inspired oxygen concentration, indicating an absence of pulmonary vasodilation in the CTEPH group. When breathing room air, 7 patients in the PPH + CoPH group (38.9%) and 10 in the CTEPH group (55.6%) demonstrated mixed venous oxygen tension (PvO2) values of less than 35 Torr. Extra attention should be paid to PvO2 when administering oxygen therapy to patients with severe pulmonary hypertension.