Additionally, the study of Weitzenblum etal, which demonstrated that LTOT resulted in a reduction in the progression of pulmonary hypertension in patients with stable COPD, was analyzed in regard to changes in arterial Po, after oxygen therapy was initiated. In this study, all patients had been examined at least one year prior to the initiation of oxygen therapy, and each had a PaO, constantly less than 60 mm Hg during three consecutive control measurements (with a delay of one month between each measurement to assure clinical stability). Both ABGs breathing room air and pulmonary artery catheterization were performed when oxygen therapy was begun (TJ and after one year (Tj).
Pertinent laboratory studies for the 20 patients who completed six months of TT02 therapy are presented in Table 1. Croup A contains the four subjects (20 percent) who demonstrated an arterial Po2 greater than 55 mm Hg after six months of therapy, while group B includes those individuals in whom the PaO£ remained equal to or less than 55 mm Hg. None of the patients with an increase in Pa02 above 55 mm Hg had erythrocytosis or manifestations of cor pulmonale which would have allowed recertification if this had been required at the end of six months; yet, all of these patients had stable severe COPD and had been receiving oxygen therapy for at least seven months before TT02 was begun (mean, 25.8 months).
Table 1—Characteristics of Patients Receiving Transtracheal Oxygen Therapy
|Patient NoVAge, yr/Sex||FEV„L||FEV„ % pred||Duration of Oa Therapy before Study||Po, T., mm Hg||Po, T„ mm Hg||Pcoa T„ mm Hg||Pco2 Ta, mm Hg||APfA-aX), Tj-Ta, mm Hg|
|2/61/F||0.67||29||9 mo||50||61||51||54||— 14.6|
|20/58/F||0.87||33||11 yr||40||34||55||51||+ 10.8|