Pulmonary embolism associated with postoperative deep breathing.

1 am pleased to see that Dr Schachter and Dr Domingo and colleagues confirm OU observation relative to an increase in arterial Po2 occurring three to six months after initiation of oxygen therapy in stable patients with ‘ However, Dr Schachter takes issue with the recommendation that supplemental oxygen not he discontinned when the arterial Po, increases as a result of the beneficial effects of oxygen therapy. Dr Schachter further comments that in his experience once the I)2ttient ha.s been able to discontinue the supplemental oxygen, the hvpoxemia and cor pulmonale do not recur, barring an acute exacerbation of the COPD. First of all, it is extremely uncommon for patients with a Po2 of 55 mm hg or less (when clinically stable) not to experience stll)sequent exacerl)atiofls of their COPD, even with what would be a minor respiratory illness for normal individuals. Even more important is the fact that the multicenter clinical trial funded by the National Institutes of llealth (the NO1’T study)2 found that patients with an arterial Po2 of55 mm Hg or less (or 56 to 59 mm Hg with cor pulmonale or erythrocytosis) who qualified after only three weeks of observation experienced a significant reduction in mortality that was evident by the end ofone year and that persisted for the three-year period of study None of these patients was retested, and there is flO evidence or assurance that discontinuing oxygen during the course of this study would have resulted in the same survival statistics for these individuals. It also should be noted that all of the patients in OU study who had an increase in PaO2 at six months continued to demonstrate desaturation with walking, indicating that they would have experienced periods of desaturation during their daily living cycle without supplemental oxygen. The bottom line is that the only conclusive scientific data currently available indicate that if patients (1ualify for long-term oxygen therapy in a stable clinical state, then continued oxygen therapy results in improved survival and an improved quality of life. Until a multicenter study specifically examines those patients who show improvement in PaO2 attributable to the beneficial effects of the therapy and it has been demonstrated that stopping therapy does not jeopardize any of the positive results found in the NOTT study, then it is my strong conviction that termination of therapy is not scientifically justified. It may be that some patients can safely terminate oxygen therapy after a period oftime ifthe PaO2 increases, but currently we are uncertain about the effect of exercise or nocturnal desaturation in these individuals and what would be the long-term prognosis when compared with a group ofsimilar patients who are allowed to continue oxygen therapy. The findings of the NOT’!’ study appear to be conclusive as far as the study was taken, and until new data from controlled studies are available the lives and welfare of patients with COPD and hypoxemia should not be jeopardized OI the basis of uncontrolled observations that patients appear to do well as long as they do not experience an acute exacerbation oftheir disease. After all, we were unable to recognize the significant benefit of nearly continuous oxygen (19 bId) over nocturnal oxygen until a multicenter study was conducted. Let us iiot discard these findings simply because we flOW recognise that oxygen has a reparative effect after months of therapy