Blog
About

7
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Risk factors for developing hypoxic respiratory failure in COPD

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Hypoxemia is associated with worse outcomes in COPD. The aim of the study was to investigate the prevalence, incidence, and risk factors of hypoxic respiratory failure (HRF) in COPD.

          Patients and methods

          This was a longitudinal analysis of data from the Swedish National Register of COPD. HRF was defined as resting saturation ≤88% or long-term oxygen therapy. Risk factors for developing HRF were analyzed using multiple logistic regression and receiver operating characteristic curve analysis.

          Results

          A total of 3,061 patients were included; mean forced expiratory volume in 1 second was 1.47 L; mean age was 70 years; and 54% were females. Median follow-up time was 1.8 years (interquartile range 1.3–2.4 years). HRF was present in 43 (1.4%) patients at baseline and 74 (2.4%) patients at follow-up. Among patients without HRF at baseline, 49 (1.6%) developed HRF during follow-up. The risk was highest for patients in Global initiative for Chronic Obstructive Lung Disease (GOLD) 2017 stage IV or groups C or D at baseline. Developing HRF was independently predicted by lower forced expiratory volume in 1 second and lower COPD Assessment Test score, with a c-statistic of 0.84 (95% CI, 0.70–0.91). When the multivariable model used the GOLD 2017 variables stages I–IV and the dichotomized variables frequent exacerbations and COPD Assessment Test ≥10; the c-statistic increased slightly to 0.86 (95% CI, 0.80–0.92; P<0.0001).

          Conclusion

          In patients with COPD, the prevalence and incidence of HRF was low and was predicted well by more severe air flow limitation and worse health status. The risk is highest in patients with GOLD stage IV and GOLD groups C or D.

          Related collections

          Most cited references 18

          • Record: found
          • Abstract: found
          • Article: not found

          Measuring the accuracy of diagnostic systems.

           J Swets (1988)
          Diagnostic systems of several kinds are used to distinguish between two classes of events, essentially "signals" and "noise". For them, analysis in terms of the "relative operating characteristic" of signal detection theory provides a precise and valid measure of diagnostic accuracy. It is the only measure available that is uninfluenced by decision biases and prior probabilities, and it places the performances of diverse systems on a common, easily interpreted scale. Representative values of this measure are reported here for systems in medical imaging, materials testing, weather forecasting, information retrieval, polygraph lie detection, and aptitude testing. Though the measure itself is sound, the values obtained from tests of diagnostic systems often require qualification because the test data on which they are based are of unsure quality. A common set of problems in testing is faced in all fields. How well these problems are handled, or can be handled in a given field, determines the degree of confidence that can be placed in a measured value of accuracy. Some fields fare much better than others.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Pulmonary hypertension in COPD.

            Mild-to-moderate pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD); such a complication is associated with increased risks of exacerbation and decreased survival. Pulmonary hypertension usually worsens during exercise, sleep and exacerbation. Pulmonary vascular remodelling in COPD is the main cause of increase in pulmonary artery pressure and is thought to result from the combined effects of hypoxia, inflammation and loss of capillaries in severe emphysema. A small proportion of COPD patients may present with "out-of-proportion" pulmonary hypertension, defined by a mean pulmonary artery pressure >35-40 mmHg (normal is no more than 20 mmHg) and a relatively preserved lung function (with low to normal arterial carbon dioxide tension) that cannot explain prominent dyspnoea and fatigue. The prevalence of out-of-proportion pulmonary hypertension in COPD is estimated to be very close to the prevalence of idiopathic pulmonary arterial hypertension. Cor pulmonale, defined as right ventricular hypertrophy and dilatation secondary to pulmonary hypertension caused by respiratory disorders, is common. More studies are needed to define the contribution of cor pulmonale to decreased exercise capacity in COPD. These studies should include improved imaging techniques and biomarkers, such as the B-type natriuretic peptide and exercise testing protocols with gas exchange measurements. The effects of drugs used in pulmonary arterial hypertension should be tested in chronic obstructive pulmonary disease patients with severe pulmonary hypertension. In the meantime, the treatment of cor pulmonale in chronic obstructive pulmonary disease continues to rest on supplemental oxygen and a variety of measures aimed at the relief of airway obstruction.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Report of the Medical Research Council Working Party.

               Research Medical (corresponding) (1981)
              A controlled trial of long term domiciliary oxygen therapy has been carried out in three centres in the U.K. The 87 patients, all under 70 years of age, who took part had chronic bronchitis or emphysema with irreversible airways obstruction, severe arterial hypoxaemia, carbon dioxide retention, and a history of congestive heart failure. The patients were randomised to oxygen therapy (treated) or no oxygen (controls). Oxygen was given by nasal prongs for at least 15 h daily, usually at 2 1/min. The two groups were well matched, both clinically and in terms of lung function and other laboratory findings. 19 of the 42 oxygen treated patients died in the five years of survival follow-up compared with 30 out of 45 controls: in the 66 men in this trial the survival advantage of oxygen did not emerge until 500 days had elapsed. Survival for the 12 female controls was surprisingly poor, 8 of them being dead at 3 years. Mortality was not easy to predict, though a summation of arterial carbon dioxide tension and red cell mass was helpful. Neither time spent in hospital because of exacerbations of respiratory failure nor work attendance were affected by oxygen therapy, but these patients were very ill at the start of the trial and many had already retired on grounds of age or ill-health. Physiological measurements suggested that oxygen did not slow the progress of respiratory failure in those who died early. However, in longer term survivors on oxygen, arterial oxygenation did seem to stop deterioration.
                Bookmark

                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2017
                20 July 2017
                : 12
                : 2095-2100
                Affiliations
                [1 ]Department of Respiratory Medicine, School of Medical Sciences, Örebro University, Örebro
                [2 ]Department of Clinical Sciences, Division of Respiratory Medicine and Allergology, Lund University, Lund, Sweden
                Author notes
                Correspondence: Josefin Sundh, Department of Respiratory Medicine, School of Medical Sciences, Örebro University, 70182 Örebro, Sweden, Tel +46 70 234 9517, Fax +46 19 186 526, Email josefin.sundh@ 123456oru.se
                Article
                copd-12-2095
                10.2147/COPD.S140299
                5530070
                © 2017 Sundh and Ekström. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Comments

                Comment on this article