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      International Journal of COPD (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on pathophysiological processes underlying Chronic Obstructive Pulmonary Disease (COPD) interventions, patient focused education, and self-management protocols. Sign up for email alerts here.

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      Hypoxemia in patients with COPD: cause, effects, and disease progression

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          Abstract

          Chronic obstructive pulmonary disease (COPD) is a leading cause of death and disability internationally. Alveolar hypoxia and consequent hypoxemia increase in prevalence as disease severity increases. Ventilation/perfusion mismatch resulting from progressive airflow limitation and emphysema is the key driver of this hypoxia, which may be exacerbated by sleep and exercise. Uncorrected chronic hypoxemia is associated with the development of adverse sequelae of COPD, including pulmonary hypertension, secondary polycythemia, systemic inflammation, and skeletal muscle dysfunction. A combination of these factors leads to diminished quality of life, reduced exercise tolerance, increased risk of cardiovascular morbidity, and greater risk of death. Concomitant sleep-disordered breathing may place a small but significant subset of COPD patients at increased risk of these complications. Long-term oxygen therapy has been shown to improve pulmonary hemodynamics, reduce erythrocytosis, and improve survival in selected patients with severe hypoxemic respiratory failure. However, the optimal treatment for patients with exertional oxyhemoglobin desaturation, isolated nocturnal hypoxemia, or mild-to-moderate resting daytime hypoxemia remains uncertain.

          Most cited references26

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          Controlled oxygen therapy and carbon dioxide retention during exacerbations of chronic obstructive pulmonary disease.

          Hypoxaemic patients with exacerbations of chronic obstructive pulmonary disease (COPD) are at some risk of carbon dioxide (CO2) retention during oxygen therapy. We quantified the risk of CO2 retention with oxygen therapy in COPD in 24 consecutive patients presenting to the accident and emergency department with acute exacerbations associated with hypercapnic respiratory failure (partial arterial pressure of oxygen [PaO2] or = 6.5 kPa). Only three patients developed clinically important CO2 retention (defined as a rise in PaCO2 > 1 kPa) with controlled oxygen therapy (24-40% by Venturi mask to maintain the oxygen saturation at 91-92%). These patients presented with more severe hypercapnia, but all three required only low-flow oxygen (24-28%). These findings suggest only a small risk of aggravating hypercapnia with controlled oxygen supplementation.
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            Effects of salmeterol on sleeping oxygen saturation in chronic obstructive pulmonary disease.

            Sleep is associated with important adverse effects in patients with chronic obstructive pulmonary disease (COPD), such as disturbed sleep quality and gas exchange, including hypoxemia and hypercapnia. The effects of inhaled long-acting beta(2)-agonist therapy (LABA) on these disturbances are unclear. The aim of the study was to assess the effect of inhaled salmeterol on nocturnal sleeping arterial oxygen saturation (SaO(2)) and sleep quality. In a randomized, double-blind, placebo-controlled, crossover study of moderate/severe stable COPD patients, we compared the effects of 4 weeks of treatment with salmeterol 50 microg b.d. and matching placebo on sleeping SaO(2) and sleep quality. Overnight polysomnography (PSG) was performed at baseline, and after 4 and 8 weeks in addition to detailed pulmonary function testing. Of 15 patients included, 12 completed the trial (median age 69 years, forced expiratory volume in 1 s, FEV(1): 39%). Both mean SaO(2) [salmeterol vs. placebo: 92.9% (91.2, 94.7) vs. 91.0% (88.9, 94.8); p = 0.016] and the percentage of sleep spent below 90% of SaO(2) [1.8% (0.0, 10.8) vs. 25.6% (0.5, 53.5); p = 0.005] improved significantly with salmeterol. Sleep quality was similar with both salmeterol and placebo on PSG. Static lung volumes, particularly trapped gas volume, tended to improve with salmeterol. We conclude that inhaled LABA therapy improves sleeping SaO(2) without significant change in sleep quality. Copyright 2009 S. Karger AG, Basel.
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              Effect of supplemental nocturnal oxygen on gas exchange in patients with severe obstructive lung disease.

              We studied the effect of supplemental nocturnal oxygen on blood gases in 15 patients with severe but stable chronic obstructive lung disease (ratio of forced expired volume in one second to forced vital capacity, 37.2 +/- 1.8 [mean +/- S.E.] per cent of predicted; arterial oxygen tension, 50.7 +/- 1.4 mm Hg; and arterial carbon dioxide tension [PCO2], 53.1 +/- 1.5 mm Hg). Sleep variables and measures of gas exchange were determined on two consecutive nights; on the first night the subjects breathed supplemental oxygen, and on the second they breathed room air. Transcutaneous PCO2 was measured with an infrared sensor, and arterial oxygen saturation with an ear oximeter. Breathing of supplemental oxygen sufficient to keep oxygen saturation at or above 90 per cent was associated with only small increases (less than 6 mm Hg) in PCO2 throughout sleep, as compared with values while subjects were breathing room air. The increase in PCO2 occurred early in the night and was not progressive. Only three patients, who were found to have obstructive sleep apnea in addition to obstructive lung disease, had larger increases in PCO2 during sleep and reported morning headaches. We conclude that nocturnal oxygen does not induce clinically important increases in PCO2 during sleep in patients with stable obstructive lung disease and therefore can safely be used to prevent the dangerous consequences of hypoxia.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2011
                2011
                14 March 2011
                : 6
                : 199-208
                Affiliations
                [1 ]Pulmonary and Sleep Disorders Unit, St. Vincent’s University Hospital, Dublin;
                [2 ]Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Ireland
                Author notes
                Correspondence: Brian Kent, Pulmonary and Sleep Disorders Unit, St. Vincent’s University Hospital, Dublin 4, Ireland, Tel +353 1221 3702, Fax +353 1221 3576, Email brian.kent@ 123456ucd.ie
                Article
                copd-6-199
                10.2147/COPD.S10611
                3107696
                21660297
                bd5f1831-a788-461e-be90-d4165a217c72
                © 2011 Kent et al, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                History
                : 11 March 2011
                Categories
                Review

                Respiratory medicine
                hypoxia,copd,sleep,pulmonary hypertension,inflammation
                Respiratory medicine
                hypoxia, copd, sleep, pulmonary hypertension, inflammation

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