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dc.contributor.authorKent, Brian D
dc.contributor.authorMitchell, Patrick D
dc.contributor.authorMcNicholas, Walter T
dc.date.accessioned2012-02-01T10:30:12Z
dc.date.available2012-02-01T10:30:12Z
dc.date.issued2012-02-01T10:30:12Z
dc.identifier.citationInt J Chron Obstruct Pulmon Dis. 2011;6:199-208. Epub 2011 Mar 14.en_GB
dc.identifier.issn1178-2005 (Electronic)en_GB
dc.identifier.issn1176-9106 (Linking)en_GB
dc.identifier.pmid21660297en_GB
dc.identifier.doi10.2147/COPD.S10611en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207522
dc.description.abstractChronic 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.
dc.language.isoengen_GB
dc.subject.meshAnoxia/*etiology/physiopathology/therapyen_GB
dc.subject.meshDisease Progressionen_GB
dc.subject.meshExerciseen_GB
dc.subject.meshHumansen_GB
dc.subject.meshHypertension, Pulmonary/etiology/physiopathologyen_GB
dc.subject.meshInflammation/etiology/physiopathologyen_GB
dc.subject.meshMuscle, Skeletal/physiopathologyen_GB
dc.subject.meshOxygen Inhalation Therapyen_GB
dc.subject.meshPolycythemia/etiology/physiopathologyen_GB
dc.subject.meshPulmonary Alveoli/*physiopathologyen_GB
dc.subject.meshPulmonary Disease, Chronic Obstructive/*complications/physiopathology/therapyen_GB
dc.subject.mesh*Pulmonary Gas Exchangeen_GB
dc.subject.meshSeverity of Illness Indexen_GB
dc.subject.meshSleepen_GB
dc.subject.meshTreatment Outcomeen_GB
dc.titleHypoxemia in patients with COPD: cause, effects, and disease progression.en_GB
dc.contributor.departmentPulmonary and Sleep Disorders Unit, St. Vincent's University Hospital, Dublin,, Ireland. brian.kent@ucd.ieen_GB
dc.identifier.journalInternational journal of chronic obstructive pulmonary diseaseen_GB
dc.description.provinceLeinster
html.description.abstractChronic 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.


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