It is also available at domiciliary settings for patients with chronic type II respiratory failure (i.e., hypoxemia with hypercapnia), including those with COPD. Correction of hypoventilation and acute respiratory acidosis using noninvasive ventilation (NIV) is a widely used and evidence-based treatment for acute hypercapnic respiratory failure (AHRF). Several mechanisms, which are detailed in this review article, may lead to alveolar hypoventilation and result in hypercapnia in COPD. Overall, chronic hypercapnia is an independent risk factor for hospitalizations and mortality in COPD and has thus attracted attention as a possible treatable trait.
Moreover, the repair mechanisms of the airway epithelial cells are also damaged as hypercapnia causes mitochondrial dysfunction and impaired cell proliferation.
Hypercapnia causes alveolar epithelial dysfunction, which results in alveolar oedema formation and further deterioration in gas exchange. Although hypercapnia may be beneficial to mitigate pulmonary inflammation, there is an increasing amount of evidence suggesting that the deleterious effects outweigh the protective ones. The prevalence of hypercapnia is around 30–50% in patients with very severe COPD (predicted forced expiratory volume in the first second (FEV 1) <30%). The presence of alveolar hypoventilation, and therefore the development of consequential hypercapnia, is more common in severe forms of COPD, although hypercapnia is present in even moderate disease in a proportion of patients.
It is usually considered to be a progressive disease, and the ultimate worsening of airflow limitation and impaired gas exchange may result in the development of hypercapnia. COPD is responsible for 250,000 deaths yearly in the European Union and is the third leading cause of mortality worldwide. Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease that is caused by aberrant airway inflammation due to chronic exposure to noxious gases or particles, such as tobacco or biomass fuel smoke.
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