Chronic obstructive pulmonary disease (COPD) is projected to be the third leading cause of mortality worldwide in 2020, with an annual healthcare expenditure of $50 billion in the United States alone. Acute exacerbation of COPD (AECOPD), characterized by worsening cough, sputum production, and breathlessness (beyond day-to-day variation), is frequently associated with hypoxic and hypercapnic respiratory failure. The inpatient mortality of patients with hypercapnic respiratory failure approaches 10%. Severe exacerbations requiring hospitalizations are commonly treated with bronchodilators, oxygen supplementation, systemic steroids, and antibiotics. Oxygen supplementation for hypoxia with concomitant hypercapnia has been a matter of relative uncertainty for many decades. The concern is that the correction of hypoxia will abolish hypoxic respiratory drive, leading to worsening hypercapnia.
Several researchers have assessed the consequences of oxygen supplementation in hypoxic AECOPD and, interestingly, hypercapnia was observed in all of these studies. Based on the available data, three potential mechanisms were responsible for the development of hypercapnia. This article discusses the pathophysiology and the relative contribution of each mechanism.
Links: Medscape (10/2021) (article is available open access on Medscape with free registration)