Oxygen Supplementation in COPD Exacerbation With Hypoxia and Hypercapnia

What Does the Evidence Show?

Biplab K. Saha, MD; Alyssa Bonnier, RN, BSN; Woon H. Chong, MD


South Med J. 2021;114(9):620-622. 

In This Article

Abstract and Introduction


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.[1,2] 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.[3] The inpatient mortality of patients with hypercapnic respiratory failure approaches 10%.[1] 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. Whether supplemental oxygen results in worsening hypercapnia and respiratory acidosis is still debatable. The mechanisms responsible for such observations have been a source of confusion among healthcare providers, respiratory therapists, nurses, and paramedics.

AECOPD is most often precipitated by an infectious process. The inflammatory response in the airways causes mucosal edema, bronchial narrowing, bronchospasm, mucus hypersecretion, and airway closure. These changes cause acute deterioration of ventilation perfusion (V/Q) matching, promote right to left shunting, and result in alveolar hypoventilation. To complicate the matter further, AECOPD is associated with significantly increased ventilatory drive and tachypnea, which can culminate in the vicious cycle of dynamic hyperinflation.[4] Several researchers have assessed the consequences of oxygen supplementation in hypoxic AECOPD and, interestingly, hypercapnia was observed in all of these studies.[4–6] Based on the available data, three potential mechanisms were responsible for the development of hypercapnia. In the following sections, we discuss the pathophysiology and the relative contribution of each mechanism.