Oxygen-induced hypercapnia: physiological mechanisms and clinical implications

Abstract

Oxygen is probably the most commonly prescribed drug in the emergency setting and is a life-saving modality as well. However, like any other drug, oxygen therapy may also lead to various adverse effects. Patients with chronic obstructive pulmonary disease (COPD) may develop hypercapnia during supplemental oxygen therapy, particularly if uncontrolled. The risk of hypercapnia is not restricted to COPD only; it has also been reported in patients with morbid obesity, asthma, cystic fibrosis, chest wall skeletal deformities, bronchiectasis, chest wall deformities, or neuromuscular disorders. However, the risk of hypercapnia should not be a deterrent to oxygen therapy in hypoxemic patients with chronic lung diseases, as hypoxemia may lead to life-threatening cardiovascular complications. Various mechanisms leading to the development of oxygen-induced hypercapnia are the abolition of ‘hypoxic drive’, loss of hypoxic vasoconstriction and absorption atelectasis leading to an increase in dead-space ventilation and Haldane effect. The international guideline recommends a target oxygen saturation of 88% to 92% in patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) and other chronic lung diseases at risk of hypercapnia. Oxygen should be administered only when oxygen saturation is below 88%. We searched PubMed, EMBASE, and the CINAHL from inception to June 2022. We used the following search terms: “Hypercapnia”, “Oxygen therapy in COPD”, “Oxygen-associated hypercapnia”, “oxygen therapy”, and “Hypoxic drive”. All types of study are selected. This review will focus on the physiological mechanisms of oxygen-induced hypercapnia and its clinical implications.

Oxygen-Associated Hypercapnia after both side Video-Assisted Thoracoscopic Surgery – A Case Report

“…In patients undergoing bilateral thoracic surgery, the use of oxygen concentration >50% during surgery can lead to hypoxic pulmonary vasoconstriction and absorption atelectasis, resulting in an increase in dead space. Pain and continuous oxygen inhalation are primary contributors to the loss of hypoxic pulmonary vasoconstriction, ventilation/perfusion mismatch, and an increase in PaCO 2 levels [6,7]. Therefore, for these patients, a shift in the ventilation strategy during the recovery period from a target oxygen saturation (SPO 2 ) of >95% to controlled oxygen therapy that corrects hypoxemia and prevents oxygen-induced hypercapnia is recommended.…”

Oxygen Overshoot: A Case Report Navigating the Perils of Unsupervised Supplementation in Chronic Obstructive Pulmonary Disease (COPD)

“…Even though COPD is recognized as a common cause of hypercapnia caused by oxygen delivery, other disease processes can also make patients vulnerable to oxygen-induced hypercapnia [ 1 , 4 ]. The improper use of oxygen in patients with COPD exacerbations can be fatal, especially when high-flow oxygen concentrations are associated with increased mortality [ 5 , 6 ].…”

“…Providing supplemental oxygen can be a careful balance between treating chronic hypoxemia and exacerbating hypercapnia in patients with chronic obstructive pulmonary disease (COPD) [ 1 , 2 ]. Uncontrolled administration of oxygen can induce hypercapnia in patients who are at high risk [ 1 ]. Careful consideration should be taken when companies directly advertise supplemental oxygen as a commercially available respiratory therapy.…”

Supplemental oxygen therapy in chronic obstructive pulmonary disease: is less is more? How much is too much?

“…To the best of our knowledge, there are no data on the critical upper limit of oxygenation under LTOT in patients with stable COPD. However, p a O 2 of 60–65 mmHg (7.98–8.65 kPa) or peripheral oxygen saturation (SpO 2 ) of 90–92% is generally considered an acceptable target [8], and most guidelines recommend a target SpO 2 of 88–92% in patients at risk of hypercapnia [9]. This represents clinically ‘adequate’ correction of hypoxemia for most patients and is unlikely to cause significant carbon dioxide (CO 2 ) retention.…”