Hypercapnia From Hyperoxia in COPD: Another Piece of the Puzzle or Another Puzzle Entirely?

Embarrassment is a powerful teacher. I was barely 3 months into my internship, on night float at my residency’s Veterans Affairs hospital, when I received a page from a concerned ward nurse. A patient was unresponsive. He was admitted for a severe COPD exacerbation. I examined him, and he only groaned with a vigorous sternal rub. Suspecting hypercapnic narcosis, I drew an arterial blood gas. The results confirmed my suspicion. The patient was suffering from acute respiratory acidosis. In a panic, I paged the resident taking ICU admissions. The patient needed to go to the ICU and be intubated. The resident said he would see the patient. He wordlessly slipped into the room and went straight to the oxygen flow meter. He turned the flow down several liters and waited. He did not have to wait long: it was as if the patient had received a naloxone injection. Within 90 seconds, he woke suddenly and looked around the room, puzzled. “What is everyone doing in here?” he asked. The resident, again wordlessly, slipped out of the room. I learned my lesson, and I will never forget it. I take minor consolation in Tobin and Jubran’s1 grievance, “This perennial problem apparently must be rediscovered by each new rotation of house-staff personnel.” I have heard anecdotal reports of internal medicine and emergency department attending physicians doubting the existence of this phenomenon: hyperoxia-induced hypercapnia in patients with COPD. Why are we so recalcitrant? Part of the reason may be that the pathophysiologic mechanism behind it defies a simple explanation. In this issue of RESPIRATORY CARE, Rialp et al2 address the complicated mechanisms behind this phenomenon. Campbell3 first hypothesized about the mechanism in 1960. His hypothesis was attractive in its simplicity: chronically hypercapnic COPD patients are dependent solely on their hypoxic respiratory drive, as the chronic hypercapnia blunts their hypercapnic respiratory drive. Unfortunately, this hypothesis was too simple. When it was tested, Aubier et al4 found that the reduction in minute ventilation (V̇E) was transient and inadequate to explain the degree of hypercapnia. In another study, Aubier et al5 found no correlation between the degree of hypercapnia and the decrease in V̇E. Instead, they hypothesized that the excess hypercapnia was caused by 2 factors. The first was the Haldane effect (ie, the release of CO2 when deoxyhemoglobin converts to