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

Abstract

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's 1 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 RESPI-RATORY CARE, Rialp et al 2 address the complicated mechanisms behind this phenomenon.Campbell 3 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 al 4 found that the reduction in minute ventilation (V E ) was transient and inadequate to explain the degree of hypercapnia.In another study, Aubier et al 5 found no correlation between the degree of hypercapnia and the decrease in V E . Instead, they hypothesized that the excess hypercapnia was caused by 2 factors. The first was the Haldane effect (ie, the release of CO 2 when deoxyhemoglobin converts to SEE THE ORIGINAL STUDY ON PAGE 328 oxyhemoglobin). This mechanism was later confirmed by Luft et al. 6 The second was a decrease in pulmonary ventilation/perfusion matching due to the release of hypoxic pulmonary arterial vasoconstriction. This leads to a subsequent increase in functional dead space. This hypothesis was supported in a later study by Robinson et al. 7 Others found that hyperoxia also lessens the hyperventilation that follows acute hypercapnia in subjects with COPD. 8 Still others found the increase in P aCO 2 from hyperoxia to be a function of both increased functional dead space and decreased ventil...

Acute oxygen therapy: a review of prescribing and delivery practices

“…Resulting in a worse ventilation/perfusion mismatch, and a right-hand shift of the CO 2 dissociation curve (Haldane effect), further increasingP a CO 2 . 13 , 16 Other mechanisms for this phenomenon include further increases in ventilation/perfusion mismatching due to absorption atelectasis and an increased work of breathing due to the higher density of oxygen over air. 17 Initial beliefs that hypercapnia was primarily caused as a result of a “reduced hypoxic drive” have been largely disproved, 18 following the publication of results challenging these earlier hypothesis.…”

Acute oxygen use in hospitalised patients with chronic obstructive pulmonary disease is guideline discordant

“…Patients were universally over‐oxygenated and complications occurred in association with this over‐oxygenation. Supra‐therapeutic oxygenation has been shown to have several deleterious effects including worsening ventilation‐perfusion mismatch, reduced ventilatory drive, the Haldane effect and increased atelectasis 8 . The net effect of these is the propensity for complications, which we could not definitively attribute to over‐oxygenation in this retrospective study.…”