Hyperoxic-Induced Hypercapnia in Stable Chronic Obstructive Pulmonary Disease<sup>1–</sup><sup>3</sup>

Sassoon, Catherine S. H.; Hassell, Kathleen; Mahutte, C. K.

doi:10.1164/arrd.1987.135.4.907

Cited by 148 publications

(52 citation statements)

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“…In accordance, although being reduced to some extent, ⌬P 0.1 /⌬P aCO 2 in hyperoxia did not change significantly compared with normoxia, as found in other studies. 3,5,11 Our results suggest that an attenuation of respiratory drive functioning would not be the main mechanism to explain the hyperoxia-induced hypercapnia in normoxic, ready-to-wean subjects with COPD.…”

Section: Discussionmentioning

confidence: 75%

“…Other studies on subjects with COPD observed similar results. 4,5 The hyperoxia-induced hypercapnia observed in these studies was assumed to result principally from an increase in the dead-space-to-V T ratio or from alterations in ventilation/perfusion matching rather than from a reduction in ventilation. 4,5 Because dead space is sensitive to changes in P aCO 2 , the Haldane effect on P aCO 2 might be responsible, in part, for the increase in dead space during hyperoxia.…”

Section: Discussionmentioning

confidence: 99%

“…4,5 The hyperoxia-induced hypercapnia observed in these studies was assumed to result principally from an increase in the dead-space-to-V T ratio or from alterations in ventilation/perfusion matching rather than from a reduction in ventilation. 4,5 Because dead space is sensitive to changes in P aCO 2 , the Haldane effect on P aCO 2 might be responsible, in part, for the increase in dead space during hyperoxia. 25 Interestingly and in accordance with these results, Santos et al 10 observed an increase in P aCO 2 of 4 mm Hg while breathing 100% oxygen in 4 subjects with COPD connected to mechanical ventilation, sedated, and paralyzed, keeping V E constant.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 From 1980 onward, several studies investigated the mechanisms by which hyperoxia induces hypercapnia in subjects with COPD. [3][4][5][6][7][8][9][10] Most of these studies were conducted in non-intubated subjects with COPD through a mouthpiece, either in stable 5,8 or unstable 3,4,6 respiratory conditions. Most concluded that the control of ventilation played a minor role and suggested that the main mechanism to impair gas exchange during hyperoxia was a release of hypoxic pulmonary vasoconstriction that induced changes in the ventilation-perfusion distribution and entailed an increase in the dead-space-to-tidal-volume (V T ) ratio.…”

Section: Introductionmentioning

confidence: 99%

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Role of Respiratory Drive in Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With COPD

et al. 2014

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BACKGROUND: Hyperoxia-induced hypercapnia in subjects with COPD is mainly explained by alterations in the ventilation/perfusion ratio. However, it is unclear why respiratory drive does not prevent CO 2 retention. Some authors have highlighted the importance of respiratory drive in CO 2 increases during hyperoxia. The aim of the study was to examine the effects of hyperoxia on respiratory drive in subjects with COPD. METHODS: Fourteen intubated, ready-to-wean subjects with COPD were studied during normoxia and hyperoxia. A CO 2 response test was then performed with the rebreathing method to measure the hypercapnic drive response, defined as the ratio of change in airway-occlusion pressure 0.1 s after the start of inspiratory flow (⌬P 0.1 ) to change in P aCO 2 (⌬P aCO 2 ), and the hypercapnic ventilatory response, defined as the ratio of change in minute volume (⌬V E ) to ⌬P aCO 2 . RESULTS: Hyperoxia produced a significant increase in P aCO 2 (55 ؎ 9 vs 58 ؎ 10 mm Hg, P ‫؍‬ .02) and a decrease in pH (7.41 ؎ 0.05 vs 7.38 ؎ 0.05, P ‫؍‬ .01) compared with normoxia, with a non-significant decrease in V E (9.9 ؎ 2.9 vs 9.1 ؎ 2.3 L/min, P ‫؍‬ .16) and no changes in In ready-to-wean subjects with COPD exacerbations, hyperoxia is followed by an increase in P aCO 2 , but it does not significantly modify the respiratory drive or the ventilatory response to hypercapnia.

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Role of Respiratory Drive in Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With COPD

et al. 2014

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“…5 The respiratory drive was unchanged between the 2 conditions, also similar to previous findings. 5,12 Additionally, hyperoxia did not affect the rate of change in V E and respiratory drive per mm Hg increase in P aCO 2 . In other words, the slope of the relationship was unchanged.…”

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confidence: 86%

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

Littleton

2015

Respir Care

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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...

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Acute on Chronic Respiratory Failure

Schmidt

Hall²

1989

JAMA

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Patients with acute or chronic respiratory failure exhibit severe pulmonary impairment as a baseline characteristic. Additional minor insults can precipitate cardiopulmonary failure that requires hospital admission and possibly mechanical ventilation. Our approach to these patients emphasizes evaluation of the imbalance between neuromuscular competence and mechanical load on the respiratory system. In this way, reversible factors can be identified and corrected before they progress to inspiratory muscle fatigue and respiratory failure. For cases in which deterioration is inexorable, guidelines for mechanical ventilation are given and approaches to eventual liberation from the ventilator are reviewed.

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Hyperoxic-Induced Hypercapnia in Stable Chronic Obstructive Pulmonary Disease^1–³

Cited by 148 publications

References 16 publications

Role of Respiratory Drive in Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With COPD

Role of Respiratory Drive in Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With COPD

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

Acute on Chronic Respiratory Failure

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Hyperoxic-Induced Hypercapnia in Stable Chronic Obstructive Pulmonary Disease1–3

Cited by 148 publications

References 16 publications

Role of Respiratory Drive in Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With COPD

Role of Respiratory Drive in Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With COPD

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

Acute on Chronic Respiratory Failure

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Hyperoxic-Induced Hypercapnia in Stable Chronic Obstructive Pulmonary Disease^1–³