The Role of Hypoventilation and Ventilation-Perfusion  Redistribution in Oxygen-induced Hypercapnia during Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Robinson, Tracey D.; Freiberg, David B.; Regnis, Jeff A.; Young, Iven H.

doi:10.1164/ajrccm.161.5.9904119

Cited by 149 publications

(104 citation statements)

References 14 publications

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“…This is only a significant risk when the inspired oxygen concentration exceeds y30% (30 kPa). The mechanism underlying this process has been hotly debated since the 1960s [27], with evidence supporting ventilation/perfusion mismatching in very severe cases [28], whereas CO 2 retention in less severe episodes involves an element of hypoventilation secondary to a reduction in hypoxic drive to breathing [29]. Controlled oxygen can be safely administered via a Venturi-based face mask or through nasal prongs.…”

Section: Maintaining Gas Exchangementioning

confidence: 99%

Respiratory failure in chronic obstructive pulmonary disease

Calverley¹

2003

Eur Respir J

107

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Respiratory failure in chronic obstructive pulmonary disease. P.M.A. Calverley. #ERS Journals Ltd 2003. ABSTRACT: Respiratory failure is still an important complication of chronic obstructive pulmonary disease (COPD) and hospitalisation with an acute episode being a poor prognostic marker. However, other comorbid conditions, especially cardiovascular disease, are equally powerful predictors of mortality.The physiological basis of acute respiratory failure in COPD is now clear. Significant ventilation/perfusion mismatching with a relative increase in the physiological dead space leads to hypercapnia and hence acidosis. This is largely the result of a shift to a rapid shallow breathing pattern and a rise in the dead space/tidal volume ratio of each breath. This breathing pattern results from adaptive physiological responses which lessen the risk of respiratory muscle fatigue and minimise breathlessness.Treatment is directed at reducing the mechanical load applied to each breath, correcting specific precipitating factors, e.g. bacterial infection, and maintaining gas exchange. Both bronchodilators and oral corticosteroids can improve spirometric results in exacerbations of COPD and should be routinely offered to patients with respiratory failure. Controlled oxygen is still not always prescribed appropriately and high inspired oxygen concentrations can lead to severe acidosis by either worsening ventilation/perfusion mismatching and/or inducing a degree of hypoventilation. Ventilatory support using noninvasive ventilation has revolutionised the approach to these patients.Acute respiratory failure due to chronic obstructive pulmonary disease remains a common medical emergency that can be effectively managed. More attention should be focused on the prevention of these episodes and identifying the factors which cause early relapse. Eur Respir J 2003; 22: Suppl. 47, 26s-30s.

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Section: Maintaining Gas Exchangementioning

confidence: 99%

Respiratory failure in chronic obstructive pulmonary disease

Calverley¹

2003

Eur Respir J

107

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“…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 ventilatory response to hypercapnia.…”

mentioning

confidence: 64%

“…9 Additionally, patients with COPD are not a homogenous group; it seems that there are subjects who retain (ie, become hypercapnic when hyperoxemic) and those who do not. 7 We know that subjects who are more hypoxemic and hypercapnic on room air experience greater degrees of hypercapnia with hyperoxia. 10 In this issue of RESPIRATORY CARE, we add a new study to the existing disarray.…”

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confidence: 99%

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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“…Robinson et al 26 used the multiple inert gas elimination technique to measure ventilation, cardiac output, and the distribution of ventilation-perfusion ratio in patients with a COPD exacerbation. They found that in patients in whom P aCO 2 rises in response to 100% oxygen, ventilation decreases and alveolar dead space increases.…”

Section: Discussionmentioning

confidence: 99%

Influence of F_IO₂on P_aCO₂During Noninvasive Ventilation in Patients With COPD

et al. 2013

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BACKGROUND:The administration of a high F IO 2 to COPD patients breathing spontaneously may result in hypercapnia, due to reversal of preexisting regional hypoxic pulmonary vasoconstriction, resulting in a greater dead space. Arterial blood gas trends have not been reported in these patients. In a 31-bed medical ICU in a teaching hospital we prospectively investigated the response of 17 CO 2 -retaining COPD patients, after acute respiratory crisis stabilization with noninvasive ventilation, to an F IO 2 of 1.0 for 40 min, after having been noninvasively ventilated with an F IO 2 of < 0.50 for 40 min. RESULTS: The mean ؎ SD baseline findings were: P aO 2 101.4 ؎ 21.7 mm Hg, P aCO 2 52.6 ؎ 10.4 mm Hg, breathing frequency 17.8 ؎ 3.7 breaths/min, tidal volume 601 ؎ 8 mL, and Glasgow coma score of 14.8 ؎ 0.3. P aO 2 significantly increased (P < .001) when F IO 2 was increased to 1.0, but there was no significant change in P aCO 2 , breathing frequency, tidal volume, or Glasgow coma score. CONCLUSIONS: During noninvasive ventilation with an F IO 2 sufficient to maintain a normal P aO 2 , a further increase in F IO 2 did not increase P aCO 2 in our CO 2 -retaining COPD patients.

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The Role of Hypoventilation and Ventilation-Perfusion Redistribution in Oxygen-induced Hypercapnia during Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Cited by 149 publications

References 14 publications

Respiratory failure in chronic obstructive pulmonary disease

Respiratory failure in chronic obstructive pulmonary disease

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

Influence of F_IO₂on P_aCO₂During Noninvasive Ventilation in Patients With COPD

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The Role of Hypoventilation and Ventilation-Perfusion Redistribution in Oxygen-induced Hypercapnia during Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Cited by 149 publications

References 14 publications

Respiratory failure in chronic obstructive pulmonary disease

Respiratory failure in chronic obstructive pulmonary disease

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

Influence of FIO2on PaCO2During Noninvasive Ventilation in Patients With COPD

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Influence of F_IO₂on P_aCO₂During Noninvasive Ventilation in Patients With COPD