Pulmonary Oxygen Toxicity

Jackson, Robert M.

doi:10.1378/chest.88.6.900

Cited by 205 publications

(111 citation statements)

References 40 publications

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“…The overall result is death and lysis of the oxygen-sensitive cells, which result in microvascular and alveolar cell injuries which are typical of the oxygen toxicity. The rate at which the oxygen toxicity develops is directly related to the partial pressure of the inspired oxygen [56].…”

Section: The Pathobiology Of Copdmentioning

confidence: 99%

Oxidative/Nitrosative Stress and the Pathobiology of Chronic Obstructive Pulmonary Disease

Pandey

Singh²,

Singhal³

et al. 2013

JCDR

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The understanding of the pathobiology of Chronic Obstructive Pulmonary Disease (COPD) has undergone a major change in the past three decades. The classical 'protease-antiprotease' hypothesis still holds true, nevertheless, the sequence of the biochemical events which lead to the protease/antiprotease imbalance have been unraveled. For instance, tobacco smoke, a primary risk factor for COPD, contains a plethora of reactive Oxygen/ Nitrogen Species (ROS/RNS) that serve to initiate the oxidant/ antioxidant imbalance in the respiratory tract of chronic smokers, a phenomenon that is amplified if certain other risk factors co-exist (e.g. a genetic deficiency of the major antiproteases, a suboptimal antioxidant defense system, airway hyper responsiveness etc.). The inflammatory response that ensues as a result of the initial occult exogenous oxidative/ nitrosative stress becomes a secondary endogenous source of ROS/RNS. This perpetuates the ongoing lung damage, even though the primary insult may no longer be present (abstinence). Depletion of the pulmonary antioxidants, damage to the local antiprotease protective screen, a decreased immune response, hypersecretion of mucus, superadded infections, oxygen therapy-induced oxidant production, etc. are some of the critical factors which account for the oxidative/ nitrosative stressmediated pulmonary as well as extrapulmonary features of COPD. In the light of the recent developments, remarkable efforts are being made, either to develop novel therapeutic strategies or to improve the existing ones, which are aimed at treating different aspects of the disease. Thus, it is reasonable to recommend antioxidants as a useful adjunct to the more conventional treatment options, keeping in view the 'oxidant/antioxidant' hypothesis as a unifying theme for the 'protease/antiprotease' theory of COPD. INTRODUCTIONChronic Obstructive Pulmonary Disease (COPD) is characterized by a poorly reversible airflow limitation that is usually progressive and associated with the abnormal inflammatory response of the lung to noxious particles and/ or gases which are present in cigarette smoke [1,2]. The characteristic features of the disease are chronic inflammation of the peripheral airways, chronic bronchitis and destruction of the lung parenchyma (emphysema), which include systemic extra-pulmonary manifestations [3]. The patients can suffer from one, some or all of these conditions. The peripheral airways inflammation or small-airway disease involves various morphological abnormalities such as airway narrowing with goblet cell hyperplasia, smooth muscle hypertrophy, excess mucous, oedema and inflammatory cellular infiltration. Airway remodeling with sub-epithelial and peribronchial fibrosis has been postulated as the critical factor in the small-airway narrowing and the fixed airway obstruction in the small-airways of the patients with COPD [4].Anatomically, the disease can be viewed as a part of a spectrum, with chronic bronchitis at one end and emphysema at the other. Chronic bronchitis is ...

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Section: The Pathobiology Of Copdmentioning

confidence: 99%

Oxidative/Nitrosative Stress and the Pathobiology of Chronic Obstructive Pulmonary Disease

Pandey

Singh²,

Singhal³

et al. 2013

JCDR

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“…Second, during mechanical ventilation, unrecognized spurious hypoxemia may trigger inappropriate increase in F IO 2 and expose patients who are already prone to respiratory complications to additional pulmonary oxygen toxicity. 30 Third, P aO 2 is part of severity scores widely used in critically ill patients (APACHE [Acute Physiology and Chronic Health Evaluation] and SOFA [Sequential Organ Failure Assessment]), 31 and low recorded P aO 2 may falsely increase those scores. Finally, initial P aO 2 has been shown to be an independent predictor of mortality in immunocompromised populations with pulmonary infiltrates.…”

Section: Discussionmentioning

confidence: 99%

Hypoxemia During Extreme Hyperleukocytosis: How Spurious?

Louw

Desai²,

Schneider³

et al. 2015

Respir Care

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BACKGROUND: Spurious hypoxemia has been described in case reports during extreme hyperleukocytosis and has led to recommendations for immediate cooling and analysis of arterial blood gases (ABGs). We sought to determine, in samples processed as recommended, the magnitude of spurious hypoxemia in acute leukemia subjects with hyperleukocytosis. METHODS: A retrospective chart review was conducted of all subjects admitted between 2003 and July 2014 for acute leukemia, who presented with white blood cell (WBC) count > 50 ؋ 10 9 cells/L and had ABGs performed. For each ABG, we collected P aO 2 , S aO 2 , simultaneous WBC count, and S pO 2 when available. Bland and Altman analysis was used to assess the agreement between S pO 2 and S aO 2 . RESULTS: One-hundred forty-six samples (from 45 subjects) were included, of which 57 samples (from 18 subjects) had data available for Bland and Altman analysis. Mean (S pO 2 ؊ S aO 2 ) was 2.5%, and 95% CI for limits of agreement between S pO 2 and S aO 2 was (؊10.1,15.1)%. The mean (S pO 2 -S aO 2 ) was significantly higher for WBC count > 100 ؋ 10 9 /L as compared with WBC count < 100 ؋ 10 9 /L (3.8% vs 0.4%, P ‫؍‬ .04), and the 95% CIs for limits of agreement were (؊10.3,18)% versus (؊7.9,8.6)%. S pO 2 and S aO 2 were poorly correlated (r 2 ‫؍‬ 0.19), whereas the difference (S pO 2 -S aO 2 ) was fairly correlated with WBC count (r 2 ‫؍‬ 0.44). Overall, 11 of 19 samples with WBC count > 150 ؋ 10 9 /L had P aO 2 < 55 mm Hg whereas S pO 2 was > 94%, the proportion being 5 of 62 samples for WBC count < 150 ؋ 10 9 /L (P < .001). Three subjects with WBC count > 150 ؋ 10 9 /L exhibited large S pO 2 to S aO 2 differences (10 -20%) before leukapheresis, which decreased to below 5% afterward. CONCLUSIONS: In subjects with acute leukemia and hyperleukocytosis, despite cooling and quickly analyzing the samples, we observed poor correlation and agreement between S pO 2 and S aO 2 , unacceptably low for WBC count > 100 ؋ 10 9 /L. Our results suggest that current guidelines may not totally prevent the diagnosis of spurious hypoxemia.

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“…Oxygen therapy has been used in the care of critically ill patients since early years of the last century. However, from the beginnings of the 1970s an increasing understanding emerged that oxygen therapy can cause pulmonary toxicity [7]. Hyperoxia is detrimental for mechanically ventilated patients and even fraction of inspired oxygen (FiO 2 ) levels of 0.40 and lower can provoke pulmonary toxicity, thus leading to VILI.…”

Section: Introductionmentioning

confidence: 99%

“…Endothelial and epithelial cells injury, increased pulmonary capillary permeability and a marked increase in the inflammatory cells are the main manifestations of HALI [10]. Microscopically the prominent findings are: hyaline membrane formation in alveoli, alveolar septal edema and fibrosis, and diffuse hyperplasia of the alveolar lining layer with formation of a cuboidal epithelial lining [7]. The combination of high Vt and hyperoxia causes significantly greater reductions in the lung compliance, increased alveolar-capillary membrane permeability, gives more severe pulmonary surfactant dysfunction [11], and increases expression of pro-inflammatory mediators [12,13].…”

Section: Introductionmentioning

confidence: 99%

Synergistic Effect of Hyperoxia and Biotrauma On Ventilator-Induced Lung Injury

Shosholcheva

Јankulovski

Карталов

et al. 2017

Prilozi

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Patients undergoing mechanical ventilation in intensive care units (ICUs) may develop ventilator-induced lung injury (VILI). Beside the high tidal volume (Vt) and plateau pressure (Pplat), hyperoxia is supposed to precipitate lung injury. Oxygen toxicity is presumed to occur at levels of fraction of inspired oxygen (FiO 2 ) exceeding 0.40. The exposure time to hyperoxia is certainly very important and patients who spend extended time on mechanical ventilation (MV) are probably more exposed to severe hyperoxic acute lung injury (HALI). Together, hyperoxia and biotrauma (release of cytokines) have a synergistic effect and can induce VILI. In the clinical practice, the reduction of FiO 2 to safe levels through the appropriate use of the positive end expiratory pressure (PEEP) and the alignment of mean airway pressure is an appropriate goal. The strategy for lung protective ventilation must include setting up FiO 2 to a safe level that is accomplished by using PaO 2 /FiO 2 ratio with a lower limit of FiO 2 to achieve acceptable levels of PaO 2 , which will be safe for the patient without local (lungs) or systemic inflammatory response. The protocol from the ARDS-net study is used for ventilator setup and adjustment. Cytokines (IL-1, IL-6, TNFα and MIP-2) that are involved in the inflammatory response are determined in order to help the therapeutic approach in counteracting HALI. Computed tomography findings reflect the pathological phases of the diffuse alveolar damage. At least preferably the lowest level of FiO 2 should be used in order to provide full lung protection against the damage induced by MV.

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Pulmonary Oxygen Toxicity

Cited by 205 publications

References 40 publications

Oxidative/Nitrosative Stress and the Pathobiology of Chronic Obstructive Pulmonary Disease

Oxidative/Nitrosative Stress and the Pathobiology of Chronic Obstructive Pulmonary Disease

Hypoxemia During Extreme Hyperleukocytosis: How Spurious?

Synergistic Effect of Hyperoxia and Biotrauma On Ventilator-Induced Lung Injury

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