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      Dose variability of supplemental oxygen therapy with open patient interfaces based on in vitro measurements using a physiologically realistic upper airway model

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          Abstract

          Background

          Supplemental oxygen therapy is widely used in hospitals and in the home for chronic care. However, there are several fundamental problems with the application of this therapy such that patients are often exposed to arterial oxygen concentrations outside of the intended target range. This paper reports volume-averaged tracheal oxygen concentration measurements (FtO2) from in vitro experiments conducted using a physiologically realistic upper airway model. The goal is to provide data to inform a detailed discussion of the delivered oxygen dose.

          Methods

          A baseline FtO2 dataset using a standard, straight adult nasal cannula was established by varying tidal volume (V t), breathing frequency (f), and continuous oxygen flow rate (Q O2) between the following levels to create a factorial design: V t = 500, 640, or 800 ml; f = 12, 17, or 22 min − 1; Q O2 = 2, 4, or 6 l/min. Further experiments were performed to investigate the influence on FtO2 of variation in inspiratory/expiratory ratio, inclusion of an inspiratory or expiratory pause, patient interface selection (e.g. nasal cannula versus a facemask), and rapid breathing patterns in comparison with the baseline measurements.

          Results

          Oxygen concentration measured at the trachea varied by as much as 60% (i.e. from 30.2 to 48.0% of absolute oxygen concentration) for the same oxygen supply flow rate due to variation in simulated breathing pattern. Among the baseline cases, the chief reasons for variation were 1) the influence of variation in tidal volume leading to variable FiO2 and 2) variation in breathing frequency affecting volume of supplemental oxygen delivered through the breath.

          Conclusion

          For oxygen administration using open patient interfaces there was variability in the concentration and quantity of oxygen delivered to the trachea over the large range of scenarios studied. Of primary importance in evaluating the oxygen dose is knowledge of the breathing parameters that determine the average inhalation flow rate relative to the oxygen flow rate. Otherwise, the oxygen dose cannot be determined.

          Electronic supplementary material

          The online version of this article (10.1186/s12931-019-1104-0) contains supplementary material, which is available to authorized users.

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          Most cited references26

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          Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality.

          Laboratory investigations suggest that exposure to hyperoxia after resuscitation from cardiac arrest may worsen anoxic brain injury; however, clinical data are lacking. To test the hypothesis that postresuscitation hyperoxia is associated with increased mortality. Multicenter cohort study using the Project IMPACT critical care database of intensive care units (ICUs) at 120 US hospitals between 2001 and 2005. Patient inclusion criteria were age older than 17 years, nontraumatic cardiac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following ICU arrival. Patients were divided into 3 groups defined a priori based on PaO(2) on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO(2) of 300 mm Hg or greater; hypoxia, PaO(2) of less than 60 mm Hg (or ratio of PaO(2) to fraction of inspired oxygen <300); and normoxia, not classified as hyperoxia or hypoxia. In-hospital mortality. Of 6326 patients, 1156 had hyperoxia (18%), 3999 had hypoxia (63%), and 1171 had normoxia (19%). The hyperoxia group had significantly higher in-hospital mortality (732/1156 [63%; 95% confidence interval {CI}, 60%-66%]) compared with the normoxia group (532/1171 [45%; 95% CI, 43%-48%]; proportion difference, 18% [95% CI, 14%-22%]) and the hypoxia group (2297/3999 [57%; 95% CI, 56%-59%]; proportion difference, 6% [95% CI, 3%-9%]). In a model controlling for potential confounders (eg, age, preadmission functional status, comorbid conditions, vital signs, and other physiological indices), hyperoxia exposure had an odds ratio for death of 1.8 (95% CI, 1.5-2.2). Among patients admitted to the ICU following resuscitation from cardiac arrest, arterial hyperoxia was independently associated with increased in-hospital mortality compared with either hypoxia or normoxia.
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            Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest

            Introduction Hyperoxia has recently been reported as an independent risk factor for mortality in patients resuscitated from cardiac arrest. We examined the independent relationship between hyperoxia and outcomes in such patients. Methods We divided patients resuscitated from nontraumatic cardiac arrest from 125 intensive care units (ICUs) into three groups according to worst PaO2 level or alveolar-arterial O2 gradient in the first 24 hours after admission. We defined 'hyperoxia' as PaO2 of 300 mmHg or greater, 'hypoxia/poor O2 transfer' as either PaO2 400 mmHg, hyperoxia had no independent association with mortality. Importantly, after adjustment for FiO2 and the relevant covariates, PaO2 was no longer predictive of hospital mortality (P = 0.21). Conclusions Among patients admitted to the ICU after cardiac arrest, hyperoxia did not have a robust or consistently reproducible association with mortality. We urge caution in implementing policies of deliberate decreases in FiO2 in these patients.
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              Systematic review of studies of the effect of hyperoxia on coronary blood flow.

              International guidelines recommend the routine use of oxygen in the initial treatment of myocardial infarction, yet it is uncertain what effect this might have on physiologic and clinical outcomes. We undertook a systematic search of Medline, Cochrane Database of Systematic Reviews, EMBASE, and CINHAL using the key words "oxygen," "coronary blood flow," "hyperoxia," and "coronary circulation" to identify human studies involving a measure of coronary blood flow while breathing oxygen and room air. The primary outcome measure was coronary blood flow; secondary outcomes included coronary vascular resistance and myocardial oxygen consumption. From 2,072 potential publications, there were 6 studies from 4 publications that met the inclusion criteria, with 6 healthy subjects and 61 subjects with cardiac disease. It was not possible to undertake a meta-analysis due to methodological limitations. In the 6 studies, high-concentration oxygen therapy resulted in hyperoxia, with a range in mean Pao(2) of 273 to 425 mm Hg. Hyperoxia caused a significant reduction in coronary blood flow (mean change -7.9% to -28.9%, n = 6 studies). Hyperoxia caused a significant increase in coronary vascular resistance (mean change 21.5% to 40.9%, n = 4 studies) and a significant reduction in myocardial oxygen consumption (mean change -15.3% to -26.9%, n = 3 studies). Hyperoxia from high-concentration oxygen therapy causes a marked reduction in coronary blood flow and myocardial oxygen consumption. These physiologic effects may have the potential to cause harm and are relevant to the use of high-concentration oxygen therapy in the treatment of cardiac and other disorders.
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                Author and article information

                Contributors
                +33 7 72 11 27 93 , ira.katz@airliquide.com
                jzc@ualberta.ca
                Kelvin@ualberta.ca
                Kaixian.ZHU@airliquide.com
                marine.pichelin@airliquide.com
                Georges.Caillibotte@airliquide.com
                armartin@ualberta.ca
                Journal
                Respir Res
                Respir. Res
                Respiratory Research
                BioMed Central (London )
                1465-9921
                1465-993X
                12 July 2019
                12 July 2019
                2019
                : 20
                : 149
                Affiliations
                [1 ]Medical R&D, Air Liquide Santé International, Paris Innovation Campus, Les loges-en-Josas, France
                [2 ]GRID grid.17089.37, Department of Mechanical Engineering, , University of Alberta, ; Edmonton, Canada
                [3 ]ISNI 0000 0001 2247 9727, GRID grid.423839.7, Air Liquide Healthcare, ; Gentilly, France
                [4 ]Technical Innovation, Air Liquide Santé International, Paris Innovation Campus, Les Loges-en-Josas, France
                Author information
                http://orcid.org/0000-0001-6755-9739
                Article
                1104
                10.1186/s12931-019-1104-0
                6625031
                31299963
                debc414e-b716-4b01-b581-b0512832c0ef
                © The Author(s). 2019

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 12 February 2019
                : 18 June 2019
                Categories
                Research
                Custom metadata
                © The Author(s) 2019

                Respiratory medicine
                oxygen,nasal cannula,facemask,fraction of inspired oxygen,supplemental oxygen,oxygen therapy

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