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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">The current SARS-CoV-2 pandemic offers an opportunity to reflect on the use of oxygen therapy in the management of acute respiratory failure that often accompanies Covid-19&#46; At a time when scientific evidence filters all clinical practice&#44; it is easy to see that oxygen therapy is often implemented in patients with acute respiratory failure with no real scientific basis<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a>&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Retrospective studies already show that excessive oxygen use does not improve the prognosis of critically ill patients&#44; and that hyperoxia is associated with higher mortality<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;3</span></a>&#46; In the 1970s&#44; Douglas et al&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> found that high oxygen levels &#40;FiO<span class="elsevierStyleInf">2</span>&#8239;&#62;&#8239;0&#46;7&#41; increased pulmonary venous admixture due to the appearance of absorption atelectasis and the suppression of the hypoxic pulmonary vasoconstriction reflex&#46; Other authors have shown that lower FiO<span class="elsevierStyleInf">2</span> levels &#40;even only 0&#46;3&#41; can cause the same alterations in patients with pre-existing lung disease<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a>&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Excessive oxygen intake can impair gas exchange by increasing oxidative stress and inflammation &#40;the Lorrain-Smith effect&#41;&#46; In the current epidemiological context&#44; oxidative stress has been placed in the spotlight by the recent description of the hypercytokinemia associated with SARS-CoV-2 pneumonia<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a>&#46; Excessive doses of oxygen increase the production of reactive nitrogen and oxygen species &#40;RNS&#44; ROS&#41;&#44; the recruitment and activation of inflammatory cells&#44; and the release of pro-inflammatory mediators &#40;IL-1&#945;&#44; IL-6&#44; IL-8&#44; or TNF-&#945;&#41;&#44; with local &#40;lung damage and infection and sepsis&#41; and distant &#40;tissue damage and multiorgan failure&#41; consequences&#46; Although these effects are magnified when high FiO<span class="elsevierStyleInf">2</span> levels are maintained for prolonged periods &#40;&#62;12&#8211;24&#8239;h&#41;&#44; shorter periods of hyperoxia are also associated with increased morbidity and mortality<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a>&#46; Hyperoxia&#44; then&#44; could be an indirect marker of poor prognosis in severe patients<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a>&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Paradoxically&#44; hyperoxia can reduce systemic oxygen consumption&#44; probably due to the redistribution of blood flow to protect vital organs from the non-physiological effects of high FiO<span class="elsevierStyleInf">2</span> &#40;functional shunt&#41;&#46; Higher than normal levels of PaO<span class="elsevierStyleInf">2</span> also trigger arteriolar vasoconstriction by local mechanisms&#44; a phenomenon that could explain the worse progress of some patients with myocardial infarction&#44; stroke&#44; head injury&#44; cardiac arrest&#44; or sepsis&#46; Tissue hyperoxia&#44; furthermore&#44; promotes lesion development in ischemia-reperfusion situations<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a>&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In short&#44; hyperoxia can be as dangerous as hypoxemia&#46; A multicenter retrospective study of 36&#44;307 patients hospitalized in intensive care units &#40;ICU&#41; showed that PaO<span class="elsevierStyleInf">2</span> during the first 24 hours of admission was an independent predictor of hospital mortality<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a>&#46; PaO<span class="elsevierStyleInf">2</span>-related mortality formed an asymmetric U with a clear plateau at the end of the lowest PaO<span class="elsevierStyleInf">2</span> values&#44; linear increase on the hyperoxia side&#44; and lowest mortality rates at a PaO<span class="elsevierStyleInf">2</span> value between 110 and 150&#8239;mmHg &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">When expressed as a standardized mortality ratio<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a>&#44; hyperoxia was a predictor of mortality at PaO<span class="elsevierStyleInf">2</span> values &#62;125&#8239;mmHg&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">A recent clinical trial in patients with septic shock had to be discontinued prematurely after evidence emerged of excess in-hospital mortality in hyperoxic patients<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a>&#46; Hyperoxia also appears to be of little benefit during recovery after cardiac arrest&#46; Helmerhorst et al&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> showed in an observational study that in-hospital mortality after cardiorespiratory arrest was the same as in patients with normal oxygen levels &#40;PaO<span class="elsevierStyleInf">2</span> 55&#8211;80&#8239;mmHg&#41;&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Hyperoxia does not benefit patients with severe acute respiratory failure&#46; The effect of exposure to excess FiO<span class="elsevierStyleInf">2</span> &#40;FiO<span class="elsevierStyleInf">2</span>&#8239;&#62;&#8239;0&#46;5 when PaO<span class="elsevierStyleInf">2</span> was &#62;80&#8239;mmHg&#41; was analyzed in a study in 2994 patients with acute respiratory distress syndrome &#40;ARDS&#41;&#46; This study found that the higher the cumulative exposure at 5 days&#44; the higher the mortality&#44; the number of days with mechanical ventilation&#44; and the length of hospital stay&#46; Mortality also affected patients with mild&#44; moderate&#44; or severe ARDS&#44; which meant that the relationship observed between mortality and cumulative exposure to high FiO<span class="elsevierStyleInf">2</span> was independent of disease severity<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a>&#46; A recent multicenter randomized trial in patients with ARDS confirmed that controlled oxygen therapy &#40;PaO<span class="elsevierStyleInf">2</span> 55&#8211;70&#8239;mmHg or SpO<span class="elsevierStyleInf">2</span> 88&#37;&#8211;92&#37;&#41; did not increase mortality at 28 days<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a>&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Evidence in patients with acute chronic respiratory failure also supports controlling SpO<span class="elsevierStyleInf">2</span> values&#46; Plant et al&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> showed that excessive use of oxygen therapy in patients with chronic obstructive pulmonary disease exacerbations was associated with respiratory acidosis and a greater number of ICU admissions&#46; The authors pointed out that therapy should focus on maintaining PaO<span class="elsevierStyleInf">2</span> and SaO<span class="elsevierStyleInf">2</span> at 55&#8211;75&#8239;mmHg and SaO<span class="elsevierStyleInf">2</span> 85&#8211;92&#37;&#44; respectively&#46; A subsequent controlled trial showed higher mortality among patients receiving oxygen therapy not adjusted to achieve SaO<span class="elsevierStyleInf">2</span> values of 88&#37;&#8211;92&#37;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a>&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">Acute respiratory care should&#44; therefore&#44; focus on improving lung function with the proper use of oxygen therapy&#44; an approach that differs considerably from standard practice&#46; Unnecessarily high FiO<span class="elsevierStyleInf">2</span> levels reduce the window of opportunity for switching treatment or adjusting FiO<span class="elsevierStyleInf">2</span> levels in the case of worsening respiratory status<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a>&#46; In acutely hypoxic patients&#44; an SpO<span class="elsevierStyleInf">2</span> of 90&#37;&#8211;94&#37; seems to be a reasonable range&#46; It accommodates normal fluctuations and is safe enough to prevent damage&#46; High-flow systems &#40;e&#46;g&#46;&#44; Venturi masks&#41; that can be adjusted to achieve stable FiO<span class="elsevierStyleInf">2</span> are recommended for oxygen administration&#46; The idea of setting a minimum PaO<span class="elsevierStyleInf">2</span> value to avoid tissue hypoxia should be discarded&#44; and emphasis should be placed on setting a maximum safety value to avoid systemic toxicity &#40;PaO<span class="elsevierStyleInf">2</span> &#60;120&#8239;mmHg&#41;&#46; In patients with hypercapnic respiratory failure&#44; the SpO<span class="elsevierStyleInf">2</span> ranges should be lower &#40;88&#37;&#8211;92&#37;&#41; and ventilatory support &#40;preferably non-invasive mechanical ventilation&#41; should be considered if greater oxygen transport is needed &#40;e&#46;g&#46;&#44; associated failure of other organs&#41; or if hypercapnia persists despite controlled FiO<span class="elsevierStyleInf">2</span> &#40;0&#46;24&#8211;0&#46;4&#41;&#46; High-flow nasal cannula may be an alternative or a supplement to non-invasive mechanical ventilation in more severe patients<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a>&#46; In the specific case of patients with chronic obstructive pulmonary disease exacerbations&#44; some guidelines recommend a maximum FiO<span class="elsevierStyleInf">2</span> of 0&#46;28&#44; a practice that is also advisable in the prehospital setting<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a>&#46; In the absence of hypoxemia&#44; oxygen therapy should be avoided in patients with acute myocardial infarction&#44; stroke&#44; head injury&#44; after cardiorespiratory arrest&#44; and in patients with sepsis&#46; In patients admitted to the ICU&#44; restrictive oxygen therapy protocols &#40;aimed at maintaining PaO<span class="elsevierStyleInf">2</span> within the physiological range&#41; are well tolerated and may improve prognosis<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a>&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">In conclusion&#44; a more liberal oxygen prescription is at odds with modern requirements for the development and approval of a treatment of any type&#46; The use of automated oxygen flow titration devices could improve morbidity and mortality and reduce care costs&#44; although they are unlikely to replace clinical monitoring<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a>&#46; In the meantime&#44; we must stress that oxygen is a drug that must be prescribed for defined indications where the benefits outweigh the risks&#44; and that the dose&#44; the delivery system&#44; the duration of administration&#44; and response monitoring must be clearly specified<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a>&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0060" class="elsevierStylePara elsevierViewall">The authors declare that they have not received funding for this study&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflict of interests</span><p id="par0065" class="elsevierStylePara elsevierViewall">The authors state that they have no conflict of interests&#46;</p></span></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Valencia Gallardo JM&#44; Sol&#233; Viol&#225;n J&#44; Rodr&#237;guez de Castro F&#46; Oxigenoterapia&#46; Consideraciones sobre su uso en el enfermo agudo&#46; Arch Bronconeumol&#46; 2022&#59;58&#58;102&#8211;3&#46;</p>"
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">In-hospital mortality values&#44; on average&#44; according to PaO<span class="elsevierStyleInf">2</span> &#40;mmHg&#41;&#46; The size of the circles represents the number of patients with the same PaO<span class="elsevierStyleInf">2</span> value&#46; Adapted from De Jonge et al&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> with permission&#46;</p>"
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Scientific Letter
Oxygen therapy. Considerations regarding its use in acute ill patients
Oxigenoterapia. Consideraciones sobre su uso en el enfermo agudo
José Manuel Valencia Gallardoa,
Corresponding author
jvalgal@gmail.com

Corresponding author.
, Jordi Solé Violánb, Felipe Rodríguez de Castroa
a Servicio de Neumología, Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas, Spain
b Servicio de Medicina Intensiva, Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">The current SARS-CoV-2 pandemic offers an opportunity to reflect on the use of oxygen therapy in the management of acute respiratory failure that often accompanies Covid-19&#46; At a time when scientific evidence filters all clinical practice&#44; it is easy to see that oxygen therapy is often implemented in patients with acute respiratory failure with no real scientific basis<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a>&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">Retrospective studies already show that excessive oxygen use does not improve the prognosis of critically ill patients&#44; and that hyperoxia is associated with higher mortality<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;3</span></a>&#46; In the 1970s&#44; Douglas et al&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> found that high oxygen levels &#40;FiO<span class="elsevierStyleInf">2</span>&#8239;&#62;&#8239;0&#46;7&#41; increased pulmonary venous admixture due to the appearance of absorption atelectasis and the suppression of the hypoxic pulmonary vasoconstriction reflex&#46; Other authors have shown that lower FiO<span class="elsevierStyleInf">2</span> levels &#40;even only 0&#46;3&#41; can cause the same alterations in patients with pre-existing lung disease<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a>&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Excessive oxygen intake can impair gas exchange by increasing oxidative stress and inflammation &#40;the Lorrain-Smith effect&#41;&#46; In the current epidemiological context&#44; oxidative stress has been placed in the spotlight by the recent description of the hypercytokinemia associated with SARS-CoV-2 pneumonia<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a>&#46; Excessive doses of oxygen increase the production of reactive nitrogen and oxygen species &#40;RNS&#44; ROS&#41;&#44; the recruitment and activation of inflammatory cells&#44; and the release of pro-inflammatory mediators &#40;IL-1&#945;&#44; IL-6&#44; IL-8&#44; or TNF-&#945;&#41;&#44; with local &#40;lung damage and infection and sepsis&#41; and distant &#40;tissue damage and multiorgan failure&#41; consequences&#46; Although these effects are magnified when high FiO<span class="elsevierStyleInf">2</span> levels are maintained for prolonged periods &#40;&#62;12&#8211;24&#8239;h&#41;&#44; shorter periods of hyperoxia are also associated with increased morbidity and mortality<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a>&#46; Hyperoxia&#44; then&#44; could be an indirect marker of poor prognosis in severe patients<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a>&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Paradoxically&#44; hyperoxia can reduce systemic oxygen consumption&#44; probably due to the redistribution of blood flow to protect vital organs from the non-physiological effects of high FiO<span class="elsevierStyleInf">2</span> &#40;functional shunt&#41;&#46; Higher than normal levels of PaO<span class="elsevierStyleInf">2</span> also trigger arteriolar vasoconstriction by local mechanisms&#44; a phenomenon that could explain the worse progress of some patients with myocardial infarction&#44; stroke&#44; head injury&#44; cardiac arrest&#44; or sepsis&#46; Tissue hyperoxia&#44; furthermore&#44; promotes lesion development in ischemia-reperfusion situations<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a>&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In short&#44; hyperoxia can be as dangerous as hypoxemia&#46; A multicenter retrospective study of 36&#44;307 patients hospitalized in intensive care units &#40;ICU&#41; showed that PaO<span class="elsevierStyleInf">2</span> during the first 24 hours of admission was an independent predictor of hospital mortality<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a>&#46; PaO<span class="elsevierStyleInf">2</span>-related mortality formed an asymmetric U with a clear plateau at the end of the lowest PaO<span class="elsevierStyleInf">2</span> values&#44; linear increase on the hyperoxia side&#44; and lowest mortality rates at a PaO<span class="elsevierStyleInf">2</span> value between 110 and 150&#8239;mmHg &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">When expressed as a standardized mortality ratio<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a>&#44; hyperoxia was a predictor of mortality at PaO<span class="elsevierStyleInf">2</span> values &#62;125&#8239;mmHg&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">A recent clinical trial in patients with septic shock had to be discontinued prematurely after evidence emerged of excess in-hospital mortality in hyperoxic patients<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a>&#46; Hyperoxia also appears to be of little benefit during recovery after cardiac arrest&#46; Helmerhorst et al&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> showed in an observational study that in-hospital mortality after cardiorespiratory arrest was the same as in patients with normal oxygen levels &#40;PaO<span class="elsevierStyleInf">2</span> 55&#8211;80&#8239;mmHg&#41;&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Hyperoxia does not benefit patients with severe acute respiratory failure&#46; The effect of exposure to excess FiO<span class="elsevierStyleInf">2</span> &#40;FiO<span class="elsevierStyleInf">2</span>&#8239;&#62;&#8239;0&#46;5 when PaO<span class="elsevierStyleInf">2</span> was &#62;80&#8239;mmHg&#41; was analyzed in a study in 2994 patients with acute respiratory distress syndrome &#40;ARDS&#41;&#46; This study found that the higher the cumulative exposure at 5 days&#44; the higher the mortality&#44; the number of days with mechanical ventilation&#44; and the length of hospital stay&#46; Mortality also affected patients with mild&#44; moderate&#44; or severe ARDS&#44; which meant that the relationship observed between mortality and cumulative exposure to high FiO<span class="elsevierStyleInf">2</span> was independent of disease severity<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a>&#46; A recent multicenter randomized trial in patients with ARDS confirmed that controlled oxygen therapy &#40;PaO<span class="elsevierStyleInf">2</span> 55&#8211;70&#8239;mmHg or SpO<span class="elsevierStyleInf">2</span> 88&#37;&#8211;92&#37;&#41; did not increase mortality at 28 days<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a>&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Evidence in patients with acute chronic respiratory failure also supports controlling SpO<span class="elsevierStyleInf">2</span> values&#46; Plant et al&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> showed that excessive use of oxygen therapy in patients with chronic obstructive pulmonary disease exacerbations was associated with respiratory acidosis and a greater number of ICU admissions&#46; The authors pointed out that therapy should focus on maintaining PaO<span class="elsevierStyleInf">2</span> and SaO<span class="elsevierStyleInf">2</span> at 55&#8211;75&#8239;mmHg and SaO<span class="elsevierStyleInf">2</span> 85&#8211;92&#37;&#44; respectively&#46; A subsequent controlled trial showed higher mortality among patients receiving oxygen therapy not adjusted to achieve SaO<span class="elsevierStyleInf">2</span> values of 88&#37;&#8211;92&#37;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a>&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">Acute respiratory care should&#44; therefore&#44; focus on improving lung function with the proper use of oxygen therapy&#44; an approach that differs considerably from standard practice&#46; Unnecessarily high FiO<span class="elsevierStyleInf">2</span> levels reduce the window of opportunity for switching treatment or adjusting FiO<span class="elsevierStyleInf">2</span> levels in the case of worsening respiratory status<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a>&#46; In acutely hypoxic patients&#44; an SpO<span class="elsevierStyleInf">2</span> of 90&#37;&#8211;94&#37; seems to be a reasonable range&#46; It accommodates normal fluctuations and is safe enough to prevent damage&#46; High-flow systems &#40;e&#46;g&#46;&#44; Venturi masks&#41; that can be adjusted to achieve stable FiO<span class="elsevierStyleInf">2</span> are recommended for oxygen administration&#46; The idea of setting a minimum PaO<span class="elsevierStyleInf">2</span> value to avoid tissue hypoxia should be discarded&#44; and emphasis should be placed on setting a maximum safety value to avoid systemic toxicity &#40;PaO<span class="elsevierStyleInf">2</span> &#60;120&#8239;mmHg&#41;&#46; In patients with hypercapnic respiratory failure&#44; the SpO<span class="elsevierStyleInf">2</span> ranges should be lower &#40;88&#37;&#8211;92&#37;&#41; and ventilatory support &#40;preferably non-invasive mechanical ventilation&#41; should be considered if greater oxygen transport is needed &#40;e&#46;g&#46;&#44; associated failure of other organs&#41; or if hypercapnia persists despite controlled FiO<span class="elsevierStyleInf">2</span> &#40;0&#46;24&#8211;0&#46;4&#41;&#46; High-flow nasal cannula may be an alternative or a supplement to non-invasive mechanical ventilation in more severe patients<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a>&#46; In the specific case of patients with chronic obstructive pulmonary disease exacerbations&#44; some guidelines recommend a maximum FiO<span class="elsevierStyleInf">2</span> of 0&#46;28&#44; a practice that is also advisable in the prehospital setting<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a>&#46; In the absence of hypoxemia&#44; oxygen therapy should be avoided in patients with acute myocardial infarction&#44; stroke&#44; head injury&#44; after cardiorespiratory arrest&#44; and in patients with sepsis&#46; In patients admitted to the ICU&#44; restrictive oxygen therapy protocols &#40;aimed at maintaining PaO<span class="elsevierStyleInf">2</span> within the physiological range&#41; are well tolerated and may improve prognosis<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a>&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">In conclusion&#44; a more liberal oxygen prescription is at odds with modern requirements for the development and approval of a treatment of any type&#46; The use of automated oxygen flow titration devices could improve morbidity and mortality and reduce care costs&#44; although they are unlikely to replace clinical monitoring<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a>&#46; In the meantime&#44; we must stress that oxygen is a drug that must be prescribed for defined indications where the benefits outweigh the risks&#44; and that the dose&#44; the delivery system&#44; the duration of administration&#44; and response monitoring must be clearly specified<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a>&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0060" class="elsevierStylePara elsevierViewall">The authors declare that they have not received funding for this study&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflict of interests</span><p id="par0065" class="elsevierStylePara elsevierViewall">The authors state that they have no conflict of interests&#46;</p></span></span>"
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">In-hospital mortality values&#44; on average&#44; according to PaO<span class="elsevierStyleInf">2</span> &#40;mmHg&#41;&#46; The size of the circles represents the number of patients with the same PaO<span class="elsevierStyleInf">2</span> value&#46; Adapted from De Jonge et al&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> with permission&#46;</p>"
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ISSN: 03002896
Original language: English
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