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Should Oxygen Therapy Be Tightly Regulated to Minimize Hyperoxia in Critically Ill Patients?

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Should Oxygen Therapy Be Tightly Regulated to Minimize Hyperoxia in Critically Ill Patients? Should Oxygen Therapy Be Tightly Regulated to Minimize Hyperoxia in Critically Ill Patients? Richard H Kallet MSc RRT FAARC Richard D Branson MSc RRT FAARC Introduction Pro Argument: Oxygen Therapy Should Be Tightly Regulated to Avoid Hyperoxia Historical Context Evolution and Genetic Influences on the Response to Hyperoxia Overview: Cellular Signaling in VILI and the Role of ROS Impact of VILI and Hyperoxic Acute Lung Injury Long-Term Impact of Supplemental Oxygen Therapy in Chronic Lung Disease Systemic Effects of Hyperoxia Permissive Hypoxemia as a Strategy to Control Hyperoxia Summary of the Pro Argument The Argument Against Strict Control of F IO2 Oxygen and Outcomes in Ventilated Patients The Conservative Oxygen Therapy Trials The Con Summary Excessive F in Other Conditions IO2 Myocardial Infarction/Cardiac Arrest Traumatic Brain Injury Stroke Conclusions Oxygen is both lifesaving and toxic. Appropriate use of oxygen aims to provide a balance between the two effects. Although local oxygen toxicity to the lung is well accepted, recent evidence has called into question the negative consequences of hyperoxemia in other organ beds. Hyperoxia following cardiac arrest, traumatic brain injury, and stroke has been shown to worsen outcomes. The role of hyperoxemia in mechanically ventilated patients, in the face of non-toxic inspired oxygen concen- trations, is less clear. This paper will review the data for and against the use of conservative oxygen targets and the avoidance of hyperoxemia in mechanically ventilated patients. Key words: hyperoxia; hyperoxic acute lung injury; lung protective ventilation; oxygen toxicity; reactive oxygen species; ven- tilator-induced lung injury. [Respir Care 2016;61(6):801–817. © 2016 Daedalus Enterprises] Introduction lematic for several reasons. These include the complexity of tissue injury and related inflammatory processes, the Several years ago during a RESPIRATORY CARE Journal impact of therapeutic interventions, and inter-individual Conference on oxygen,1 Editor Emeritus Dr David Pierson genetic variability. In addition, the issue is influenced by quipped that “oxygen toxicity is like Bigfoot, everyone has how the debate over hyperoxia has played out over the heard of it, but nobody has actually seen it”. The question past 60 years. That historical context continues to color of whether hyperoxia is a relevant clinical concern is prob- contemporary perceptions and attitudes regarding the clin- RESPIRATORY CARE • JUNE 2016 VOL 61 NO 6 801 REGULATION OF O2 THERAPY IN CRITICALLY ILL PATIENTS ical importance of hyperoxia. Even now, when interest in ning in the 1950s, the first reports of hyperoxic acute lung ventilator-induced lung injury (VILI) dominates the dis- injury in humans began to appear in the medical litera- cussion of mechanical ventilation, the contributory role of ture.4,5 However, it was only in the 1960s, with the estab- hyperoxia is still considered to be of secondary impor- lishment of the ICU and prolonged mechanical ventilation 2 tance. In this paper, we debate both sides of this issue. as well as hyperbaric O2 therapy, that serious concern over The pro argument incorporates background information clinical O2 toxicity arose in response to numerous case necessary to appreciate the complexity of the topic. reports in both adults and neonates.1 However, these early reports implicating hyperoxia Pro Argument: Oxygen Therapy Should Be Tightly grossly overstated the problem and virtually ignored over Regulated to Avoid Hyperoxia a century of animal research. The excessive attribution of the development or perpetuation of acute respiratory fail- Pulmonary oxygen toxicity, now referred to as hyper- ure to hyperoxia was in part due to the pervasive lack of oxic acute lung injury, has been consistently reproduced in knowledge regarding ARDS and VILI as well as the lim- numerous animal models since Antoine Lavoisier’s exper- itations of O2 delivery in early mechanical ventilators. It iments in 1783.1 In essence, exposure to F Ն0.70 for was only with the publication of the seminal report de- IO2 several days leads to progressive lung injury; the severity scribing ARDS6 as well as other studies examining the of symptoms and pulmonary lesions are dependent upon pathophysiology of ARDS,7-9 the technical problems as- both the concentration and duration. Breathing an F Ն0.80 sociated with respiratory care equipment,10-12 and the elu- IO2 for approximately 3–6 d typically is fatal to most animals. cidation of VILI13-15 that the role of hyperoxia was placed However, there also appear to be pronounced interspecies into a more realistic perspective. Unfortunately, when mis- and even subspecies differences in the inflammatory re- conceptions cloaking a particular phenomenon are dis- sponse to hyperoxia. Hyperoxic acute lung injury is almost pelled, an overreaction tends to occur in the opposite di- uniformly fatal in smaller species (eg, mice, rats, guinea rection, fostering an attitude of excessive skepticism. The pigs, rabbits), whereas humans appear more resistant, tend- current debate must be framed within this context. The ing to acclimate after a period of approximately 7–10 d overarching question in 2016 is how, to what extent, and through hyperplasia of alveolar type-II cells.1 Nonetheless, in which context does hyperoxic acute lung injury (and, over 230 years of data strongly suggest that breathing therefore, the need for tightly controlling F ) impact mor- IO2 hyperoxic gas mixtures is toxic to human lungs, and there bidity and mortality during critical illness. looms the distinct possibility that hyperoxia may be fatal in patients possessing a genetic predisposition.3 Evolution and Genetic Influences on the Response to Hyperoxia Historical Context The influence of hyperoxia on patient outcomes, partic- Medical interest in hyperoxia resulted from the inter- ularly in ARDS, is difficult to isolate because of the com- section of several events in the mid-20th century, namely plex interplay of mechanisms that activate the same injury military demands related to high-altitude aviation and scuba response pathways. Recent advances in our understanding diving during World War II and the increasing availability of both inflammation and the role of genetics suggest that of O2 therapy to treat cardiopulmonary diseases. Begin- the problem presented by hyperoxia transcends the imbal- ance between reactive oxygen species (ROS) production and antioxidant defense mechanisms. Rather, hyperoxia Mr Kallet is affiliated with Respiratory Care Services, University of Cali- acts as an external stressor that strongly influences genet- fornia San Francisco Department of Anesthesia at San Francisco General ic-environmental interactions. One sobering example is Hospital, San Francisco, California. Mr Branson is affiliated with the De- that exposure to hyperoxia during perinatal life profoundly partment of Surgery, University of Cincinnati, Cincinnati, Ohio. impacts the development of several diseases later in life, Mr Kallet and Mr Branson presented a version of this paper at the 54th believed to be mediated by subsequent alterations in ge- RESPIRATORY CARE Journal Conference, “Respiratory Care Controversies netic expression that follows exposure.16 III,” held June 5–6, 2015, in St Petersburg, Florida. Biological evolution has been intertwined with the rise Mr Branson has disclosed relationships with Mallickrodt, Medtronic, Meiji of planetary O2 concentrations, which have fluctuated cy- 17,18 Pharmaceuticals, Bayer, and Ventec. Mr Kallet has no conflicts to disclose. clically with extremes between ϳ10 and 35%. This exerted evolutionary pressure for life forms to devise adap- Correspondence: Richard H Kallet MSc RRT FAARC, Department of tive strategies for successfully maintaining aerobic metab- Anesthesia, University of California San Francisco at San Francisco Gen- eral Hospital NH:GA-2, 1001 Potrero Avenue, San Francisco, CA 94110. olism. Implications for the current debate stem from the fact that the explosion in mammalian evolution began ap- DOI: 10.4187/respcare.04933 proximately 200 million years ago. During this period (Tri- 802 RESPIRATORY CARE • JUNE 2016 VOL 61 NO 6 REGULATION OF O2 THERAPY IN CRITICALLY ILL PATIENTS assic-Jurassic), atmospheric O2 concentrations plummeted ascertain whether an optimal balance between supplemental from approximately 35% to 10%, so that selective pressures O2 therapy and mechanical ventilation can be achieved to encoded in the genome favored animals with efficient respi- minimize the deleterious effects of both. ratory systems. What characterized this period in eukaryote evolution was an enhanced ability to adjust metabolism Impact of VILI and Hyperoxic Acute Lung Injury through hypoxic-responsive gene expression. Another (pre- ceding) evolutionary characteristic was segregating metabolic Several additional animal models found that either function (oxidation-reduction) away from cellular DNA to pretreating the lungs with hyperoxia before high-stretch 19 prevent oxidative stress and genetic damage. tidal volume (VT) or combining hyperoxia with high- Thus, coping with hypoxia, rather than hyperoxia, fa- stretch ventilation significantly magnifies the degree of vored natural selection. But this raises questions regarding VILI.24,26-36 These models mimic common clinical strate- the efficiency of co-evolving antioxidant defense mecha- gies in managing ARDS and other forms of acute respi- nisms in mammals whose evolutionary journey began breath- ratory failure before
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