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Edited "Storages and sources" and "Delivery" subsection to be more succinct/clear; grammar edits
Alex Nhan (talk | contribs)
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Added section on physiologic effects of hyperoxia and normobaric/hyperbaric hyperoxia, checkpoint, will revise
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*{{Cite journal| last1 = O'Driscoll | first1 = B. R.| last2 = Howard | first2 = L. S.| last3 = Davison | first3 = A. G.| last4 = British Thoracic | first4 = S.| title = BTS guideline for emergency oxygen use in adult patients | doi = 10.1136/thx.2008.102947| journal = Thorax| volume = 63| pages = vi1–v68| year = 2008| pmid = 18838559| doi-access = free}}
*{{Cite journal| last1 = O'Driscoll | first1 = B. R.| last2 = Howard | first2 = L. S.| last3 = Davison | first3 = A. G.| last4 = British Thoracic | first4 = S.| title = BTS guideline for emergency oxygen use in adult patients | doi = 10.1136/thx.2008.102947| journal = Thorax| volume = 63| pages = vi1–v68| year = 2008| pmid = 18838559| doi-access = free}}
*{{Cite journal| last1 = MacNee | first1 = W.| title = Prescription of Oxygen | doi = 10.1164/rccm.2506007| journal = American Journal of Respiratory and Critical Care Medicine| volume = 172| issue = 5| pages = 517–18| year = 2005| pmid = 16120712}}</ref> If the initial hypoxemia has resolved, additional treatment may be an unnecessary use of resources.<ref name="ACCPandATSfive"/>
*{{Cite journal| last1 = MacNee | first1 = W.| title = Prescription of Oxygen | doi = 10.1164/rccm.2506007| journal = American Journal of Respiratory and Critical Care Medicine| volume = 172| issue = 5| pages = 517–18| year = 2005| pmid = 16120712}}</ref> If the initial hypoxemia has resolved, additional treatment may be an unnecessary use of resources.<ref name="ACCPandATSfive"/>

== Physiologic Effects of Oxygen Therapy ==
Oxygen supplementation has a variety of physiologic effects on the human body. These physiologic effects are typically considered adverse in nature (with exception of vasoconstriction, which varies upon clinical context).

=== Vasoconstriction ===
Hypoxia is observed to be a potent pulmonary vasoconstrictor, due to inhibition of an outward potassium current and activation of inward sodium current leading to contraction of pulmonary vascular musculature.<ref>{{Cite journal|last=Sylvester|first=J. T.|last2=Shimoda|first2=Larissa A.|last3=Aaronson|first3=Philip I.|last4=Ward|first4=Jeremy P. T.|date=2012-01|title=Hypoxic Pulmonary Vasoconstriction|url=https://www.physiology.org/doi/10.1152/physrev.00041.2010|journal=Physiological Reviews|language=en|volume=92|issue=1|pages=367–520|doi=10.1152/physrev.00041.2010|issn=0031-9333}}</ref> However, the effects of hyperoxia do not seem to have a particularly strong vasodilatory effect from the few studies that have been performed on this topic in patients with pulmonary hypertension.<ref>{{Cite journal|last=Groves|first=B. M.|last2=Reeves|first2=J. T.|last3=Sutton|first3=J. R.|last4=Wagner|first4=P. D.|last5=Cymerman|first5=A.|last6=Malconian|first6=M. K.|last7=Rock|first7=P. B.|last8=Young|first8=P. M.|last9=Houston|first9=C. S.|date=1987-08-01|title=Operation Everest II: elevated high-altitude pulmonary resistance unresponsive to oxygen|url=https://journals.physiology.org/doi/abs/10.1152/jappl.1987.63.2.521|journal=Journal of Applied Physiology|volume=63|issue=2|pages=521–530|doi=10.1152/jappl.1987.63.2.521|issn=8750-7587}}</ref><ref>{{Cite journal|last=Day|first=Ronald W.|date=2015|title=Comparison between the Acute Pulmonary Vascular Effects of Oxygen with Nitric Oxide and Sildenafil|url=https://www.frontiersin.org/article/10.3389/fped.2015.00016|journal=Frontiers in Pediatrics|volume=3|pages=16|doi=10.3389/fped.2015.00016|issn=2296-2360}}</ref>

In the systemic vasculature, oxygen serves as a vasoconstrictor leading to mildly increased blood pressure and decreased cardiac output and heart rate; increased baricity does not seem to have a significant effect on the overall physiologic effect.<ref>{{Citation|last=Mathieu|first=Daniel|title=Physiologic Effects of Hyperbaric Oxygen on Hemodynamics and Microcirculation|date=2006|url=https://doi.org/10.1007/1-4020-4448-8_6|work=Handbook on Hyperbaric Medicine|pages=75–101|editor-last=Mathieu|editor-first=Daniel|place=Dordrecht|publisher=Springer Netherlands|language=en|doi=10.1007/1-4020-4448-8_6|isbn=978-1-4020-4448-9|access-date=2021-10-28|last2=Favory|first2=Raphael|last3=Collet|first3=François|last4=Linke|first4=Jean-Christophe|last5=Wattel|first5=Francis}}</ref> As a result this may lead to increased left-to-right shunting in particular patient populations, such as those with atrial septal defects. While the mechanism of the vasoconstriction is unknown, one plausible theory is that increased reactive oxygen species from oxygen therapy accelerates the degradation of endothelial nitric oxide, a vasodilator.<ref>{{Cite journal|last=McNulty|first=Patrick H.|last2=King|first2=Nicholas|last3=Scott|first3=Sofia|last4=Hartman|first4=Gretchen|last5=McCann|first5=Jennifer|last6=Kozak|first6=Mark|last7=Chambers|first7=Charles E.|last8=Demers|first8=Laurence M.|last9=Sinoway|first9=Lawrence I.|date=2005-03-01|title=Effects of supplemental oxygen administration on coronary blood flow in patients undergoing cardiac catheterization|url=https://journals.physiology.org/doi/full/10.1152/ajpheart.00625.2004|journal=American Journal of Physiology-Heart and Circulatory Physiology|volume=288|issue=3|pages=H1057–H1062|doi=10.1152/ajpheart.00625.2004|issn=0363-6135}}</ref>

=== Hypercapnea ===
Among CO2 retainers, excess exposure to oxygen in context of the Haldane effect leads to loss of affinity of deoxyhemoglobin to CO2.<ref>{{Cite journal|last=Christiansen|first=Johanne|last2=Douglas|first2=C. G.|last3=Haldane|first3=J. S.|date=1914-07-14|title=The absorption and dissociation of carbon dioxide by human blood|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1420520/|journal=The Journal of Physiology|volume=48|issue=4|pages=244–271|issn=0022-3751|pmc=1420520|pmid=16993252}}</ref> This may contribute to acid-base disorders due to the increase in PaCO2 (hypercapnea), and patients with lung disease they may not be able to adequately clear CO2.<ref>{{Cite journal|last=Hanson|first=C. W.|last2=Marshall|first2=B. E.|last3=Frasch|first3=H. F.|last4=Marshall|first4=C.|date=1996-01|title=Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease|url=https://pubmed.ncbi.nlm.nih.gov/8565533/|journal=Critical Care Medicine|volume=24|issue=1|pages=23–28|doi=10.1097/00003246-199601000-00007|issn=0090-3493|pmid=8565533}}</ref>

=== Absorption atelectasis ===
It has been theorized that oxygen administration can promote accelerated development of atelectasis.<ref>{{Cite journal|last=Hedenstierna|first=Göran|last2=Edmark|first2=Lennart|date=2010-06|title=Mechanisms of atelectasis in the perioperative period|url=https://pubmed.ncbi.nlm.nih.gov/20608554/|journal=Best Practice & Research. Clinical Anaesthesiology|volume=24|issue=2|pages=157–169|doi=10.1016/j.bpa.2009.12.002|issn=1521-6896|pmid=20608554}}</ref> The concept is based on the idea that oxygen is more quickly absorbed over nitrogen, leading oxygen-rich areas that are poorly ventilated to be rapidly absorbed leading to atelectasis.<ref>{{Cite journal|last=Hedenstierna|first=Göran|last2=Edmark|first2=Lennart|date=2010-06|title=Mechanisms of atelectasis in the perioperative period|url=https://pubmed.ncbi.nlm.nih.gov/20608554/|journal=Best Practice & Research. Clinical Anaesthesiology|volume=24|issue=2|pages=157–169|doi=10.1016/j.bpa.2009.12.002|issn=1521-6896|pmid=20608554}}</ref> It is suggested that higher fractions of inhaled oxygen will be associated with increasing rates of atelectasis.<ref>{{Cite journal|last=Dale|first=W. Andrew|last2=Rahn|first2=Hermann|date=1952-09-01|title=Rate of Gas Absorption During Atelectasis|url=https://journals.physiology.org/doi/abs/10.1152/ajplegacy.1952.170.3.606|journal=American Journal of Physiology-Legacy Content|volume=170|issue=3|pages=606–615|doi=10.1152/ajplegacy.1952.170.3.606|issn=0002-9513}}</ref>

=== Oxidative Stress ===
Sustained exposure to oxygen overwhelms the capacity to deal with oxidant stress.<ref>{{Cite journal|last=Heffner|first=John E.|last2=Repine|first2=John E.|date=1989-08-01|title=Pulmonary Strategies of Antioxidant Defense|url=https://www.atsjournals.org/doi/abs/10.1164/ajrccm/140.2.531|journal=American Review of Respiratory Disease|volume=140|issue=2|pages=531–554|doi=10.1164/ajrccm/140.2.531|issn=0003-0805}}</ref>  Rate of oxidant stress appears to be influenced by both oxygen concentration and length of exposure, with general toxicity observed to occur within hours in hyperoxic conditions.<ref>{{Cite journal|last=Clark|first=J M|last2=Lambertsen|first2=C J|date=1971-05-01|title=Rate of development of pulmonary O2 toxicity in man during O2 breathing at 2.0 Ata.|url=https://journals.physiology.org/doi/abs/10.1152/jappl.1971.30.5.739|journal=Journal of Applied Physiology|volume=30|issue=5|pages=739–752|doi=10.1152/jappl.1971.30.5.739|issn=8750-7587}}</ref>

=== Reduction in erythropoiesis ===
Hyperoxia is observed to result in a serum reduction in erythropoietin, resulting in reduced stimulus for erythropoiesis.<ref name=":0">{{Cite journal|last=Kokot|first=M|last2=Kokot|first2=F|last3=Franek|first3=E|last4=Wiecek|first4=A|last5=Nowicki|first5=M|last6=Duława|first6=J|date=1994-10|title=Effect of isobaric hyperoxemia on erythropoietin secretion in hypertensive patients.|url=https://www.ahajournals.org/doi/10.1161/01.HYP.24.4.486|journal=Hypertension|language=en|volume=24|issue=4|pages=486–490|doi=10.1161/01.HYP.24.4.486|issn=0194-911X}}</ref> However, hyperoxia at normobaric measurements does not appear to be able to stop erythropoiesis completely.<ref name=":0" />

=== Immunosuppressant effects ===
Hyperoxic environments have been observed to decrease granulocyte rolling and diapedesis in specific circumstances.<ref>{{Cite journal|last=Waisman|first=Dan|last2=Brod|first2=Vera|last3=Wolff|first3=Rafael|last4=Sabo|first4=Edmond|last5=Chernin|first5=Mark|last6=Weintraub|first6=Zalman|last7=Rotschild|first7=Avi|last8=Bitterman|first8=Haim|date=2003-08-01|title=Effects of hyperoxia on local and remote microcirculatory inflammatory response after splanchnic ischemia and reperfusion|url=https://journals.physiology.org/doi/full/10.1152/ajpheart.00900.2002|journal=American Journal of Physiology-Heart and Circulatory Physiology|volume=285|issue=2|pages=H643–H652|doi=10.1152/ajpheart.00900.2002|issn=0363-6135}}</ref>

=== Anaerobic activity ===
Cases of necrotizing fasciitis have been observed to require fewer debridement operations and have improvement in regard to mortality in patients treated with hyperbaric oxygen therapy.<ref>{{Cite journal|last=Riseman|first=Jay A.|last2=Zamboni|first2=William A.|last3=Curtis|first3=Anne|last4=Graham|first4=Donald R.|last5=Konrad|first5=Horst R.|last6=Ross|first6=Donald S.|date=1990-11-01|title=Hyperbaric oxygen therapy for necrotizing fasciitis reduces mortality and the need for debridements|url=https://www.surgjournal.com/article/0039-6060(90)90280-F/abstract|journal=Surgery|language=English|volume=108|issue=5|pages=847–850|doi=10.5555/uri:pii:003960609090280F|issn=0039-6060|pmid=2237764}}</ref>

== Impact of Hyperoxia ==
Hyperoxia is defined as an excess amount of oxygen available to tissues and organs.<ref>{{Cite journal|last=Mach|first=William J.|last2=Thimmesch|first2=Amanda R.|last3=Pierce|first3=J. Thomas|last4=Pierce|first4=Janet D.|date=2011-06-05|title=Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung|url=https://www.hindawi.com/journals/nrp/2011/260482/|journal=Nursing Research and Practice|language=en|volume=2011|pages=e260482|doi=10.1155/2011/260482|issn=2090-1429}}</ref> This is associated with a myriad of adverse effects, which may be exacerbated in cases when individuals are exposed to excessive pressures of oxygen (hyperbaric hyperoxia).

=== Normobaric Hyperoxia ===
At normal pressures, hyperoxia is associated with a myriad of adverse effects, stemming from the physiological effects of oxygen on the body. In regard to the airway, both tracheobronchitis and mucositis have been observed.<ref>{{Cite journal|last=Kallet|first=Richard H|last2=Matthay|first2=Michael A|date=2013-1|title=Hyperoxic Acute Lung Injury|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3915523/|journal=Respiratory care|volume=58|issue=1|pages=123–141|doi=10.4187/respcare.01963|issn=0020-1324|pmc=3915523|pmid=23271823}}</ref> Within the lungs, high concentrations of oxygen is associated with alveolar toxicity (coined the Lorrain-Smith effect).<ref>{{Cite journal|last=Mach|first=William J.|last2=Thimmesch|first2=Amanda R.|last3=Pierce|first3=J. Thomas|last4=Pierce|first4=Janet D.|date=2011-06-05|title=Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung|url=https://www.hindawi.com/journals/nrp/2011/260482/|journal=Nursing Research and Practice|language=en|volume=2011|pages=e260482|doi=10.1155/2011/260482|issn=2090-1429}}</ref> Increased oxygen absorption leads to predisposition to absorption atelectasis (as well as denitrogenation of gas cavities) and decreased respiratory drive.<ref>{{Cite journal|last=Domino|first=Karen B.|date=2019-10-01|title=Pre-emergence Oxygenation and Postoperative Atelectasis|url=https://doi.org/10.1097/ALN.0000000000002875|journal=Anesthesiology|volume=131|issue=4|pages=771–773|doi=10.1097/ALN.0000000000002875|issn=0003-3022}}</ref> Pulmonary vasodilation is observed along with systemic vasoconstriction, thought to be due to accelerated degradation of nitric oxide which typically functions as a vasodilator.<ref>{{Cite journal|last=Brugniaux|first=Julien Vincent|last2=Coombs|first2=Geoff B.|last3=Barak|first3=Otto F.|last4=Dujic|first4=Zeljko|last5=Sekhon|first5=Mypinder S.|last6=Ainslie|first6=Philip N.|date=2018-07-01|title=Highs and lows of hyperoxia: physiological, performance, and clinical aspects|url=https://journals.physiology.org/doi/full/10.1152/ajpregu.00165.2017|journal=American Journal of Physiology-Regulatory, Integrative and Comparative Physiology|volume=315|issue=1|pages=R1–R27|doi=10.1152/ajpregu.00165.2017|issn=0363-6119}}</ref> Decreased cerebral blood flow is also observed, with mixed results regarding impact on cognition.<ref>{{Cite book|last=Cipolla|first=Marilyn J.|url=https://www.ncbi.nlm.nih.gov/books/NBK53082/|title=Control of Cerebral Blood Flow|date=2009|publisher=Morgan & Claypool Life Sciences|language=en}}</ref><ref>{{Cite journal|last=Sheng|first=Min|last2=Liu|first2=Peiying|last3=Mao|first3=Deng|last4=Ge|first4=Yulin|last5=Lu|first5=Hanzhang|date=2017-05-02|title=The impact of hyperoxia on brain activity: A resting-state and task-evoked electroencephalography (EEG) study|url=https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0176610|journal=PLOS ONE|language=en|volume=12|issue=5|pages=e0176610|doi=10.1371/journal.pone.0176610|issn=1932-6203|pmc=PMC5412995|pmid=28464001}}</ref><ref>{{Cite journal|last=Seo|first=Ho-Jun|last2=Bahk|first2=Won-Myong|last3=Jun|first3=Tae-Yun|last4=Chae|first4=Jeong-Ho|date=2007-02-01|title=The Effect of Oxygen Inhalation on Cognitive Function and EEG in Healthy Adults|url=https://www.cpn.or.kr/journal/view.html?spage=25&volume=5&number=1|language=en|volume=5|issue=1|pages=25–30|issn=1738-1088}}</ref> From a hematological standpoint, hyperoxia may have an immunosuppressant effect, as well as an associated with decreased erythropoesis.

=== Hyperbaric Hyperoxia ===
At higher pressures, many of the effects are magnified. Mucosal damage is observed to increase with increased pressure/exposure to high oxygen concentrations, leading to possible ARDS.<ref>{{Cite journal|last=Mach|first=William J.|last2=Thimmesch|first2=Amanda R.|last3=Pierce|first3=J. Thomas|last4=Pierce|first4=Janet D.|date=2011|title=Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3169834/|journal=Nursing Research and Practice|volume=2011|pages=260482|doi=10.1155/2011/260482|issn=2090-1429|pmc=3169834|pmid=21994818}}</ref> Dissolved O2 also may make a significant contribution to total gas transport.<ref>{{Cite web|last=Jaih|first=K. K.|date=2009|title=Physical , Physiological , and Biochemical Aspects of Hyperbaric Oxygenation|url=https://www.semanticscholar.org/paper/Physical-%2C-Physiological-%2C-and-Biochemical-Aspects-Jaih/ce2b40f42dea0e2003aad2ae775deb177dae812a|access-date=2021-10-28|website=www.semanticscholar.org|language=en}}</ref> Physiologically hypertension, bradycardia, and decreased cardiac output have also been observed.<ref name=":1">{{Cite journal|last=Brugniaux|first=Julien Vincent|last2=Coombs|first2=Geoff B.|last3=Barak|first3=Otto F.|last4=Dujic|first4=Zeljko|last5=Sekhon|first5=Mypinder S.|last6=Ainslie|first6=Philip N.|date=2018-07-01|title=Highs and lows of hyperoxia: physiological, performance, and clinical aspects|url=https://journals.physiology.org/doi/full/10.1152/ajpregu.00165.2017|journal=American Journal of Physiology-Regulatory, Integrative and Comparative Physiology|volume=315|issue=1|pages=R1–R27|doi=10.1152/ajpregu.00165.2017|issn=0363-6119}}</ref> Hyperoxia is associated with seizures, cataract formation, and reversible myopia.<ref>{{Cite journal|last=Tibbles|first=Patrick M.|last2=Edelsberg|first2=John S.|date=1996-06-20|title=Hyperbaric-Oxygen Therapy|url=https://doi.org/10.1056/NEJM199606203342506|journal=New England Journal of Medicine|volume=334|issue=25|pages=1642–1648|doi=10.1056/NEJM199606203342506|issn=0028-4793|pmid=8628361}}</ref> Decreased ICP and cerebral blood flow are also present.<ref name=":1" /> Increased immunosuppressant effect, toxicity to anaerobes is observed.<ref>{{Cite journal|last=Leach|first=R M|last2=Rees|first2=P J|last3=Wilmshurst|first3=P|date=1998-10-24|title=Hyperbaric oxygen therapy|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1114115/|journal=BMJ : British Medical Journal|volume=317|issue=7166|pages=1140–1143|issn=0959-8138|pmc=1114115|pmid=9784458}}</ref>


==Side effects==
==Side effects==

Revision as of 22:30, 28 October 2021

Oxygen therapy
A person wearing a simple face mask
Clinical data
Other namessupplemental oxygen, enriched air
AHFS/Drugs.comFDA Professional Drug Information
Routes of
administration		inhaled
Drug classmedical gas
ATC code
Identifiers
CAS Number
ChemSpider
  • none
UNII
Chemical and physical data
FormulaO2

Oxygen therapy, also known as supplemental oxygen, is the use of oxygen as a medical treatment.[1] Indications for treatment may include low blood oxygen, carbon monoxide toxicity, cluster headaches, and maintenance of oxygen levels during inhaled anesthetics.[2] Long-term oxygen is often useful in people with conditions predisposing them to chronically low oxygen levels such as severe COPD or cystic fibrosis.[3][1] Oxygen can be given in a number of ways, including nasal cannula, face mask, and hyperbaric chamber.[4][5]

Oxygen is required for normal cell metabolism.[6] Excessively high concentrations can cause oxygen toxicity leading to lung damage or respiratory failure in those who are predisposed.[2][7] Higher oxygen concentrations also increase the risk of airway fires, particularly while smoking.[1] In the absence of humidification oxygen therapy may also dry out the nose.[1] The target oxygen saturation recommended depends on the condition being treated.[1] In most conditions a saturation of 94–96% is recommended, while in those at risk of carbon dioxide retention saturations of 88–92% are preferred, and in those with carbon monoxide toxicity or cardiac arrest they should be as high as possible.[1][8] While air is typically 21% oxygen by volume, oxygen therapy can increase O2 delivery up to 100%.[7]

The medical use of oxygen became common around 1917.[9][10] Template:WHO LEM The cost of home oxygen is about US$150 per month in Brazil and US$400 per month in the United States.[3] Home oxygen can be provided either by oxygen tanks or an oxygen concentrator.[1] Oxygen therapy is believed to be the most common hospital treatment in the developed world.[11][1]

Medical uses

Nasal cannula
Oxygen piping and regulator with flow meter, for oxygen therapy, mounted in an ambulance
Pin-indexed Oxygen Regulator for portable D-Cylinder, usually carried in an ambulance's resuscitation kit
Pin index medical oxygen cylinder valve

Oxygen is used as a medical treatment in a variety of acute and chronic conditions. It may be used in hospital, en route, or outside of the hospital.

Chronic conditions

Common conditions predisposing to use of supplementary oxygen include chronic obstructive pulmonary disease (COPD), chronic bronchitis, and emphysema, which are common long-term effects of smoking. These conditions may require additional oxygen during an acute exacerbation, or throughout the day and night. Physiologically, it may be indicated in people with arterial oxygen partial pressure PaO
2 ≤ 55 mmHg (7.3 kPa) or arterial oxygen saturation SaO
2 ≤ 88%, and it has been shown to increase lifespan.[12][13][14]

Oxygen may be prescribed for breathlessness, end-stage cardiac failure, respiratory failure, advanced cancer, or neurodegenerative disease in spite of relatively normal blood oxygen levels. A 2010 trial of 239 subjects found no significant difference in reduction of breathlessness between oxygen and air delivered in the same way.[15]

Acute conditions

Oxygen is widely used in emergency medicine, both by emergency medical services and in-hospital, among those giving advanced first aid.

In the pre-hospital environment, high-flow oxygen is indicated for use in resuscitation, major trauma, anaphylaxis, major bleeding, shock, active convulsions, and hypothermia.[16][17]

It may also be indicated where injury or illness has caused low oxygen levels, although oxygen flow should be titrated to achieve target oxygen saturation levels based on pulse oximetry (with a target level of 94–96% in most, or 88–92% in people with COPD).[16][8] Excessive use of oxygen in those who are acutely ill however increases the risk of death.[8] In 2018, the British Medical Journal recommended that oxygen therapy should be stopped when saturations are greater than 96% and should not be started if above 90 to 93%.[18] Exceptions included patients with carbon monoxide poisoning, cluster headaches, attacks of sickle cell disease, and pneumothorax.[18]

For personal use, high concentration oxygen is sometimes used as home therapy to abort cluster headache attacks due to its vaso-constrictive effects.[19]

People receiving oxygen therapy for hypoxemia following acute illness or hospitalization should be re-assessed by a physician prior to prescription renewal to gauge the necessity of oxygen therapy.[20] If the initial hypoxemia has resolved, additional treatment may be an unnecessary use of resources.[20]

Physiologic Effects of Oxygen Therapy

Oxygen supplementation has a variety of physiologic effects on the human body. These physiologic effects are typically considered adverse in nature (with exception of vasoconstriction, which varies upon clinical context).

Vasoconstriction

Hypoxia is observed to be a potent pulmonary vasoconstrictor, due to inhibition of an outward potassium current and activation of inward sodium current leading to contraction of pulmonary vascular musculature.[21] However, the effects of hyperoxia do not seem to have a particularly strong vasodilatory effect from the few studies that have been performed on this topic in patients with pulmonary hypertension.[22][23]

In the systemic vasculature, oxygen serves as a vasoconstrictor leading to mildly increased blood pressure and decreased cardiac output and heart rate; increased baricity does not seem to have a significant effect on the overall physiologic effect.[24] As a result this may lead to increased left-to-right shunting in particular patient populations, such as those with atrial septal defects. While the mechanism of the vasoconstriction is unknown, one plausible theory is that increased reactive oxygen species from oxygen therapy accelerates the degradation of endothelial nitric oxide, a vasodilator.[25]

Hypercapnea

Among CO2 retainers, excess exposure to oxygen in context of the Haldane effect leads to loss of affinity of deoxyhemoglobin to CO2.[26] This may contribute to acid-base disorders due to the increase in PaCO2 (hypercapnea), and patients with lung disease they may not be able to adequately clear CO2.[27]

Absorption atelectasis

It has been theorized that oxygen administration can promote accelerated development of atelectasis.[28] The concept is based on the idea that oxygen is more quickly absorbed over nitrogen, leading oxygen-rich areas that are poorly ventilated to be rapidly absorbed leading to atelectasis.[29] It is suggested that higher fractions of inhaled oxygen will be associated with increasing rates of atelectasis.[30]

Oxidative Stress

Sustained exposure to oxygen overwhelms the capacity to deal with oxidant stress.[31]  Rate of oxidant stress appears to be influenced by both oxygen concentration and length of exposure, with general toxicity observed to occur within hours in hyperoxic conditions.[32]

Reduction in erythropoiesis

Hyperoxia is observed to result in a serum reduction in erythropoietin, resulting in reduced stimulus for erythropoiesis.[33] However, hyperoxia at normobaric measurements does not appear to be able to stop erythropoiesis completely.[33]

Immunosuppressant effects

Hyperoxic environments have been observed to decrease granulocyte rolling and diapedesis in specific circumstances.[34]

Anaerobic activity

Cases of necrotizing fasciitis have been observed to require fewer debridement operations and have improvement in regard to mortality in patients treated with hyperbaric oxygen therapy.[35]

Impact of Hyperoxia

Hyperoxia is defined as an excess amount of oxygen available to tissues and organs.[36] This is associated with a myriad of adverse effects, which may be exacerbated in cases when individuals are exposed to excessive pressures of oxygen (hyperbaric hyperoxia).

Normobaric Hyperoxia

At normal pressures, hyperoxia is associated with a myriad of adverse effects, stemming from the physiological effects of oxygen on the body. In regard to the airway, both tracheobronchitis and mucositis have been observed.[37] Within the lungs, high concentrations of oxygen is associated with alveolar toxicity (coined the Lorrain-Smith effect).[38] Increased oxygen absorption leads to predisposition to absorption atelectasis (as well as denitrogenation of gas cavities) and decreased respiratory drive.[39] Pulmonary vasodilation is observed along with systemic vasoconstriction, thought to be due to accelerated degradation of nitric oxide which typically functions as a vasodilator.[40] Decreased cerebral blood flow is also observed, with mixed results regarding impact on cognition.[41][42][43] From a hematological standpoint, hyperoxia may have an immunosuppressant effect, as well as an associated with decreased erythropoesis.

Hyperbaric Hyperoxia

At higher pressures, many of the effects are magnified. Mucosal damage is observed to increase with increased pressure/exposure to high oxygen concentrations, leading to possible ARDS.[44] Dissolved O2 also may make a significant contribution to total gas transport.[45] Physiologically hypertension, bradycardia, and decreased cardiac output have also been observed.[46] Hyperoxia is associated with seizures, cataract formation, and reversible myopia.[47] Decreased ICP and cerebral blood flow are also present.[46] Increased immunosuppressant effect, toxicity to anaerobes is observed.[48]

Side effects

EMS protocols vary in regard to oxygen therapy indications. There are certain situations in which oxygen therapy has been shown to negatively impact a person's condition.[49]

Oxygen therapy can exacerbate the effects of paraquat poisoning and should be withheld except in cases of severe respiratory distress or respiratory arrest. Paraquat poisoning is rare, with about 200 deaths globally from 1958 to 1978.[50] Oxygen therapy is not recommended for people with pulmonary fibrosis or bleomycin-associated lung damage.[51]

High levels of oxygen given to infants can promote overgrowth of new blood vessels in the eye leading to blindness. This phenomenon is known as retinopathy of prematurity (ROP).

Oxygen has vasoconstrictive effects on the circulatory system, which was once thought to exacerbate the effects of stroke. However, with oxygen therapy, additional oxygen dissolves in the plasma, providing oxygen support to hypoxic neurons, leading to a reduction in both inflammation and post-stroke cerebral edema. Since 1990, hyperbaric oxygen therapy has been used worldwide for stroke treatment. In rare instances, people receiving hyperbaric oxygen therapy have had seizures. Such seizures are generally attributed to oxygen toxicity,[52][53] although hypoglycemia may play a role as well. The risk of hypoglycemia may be reduced by careful monitoring the patient's blood glucose.

Oxygen therapy has also been used as an emergency treatment for diving injuries for years.[54] Recompression in a hyperbaric chamber with 100% oxygen exposure is the standard hospital and military medical treatment to decompression illness.[54][55][56] The success of recompression therapy is greatest if given within four hours after resurfacing, with earlier treatment associated with a decrease in the number of recompression treatments required.[57] It has been suggested in literature that heliox may be a better alternative to oxygen therapy.[58]

Chronic obstructive pulmonary disease and emphysema

Patients with chronic obstructive pulmonary disease and emphysema are especially known to retain carbon dioxide (type II respiratory failure). Oxygen therapy may decrease respiratory drive, leading to accumulation of carbon dioxide (hypercapnia) and thus decreased blood pH, affecting mortality by potentially precipitating respiratory failure.[59] Improved outcomes are seen when oxygen treatment is titrated. [59] This is primarily as a result of ventilation–perfusion imbalance (see Effect of oxygen on chronic obstructive pulmonary disease).[60] However, the risks associated with loss of respiratory drive are far outweighed by the risks of withholding emergency oxygen; therefore, emergency administration of oxygen is never contraindicated. Transfer from field care to definitive care where oxygen use can be carefully calibrated typically occurs long before significant reductions to the respiratory drive are observed.

A 2010 study has shown that titrated oxygen therapy is less dangerous in COPD patients compared to high-flow therapy, and that other patients without COPD may benefit more from titrated therapy in specific circumstances.[59]

Fire risk

Highly concentrated sources of oxygen increase risk for rapid combustion. Oxygen itself is not flammable, but the addition of concentrated oxygen to a fire greatly increases its intensity, and can aid the combustion of materials (such as metals) which are relatively inert under normal conditions. Fire and explosion hazards exist when concentrated oxidants and fuels are brought together in close proximity, although an ignition event (e.g., heat or spark) is needed to trigger combustion.[61] A well-known example of an accidental fire accelerated by pure oxygen occurred in the Apollo 1 spacecraft in January 1967 during a ground test, killing all three astronauts.[62] A similar accident killed Soviet cosmonaut Valentin Bondarenko in 1961.

Combustion hazards also apply to compounds of oxygen with a high oxidative potential, such as peroxides, chlorates, nitrates, perchlorates, and dichromates because they can donate oxygen to a fire.[relevant?]

Concentrated O
2 will allow combustion to proceed rapidly and energetically.[61] Steel pipes and storage vessels used to store and transmit both gaseous and liquid oxygen will act as a fuel; and therefore the design and manufacture of O
2 systems requires special training to ensure that ignition sources are minimized.[61] Highly concentrated oxygen in a high-pressure environment can spontaneously ignite hydrocarbons such as oil and grease, resulting in fire or explosion. The heat caused by rapid pressurization serves as the ignition source. For this reason, storage vessels, regulators, piping and any other equipment used with highly concentrated oxygen must be "oxygen-clean" prior to use, to ensure the absence of potential fuels. This does not only apply to pure oxygen; any concentration significantly higher than atmospheric (approximately 21%) carries a potential ignition risk.

Some hospitals have instituted "no-smoking" policies which help support the aim of keeping ignition sources away from medical piped oxygen. Recorded sources of ignition of medically prescribed oxygen include candles, aromatherapy, medical equipment, cooking, and deliberate vandalism. Smoking of pipes, cigars, and cigarettes is of special concern. These policies do not entirely eliminate the risk of injury with portable oxygen systems, especially among patients who smoke at home.[63]

Alternative medicine

Some practitioners of alternative medicine have promoted "oxygen therapy" as a cure for many human ailments including AIDS, Alzheimer's disease and cancer. Associated procedures may include injecting hydrogen peroxide, oxygenating blood, or administering pressurized oxygen to the rectum, vagina, or other bodily openings.[citation needed] According to the American Cancer Society, "available scientific evidence does not support claims that putting oxygen-releasing chemicals into a person's body is effective in treating cancer", and some of these treatments can be dangerous.[64]

Storage and sources

Gas cylinders containing oxygen to be used at home. When in use a pipe is attached to the cylinder's regulator and then to a mask that fits over the person's nose and mouth.
A home oxygen concentrator for a person with emphysema

Oxygen can be separated by a number of methods, including chemical reaction and fractional distillation, and then used immediately or stored for future use. The main methods utilized for oxygen therapy include:

  1. Liquid storage – Liquid oxygen is stored in chilled tanks until required, and then allowed to boil (at a temperature of 90.188 K (−182.96 °C)), releasing oxygen as a gas. This method is widely utilized at hospitals due to their high usage requirements, but it can also be used in other settings. See Vacuum Insulated Evaporator for more information on this method of storage.
  2. Compressed gas storage – The oxygen gas is compressed in a gas cylinder, which provides a convenient storage method not requiring refrigeration (e.g., liquid storage). Large oxygen cylinders hold 6,500 litres (230 cu ft) and can last about two days at a flow rate of 2 litres per minute. A small portable M6 (B) cylinder holds 164 or 170 litres (5.8 or 6.0 cu ft) and weighs about 1.3 to 1.6 kilograms (2.9 to 3.5 lb).[65] These tanks can last 4–6 hours when used with a conserving regulator, which senses the person's breathing rate and sends pulses of oxygen. Conserving regulators may not be usable by people who breathe through their mouths.
  3. Instant usage – The use of an electrically powered oxygen concentrator[66] or a chemical reaction based unit[67] can create sufficient oxygen for immediate personal use. These units (especially the electrically powered versions) are widely used for home oxygen therapy as portable personal oxygen, with an advantage of being continuous supply without the need for additional deliveries of bulky cylinders.

Delivery

Various devices are used for administration of oxygen. In most cases, the oxygen will first pass through a pressure regulator, used to control the high pressure of oxygen delivered from a cylinder (or other source) to a lower pressure. This lower pressure is then controlled by a flowmeter, which may be preset or selectable, which controls the flow at a measured rate (e.g., litres per minute [LPM]). The typical flowmeter range for medical oxygen is between 0 and 15 LPM with some units capable of obtaining up to 25 liters per minute. Many wall flowmeters using a Thorpe tube design are able to be dialed to "flush" oxygen which is beneficial in emergency situations.

Low-dose oxygen

Many people only require slight increases in inhaled oxygen, rather than pure or near-pure oxygen.[68] These requirements can be met through a number of devices dependent on situation, flow requirements, and personal preference.

A nasal cannula (NC) is a thin tube with two small nozzles inserted into a person's nostrils. It can provide oxygen at low flow rates, 2–6 litres per minute (LPM), delivering an oxygen concentration of 24–40%.

There are also a number of face mask options, such as the simple face mask, often used at between 5 and 8 LPM, capable of deliverying oxygen concentrations between 28% and 50%. This is closely related to the more controlled air-entrainment masks, also known as Venturi masks, which can accurately deliver a predetermined oxygen concentration up to 40%.

In some instances, a partial rebreathing mask can be used, which is based on a simple mask, but features a reservoir bag, which can provide oxygen concentrations of 40–70% at 5–15 LPM.

Non-rebreather masks draw oxygen from attached reservoir bags with one-way valves that direct exhaled air out of the mask. When properly fitted and used at flow rates of 8–10 LPM or higher, they can deliver close to 100% oxygen. This type of mask is indicated for acute medical emergencies.

Demand oxygen delivery systems (DODS) or oxygen resuscitators deliver oxygen only when the person inhales or the caregiver presses a button on the mask (e.g., nonbreathing patient). These systems greatly conserve oxygen compared to steady-flow masks, which are useful in emergency situations when a limited supply of oxygen is available and there is a delay in transporting the person to higher care. They are very useful in CPR, as the caregiver can deliver rescue breaths composed of 100% oxygen with the press of a button. Care must be taken not to over-inflate the person's lungs, and some systems employ safety valves to help prevent this. These systems may not be appropriate for people who are unconscious or in respiratory distress because of the effort required to breathe from them.

High flow oxygen delivery

In cases where the person requires a high concentration of up to 100% oxygen, a number of devices are available. The most common is the non-rebreather mask (or reservoir mask) which has a series of one-way valves preventing exhaled air from returning to the bag. There should be a minimum flow of 10 L/min. The delivered FIO2 (Inhalation volumetric fraction of molecular oxygen) of this system is 60–80%, depending on the oxygen flow and breathing pattern.[69][70] Another type of device is a humidified high flow nasal cannula which enables flows exceeding a person's peak inspiratory flow demand to be delivered via nasal cannula, thus providing FIO2 of up to 100% because there is no entrainment of room air, even with the mouth open.[71] This also allows the person to continue to talk, eat, and drink while still receiving therapy.[72] This type of delivery method is associated with greater overall comfort, improved oxygenation, and respiratory rates compared with face mask oxygen.[73]

In specialist applications such as aviation, tight-fitting masks can be used. These masks also have applications in anaesthesia, carbon monoxide poisoning treatment and in hyperbaric oxygen therapy.

Positive pressure delivery

Patients who are unable to breathe on their own will require positive pressure to move oxygen into their lungs for gaseous exchange to take place. Systems for delivery vary in complexity and cost, starting with a basic pocket mask adjunct which can be used to manually deliver artificial respiration with supplemental oxygen delivered through a mask port.

Many emergency medical service members, first aid personnel, and hospital staff may use a bag-valve-mask (BVM), which is a malleable bag attached to a face mask (or invasive airway such as an endotracheal tube or laryngeal mask airway), usually with a reservoir bag attached, which is manually manipulated by the healthcare professional to push oxygen (or air) into the lungs. This is the only procedure allowed for initial treatment of cyanide poisoning in the UK workplace.[74]

Automated versions of the BVM system, known as a resuscitator or pneupac can also deliver measured and timed doses of oxygen directly to people through a facemask or airway. These systems are related to the anaesthetic machines used in operations under general anaesthesia that allow a variable amount of oxygen to be delivered, along with other gases including air, nitrous oxide and inhalational anaesthetics.

As a drug delivery route

Oxygen and other compressed gasses are used in conjunction with a nebulizer to allow the delivery of medications to the upper and/or lower airways. Nebulizers use compressed gas to propel liquid medication into therapeutically sized aerosol droplets for deposition in the appropriate desired portion of the airway. A typical compressed gas flow rate of 8–10 L/min is used to nebulize medications, saline, sterile water, or a combination these treatments into a therapeutic aerosol for inhalation. In the clinical setting, room air (ambient mix of several gasses), molecular oxygen, and Heliox[citation needed] are the most common gases used to nebulize a bolus treatment or a continuous volume of therapeutic aerosols.

Exhalation filters for oxygen masks

Filtered oxygen masks have the ability to prevent exhaled, potentially infectious particles from being released into the surrounding environment. These masks are normally of a closed design such that leaks are minimized and breathing of room air is controlled through a series of one-way valves. Filtration of exhaled breaths is accomplished either by placing a filter on the exhalation port or through an integral filter that is part of the mask itself. These masks first became popular in the Toronto (Canada) healthcare community during the 2003 SARS Crisis. SARS was identified as being respiratory based, and it was determined that conventional oxygen therapy devices were not designed for the containment of exhaled particles.[75][76][77] Common practices of having suspected people [clarification needed] wear a surgical mask was confounded by the use of standard oxygen therapy equipment. In 2003, the HiOx80 oxygen mask was released for sale. The HiOx80 mask is a closed design mask that allows a filter to be placed on the exhalation port. Several new designs have emerged in the global healthcare community for the containment and filtration of potentially infectious particles. Other designs include the ISO-O
2 oxygen mask, the Flo2Max oxygen mask, and the O-Mask. The use of oxygen masks that are capable of filtering exhaled particles is gradually becoming a recommended practice for pandemic preparation in many jurisdictions.[citation needed]

Typical oxygen masks allow a person to breathe in a mixture of room air and therapeutic oxygen. However, as filtered oxygen masks use a closed design that minimizes or eliminates the person's contact with and ability to inhale room air, delivered oxygen concentrations in such devices have been found to be elevated, approaching 99% using adequate oxygen flows.[citation needed] Because all exhaled particles are contained within the mask, nebulized medications are also prevented from releasing into the surrounding atmosphere, decreasing the occupational exposure to healthcare staff and other people.[citation needed]

Aircraft

In the United States, most airlines restrict the devices allowed onboard an aircraft. As a result, passengers are restricted in what devices they can use. Some airlines will provide cylinders for passengers with an associated fee. Other airlines allow passengers to carry on approved portable concentrators. However, the lists of approved devices varies by airline so passengers may need to check with any airline they are planning to fly on. Passengers are generally not allowed to carry on personal cylinders. In all cases, passengers need to notify the airline in advance of their equipment.

Effective May 13, 2009, the Department of Transportation and FAA ruled that a select number of portable oxygen concentrators are approved for use on all commercial flights.[78] FAA regulations require larger airplanes to carry D-cylinders of oxygen for use in case of an emergency.

See also

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Further reading

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