Category: CONVERSATION

Medical Oxygen

 

Outside of industry, oxygen’s main commercial use is medical. Odd as it seems to label medical oxygen use commercial, every breath supplemented by oxygen, whether in an ambulance, in an emergency room, on a ward, in labor and delivery, in an operating room or recovery room, in an intensive care unit, or as home oxygen therapy, a financial cost is incurred.

The infrastructure required to support medical oxygen use is elaborate, varied, complicated, and often taken for granted. Medical oxygen, like water in a hospital or clinic, is expected to be readily available, free flowing, and cheap. Rarely is cost consideration a factor in oxygen use decisions.

On a per dose basis oxygen is inexpensive. However, the total number of “oxygen doses” administered plus the personnel and equipment required to administer and monitor it make oxygen a costly drug  for hospitals in the aggregate. Rarely is the cost of respiratory therapy services or pulse oximetry or blood gas analysis or oxygen sensor maintenance considered when the total cost of medical oxygen supplementation is assessed.

Surprisingly, it is difficult to get cost data about medical oxygen. It is supplied under contracts that are specific to institutions. As contracts may contain proprietary information, cost accounting estimates hard to calculate. Perhaps a future post will provide more information as it becomes available.

If you are a visitor with specific, accurate information about oxygen cost accounting, please, join the conversation.

What Happens After Your Last Breath: The Short Version

Breathing unites respiration with ventilation. While respiration occurs in all organisms, ventilation does not.  The coupling of respiration to ventilation increases an organism’s capacity for complexity. The price of complexity, however, is constrained adaptation—limitation to a specific environment where respiration and ventilation remain possible.

Breathing removes gaseous metabolic wastes produced by respiration—mostly, but not exclusively, carbon dioxide and water. Breathing moves nitrogen and oxygen into the body: nitrogen to hold open alveolar spaces required to match ventilation to blood perfusion; oxygen to be sequestered in blood before transfer into tissues for reduction to water during adenosine triphosphate (ATP) generation by mitochondrial electron transport. As all gas transfers follow pressure gradients, differences in partial pressure determine how a gas moves throughout a body.

A body’s internal ecology— its milieu intérieur—depends on respiration coupled to ventilation: respiration to generate energy inside mitochondria, ventilation to move gasses around. Aerobic biology ultimately depends on this sequence: oxygen intake, oxygen sequestration, oxygen diffusion, reactive oxygen species (ROS) generation from electron transfers in mitochondria during carbohydrate and lipid oxidation, oxygen reduction during ATP generation, carbon dioxide and water production, carbon dioxide and water elimination, antioxidant correction of any collateral damage.

So imagine you’ve taken your last breath. What happens? The simple version goes something like this:

As ventilation ceases, carbon dioxide accumulates in tissues and blood. Tissues become more acidic and electrochemically unstable. Respiration shifts from the efficient aerobic to less efficient anaerobic form. Nitrogen- and oxygen-filled alveoli accumulate carbon dioxide; they also collapse as the last oxygen is extracted and diaphragm motion ceases. As oxygen intake ceases, blood oxygen reservoirs decrease. As long as the heart keeps beating whatever oxygen is sequestered in the blood will be extracted by perfused tissues. After oxygen drops below the supply threshold required to support ATP formation at Complex IV in mitochondria, electron transport chain efficiency collapses and ROS production increases. As oxygen is too low to receive any generated electrons, the all-important electrochemical or chemiosmotic gradient that supports electron transfer and hydrogen ion transport across the inner mitochondrial membrane collapses.  With hydrogen ion accumulation mitochondrial acidity increases and calcium regulation is disrupted. Generated reactive species overwhelm any remaining antioxidant capacity. Unchecked, chain reactions with fats, proteins, and nucleic acids further destroy tissue capacity to regulate and repair damage.

The net effect of stopping ventilation, then, is cessation of respiration. Artificial ventilation must be imposed if any possibility of salvaging undamaged tissues exists. In the absence of such an intervention, biological collapse ensues for us—but not our microbiomes. Our microbiomes, much of which is anaerobic to begin with, continue to respire until their unique metabolic needs can no longer be met either.

 

 

A Perspective on Oxygen in Clinical Use

Over the past seven to ten years or so concern has increased among pediatric anesthesiologists about developmental delay risks in young children exposed to “anesthesia.” A corresponding concern has developed among adult specialists about post operative cognitive dysfunction and the late onset of dementia in patients who have “anesthesia” after age 60 or so.
The anesthesiology literature is just now filling with articles on these subjects but no biomarker-based studies have been conducted or published yet, to my knowledge, that can help point toward the cause or causes of these vexing and delayed neurological conditions.
Clearly “anesthesia” works by influencing synaptic functions or at least the interconnectivity of brain regions that otherwise need to be connected for consciousness and movement to be experienced. Common denominators in the background of every “anesthetic” are supplemental oxygen, reactive oxygen and nitrogen species (RONS), antioxidant ecology disruption, inflammation, and “transcriptome” activation/deactivation.
I have been stunned especially by the increase in autism rates since the mid-80s. Interestingly, increases in Alzheimer Disease and other oxidative stress-driven conditions have tracked autism, more or less. Some clinical historical perspective may be illuminating.
Administering ‘anesthesia” involves producing amnesia, analgesia, akinesis, and autonomic stability while guaranteeing oxygen delivery by using artificial atmospheres composed of air, nitrous oxide, oxygen, and volatile anesthetic drugs in combination with a variety of injectable fixed agents to allow patients to undergo noxious procedures without undue suffering.
Modern society’s reliance on these intensely unnatural combinations of gasses and drugs for an increasing array of diagnostic and invasive procedures constitutes one of civilizations most remarkable achievements, dependence upon which has accelerated over the past 50 years. It is however, probably not without (as yet) undetected cost to health, especially to children and adolescents, but also to the old and aging. More research is needed to point a way toward some answers to emerging questions about mental functional changes after anesthesia in all of these patient populations.
In the mid-1980s the first commercially viable pulse-oximeters came into use. This improved physicians’ abilities to continuously monitor arterial oxygen saturation without reliance on serial painful arterial blood gasses. Because it was now convenient to track immediate responses to even small changes in oxygen supplementation, empirical oxygen use became more popular in many medical specialties — pediatrics, anesthesiology, obstetrics, emergency and intensive care in particular.
An overlooked problem was that “O2 sat” is a proxy for arterial oxygen partial pressure, a phenomenon tightly regulated by both a finite natural atmospheric oxygen partial pressure, a delicate pro-oxidant/antioxidant balance, and the titration effects of hemoglobin’s function as the blood’s buffer against too much dissolved oxygen content being released to tissues. Under clinical hyperoxemic conditions of supplemental oxygen administration “O2 sat” readings max out at 100% while the measurable arterial oxygen partial pressure might range from 100 mmHg to almost 700 mmHg — a > 6 fold range equal to a toxic overdose.
It is no exaggeration to say that for the first time in history large numbers of patients could be routinely exposed to gasses/artificial atmospheric mixtures that evolution has equipped them to tolerate at much lower concentrations, if at all. With respect to oxygen in particular, in evolutionary terms, 500 million years of adaptation to 21% ambient oxygen could now be routinely offset on a medical whim by health care providers to achieve an “O2 sat” of 100%, a saturation that is almost always abnormal in itself from a physiological perspective.
It is also not an exaggeration to suggest injury homology exists at both the RONS and transcriptome level (eg. p53 activation) between hyperoxic and radiation exposures and that these might be additive over time.
Beginning with OB practices and extending beyond pediatric and anesthesia practices into intensive and emergency care settings it is plausible that oxidative stress induced by oxygen supplementation constitutes an overlooked historical thread in forms of cognitive neurological diseases.
Oxygen, as a supplemental drug, gets administered to mothers carrying vulnerable fetuses during labor and then to infants delivered in the delivery room. On induction and during maintenance of anesthesia hyperoxic gas mixtures are used despite the tendency of anesthetics to reduce oxygen consumption. In intensive care units patients are maintained on hyperoxic gas mixtures despite good blood gasses or in lieu of other maneuvers such as increased PEEP or ventilation mode changes that can support oxygenation. In the backs of ambulances patients are getting oxygen via masks even when data and clinical situations show it was not needed.
Unfortunately, audit studies of such practices are few and the clinical literature does not reflect what happens numerous times daily in practice. In the domain of understanding the science beneath iatrogenic oxygen use, basic science is way out in front of clinical practice. The consequences are macromolecular and their recognition is delayed if not overlooked entirely.

 

The Oxygen Paradox

Oxygen’s three major forms are dynamically interrelated: molecular oxygen (O2), atomic oxygen (O), and ozone (O3). Each form has a more or less dominant role in different layers of the atmosphere: O2 in the troposphere (< 8 km over the Poles to > 16km over the Equator), O3 in the stratosphere (< 50 km), and O in the exosphere (> 500 km) where most O2 and O3 are photo-dissociated by ultraviolet radiation. About 90% of Earth’s atmospheric mass, estimated at 5.2 x 1021 g, of which 1.18 x 1021 g is oxygen, is located < 15 km above its surface. Gravity, temperature, radiation, and planetary rotation influence oxygen distribution variously at different atmospheric levels.*

Oxygen’s chemical reactivity is determined by the unpaired electron’s spin pattern in O’s outer orbital. When two Os form O2 the parallel spin pattern of each outer orbital electron is maintained even as the electrons are shared. This anomaly confers relative stability to ground state O2. Because the Pauli exclusion principle holds that anti-parallel spin electrons must pair with parallel spin electrons, the two parallel spin electrons occupying O2’s outer domain do not readily react with other moieties at the same time. Energy must be expended to overcome this electron restriction to produce spin reversal for O2 to react. Thus, reduction of O2 to H2O progresses stepwise via energy-dependent serial electron transfers that create distinct reactive intermediaries with different half-lives, diffusion capabilities, biological significance, and toxicity.

It is this oxygen property related to outer orbital electron spin restriction that frames the “oxygen paradox,” defined here as obligate aerobic life-form dependency on a chemical reduction process that produces invariably harmful intermediaries hazardous to the very life forms that produce them. Implicit in the oxygen paradox is another paradox – free radical (FR) production amounts to self-generated “inner radiation,” protection from which is conferred by intrinsic antioxidant capacity.

 

*The technically minded reader may want to review or read:

Stepniewski W, Stepniewski Z, Bennicelli RP, Glinski J. Oxygenology in Outline. Institute of Agrophysics PAS, Lublin 2005

Early Clinical Oxygen Supplementation

Early Clinical Oxygen Supplementation

Oxygen supplementation grew gradually in medicine. First Mayow then Boyle demonstrated absence of air made mammalian life impossible by 1666. Priestly in 1774 and Lavoisier in 1777 isolated and demonstrated oxygen as air’s vital component. Beddoes medicalized oxygen as a panacea in 1789 through his Pneumatic Institute in Bristol, which closed in 1800. Thereafter oxygen use fell out of favor. (Warnock E, Tovell RM. Oxygen therapy and resuscitation. Anesthesiology. 1940; 1:187-204)

The roots of oxygen supplementation in anesthesia are also instructive. Availability, purity, equipment, logistics, and indications for use factored into acceptance. Most early anesthetics using ether, chloroform, and nitrous oxide were delivered in room air (FiO2 0.21) with the patient breathing spontaneously. The first inhaled ether anesthetic was reported in 1846. (Bigelow HJ. Insensibility during surgical operations produced by inhalation. Boston Med Surg J. 1846; 35:309-17) Hooper reported using oxygen after ether anesthesia to aid recovery in April 1847. (Hooper W. Inhalation of oxygen for resuscitating etherized patients. The Pharmaceutical Journal. 1847; 6:508-9)

Supplemental oxygen was first used to treat nitrous oxide poisoning in the 1860s. (Andrews E. The Oxygen Mixture, a new anaesthetic combination. Chicago Medical Examiner. 1868; 9:656-61) A common anesthetic technique then relied on 100% nitrous oxide inhalation until signs of adequate anesthesia appeared—stretor, jacitation, and lividity. With the patient obtunded near asphyxiation the procedure was performed. Blood loss was minimal as death was near. At surgery’s end oxygen was given for rescue treatment. (Smith WDA, The introduction of nitrous oxide and oxygen anaesthesia. Brit J Anaesth. 1966; 38: 950-62)

Volatile agent-oxygen combinations surfaced in the late 19th C. Who to credit is a matter of dispute. Kreutzmann cited Neudorfer in Vienna in his 1887 report. (Kreutzmann H. Anaesthesia by choloroform and oxygen combined: preliminary report. Pacif Med Surg J. 1887; 30:462-3) Suarez published his “Spanish method” in 1898. (Diz JC, Franco A. A Spanish pioneer in the use of oxygen in anaesthesia. International Congress Series. 2002; 1242:121-5) Routine oxygen supplementation during and after inhalation anesthesia grew in the mid-20th C. Increased muscle relaxant use likely hastened oxygen’s acceptance as part of anesthesia.

Awareness about how too little and too much oxygen affects life also grew gradually. Claude Bernard’s early lectures on anesthetics and asphyxia were published in 1875. (Bernard C. Lectures on anesthetics and on asphyxia. Translated by BR Fink. Park Ridge, IL:Wood Library-Museum of Anesthesiology. 1989) Paul Bert, a Bernard protégé, reported central nervous system oxygen toxicity effects in animals and other toxic effects on plants and animals in 1878. William Osler’s first textbook edition published in 1892 made no reference to supplemental oxygen. Lorrain Smith induced fatal pneumonia in rabbits with two to four days of 80% oxygen exposure in 1899. (Barach AL. Widening scope of oxygen therapy in the treatment of disease. Anesth Analg. 1932; :71-7)

Oxygen supplementation got a boost with efficacious poison gas-induced pulmonary injury treatment with 40% to 50 % oxygen during WW I. Barcroft and Haldane demonstrated hypoxemia’s relationship to harmful effects between 1914 and 1922. Enthusiasm built afterward to where Cohen, quoted by Buettner, said in 1931: “Oxygen to be efficacious must be used freely, frequently, fearlessly, and almost constantly, nor must its use be postponed until the patient is moribund for it will not revive the dead.” (Buettner JJ. Oxygen therapy. Anesth Analg. 193; 10:39-44) A new “oxygen culture” was thus born out of war-time experience.

By 1932 Barach endorsed specific indications for oxygen supplementation: lobar and bronchopneumonia; postoperative atelectasis; atelectasis of the new-born; acute and chronic cardiac failure; chronic pulmonary fibrosis; and (in combination with carbon dioxide) carbon monoxide poisoning and morphine poisoning. For these conditions he advocated an oxygen therapy range of between 30% and 60%. (Barach AL. Widening scope of oxygen therapy in the treatment of disease. Anesth Analg. 1932; :71-7) By 1940-41 the indications and physiological considerations applicable to oxygen supplementation were defined for cardiac disease, resuscitation, and “asphyxia neonatorum.” (Warnock E, Tovell RM. Oxygen therapy and resuscitation. Anesthesiology. 1940; 1:187-204) (Behkne AR. Certain physiological principles underlying resuscitation and oxygen therapy. Anesthesiology. 1941; 2:245-60)

 

 

Origins of Artificial Oxygen Atmospheres

The creation and use of artificial oxygen atmospheres is of extremely recent origin by evolutionary standards. Indeed, the capacity of organisms to adapt to artificial oxygen atmospheres is constrained by the fact that extreme concentration exposures are artificial, usually acute and abrupt, mostly post-reproductive, and ultimately unsustainable for long periods of time. Much as wood cannot evolve protections against intense thermal injury (burning), eucaryotic cells have not evolved — and possibly cannot evolve unequivocally — to withstand even short term, serious oxidative injuries induced by extreme oxygen exposures.

While the word “oxygen” dates to the 18th C, knowledge about oxygen’s production and properties dates to the 8th C or earlier.* Credit for oxygen’s “discovery” should not be ascribed to any one person, place, or time but regarded as a metaphor based in fact for how we come to know what we know — and may still come to know in the future.

Chinese experimenters recognized as early as the 8th C that a substance released by heating potassium nitrate could react with carbon and sulfur but not gold. Italian scientist, artist, and inventor Leonardo da Vinci (1452-1519) postulated in the 15th C that air consisted of two parts: one consumed by burning and one not, corresponding to oxygen and nitrogen, respectively. Polish alchemist Michael Sendivogius Polonos (1566-1636) postulated in the early 1600s that an “areal food of life” circulated from earth to air via the same potassium nitrate — saltpeter — pathway that, when heated, released the “Elixir of Life.” His concept was put to a practical test in 1621 when a Dutchman, Cornelius Drebbel (1572-1633), created the first known artificial oxygen atmosphere, one capable of sustaining 12 men who remained submerged under water in a wooden submarine for three hours.

John Mayow (1641-1679, English), who studied respiration and physiology at Oxford in the 17th C, conducted a series of experiments that shed light on the properties and nature of oxygen. He probably deserves more credit than he typically receives for his work in this empirical domain. His experiments showed that select metals increased in weight when heated in the presence of his mysterious gas; that this marvelous and wondrous gas composed about 20% of the atmosphere; and that mice kept under a bell jar in the presence of a burning candle expired soon after the candle extinguished presumably because this gas was exhausted. These observations led him to conclude that spiritus nitro-aereus — oxygen by another name — was present in the atmosphere, transfered via the lungs to the blood by breathing, and consumed in respiration so as to sustain life itself.

Other curious and intrepid proto-chemists produced the “release of oxygen” by heating various metals: Ole Borch (1626-1690, Denmark) in 1678 (saltpeter), Steven Hales (1677-1761, England) in 1731 (saltpeter), Pierre Bayen (1725-1798, France) in 1774 (mercury oxide). However, there are three names most commonly cited in connection to the isolation, characterization, and naming of oxygen, fairly or not: Carl Wilhelm Scheele (1742-1786, Swedish), Joseph Priestly (1733-1804, English), and Antoine Lavoisier (1743-1794, French). Perhaps the improved communication flow and revolutionary spirit abounding in the 18th C explains why these three scientists typically receive credit for things predecessors also accomplished in some form.

Scheele isolated oxygen from various nitrates; Priestly isolated “deflogisticated air” from mercuric oxide using sunlight as a heat source and essentially replicated Mayow’s work with bell jars, mice, and candles — with the added feature of breathing the gas himself to see how it made him feel; while Lavoisier conducted derivative investigations but ultimately gave oxygen its name, after the Greek for “acid-former,” under the misconception that anything acting like an acid had to contain oxygen.

While all three deserve credit for experiments, reports in letters, and formal publications; Lavoisier is the one who campaigned most actively to gather fame to himself for the discovery of oxygen. Beheaded during the French Revolution, he nonetheless claimed: “This theory [the oxygen theory] is not as I have heard it described, that of the French chemists (e.g, Bayen), it is mine (elle est la mienne); it is a property which I claim from my contemporaries and from posterity.”**

It was not long after Priestly published “Experiments and Observations on Different Kinds of Air” (1775) that the therapeutic potential of oxygen to treat various respiratory conditions and unrelated diseases was recognized and exploited. The first commercial use of artificial oxygen atmospheres for medical purposes was initiated by Thomas Beddoes (1760-1808) at his Pneumatic Institute in Bristol, England in 1798. This short-lived enterprise shut down in 1802. Of great interest is the fact that Humphry Davy (1778-1829, England) of nitrous oxide fame; and James Watt (1736-1819) of steam engine fame were partners with Beddoes in his enterprise — one which, practically speaking, upended the tight relationship between evolution and atmospheric oxygen content; while changing forever the way medicine would view and handle oxygen therapy in patient care settings.

 

*Technically minded readers might enjoy reading or reviewing:

Lane N. Oxygen. The Module that made the World. Oxford, 2002

Stępniewski W, Stępniewska Z, Bennicelli RP, Gliński J. Oxygenology in Outline. Institute of Agrophysics PAS, Lublin, 2005

http://www.chemistryexplained.com/elements/L-P/Oxygen.html

**http://todayinsci.com/QuotationsCategories/O_Cat/Oxygen-Quotations.htm

Ancient Oxygen Atmospheres

What drove oxygen accumulation in the earth’s atmosphere? Scientists have theories with supportive data but ultimate answers are elusive and always engender additional intriguing questions.*

What is unquestioned is that ancient oxygen atmospheres developed slowly over the eons, fluctuated before they flourished, and see-sawed before they stabilized. How atmospheric dynamism pressured various and varied organisms to adapt, evolve, dominate, die off, and otherwise reshape the barren and burning terrain of our beautiful, infant planet is both a marvelous story and germane to how we should view oxygen today.

As will become evident through future posts, evolution has equipped humans — mere blips in planetary time — with a greater capacity to withstand low oxygen levels than high oxygen levels. That’s “because” early evolution proceeded from extremely low oxygen fractions to the current 21% level with only a brief period of time spent at higher levels (a few million years) estimated to have peaked around 30% to 35% of total atmospheric pressure. In a real sense, to paraphrase the poet T.S. Eliot, “in our beginning is our end.” Not only is biology our destiny; destiny is in our biology. How true when it comes to oxygen.

As mentioned in a previous Oxygenologist entry, our late Proterozoic and early Phanerozoic eons saw oxygen levels rise enough to support complex oxygen-sustained organisms. This means life forms capable of metabolizing hydrogen sulfide, methane, and other gasses preceded, co-existed with, and probably co-operatively interacted with oxygen-dependent organisms in oxygen-rich eons and eras. It also means critical oxygen levels had to be attained before the most complex animals (metazoans) could populate and dominate our chemically volatile earth.

Planetary biogeochemical cycles saw complex interactions among minerals, water, gasses and the full spectrum of radiation (infra-red to cosmic) before a floor and a ceiling level for planetary ancient oxygen atmospheres could develop. The floor was set when saturated complex iron, carbon, sulfur, and other mineral substance “burials” permitted enough oxygen to accumulate as a measurable atmosphere in oxidative/reductive equilibrium with the volatile and volcanic surface mantle; the ceiling was set when conflagrations of organic matter (paleofires) periodically drew down maximum atmospheric oxygen levels, above which all combustibles could consumed, but below which combustibles could be cyclically restored. Between the two extremes life-forms evolved that depend on oxygen protected by a burgeoning ozone layer capable of shielding surface organisms from the highest levels of cosmic radiation capable of inducing genetic mutations.

 

*Technically-minded readers might be interested in reading:

Berner RA. Atmospheric oxygen over the Phanerozoic time. Proc Natl Acad Sci USA. 1999; 96:10955-7

Goldblatt C, Lenton TM, Watson AJ. Bistability of atmospheric oxygen and the Great Oxidation. Nature. 2006; 443:683-6

Plavansky NJ, Reinhard CT, Wang X, Thomson D, McGoldrick P, Rainbird RH, Johnson T, Fischer WW, Lyons TW. Low mid-proterozoic atmospheric oxygen levels and the delayed rise of animals. Science. 2014; 346:635-8

 

 

Oxygen Atmospheres

Oxygen atmospheres on earth have varied dramatically over the eons and eras. Scientists refer to the eons as the Hadean (4.5 to 4.0 billion years ago), Archean (4.0 to 2.5 billion years ago), Proterozoic (2.5 to 0.5 billion years ago); and Phanerozoic (0.5 billion years ago to the present). The Hadean eon is undivided; the Archean eon is subdivided into Eo-, Paleo-, Meso- and Neo- eras; the Proterozoic into Paleo-, Meso-, and Neo- eras; the Phanerozoic into Paleozoic, Mesozoic, and Cenozoic eras — this last, our current era.

Each eon, era, and subdivision marks a milestone in the remarkable story — too complex to cover here — of oxygen’s planetary equilibration amid shifting complex physical systems to accumulate and “stabilize” at the 21% atmospheric level we most naturally breathe today.  The inseparable parallel story is how life forms developed and evolved to handle oxygen within the eons’ and eras’ volatile atmospheric conditions.*

As remarkable as the story of oxygen’s past is, its present and future point in a different direction. The isolation of oxygen at various times between the 15th and the 18th centuries moved us to where we are today: capable of creating oxygen atmospheres containing levels far in excess of 21%. Attainment of this feat preceded awareness of oxygen’s biophysical significance and development of a nomenclature suitable to its medicinal properties. In brief, we used oxygen medically before we understood its importance, risks, benefits, and limitations. Interestingly, the 20th century saw humanity asking how to control “the atom” — radiation — in multiple settings. Perhaps the 21st century will see us determining how to rationally use and wisely control oxygen in medical settings.

* The technically minded reader might enjoy: Hsia CWC, Schmitz A, Lambertz M, Perry SF, Maina JN. Evolution of air breathing: oxygen homeostasis and the transition from water to land and sky. Compr Physiol. 2013; 3:849-915. doi:10.1002/cphy.c120003

Why Oxygen?

Oxygen supports life. At sea level the atmosphere is close to 21% oxygen, a condition that has taken an estimated 500,000,000 years to develop. Humans and many other multicellular aerobic organisms have evolved over shorter time periods to function optimally at this modest oxygen level. They have also developed limited abilities to withstand and repair damage caused by excessive oxygen levels. Because oxygen levels vary under different environmental and physiological conditions (high altitude, intrauterine life) adaptation to lower levels also occurs. This adaptation, evidence suggests, is more robust and evolutionarily appropriate than adaptation to high levels of oxygen.

Medical oxygen use dates to the late 18th century. It has come into sustained use since the early to mid 20th century, primarily following extension of anesthesia-type artificial ventilation methods to early intensive care settings. In the medical setting oxygen is used as a drug, primarily to reverse low blood and tissue oxygen levels as measured by oxygen saturation monitors and blood gas samples. A problem arises, however, when oxygen is used empirically or in settings where a documented need for supplemental oxygen does not exist. Though technically oxygen supplementation is prescription-governed, non-physicians often implement oxygen or make oxygen level adjustments without specific instruction. This results in inappropriate medical oxygen use. It is known that excessive or inappropriate oxygen supplementation can be harmful; what is unknown is to what specific extent or degree and by what timetable harm can become manifest in any person’s health. This blog will explore these, and related topics in the near future.