Hyperbaric Oxygen Therapy and Treatment - An Overview - Part 1 Hayden Dunstan March 2018 Copyright 2018 ?

Hyperbaric Oxygen Therapy and Treatment

An Overview

Hayden Dunstan

March 2018

Copyright 2018 ?

Contents:

Definition and Introduction – Pg. 3

Diving Physics and Physiology – Pg. 5

Boyle’s Law – Pg. 6

Henry’s Law – Pg. 9

Dalton’s Law of Partial Pressures – Pg. 10

General Gas Law – Pg. 12

Gas Exchange/Gaseous Interchange – Pg. 13

Pressure Gradients – Pg. 16

Altitude – Pg. 17

The Hyperbaric Environment and Hyperbaric Administration of Oxygen and Oxygen Enriched Gases – Pg. 21

Oxygen Tolerance – Pg. 28

Cerebral/CNS Toxicity – Pg. 28

Pulmonary Oxygen Toxicity – Pg. 33

Emergency Medicine and Oxygen Administration – Pg. 41

Cellular Metabolism – Pg. 46

Wound Healing – Pg. 50

Oxygen as an Anti-Inflammatory and Multiple Sclerosis – Pg. 52

Orthopaedic Conditions – Pg. 53

Oxygen as an Anti-Bacterial Agent – Pg. 54

A Word on Sports Injuries – Pg. 56

Dosage – Pg.56

Other Conditions – Pg. 58

Decompression Sickness – Pg. 61

Gas Embolism – Pg. 61

Acute Carbon Monoxide Poisoning (CO) – Pg. 62

Non-Indicated Off-Label Conditions – Pg. 63

Cerebral Malaria – Pg. 64

Cancer and Radiotherapy – Pg. 66

A Word on Immunotherapy - Pg. 67

 Anti-Ageing – 68

Macular Degeneration and Diabetic Retinopathy – Pg. 69

Birth Injury and Cerebral Palsy – Pg. 71

Gas Gangrene – Pg. 71

Fibromyalgia & Mild Brain Injury – Pg. 72

A Word on Sleep – Pg. 74

Dementia Stroke and Nero-Degenerative Disorders – Pg. 75

Side Effects and Contra Indications – Pg. 77

Prohibited Items and Safety – Pg. 80

Closing Thoughts – Pg. 83

Further Reading and References – Pg. 86 - 89

Definition:

The Administration of Pure Oxygen or Enriched Breathing Gas Mixes At Higher Than Atmospheric Pressure

Introduction

I wanted to start this article with a brief mention of oxygen levels during the Cretaceous period and their contribution to the size of dinosaurs. Having read some fairly recent commentary on further studies however, it seems the scientific world is in two minds about whether higher oxygen levels of roughly 30% during the Cretaceous period, (65 to 145 million years ago), and the much lower than previously thought levels of the end of the Permian period, which are now believed to have been as low as 10%, (250 million years ago) were indeed solely responsible for the size of dinosaurs. [18] University of Innsbruck 2013

It would have been convenient for me to begin with the simple question asked by many children; “Why were the dinosaurs so big?” but alas I cannot. Well not entirely.

So instead I’ll begin with this. I am no doctor. Nor do I claim to be. This is an article or essay if you will, presented by a layman in layman’s terms where possible.

While it is supposition to assume that oxygen levels alone contributed to the size of dinosaurs it certainly still would have had something to do with it. As we know from basic cell metabolism it would be reasonable to conclude that higher oxygen levels at least promoted faster growth in the presence of supporting factors.  It cannot reasonably be ruled out as at least a contributing factor among others such as consumption of huge amounts of food.

I’ve read many articles claiming this and while they clearly only look at one side of the argument they aren’t completely incorrect. Oxygen, and certainly higher concentration of oxygen does indeed affect the growth, healing, repair and proliferation of the cells within all our tissues as well as those of animals. Arguably this would affect the evolution of a species as well. [19] Berner Et al April 20017

The human animal differs little in basic function from animals of similar mammalian design. Why else would we use them so extensively in medical trials? [20] The American Physiological Society – 2001 Trials upon which a multitude of drugs and pharmacology have been approved and released into the market. The same applies to us. Increased oxygen concentration in the air or gas we breathe either by percentage at normal pressure, (baric), or by partial pressure by increasing ambient and thus delivery pressure, (hyperbaric), will most certainly affect our bodily function as it would have done with the dinosaurs of old. Both favourably in the case of higher levels, and unfavourably as in the case of the lower levels of the end of the aforementioned Permian period, which are considered as contributing factors in mass extinctions. [21] University of Washington 2003

In this article I will investigate this relationship and attempt to give an overview of how hyperbaric oxygenation (HBO) and hyperbaric oxygen therapy or treatment as some prefer to call it (HBOT), works.

I will try to explain the physiological process and physical laws responsible for the oxidative process in the body and explain why it supercharges our existing bodily function and optimises those functions.

To do this it is important to start at the beginning, and that beginning is found in the text books and student manuals of diving. And not just the elite world of special ops divers and the advanced world of commercial diving but as early as the first diving course a person may take. This being the basic instruction given in any open water diver course, and indeed content considered a minimum standard by the World Recreational SCUBA Training Council (WRSTC).

The first half of this article is dedicated largely to that, physics, physiology and discussion on the understanding of what happens in the body when we breathe oxygen under pressure. The second half details the benefits of HBOT for individual conditions and the mechanisms involved.

Diving physics and physiology is where the proof lies. There are many calls for empirical data and irrefutable evidence in the ongoing HBOT debate. Diving physics is long established and empirical fact. The effects of the laws discussed below can be observed in simple experiments or indeed by simply ignoring them at one’s own peril when diving.

For over a hundred years human beings have been applying the principals of hyperbaric oxygen therapy to patients and divers with remarkable success. From the days of the earliest caisson workers under the East River, during the construction of the Brooklyn Bridge, which began in 1869 and was completed in 1883, to the discovery by French physiologist Paul Bert in 1878 of a link between decompression sickness and nitrogen bubbles, at the time also called caisson disease, (more notably named “The Bends”), owing to the posture of the afflicted caisson workers. [22] Encyclopaedia Britannica Volume 3 1922

In fact, the first hyperbaric chamber was created in 1662 by British Clergyman and physician Nathaniel Henshaw. Known for his work and belief in the medical benefit of “fresh Air”. His chamber or “Domiclium” as he called it, was driven by bellows. [23] Dictionary of National Biography 1885 – 1900 - Volume 26 [17] US Navy Diving Manual 7th Edition Volume 1 The History of Diving 2016

Europe witnessed the use of hyperbaric oxygen treatment as a spa or wellbeing therapy in 19th century with pressure of 2 atmospheres (ATA). The French led the discipline as early as the 1830’s. [24] Hyperbaric Medicine Collections: History – Duke University Library Archives

In the 1930’s the military began testing the use of HBOT to treat deep sea divers with decompression sickness. [17] US Navy Diving Manual 7th Edition Volume 1 The History of Diving 2016

And the history goes on. Almost any website promoting the use of HBOT will detail what is reproduced here.

With that in mind, it is into the world of diving we must venture. As mentioned, not necessarily the complex world of decompression theory or military and commercial applications, (though we will touch on these), but rather let’s start where any resort tourist may start if completing a short 4-day resort course. As found in any reputable diving manual from BSAC (British Sub Aqua Club) to PADI (Professional Association of Diving Instructors), and of course the world leaders in the diving during the 70’s CMAS, (Confédération Mondiale des Activités Subaquatiques), the home of the visionary Jacques Cousteau. Also, to be found in any good commercial and military diving manual.

Whether a military, commercial or recreational sport diver, we are subject to the same physics, physiology and scientific laws as each other. A diver is a diver so to speak. A well-practiced belief at least in the world of diving I know.

To make a start we must first familiarise ourselves with 3 main principles known as the gas laws. At most this equates to a high school understanding of gas action and reaction and how pressure relates to how gases behave. We will also discuss in the early stages of the article how these gases actually get into our bodies. This is known as “Gas Exchange” or “Gaseous Interchange” in the lungs. This is particularly important in understanding the mechanisms involved with HBOT as well as diving theory, physics and physiology.

As for the dinosaurs, you decide. The jury seems out on that one for now. What follows is a discussion on known physical laws established and discovered by their namesakes. They are irrefutable fact.

Diving Physics and Physiology

In diving we come across three main gas laws. Namely; Boyles Law, Daltons Law, Henry’s Law and then a fourth law which doesn’t really feature in this discussion but worth a mention; Charles’ law. (Guy Lussac’s Law). Charles’ Law relates to the behaviour of gases when temperature and volume is considered, and while it is relevant to the people working the equipment and using the physics daily, such as diving supervisors and instructors as well as chamber operators and technicians, it features less than the 3 main laws explained below. Certainly, in a physiological way at least. Although it does explain why the chamber gets hot when blowing down (pressurising) and why it cools down when decompressing, often resulting in the formation of cloud like mist and even slight precipitation as a result of increased humidity. It is also the reason we don’t leave a compressed gas cylinder in the sun.

A good experiment to prove this is to fit a typical car tyre valve (Schrader valve) to the sealed top of an old 2 litre soda (plastic) bottle and then compress and decompress the bottle slightly with a foot pump to observe humidity and condensation forming. I’ve tested this to 2 bar gauge and it appears to handle the pressure well.

To build on the mention of the resort course mentioned in the introduction. Those who have ever been for a course or dived in any way, even a discover scuba diving, as they are called, or so much as watched a documentary on the subject, are told two main things right from the outset. These will be familiar to even those who claim to have no understanding of diving physics.

“Never, never, never hold your breath” your instructor or guide would have told you. They would have also told you something along the lines of the PADI directive “Safely Ascend From Every Dive” Or as the PADI guys call it “Be a S.A.F.E. diver”. Indeed, they would have drilled this into you. Simply because your life literally depends on getting these two things right. Those readers involved in sub marine escape training will also know all too well the importance of breathing normally inside the escape suit and exhaling while ascending should that suit fail. Again, it would have been drilled into every candidate. Deaths have occurred in those candidates ignoring or failing to follow this cardinal rule of breathing compressed air or gas. It’s interesting to note that when it comes to life and death, no one disputes the physics. No one pushes the envelope because it’s accepted un-reservedly that these laws are absolute. Statutory regulations such as “The Work in Compressed Air Regulations 1996” exist because of the following physical laws being universally accepted. [17] US Navy Diving Manual 7th Edition Volume 1 Underwater Physics 2016

Boyles Law:

States:

“For a fixed amount of an ideal gas kept at a fixed temperature, pressure and volume are inversely proportional. Boyle's law is a gas law, stating that the pressure and volume of a gas have an inverse relationship, when temperature is held constant.” [25] Oxford Refence 2009 [17] US Navy Diving Manual 7th Edition Volume 1 Underwater Physics 2016

The mathematical equation for Boyle's law is: PV = k

{\displaystyle PV=k}where:

·       P denotes the pressure of the system.

·       V denotes the volume of the gas.

·       k is a constant

It can also be expressed P1V1=P2V2 for calculating the proportionate change in a gases volume when pressure changes.

The equation shows that, as volume increases, the pressure of the gas decreases in inverse proportion. Similarly, as volume decreases, the pressure of the gas increases. The law was named after chemist and physicist Robert Boyle, who published the original law in 1662.

The above stated physical law was confirmed by Robert William Boyle (25 January 1627 – 31 December 1691), an Anglo-Irish physicist and chemist. He confirmed the earlier work on the relationship between pressure and volume which was first noted by Richard Towneley and Henry Power in the seventeenth century.

Ruling out any temperature changes covered by the above-mentioned Charles’ Law, this law defines the relationship between pressure and gas volume.

As mentioned, instructors across all disciplines will drill this into any candidate undertaking a diving course, or any other course such as, sub-marine escape training, tunnelling (under pressure), caisson worker, air lock operator etcetera. Many of these disciplines are unrelated to diving but fall into the mining disciplines. A word on tunnelling: Tunnelling works are often done in a compressed air environment to keep ground water from seeping into the works area. This is essentially the same as breathing compressed air whilst diving. Air is breathed under conditions exhibiting the same volume / density relationship. In a flexible container, volume is subject to Boyles’s Law. Volume behaves inversely proportional to pressure.

The primary consideration of this law, is that a flexible container will expand along with the expanding compressed gas it contains as pressure is relieved. Conversely the gas a flexible container contains, will be compressed along with the container as pressure increases, i.e. a balloon filled under pressure, or pair of lungs or other flexible container, will eventually rupture if internal increased volume expansion and pressure is not released or equalised when external pressure is reduced. This is where free diving and diving with compressed air differs. The Free-diver’s lungs will shrink with increasing pressure and then re-expand when the diver returns to normal pressure as they re-surface. With exception of a slight fall in the oxygen content, which will affect the volume to a degree, the final lung volume upon servicing will be the same. This is an important note. Some of the oxygen has been used by the metabolic process while the free-diver has been down and hence the volume will be slightly less upon surfacing It means nothing whatsoever to the diver or his lungs but is relevant to remember when we discuss gas exchange and cell metabolism later.

Opponents of HBOT will no doubt put this forward as a grave risk. “This law…”, they will say, “proves that HBOT and chamber compression and decompression is dangerous and should be avoided”.  Not at all.

While lung overexpansion is a physical possibility and has happened many times to divers resulting in serious injuries and death, it is so easily overcome it’s almost missed among all the techno babble we are subjected to these days. The solution is as mentioned already… “never, never, never hold your breath”. Breathe normally and you will not have a problem.

Granted, we do have other air spaces in our bodies that are affected such as sinus cavities, middle ear canals behind the ear drum, lungs of course, and any such minor gas pockets as may be present in the digestive tract. Breathing normally protects the lungs, and with simple instruction ears and sinuses are easily equalised. Gastro intestinal gas will simply compress and re-expand as in the lungs of a free-diver, unless a small amount of air is swallowed during a dive or treatment. This will assuredly find its way out along one of two paths with no ill effect, albeit a touch blushworthy.

It’s worth noting that someone with obstructed airways who is unable to equalise may be contra-indicated until such time as their air passage ways are clear enough to equalise pressure changes. That said, in cases where benefit outweighs risk it may be prudent to sacrifice and ear drum or two for the sake of avoiding further tissue damage, such as brain damage resulting from poor oxygenation. Life over limb and all that. Ear drums heal readily, brains not so much. This will be more extensively discussed under the heading “emergency medicine”.

What Boyles Law also lends itself to, is that as a volume of gas is compressed it occupies a smaller volume. In real world terms this means that a relatively small container such as a compressed gas cylinder, can hold very much greater volumes of gas once that gas is compressed. Or in other words, a large volume of free air can be made to fit into a small container by applying force (pressure), to make it fit, by squeezing the molecules closer together. Compressors, foot pumps, car tyre inflators, and suchlike, perform this function for us. Your car tyre holds a few times it’s volume in air since the air has been compressed to inflate the tyre and support the weight of the vehicle. The molecules have been pressed together to occupy a smaller space, i.e. compressed air.

It sounds rather remedial put that way, but non-divers often don’t quite appreciate that a standard 15lt diving cylinder filled to 200 bar holds 3000 litres of free air. A car tyre filled to 2 bar (roughly 30psi) holds three time the volume of air an empty tyre does.

Offshore contractors often use even higher pressures than that, and it is not uncommon to have 80 litre cylinders holding 300 bars of pressure. That amounts to an incredible 24 000 litres of free gas in each cylinder. This is explained courtesy of Mr Robert Boyle. His law dictates that more molecules of a given gas may occupy a smaller volume when compressed. It is essentially what historically made diving with stored gas possible. Indeed, it has made diving at all possible. Even surface supplied breathing gas must be compressed to a pressure greater than that of the surrounding water for the diver to receive it in some way. If not, the water will simply rush back up the hose in the absence of the now standard non-return or check valve, until equilibrium is reached between gas and water pressure. The same principal applies to a sport second stage regulator as it does to an advanced commercial reclaim heliox helmet, as is commonly used, and made by Kirby Morgan and others. Similarly, even a free flow helmet, which is not unlike an upturned bucket fed by an air hose, requires pressure to come in above the ambient pressure. Like blowing bubbles in a glass. The bubbles must exert more pressure than the drink before they can leave the end of the straw.

What this means to us as supporters of HBOT is that when a gas is compressed, such as oxygen, and delivered under pressure to a patient, we can deliver very much greater numbers of molecules in real terms to the lungs of a patient, if delivered under increased ambient pressure.

I can hear the protests already. Medical professionals refer to oxygen saturation in blood, in terms of, and to, what extent the red blood cells (largely haemoglobin but for the purposes of this discussion considered one and the same), are saturated with oxygen molecules. Or in other words, as a percentage, they express saturation (SATS) as a representation of the oxygen carrying capacity of haemoglobin. Medical professionals follow the mindset that if SATS are stable at anything above 90% or so, its normal, and the amount of extra oxygen that can be introduced into blood is insignificant, and not worth the effort and risk of moving a patient to a hyperbaric chamber. Absolutely not. Quite to the contrary in fact. A medically significant amount of oxygen can indeed be added to blood indeed over and above well saturated haemoglobin.

We do not aim to increase the oxygen carrying capacity of haemoglobin, that is a finite value. Only so many molecules of oxygen can occupy a red blood cell. No argument there. We aim to increase the amount of oxygen dissolved in solution in the blood plasma which is incidentally the greater portion of the volume pumping through our circulatory system. Current oxygen saturation monitoring equipment as found on most wards will only show haemoglobin SATS and does not indicate plasma or tissue saturation. The question is why? Subcutaneous monitoring equipment is readily available to monitor oxygen tension in tissues. This is known as Transcutaneous oximetry (TCOM or TcPO2). This too we shall re-visit under the heading gaseous interchange and when we discuss tissue saturation. As we come to saturation and how gas dissolves into a liquid, I give you Henry’s Law, the second of the three main gas laws in diving and diving medicine.

Henry’s Law:

Henry's law is one of the gas laws, formulated by the British chemist, William Henry, in 1803. It states that:

At a constant temperature, the amount of a given gas dissolved in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid. [17] US Navy Diving Manual 7th Edition Volume 1 Underwater Physics 2016 [26] Oxford Refence - 2016

Again, discounting temperature as a constant as above, and as explained by Charles’s Law, and with temperature being constant in most bodies, we can now discuss the law which explains how a gas dissolves into a liquid under pressure. This law works hand in hand with Daltons Law which we will discuss next. Briefly though, Daltons law explains that in a gas that is not a pure gas, i.e. made up of different gases, each of those gases exert a proportionate amount of pressure relative to the total pressure of the gas, proportionate to their portion (percentage) in that gas. Remembering here that air is a mix of gases, so it is particularly relevant to air.

Another way to phrase it is:

 In chemistry, Henry's law is a gas law that states that the amount of dissolved gas is proportional to its partial pressure in the gas phase. The proportionality factor is called the Henry's law constant.

Remember that we are under pressure even when not diving and not in a pressure chamber. The earth’s atmosphere exerts pressure. It could be referred to as the ultimate (hyper)baric chamber. Although we refer to atmospheric pressure as “Baric” or “Normobaric” air. In other words, barometric, or atmospheric pressure that is measurable with a barometer. In fact, we name our primary measure of ambient pressure after this great pressure chamber in the sky which surrounds us. We call it “Atmospheres Absolute (ATA)” and one ATA is equivalent to the pressure exerted by the atmosphere. This is incidentally almost equal to 1 bar at sea level. They are so close in value, that they are interchangeable in diving theory. This is measured at sea level as, 760mm of mercury (mmHg) or 100kPa or 14,7 pounds per square inch (PSI) and indeed roughly 1Kg per centimetre squared. That means that for every 1 cm squared of surface area on the earth, the atmosphere exerts 1kg. That 1cm squared column of air would extend to outermost reaches of the atmosphere, and it weighs 1Kg. The weight of two large bricks of butter.

(As an aside, I recently had a diving cylinder couriered to me. It was prudent to empty the cylinder to have it weigh, and cost less. Air has weight and therefore exerts pressure in the amount presented above.)

In a different vein, imagine a liquid, such as water, exposed to an increased pressure in a pure gas environment, for example carbon dioxide (CO2). With either a high enough pressure gradient, as discussed under “Gas Exchange”, or a long enough time, the water would become saturated with that gas. It would seek to achieve equilibrium according to Henry’s Law. This is why a bottle of pop goes Pttsshhh! It holds carbon dioxide gas in solution under a maintained pressure. This is how soda water is made, as whoever owned a Soda Stream machine will know. The bottle is sealed in place and pressurised CO2 is exposed to the water surface causing it to dissolve into the liquid and go into solution. As long as the pressure is maintained it will stay in solution. When the pressure is relieved, by opening the cap, it will come out of solution forming bubbles, which will also be discussed later when we discuss decompression sickness and pressure gradients.

Incidentally water exposed to any gas will have that gas dissolve into it. Nitrogen for example will also make soda water. Nitrogen makes finer bubbles and is not quite as soluble in water as CO2 though, and they don’t taste the same. It would take longer to make bubbly water with nitrogen. Which is why drinks companies use carbon dioxide instead. We will also discuss why oxygen does not and is not known to come out of solution in this way under cellular metabolism.

This is also brilliantly demonstrated by adding liquid to the above-mentioned soda bottle that was fitted with a car tyre valve. Fill the bottle half with water (add some red food colouring for effect), and leave it pressurised for the duration of a normal dive. Pick a 20-meter table - 2 bar on the car tyre pump (gauge pressure). It should be less than an hour to wait. Shallower depths / lower pressures, take longer. Then let the pressure out all at once and observe the bubble formation over the following minutes or even hours, and their collection on the surface as the saturated gas escapes.

Absolute proof and empirical evidence that gas dissolves into liquid under pressure and then comes out of that solution when the pressure is relieved. Henry’s Law demonstrated. Empirically.

Daltons Law of Partial Pressures

The third and possibly most relevant of the three main gas laws in diving physics and medicine, is Daltons Law of Partial Pressure which works hand in hand with Henry’s Law.

In chemistry and physics, Dalton’s law (also called Dalton’s law of partial pressures) states that in a mixture of non-reacting gases, the total pressure exerted is equal to the sum of the partial pressures of the individual gases. [27] Oxford 2016 [17] US Navy Diving Manual 7th Edition Volume 1 Underwater Physics 2016

It can be expressed mathematically as:

pTotal = p1+p2+p3…+pN

Where: pTotal is the total pressure of the gas and p1, p2 and pN represent the component gases in the mix.

“Non-reactive” gases refer to interaction between gases while in the mix, and not to metabolism (which only occurs after the fact), and any enacted mechanism explained by the gas laws, including the dissolving into solution of gas into liquid.

As mentioned above when discussing Henry’s Law, these two laws go hand in hand, as they pertain to gas exchange in the lungs which will be discussed shortly.

In layman’s terms, this law dictates that, whether a gas is pure, or a gas is made up of different components, i.e. a mix, the portions of that gas will exert their relative proportionate amount of pressure in that gas, in the gas phase. It is primarily used to calculate gas mixtures though, as it is commonly known that a pure gas with only one component exerts the full pressure of that gas. It exerts 1,0 of, or 1,0 multiplied by the gas pressure whatever that total pressure is. 1 being the highest factor possible for the “Fraction of the Gas” (fg) factor indicating a “whole” single component or pure gas.

For example, in the case of pure oxygen at atmospheric pressure, or barometric pressure, the pressure of the gas is 1 atmosphere Absolute (1 ATA), (1x1=1), and if we had pure oxygen at an ambient pressure of 2 ATA, the pressure of that gas would be 2 ATA and so on (2 ATA x 1,0 fraction of gas (fg) = 2). Because it is a free gas not contained in any form of independent container but rather within a system such as the atmosphere itself, or chamber atmosphere, it exerts a pressure equal to the ambient pressure of the atmosphere it is in, either the actual atmosphere or artificial atmosphere such as that inside a chamber. This is called the total pressure of the gas. For gases made up of component gases, each gas would exert a pressure equal to their share of that gas, or, as described above, their fraction of that gas (fg). In the case of air, which we all understand readily, we have a mix of the following: [17] US Navy Diving Manual 7th Edition Volume 1 Underwater Physics 2016

Commonly in diving we refer to air as a mix of 21% oxygen, 78% nitrogen and 1% trace gases. To further simplify this in terms of diving, we dismiss the trace gases as insignificant at the pressures commonly experienced in most diving, and we simply refer to air as 21/79. That is 21% oxygen (O2) and 79% nitrogen (N2). Or as some might even say 21/79 Nitrox. Nitrox being a mix of nitrogen and oxygen. Although we seldomly refer to air as nitrox, but commonly refer to Nitrox as “Enriched Air” or “Enriched Air Nitrox”. The Acronym EANx is commonly used in diving.

Now that we have a gas mix and know its components (air), 21% O2 and 79% N2, we can express as follows the fractions of the component gases as fractions of gas at barometric pressure, or sea level as 0,21 ATA ppO2 and 0,79 ATA ppN2. Where pp is partial pressure and sea level is 1 ATA.

And that’s the sum of it. Understanding partial pressures and fractions of a gas.

It is important to understand these 3 gas laws to some degree, in order to understand the next subject. That of gas exchange in the lungs. Also called gaseous interchange, terms which are equally as descriptive as the other. Basically, it is the process by which the gases in the air we breathe enter the bloodstream, and as a knock-on effect, enter the individual tissues of the body, and then proceed on to enter each and every cell in those systems. It governs oxygen transport, inert gas saturation and indeed any gas poisoning we may encounter, including pollution related poisoning.

General Gas Law:

For those wanting to calculate gas values, the above laws have been conveniently incorporated in a general gas law, which can be expressed mathematically as follows: [17] US Navy Diving Manual 7th Edition Volume 1 Underwater Physics 2016

It incorporates, Boyle’s Law, Charles’s Law [42] A Dictionary of Chemistry 2008 and Dalton’s Law and a fourth law not discussed in detail here. Gay Lussac’s Law. [43] A Dictionary of Chemistry 2008 Charles’s Law is sometimes confused with Guy Lussac’s Law in some instance since they both deal with pressure and volume related to temperature of gasses. Charles’s Law deals with the volume of a gas as it relates to temperature, (the temperature-volume law), and Guy Lussac’s Law deals with the temperature of a gas as it relates to pressure, (the pressure-temperature law). Loosely put: As the pressure goes up, so does the temperature and vice versa. Since Charles’s Law and Guy Lussac’s Law work in tandem it is best to use the general gas law for calculations which include factors of temperature, volume and pressure.

Where:  P = Pressure             V = Volume and             T = Temperature

With value variations being accommodated for by pressure 1 / pressure 2, volume 1 / volume 2 and so on. Personally, I prefer using them all independently, although this is a practical one to remember and is commonly used in diving to calculate temperature, volume and pressure relationships in gas.

For pressure volume calculations the T function is cross cancelled removing it from the equation, as is similarly the case for temperature calculations. Either the pressure or volume function can be cross cancelled and removed as necessary. Or it can calculate all three.

Gas Exchange / Gaseous Interchange

The lungs, as we know are essentially large sacks filled with lots of smaller sacks. Each lobe of the lungs contains increasingly smaller chambers and pathways, the smallest being the alveoli.

As can be seen from the diagram above, air enters the mouth or nasal cavity and passes through the pharynx and then the oesophagus and on to the larynx. From there the trachea carries air inward as we breathe in to the right and left bronchus, and on to the bronchiole on both sides, eventually reaching the air sacs called the alveoli. All this is driven by the contracting of the diaphragm which creates an area of lower pressure in the lungs drawing air in. The reverse happens when we breathe out again, with the help of a flexing diaphragm now causing a higher pressure in the lungs carrying air outward. [29] Anatomy and Physiology – Rice University [30] US Navy Diving Manual 7th Edition 2016

Our focus for this discussion is what happens in the air sacs or alveoli. This is where air (gas) meets liquid. It is where our singular most important biological process and mechanism exists. The process which allows us to continue living and allows oxygen in and carbon dioxide out of the body. Without it life would quickly cease. It is also where we absorb metabolically inert or non-reactive gases such as nitrogen, or helium in the case of very deep diving mixes. (Dives deeper than 50 meters are generally undertaken on a helium and oxygen mix called heliox, or a combination of air and helium called Trimix. Oxygen – Nitrogen - Helium).

On one side of the alveoli wall is blood and the other there is air/gas. Between them is tissue as little as one cell across, which is coated with surfactant on the air or alveolar space side, rendering it essentially ‘waterproof’. This surfactant prevents blood from passing into the lungs. It also facilitates the lowering of the surface tension at the point of the gas/liquid interface. Explained in the graphic below. This is important to remember as we will discuss oxygen tolerance and toxicity later on, and how it is greatly misunderstood in general, and has become probably the singularly most preventative factor in the willingness of professionals to administer hyperbaric oxygen therapy/treatment in patients who would benefit greatly from it.

“Pulmonary surfactant is a complex and highly surface-active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms” [33] Eur Respir J. 1999 Jun.

“Pulmonary surfactant is a mixture of lipids and proteins which is secreted by the epithelial type II cells into the alveolar space. Its main function is to reduce the surface tension at the air/liquid interface in the lung.” [31] Biochimica et Biophysica Acta 2000

It’s at this point I will introduce a new term describing gas pressure as we discussed already. That is “Gas tension”.

You will have seen the words, “In the gas phase”, above. “Gas phase” simply means that while a gas is actually a free gas, it is in the gas phase. When we breathe in, a gas will dissolve into the blood, and in the case of oxygen, dissolves into the blood and then attaches itself to the haemoglobin.

Alternately put, when carbon dioxide dissolves into water to make fizzy pop or soda water, it achieves a gas tension within a liquid.

Gas is then no longer in the “gas phase” at the point where it is referred to as gas tension, as it becomes solute in the solution in this example, blood or water respectively. Gas tension is the pressure a gas exerts in solution within a liquid.

In medical terms, “blood-gas”, or tissue gas tension, will almost always be measured in millimetres of mercury (mmHg). A unit of particular familiarity when considering the measurement of blood pressure using mercury calibrated manual sphygmomanometers. Conversely, in diving, we commonly use atmospheres to measure pressure either in whole atmospheres or fractions of atmospheres. They are simply different units of measurement, with mmHg being a far more accurate and precise unit used in medicine to determine very accurate measurements of pressure and tensions, as opposed to the comparatively brutish unit of atmospheres in diving.

When reading medical papers and studies, pressures or tensions of dissolved gas in tissues will almost always be presented in mmHg and this is referring to pressure that dissolved gas exerts on the tissue, and by virtue of that, the environment (the actual ambient atmosphere). The conversion factor is 760 mmHg for 1 atmosphere (1atm or 1ata).

Accordingly, barometric pressure at sea level, when normal, is 760 mmHg. For the purposes of measurements in diving we use atmospheres absolute, bars, psi and so on. Since this article won’t cover specific quantities of gas but rather the theory of mechanisms, normal pressure reference units will be used. Quantities of dissolved gasses would be measured in grams, micrograms etcetera.

This gas tension can be accurately measured in tissues using a device capable of measuring oxygen saturation below the skin. This is known as transcutaneous oxygen measurement (transcutaneous oximetry) (TCOM or TcPO2). With the TcPO2 standing for: Transcutaneous Pressure of Oxygen. The term pressure, or partial pressure of oxygen, will continue to be used a lot in this reading. It is a necessary concept and analysis method in HBOT because it allows for the understanding of, and the measurement of how much oxygen is saturated into the tissues, rather than only measuring the heamoglobin saturation. As mentioned before, tissue saturation trumps heamoglobin saturation since tissue saturation is the end goal of heamoglobin saturation. Without adequaate tissue saturation, heamoglobin saturation is largely useless.

While gas and liquid are both fluids, they interact according to a variety of factors including density and pressure. A dissolved gas in a liquid however, will still behave according to the three gas laws above. It will still exert its partial pressure in the liquid as it does in the gas phase. In the gas reducing pressure will cause gas to simply expand, in the liquid phase it will come out of solution and return to gas form, it will “off-gas”. We simply refer to it as gas tension in the liquid, and gas pressure in the gas form. For all intents and purposes of this discussion, they are one and the same.

The following explanation is the basis for decompression theory, and originates in the works of visionary, John Scott Haldane (1860 – 1936). A Scottish physiologist famous for intrepid self-experimentation, which led to many important discoveries about the human body and the nature of gases. He is sometimes referred to as the “Father of Oxygen Therapy”. [32] Encyclopaedia Britannica 2018 He developed some of the first decompression schedules or tables and his work in altitude studies in climbers, balloonists and the early stages of flight, were revolutionary to say the least. To divers is he is the father of diving as well.  We still dive today on the basis of the Haldanean model. A wrist-mount dive computer is possible because of the work of JS Haldane. He is cited in almost every diving manual I have ever read. Although his work has been built upon, the basic science is still Haldanean, and it all begins with gaseous interchange or gas exchange and the gas laws discussed above.

Pressure Gradients:

Dealing with oxygenation first, the mechanism responsible for the actual carriage of oxygen into the blood is called an inward pressure gradient and is explained as follows:

When we breathe air into our lungs and that air mixes with the last breath we breathed out, the fraction of oxygen in that air increases, thus creating a differential in the tension of the oxygen in the tissue (the blood), and the gas (the alveola air). This differential is referred to as a pressure gradient. This mechanism is explained by Henry’s Law. In the presence of a gradient that can be described as “inward”, or in other words, higher pressure on the air side than the blood side of the alveolar wall, it will facilitate Henry’s law and the oxygen will seek equilibrium and dissolve into the liquid until equilibrium is reached. It will “in-gas”. When equilibrium is achieved, no more oxygen will dissolve into the blood. Those oxygen molecules just dissolved into the blood will then attach themselves to haemoglobin in the red blood cells (RBC’s) and will be carried through the circulatory system. [29] Anatomy and Physiology -The Process of Breathing Chapter 22 - Rice University [28] Pulmonary Gas Exchange 1998 [30] United States Navy Diving Manual 7Th Edition 2016

The oxygen then travels with the bloodstream until it comes to a tissue or cell which exhibits a lower gas tension that it does, and in the same way, dissolves into that tissue or cell plasm. It’s a downstream effect. This will continue until equilibrium is again achieved. As we know, in the case of oxygenation, equilibrium fluctuation is what drives the process. Oxygen tension and pressures will constantly switch back and forth, resulting in what is termed “oxygen transport”.

We exist at a point of near equilibrium in normal atmospheric pressure. We are essentially saturated to 1 atmosphere absolute in terms of gas saturation with minor fluctuations as we breathe in and out. Because oxygen is reactive (metabolically active), a portion of it is consumed by the cell in the oxidative process and the gas tension in the cell drops compared to the passing blood. As the cells produce carbon dioxide (CO2) as a by-product of oxidative metabolism, the tension of the CO2 rises above that of the passing blood and a reverse gradient now exists. Known as an “Outward Gradient”, this will drive the removal of metabolic by-products like CO2 from the cells across the cell membrane into the blood stream. That CO2 will travel back to the lungs via the venous system and when it encounters the alveolar wall, it will have a higher gas tension than its counterpart in the alveolar air, once again facilitating Henry’s Law, and causing it to come out of solution (tension) from the blood or “out-gas” and again exist in the gas phase in the lungs. The lungs then breath out this CO2 and the process continues.

Essentially there is never a point of absolute equilibrium. It’s a see-saw process that goes on for the duration of our lives. Quite beautiful in its complexity yet simple enough. With every breath we breathe, the saturation level changes back and forth as the gas tensions change back and forth, facilitating breathing, oxygen transport, and life.

A word on metabolically inert gases is relevant at this point: These metabolically inert gases such as nitrogen (N2) and helium(He) are metabolically inert and as such, don’t react within the body. These gases will also seek equilibrium as we breathe, until such time as the gas tension in the blood and the gas pressure in the air is equal. We are then said to be saturated in as far as that gas goes.

As long as our surrounding or ambient pressure remains the same, that level of saturation will remain as it is indefinitely. In the main, and for those that remain largely at ambient barometric pressure, that’s where its ends. You needn’t know about it other than out of interest. It’s when ambient pressure changes, such as would happen in activities such as diving or flying that things change within the body and can lead to disastrous effects. For example, diving accidents and illness and altitude sickness, or, in the case of metabolically active oxygen, the contrary. It can result in the upregulation of our natural physiological processes of healing and rebuilding that has been going on since we were born.

When pressure is relieved, as noted above in the soda water and fizzy pop analogy, that inert gas we spoke of comes out of solution. This is well and fine provided the rate at which it comes out (the outward gradient) is within accepted norms and within a range an individual body can tolerate. As with the Carbon dioxide, any inert gas (nitrogen, helium etc) coming out of solution, will travel to the lungs and leave the body. In diving we call it scrubbing if we facilitate this process and accelerate it with…. you guessed it… oxygen … under pressure in the process known as “Surface Decompression” or in the case of accidents, “recompression therapy”. If it comes out of solution too fast it can and does cause decompression illness. Bubbles can form in tissues and in the blood, leading to a host of very serious medical issue better discussed under the heading “Decompression Illness”. This is not so for oxygen. Oxygen, being metabolically active is used up, and does not come back out of solution in any significant manner.

Altitude:

You may ask what altitude has to do with HBOT.  The same physics apply to altitude considerations as do increasing pressure considerations. These physics are universally accepted in the case of altitude related physiological changes and processes. Altitude sickness and hypoxia induced symptoms mimic hypoxia induced symptoms in injury and illness. [28] Pulmonary Gas Exchange 1998 [30] US Navy Diving Manual 2016

When climbers go to elevated altitudes, they experience lower air/atmospheric pressure and they can suffer altitude sickness. In short, they suffer from hypoxia, a lack of, or insufficient oxygen in the tissues. In severe cases and untreated this can lead to brain damage, loss of vision, disability and even death. It’s common knowledge to climbers and non-climbers alike who have ever watched a film about climbing, that when this happens the only solution is to increase the amount of oxygen reaching the tissues. The prescribed treatment for lack of oxygen is to give more oxygen to the tissues. There is a point at altitude when the body literally begins to die from hypoxia. [35] Medicine and Mechanisms in Altitude Sickness – Recommendations (Abstract) Coote JH September 1995

Oxygen can be increased in the tissues in one of two ways. By Increasing the fraction of oxygen being breathed, i.e. by breathing oxygen or an enriched air mix. Or, increase the partial pressure of the oxygen being breathed. Essentially these two methods achieve the same end. Increased pressures of oxygen being breathed and an increase of the inward gradient.

At great altitude, even that of high flying jets at 10 000 meters, the oxygen percentage is still 21%. So why the headaches and unconsciousness? Because oxygenation and gas exchange are driven by pressure and not by the percentage or fraction of the gas. [28] It seems contradictory that statement. I just said you could increase the fraction of oxygen being breathed. It’s not contradictory at all though. By increasing the fraction of the oxygen, you also increase the partial pressure of the oxygen, allowing better gas exchange and oxygen transport to the tissue, including and most importantly the brain.

In a medical environment this is called “Baric Oxygen” when it is administered, and if indeed it can be delivered at a true 100%, which is rare considering that standard ward equipment spills more oxygen down your clothes and bed than you benefit from. Free flow masks simply mix in a bit more oxygen in the air you’re breathing. Most of it is lost unfortunately and resulting in what could be better outcomes for current practice. The only way to get a true 100% is to use a properly sealing oral nasal mask and a demand valve.

If climbers have oxygen to breathe that’s fabulous. Breathe it and keep climbing. Because as we calculated earlier, the pressure of the oxygen when its pure is 1,0 of the gas pressure as dictated by ambient pressure. So even at 5000 meters or +/-15 000 feet (about half of atmospheric pressure), the partial pressure of the oxygen (PPO2) is still high enough to maintain consciousness and ward off ill effects. Breathing air however at 5000 meters would reduce the partial pressure of the oxygen in the air from 0,21ATA at sea level to about 0.105 at 5000 meters. Not enough to facilitate a significant inward gradient and maintain sufficient oxygen delivery to tissues resulting in hypoxia.

The other way to increase this PPO2 is to descend the climb and go to a place of higher ambient pressure to facilitate better gas exchange and oxygen transport, or make use of a hyperbaric bag, tent, or portable chamber to increase the ambient pressure artificially. [36] High Altitude Medicine Guide 2001 This is common place, and hyperbaric bags have been in use for many years. They really are just portable hyperbaric chambers designed to raise the ambient pressure a climber is subjected to, thus alleviating the symptoms of altitude sickness by effectively raising the partial pressure of the oxygen in normal air.

Such bags have been extensively used in mountaineering studies, altitude experiments and studies, as well as high altitude aviation and aerospace research.

To step back to gas exchange briefly, I mentioned that when we breathe in, we breathe in 21% oxygen and a portion of it is metabolised, producing the by-product CO2. That amount is approximately enough to reduce the oxygen content of air to about 16% down from 21%. If we venture into altitudes or areas of pressure which take that respective partial pressure much below what we can calculate for 16% (0,16 ATA), we risk becoming unconscious and suffering the onset of altitude sickness. This is the point at which altitude sickness becomes a concern. Above a PPO2 of 0,16ATA the body functions normally, i.e. we can safely breathe oxygen content as low as 0,16ATA which would equate to 16% at sea level.

This is evident in the widespread use, and global acceptance, of expired air resuscitation (EAR) in life saving and first aid taught in every first aid course available today. A crucial component of CPR. The 16% we breath out is enough to sustain normal consciousness, brain function and life. Below this level can be problematic however.

So, if we consider a climb, or unpressurised flight to 5000 meters, (at 10 000 meters there is almost no pressure and it is considered the top of the atmosphere as far as pressure goes), we experience ambient or barometric pressure at roughly half of 1 Atmosphere absolute (0,5 ATA). So, we can calculate that breathing oxygen at 0,5 ATA is still well above the low end of 0,16 ATA we can tolerate. However, breathing air at this level as calculated above, at 0,105ATA, is well below that level. Therefore, altitude sickness occurs.

And that’s why simply breathing oxygen at high altitude relieves altitude sickness. Because it raises the partial pressure of the gas. Nothing really to do with percentage. Raising the percentage of oxygen being breathed is simply the easiest way of increasing its partial pressure. Although limited by ambient barometric pressure, it is an effective measure on the side of a mountain.

Consider the opposite then in a saturation dive to 300 meters of sea water. The ambient pressure at those depths is a massive 31 ATA. Even an oxygen percentage, or fraction of gas, of 2% affords the divers a partial pressure of oxygen of 0,6ATA. Incidentally, as discussed under oxygen toxicity, this is close to the level where no toxicity will occur. It allows for extended periods at this level of oxygen concentration, while still remaining well above the required minimum of 0,16ATA for healthy physiological function, yet with only 2% oxygen in the mix. Obviously, this couldn’t be breathed at the surface, unconsciousness would be quick and certain. This type of mix is only meant for the “bottom” or “storage depth” mix.

Incidentally, 0.5ata to 0.6ata of ppO2 has historically been a partial pressure range used in space exploration as well. Further establishing pressure as the gas exchange driver, and not percentage (fraction).

Aside:

This begs the question then in patients who exhibit hypoxic symptoms following accident or illness. Why do medical professionals resist administering higher partial pressures of oxygen to better facilitate gas exchange and oxygen transport? The answer is that it would undermine years of medical teaching and strongly held opinions which echo the sentiments of generations of highly venerated medical instructors and teachers. And this simply isn’t done in medicine. It seems to be a rather emotional issue. Kind of a “pressure point” so to speak, pun intended. Questioning this leads to many professionals taking this as a personal affront to their competence.

It would also require hospitals to monitor oxygen levels in tissue saturation and not just haemoglobin SATS as they currently do. It’s an emotional button with most doctors. They perceive the suggestion that they could do more as an attack on their competency when in fact it’s not. This is not to say that doctors are closed minded to new technology, not at all. In fact, that is one of the governing principals of science is it not? To be open to new developments. Especially low-tech, cost effective modalities such as HBOT. It never ceases to amaze me that governments with limited healthcare funding refuse to see the benefit of general wellbeing in a population thus reducing at least some of the ongoing need for chronic care costs.

The fact remains though that hyperbaric medicine is not included in the standard syllabus for medical students as it stands today. The select committee responsible for deciding just what makes up the syllabus aren’t easy to convince, and unless doctors have covered some diving and hyperbaric medicine at least at university or post graduate level, it’s likely they’re unaware of the benefits of hyper-oxygenation. Hence it is dismissed as unnecessary and fruitless. They are stuck in the old science of toxicity and free radicals, which will be discussed later.

They want double blind trials based on animal human analogues which aren’t always possible and aren’t true representations of efficacy. Remember, humans are not rats or rabbits. While non-human analogues are fine for certain comparative analysis, they do not mirror human physiology in many of the ways the ways they are being used to. Physiology differs from person to person rather significantly, as shown in the absorption of something as simple as an analgesic. So certainly, using rats, mice, rabbits and piglets as human analogues in complicated trials is not entirely a true representation of findings. Further, the probability factor used to calculate the success of a trial is easily manipulated mathematically by simply using a big enough sample of participants.

The best control for a study is the patients themselves.  They should be their own control subject before and after a trial treatment period. Let the results speak for themselves as has been seen in numerous anecdotal and observational studies. Even then, where double and triple blind trials with placebo control groups do exist, they are ignored consistently. Because they challenge the status quo and are politically unpopular. Then there is the money trail of course, but we’ll leave the pharmaceutical companies and influential government lobbyists out of this for now.

Current practice is to declare a patient adequately oxygenated at above more or less 90% O2 SATS. Clearly this is only one component of oxygen monitoring that should be employed. Oxygen in the blood is not the end goal. It’s the oxygen in the tissues that matters, and this is not currently monitored at ward level.

Seemingly contrary to the above paragraph, though not strictly so because blood saturation in human and non-human subjects would be very similar, believe it or not, a subject can survive in a hyperbaric chamber breathing pure oxygen under pressure with no haemoglobin. This experiment was done in rats and swine. [37] Life Without Blood Boerema 1959 I hardly see it passing any ethical review be tested in humans (nor should it!). In the experiment, all of the subject’s haemoglobin was removed, yet, breathing oxygen, under hyperbaric conditions, they lived until they were decompressed of course. This effect was also observed in the 1960’s when the Dutch thoracic surgeon, Ite Boerema, demonstrated that one could transfuse piglets with a simulated plasma mixture of buffered normal saline (Ringer’s Lactate solution), dextrose and dextran. In this process, blood was removed from the blood vessels and the substitute liquid (without haemoglobin) replaced. The piglets were then pressurized in a hyperbaric chamber while the animals breathed 100 percent oxygen. Pressurized, enough oxygen could be dissolved in the simulated plasma to adequately meet the oxygen requirements of the tissues. This was enough to adequately sustain the subject. They survived and could be brought out of the chamber to be successfully transfused with their own blood. 

A note from the website of the Undersea & Hyperbaric Medical Society (UHMS):

“As early as 1959, Boerema demonstrated that swine which were exchanged transfused with 6% dextran/dextrose/Ringers' lactate solutions to produce Hgb levels of 0.4 to 0.6 g/dL could survive in the short-term if they underwent assisted O2 ventilation in a hyperbaric chamber at 0.3 MPa. HBO2 therapy has repeatedly allowed survival in what would have otherwise clearly been un-survivable clinical circumstance without blood transfusion.”

This shall be revisited later under emergency medicine and severe anaemia.

The Hyperbaric Environment and Hyperbaric Administration of Oxygen and Oxygen Enriched Gases:

Borrowing from my previous article “Hyperbaric Oxygen Therapy Research/Trial Proposal Obesity, Metabolic Disorders and Type 2 Diabetes”. [6] Hyperbaric Oxygen Therapy Research/Trial Proposal Obesity, Metabolic Disorders and Type 2 Diabetes – Dunstan 2017 Reproduced here is a definition of hyperbaric Oxygen Therapy/Treatment.

HyperBaric Oxygen Therapy is described as the medical administration of pure oxygen or enriched breathing gas mixes at higher than atmospheric (Normobaric) pressure

As discussed in that article, and explained above, hyper-oxygenation is facilitated by an increased pressure differential or gradient between the partial pressure of oxygen in the breathing mix (gas phase) and the tension found in the tissues (liquid phase). As explained above when an increased fraction of oxygen is breathed under increased pressure it will dissolve in greater amounts into the blood, according to Henry’s Law. [28] Pulmonary Gas Exchange – West Et al – 1998 This is not to say that the haemoglobin will suddenly be able to carry more oxygen, it means that the blood plasma becomes saturated to a higher degree. This results in a far greater saturation of oxygen in blood plasma and in turn results in greater saturation of individual tissues and cells in the body. We will investigate the importance of this under cell metabolism.

In mechanical terms, this is achieved by increasing the ambient pressure surrounding a patient’s body, facilitating the breathing of oxygen at increased pressure while maintaining pressure equilibrium inside and outside of the body so as to avoid disbaric injury or pressure differential injury. This can usually only be achieved by means of a sealed chamber capable of being pressurised and depressurised at will. That is, a hyperbaric chamber/pressure chamber. Since the body, other than its air spaces, is predominantly water, it is for all intents and purposes incompressible and this pressure is not noticeable. Even in very deep experimental dives by Comex in France, to 701 meters in saturation chambers, the occupants’ bodies tolerate the pressure well. [38] Diving Almanac Hydra 10 2018 [39] Deep Hydrogen Diving Hydra 10 Gallant 1993

This effect can also be achieved by diving under the water. Hence the alternative name for a hyperbaric chamber, AKA, diving chamber. Diving physics explains that for every 10 meters of sea water a diver dives under, an additional 1 atmosphere absolute is added to their ambient pressure, i.e. 10 meters of sea water (MSW) is equivalent of 1 ATA. [17] United States Navy Diving Manual 7th Edition 2016 This is much the same as the weight of the atmosphere already discussed. Water however, being far denser, about 800 times denser than air, exerts a far greater weight or pressure than air. Not to forget the actual atmosphere above the water, which is also equal to… yup, one atmosphere. So, at a depth of 10 MSW a diver would be under 2 atmospheres of pressure, at 20 MSW, 3 ATA and so on. 2 ATA being a common pressure used in HBOT protocols and treatment plans. These calculations are particularly important for operators, divers and supervisors as they pertain to gas flow and volumes as well as inert gas absorption and other gas management factors, but not so much to a patient. Doctors also need to have an appreciation for the ambient pressure at which oxygen is being breathed. It is an important factor in determining protocols and treatment dosages for each patient. Some conditions require higher pressures than others. Some require longer treatment regimens as well.

The technology originates in the diving sector and has gradually crossed into the medical world and shown itself useful in a variety of medical applications as discussed below. Many divers and supervisors noticed a curious correlation between medical physics and diving physics. They noted that some of the things we are warned about, and taught, could serve as therapy for some medical conditions, if not as a cure then certainly as a management tool, and complimentary therapy to control symptoms and provide better quality of life. Extensive study since those early days have indeed shown that diving chambers can benefit many medical conditions outside of the traditional “Bubble Squashing” use in diving. Some of these will be visited briefly later.

By bubble squashing, I mean the actual squashing of bubbles which can present in cases of decompression illness as described above. Henry’s Law determines the solubility of a gas in a liquid under increased pressure. In the case of metabolically inert gas, it will simply come back out of solution when pressure is reduced, as in, when a diver surfaces. This can result in the condition mentioned above. Decompression illness as it is termed these day. Essentially it is what would have been called; the bends, decompression sickness, caisson disease and so on. Boyles Law dictates that increasing pressure will reduce the volume of any bubble present and quite literally, the bubble is squashed.

When bubbles form in the circulatory system or tissues of the nervous or other systems, they cause massive tissue damage and block the flow of arteries starving sensitive tissue of oxygen. Obviously the circulatory and nervous system are of greatest importance, but while a “Pain Only” bend in a muscle or joint may not kill you immediately, it won’t be a holiday. This condition can lead to neurological trauma, cardiac arrest, localised tissue damage, and so on. There is more to decompression illness but for the purposes of the mechanical effect this will suffice for now. Later we will discuss micro emboli as well. A mechanical effect in and of itself, a mechanism of disease so to speak, however on the microscopic level. [30] United States Navy Diving Manual – Underwater Physiology and Diving Disorders 2016 

As promised earlier and will be further discussed, this is not the case with oxygen. Only inert gas comes back out of solution to any significant degree. The reason for this is that oxygen is metabolically active and is metabolised (gets used up), to a far greater degree when breathed at higher than normal partial pressures. In other words, as the pressure of oxygen increases so does the oxygen tension in tissues and cells. With this, there is an increase in the metabolic process. The glucose cycle is upregulated as is the entire metabolism. Inert gas does not get used up and remains in solution in its original quantity until the pressure is relieved.

When a diver suffers from decompression illness, the increased pressure of a recompression treatment will simply squash the bubble/bubbles according to Boyles Law [25] Boyle’s Law (volume/pressure relationship), and re-dissolve the gas into solution in the tissue or blood according to Henry’s Law [26] Henry’s Law (pressure/solubility). This is followed by a gradual reduction in pressure to avoid a re-occurrence of micro nuclei and bubble formation. It is facilitated by breathing pure oxygen in pre-determined intervals or periods know as treatment or Rx tables or protocols as they’re know to HBOT operators. This is Hyperbaric Oxygen Therapy in its simplest form and is the only indicated treatment worldwide for decompression illness. The US Navy as well as the Royal Navy have developed a wide range of Rx tables after more than half a century of research and, before the days of stricter ethical controls, experimental dives with actual human subjects. The best analogue so to speak. These are universally accepted and extensively used today in commercial, military and sport diving. [30] United States Navy Diving Manual – Underwater Physiology and Diving Disorders 2016 

This technology has shown not only to help decompression illness, but a host of other afflictions as listed below. It’s a simple concept. The primary requirement for life is oxygen. Without it life ceases fairly quickly. The primary requirement for biological process is oxygen. Without it, cell function ceases and the natural growth, repair and rebuilding processes in the body cease. Giving more of it increases cellular metabolism and enhances the body’s natural process of healing and repair. I was once told the body is its own pharmacy. It has evolved to maintain itself. In cases where normal oxygenation isn’t quite enough, hyperbaric oxygen can be administered to simply enhance what exists in nature already.

Chambers themselves are usually made of steel and are great big tubes with small portholes much like a submarine from a children’s story book. They are intimidating to the inexperienced patient to say the least. Others are made of transparent acrylic and are essentially one-man tubes in which a patient can be observed from the outside. The big chambers are usually referred to as multi-place chambers and the one-man acrylic ones are referred to as mono-place chambers for obvious reasons.

In diving we use what are called twin lock chambers. This simply means it has two compartments. The entry lock and the main lock. They have the same set of controls for each compartment inside and outside. That is called a double skinned chamber. It allows an attendant to take control of the treatment from the inside if needed. The entry lock serves as a method of entering and exiting the chamber without the need for decompressing the chamber or surfacing the chamber. Much the same way an astronaut enters and exits a space shuttle or the space station. It also allows for the delivery of medicines, food, blankets and other materials as may be needed during a treatment without surfacing the chamber. They are usually fitted with a third smaller compartment called a med lock which can be used to transfer smaller items in and out of the chamber without surfacing the chamber.

In medicine, chambers differ a little, but the principal is the same. Some facilities will use mono-place chambers as described above and some will use multi-place chambers as described but with only one compartment. They are usually used for what is termed “ambulant” patients who are not in a condition requiring emergency handling and treatment. These single lock chambers are more affordable and easier to run than their more advanced cousins. They are ultimately best suited to “walking, talking, voluntary patients”. UK law describes these as type 3 chambers and in 2008 they were deemed so safe they were deregulated by an act of parliament under the amendment of that year to the Private and Voluntary Health Care (England) Regulations 2001 [40] Private and Voluntary Health Care (England) Regulations 2001 Amended 2008

Although risk is present, and it will be discussed at the end of this article, in the millions of treatments conducted by non-medical staff and volunteers in the last 30 years, there has never been a reported serious incident. [44] Private and Voluntary Healthcare Care Standards Act 2000 - 2008

In the bigger hospitals, they have chambers which are a combination of both of the above. They have what are termed by the UK Health Department as type 1 and 2 chambers, and those chambers can offer diver treatment as well as HBOT as opposed to a type 3 chamber which may only provide HBOT under the type 3 amendment. These facilities are two compartment chambers capable of offering, in the case of type 1, advanced life support capability, and in the case of type 2, emergency life support capability. Type ones are generally within a hospital facility that has helicopter access, and type two is generally in a hospital, or sited near a hospital, that does not necessarily have helicopter reception facilities. A type 1 chamber must be sited within the hospital precinct. [4] NHS Commissioning of HBOT 2013

In keeping with the main heading of this section, the environment inside a chamber is actually rather cool. Contrary to misconceptions it is not particularly claustrophobic or cramped, even when holding lots of patients. They are comfortable, safe, warm and often the type 3 chambers will offer TV, video facilities and so on. You can read, sleep or chat to your companions though your oral nasal mask. In fact, I would argue you are safer in a chamber than out. When the inherent risk is managed properly nothing can hurt you inside a chamber. You are independent of the world outside. Much like David Bowie’s Major Tom sitting in his tin can. Ground control being your chamber operator on the outside. The old communication standard in the UK would have been something like “inside to outside… do you copy?”. To which the reply would have been “outside to inside… copy you five out of five”. Or something along those lines.

For those who have never been in a chamber, it usually starts with a briefing by either the nurse or attendant or even the operators themselves. They will instruct you on everything you need to know about safety, evacuation, what to do, what not to do, and so on. You will be monitored every second of your treatment.

Then comes what is called “blowdown” in diving. This is the pressurisation of the chamber. The operator will talk to you via a communications system and keep you informed as to what to expect. At first the operator will achieve a door seal and then stop to check everyone is ‘OK’ inside, communicated either verbally or by use of hand signals. In diving we have occupants hold a thumb against one of the viewports all the way through blowdown. That way it will be immediately obvious if someone removes a thumb indicating a problem. It can be a bit noisy and on your first run maybe a little overwhelming, but it really is just sound of air rushing into the chamber. And yes, other than some small, low pressure acrylic mono-place chambers, we pressurise the chamber with air. If your operator wants to pressurise a large multi-place chamber with pure oxygen, feel free to head in the other direction. Pure oxygen pressurisation of anything other than low pressure mono-place acrylic chambers designed for it, is not safe. [2] BHA Fire Safety 1996 [3] A European Guide to Good Practice for Hyperbaric Oxygen Therapy

During the blowdown the chamber will get pretty warm. Remember Charles’s Law [42] A Dictionary of Chemistry 2008 and Guy Lussac’s Law [43] A Dictionary of Chemistry 2008 at the top of the article? When a gas is compressed it heats up. Next time you fill your car tyres at the garage, feel the tyre wall. It will have warmed up a little if they needed more than just a small amount of air, and if the weather isn’t too cold. In saturation diving this is a serious consideration. They go to great depths exceeding 100 meters and sometimes as deep as 300 meters. If they blow down too quickly the heat can become dangerous. In HBOT however we don’t go anywhere near those pressures and the heating of the chamber will be minimal. We also take it slow to afford chamber occupants ample time to equalise air spaces as we discussed under Boyles Law. [25] Boyle’s Law The humidity may rise also. During the blowdown, any mention of “STOP” will stop the pressurisation. If an occupant for some reason cannot equalise their air spaces, we will stop and ascend until they can, then try again. While disbaric injuries are possible such as ear drum rupture, they are extremely rare, especially with well trained staff managing your treatment and comprehensive ‘pre-dive’ briefings and induction.

The temperature will stabilise after reaching the treatment pressure or depth as it is also called. Since we simulate water pressure in a dry chamber, depth is the standard term. The chamber will cool, and this will result in a slight lowering of the pressure in accordance with Charles’s Law [42] Charles’s Law above. This necessitates a topping off the pressure to fine tune the treatment depth. This is known as “chamber creep”. It happens to dive cylinders too after they have been filled. They cool a little and the pressure drops requiring a “top off”.

You will then be asked, via the communications system, to don your oral nasal mask through which you will breathe pure oxygen. The oxygen will be delivered to you at the same pressure as the ambient pressure in the chamber. It will need to be at least that to allow the gas to penetrate the chamber hull through its delivery system without being ‘pushed back’ by the pressure in the chamber. This will come to you via a demand valve in the oral nasal mask, and it will deliver oxygen only when you breathe in the same way a diving regulator delivers gas to a diver. Breathing in activates a diaphragm valve releasing oxygen.

When you breathe out, the high concentration of oxygen in your exhaled breath should not go into the chamber. It will pass through a second hose attached to the oral nasal mask and be vented outside the chamber. We call this overboard dump. It helps maintain a safe level of oxygen in the chamber atmosphere. As mentioned, chamber atmosphere should not be pure oxygen. In fact, it should not be allowed to rise above 24%. If it ever does exceed 24% your operator will likely prepare you in advance for a chamber “flush” in which they will vent the chamber and pressurise it at the same time. This will keep the pressure constant while replacing the chamber internal atmosphere with normal air thus lowering the oxygen content to a safe level. In diving we routinely flush chambers not fitted with carbon dioxide scrubbers or filters to keep carbon dioxide level at a safe level. This has the dual benefit of ensuring safe oxygen levels also.

During your treatment we will give you what are called air breaks. This is a 5-minute period in which you will remove your mask and breathe the chamber atmosphere (air). We will do this every 20 minutes usually. We do it for divers also. We always have. Even those on extreme recompression therapy tables. This will be explained in a little more detail under oxygen toxicity and tolerance and we will discuss the Repex Method of monitoring oxygen tolerance. As you will see, air breaks are important and not something mainstream medicine seems to take into account when discussing hyperbaric oxygen therapy. The usual response from medical professionals unfamiliar with HBOT is usually centred around objections based on oxygen toxicity which is eliminated by observing limits, and applying the brakes, the air breaks.

Once your treatment time has elapsed we will inform you via the communications system that we are to begin depressurising the chamber or surfacing the chamber as it’s called. You may be asked to remove your oral nasal mask and close any associated valves. The attendant can help you with this. It’s simply a reversal of the blow down procedure. Air is vented from the chamber until it is equal with normal atmospheric pressure. It can take a few minutes to do and sometimes a little longer for comfort sake. This time however, any air spaces that now contain compressed air or other gas will expand. As described in the balloon analogy under Boyles Law, [25] Boyle’s Law it is vitally important to breathe normally and…. never, never, never hold your breath. This will facilitate safe equalisation of the lungs. Other air spaces such as sinus cavities and ears will equalise naturally on their own. In the event they do not, an occupant can experience what’s called a “reverse block”. The ascent will be halted allowing a little time to relieve the problem and then try again until we are able to reach the surface comfortably and safely.

You may ask what can be done if the blockage does not and will not clear. In this extremely rare situation it is obvious we cannot leave you in the chamber indefinitely. We will at some point, some hours later even, be forced to surface the chamber. The worst-case scenario is that your ear drum may rupture. However, we are able to administer decongestants inside the chamber via the aforementioned med lock. These take effect quickly and facilitate a problem free ascent. Your attendant will likely have decongestant to hand anyway. Easier solved than any in-water problems some divers experience. Regarding lungs however, this could be very much more serious. This is why you would undergo a medical examination either at the facility or by your doctor and bring such documentation with you, declaring you fit to go under pressure. Any major signs of lung, airway or chest congestion or airway obstruction on the day will almost certainly exclude you from that treatment. Basically, if we don’t think we can bring you out safely we won’t let you in. We’ll show you how the control panel works instead, and you can talk to all the Major Tom’s inside from ground control.

Following that you go on your merry way until the next treatment. We ask you not to smoke for 20 to 30 minutes after a treatment. Indeed, as it applies to smoking anywhere near a chamber that is venting pure oxygen via the overboard dump. Your lungs will be full of pure oxygen and it takes a while to replace all that O2 with normal air again. Your clothes may also be a little “enriched” from the experience. They too “off-gas” in the same way people do. Give the fabric time to “off-gas” before lighting up. As you know, oxygen supports combustion. Many units will give you pocket-less scrubs to wear in the chamber. This is explained further under prohibited items.

You will then probably enjoy the best night’s sleep ever. Explained in a little more detail further along.

Following the mention of oxygen toxicity, it is pertinent to discuss the body’s tolerance of oxygen. Perhaps one of the more misunderstood factors in HBOT and the greatest single factor to give rise to protest.

For those unfamiliar with chambers I include some pictures of an HBO chamber I recently visited.

Oxygen Tolerance:

The medical professionals among you will notice I head this section “Oxygen Tolerance” as opposed to “Oxygen Toxicity”. Most medical doctors consider excess oxygen toxic to humans. This is partly why administration of hyperbaric oxygenation is frowned upon and misunderstood in the mainstream.

The toxicity mechanism is not extensively taught outside of post graduate modules on hyperbaric medicine. It is also taught to divers and supervisors, during chamber operator training, and is also found in deep diving instruction literature. [17] United States Diving Manual - 2016 It is also very much misunderstood from one medical discipline to another with the standard line of, “the mechanism is not fully understood”, being the party line. It is a subject seemingly better covered in diving than medicine.

Not to disagree though, oxygen in excessive quantities can be harmful indeed, and the exact mechanisms of this toxicity aren’t fully understood, but, perhaps better understood by divers more comprehensively than by medical staff. A better understanding of this is desperately needed across the medical and diving professions today.  

I call it “tolerance”, in keeping with the authors of the Repex method of determining biological tolerance levels which will be addressed shortly. [5] Tolerating Exposure to High Oxygen Levels - 1989

Medical science, and indeed most doctors, refer to oxygen as a poison or a drug. This is wholly untrue. Oxygen merely behaves in the manner a poison behaves under certain conditions. It is a naturally existing compound with absolutely zero narcotic value which doesn’t exhibit the pharmacology that “drugs” are described as having. How is it that the only gas that can safely be breathed as pure gas is a poison? And how is that the one compound singularly essential to continued life can be called a poison? Simply, it cannot. Similar can be said of vitamin A or just about anything we consume. Too much of almost anything could harm one.

Historically oxygen toxicity was only ever a problem to people exposed to either high concentrations of oxygen or to those exposed to lower elevated concentrations over a long period. These principals still apply today but the level of tolerance is where the disagreement is most evident with some imposing un-realistic limits on how much oxygen can be safely administered.

The two types of oxygen toxicity that concern us in diving and HBOT are namely, “Cerebral Toxicity” or “Central Nervous System Toxicity” (CNS) or “Pulmonary Toxicity”. [5] Tolerating Exposure to High Oxygen Levels - 1989

Cerebral/CNS Toxicity:

This is a form of toxicity that affects the central nervous system including the spinal cord and the brain. It can result in grand mal (generalized tonic-clonic seizure) like convulsions, and unconsciousness. In general, these have no lasting effect and cause no lasting damage and are essentially harmless to the patient and are completely reversible and achieved by halting oxygen breathing. Remember the air breaks? One of the reasons we give divers or HBOT patients air breaks, is to relive the oxidative stress effect of continued breathing of high concentration or pure oxygen. US Navy and Royal Navy studies show that the air break almost eliminates the all to famous oxygen “hit” when breathing pure oxygen in a chamber environment.

 Without drowning being a problem in a dry chamber, the only problem that exists is if the seizure causes the patient to injure or harm themselves by colliding with the hull of the chamber or other immovable object. Other than that, it causes no other harm. In divers using bite mouthpieces, it can almost certainly be fatal. The diver would spit the mouthpiece out and drown. This is one of the reasons commercial and military divers make use of full face masks or enclosed helmets which cannot easily come off. In a chamber environment an attendant would be present to manage this in the extremely unlikely event of it happening.

The measurement for CNS Toxicity is called the oxygen clock and is expressed in percentage. 100% being the most one can theoretically tolerate before seizure become a real risk.

That said, many a dry and wet dive has been conducted way beyond these limits with little or no occurrence of seizure. As little as 1 in 157,930 incidences are reported in studies undertaken by special ops diving units in the paper indicated in the graphic below. In other words, it’s a rare occurrence even under stress induced situations such as special forces diving. It’s even rarer and largely unheard of in HBOT chambers. [46] Oxygen Toxicity and Special Forces Operations Diving Wingelaar Et al 2017

This is a very well authored and referenced paper going into detail on the physiological causes of toxicity and well worth a read. It describes mechanisms in more detail than can be presented here for the purposes of this article though. It is far more than can be covered in this discussion.

What it does establish though is that cerebral or CNS toxicity is not quite as common as previously thought. It also establishes that what may induce seizure on one day in a given subject, may not the next day. The variables for personal susceptibility are so varied that it is very difficult to apply a standard to the general population.

Remember though that Special Operations (Spec Ops) divers are generally without doubt, far fitter than most commercial, sport or technical divers.

Accordingly, the diving industry, including recreational, technical, commercial and military, have introduced in-water limits to be observed. They are considered to be well within the safety margins provided by the original US Navy prediction and also the Royal Navy predictions. Varying organisations have slightly differing limits, but all follow in the same sort of vein.

The oxygen clock is calculated by observing the partial pressure of oxygen being breathed and the time it is breathed for.

The Royal Netherlands Navy follows the following calculations for CNS exposure to oxygen. Incidentally, the equation can be extended to VO2 and variable metabolic rates as well. [47] Model of CNS O2 toxicity in complex dives with varied metabolic rates and inspired CO2 levels – Arieli R Israel Naval Institute – June 2003

I’ll stress though that these limits are for IN-WATER application. Because of the additional risk of drowning, the in-water limits are conservative to say the least, along with other contributing susceptibility factors present in water, with many divers reporting exceeding these limits, by a huge margin, with no ill effect. Notwithstanding that, it is ill advised to exceed the limits laid out below in the National Oceanographic and Atmospheric Administration (NOAA) table for in-water application.

Commercial divers will observe slightly less conservative limits although not distant from the above table. Most recreational agencies have, these days, reduced their upper limit to 1,4ATA which is only just above the threshold at which seizure becomes possible (1,3ATA), according to the USN diving manual as well as Royal Netherlands navy documentation, rendering exposure to higher partial pressures of oxygen (ppO2) relatively safe when following guidelines.

Exceptional exposure air diving tables in the 2016 revision (revision 7) of the USN diving manual still allow dives to a depth of 300 feet or approximately 92 meters on air. The “Exceptional Exposure” part of the title refers to both the nitrogen and the oxygen exposure. At 92 meters of sea water the ambient pressure is a staggering 10,2 ATA or 10 times that of atmospheric pressure. While the body is quite ok at this depth, it is indeed an extreme exposure in terms of oxygen partial pressures. (Nitrogen also, but that’s another discussion). [30] United States Navy Diving Manual - 2016

Breathing air at this depth equates to a ppO2 of 2,14ATA (10.2ATA x 0.21 ppO2). Certainly above any limit imposed by private enterprise and mainstream diving agencies. As explained in the above cited paper, a single exposure limit of 2,5ATA is allowable in US Navy procedures in exceptional circumstances where proper training is observed and proper equipment available and no other options are available. The usual in-water diving limit imposed by recreational, technical and commercial operators is 50 meters on air. This is based on nitrogen content though. For short exposure of up to 45 minutes the ppO2 is quite tolerable. At 50 meters the ambient pressure is 6ATA and this equates to a ppO2 of 1,26. Well within limits.

In fact, as far as oxygen goes it is relatively safe to spend 45 minutes at 66 meters breathing air. The ambient pressure being 7.6ATA, breathing air equates to a ppO2 of just under 1.6ATA. The reason no one does this routinely is the nitrogen consideration including both the decompression penalty (the need to complete decompression stops on the way up), and something called nitrogen narcosis. Again, a topic for another discussion. Also known as the “Rapture of the Deep”, personal experience leads me to conclude that this is more the concern when diving deep (up to 66m), on air. The deep air limit is very much a nitrogen-based limit and not only an oxygen consideration. Once an understanding of in-water limits is achieved, it makes possible a comparison between that and the comparatively benign and safe, chamber “diving”.

This is further evidence that cerebral toxicity isn’t the unmanageable monster it is portrayed to be in mainstream medicine. Certainly, exposures of 2.0 to 2.4 ATA in a dry environment are easily tolerable by humans and easily managed with no lasting consequence in the event a chamber occupant or patient does experience symptoms of intolerance. Varying susceptibility factors do come into it though, and lower tolerance limits are observed in individuals with intra cerebral issues as well as those who are particularly unfit among many other factors. This is however easily managed by simply giving them a break - an air break. [49] United States Navy Diving Manual Volume 5 3-9.2.2.4 - 2016

Mention must be made of infants, specifically prematurely born infants who receive HBOT. Infants are more susceptible to toxicity than adults and ocular toxicity has been noted in some cases. For this reason, dosage and duration of treatment is often modified to mitigate the additional risk and susceptibility. This should not be construed as a contra indication but rather cause to monitor or modify protocols at most.

Commercial diving is usually, or rather should be, undertaken on either full face masks or some kind of securely fitted enclosed helmet. This reduces the risk of drowning owing to an oxygen induced seizure. Nonetheless, diving on pure oxygen is limited to 6 meters, (1,6ATA), in general and the maximum oxygen clock exposure of 100% is still recognised at 45 minutes when breathing oxygen at a partial pressure of 1,6ATA. If you recall we discussed pure oxygen has a pressure factor of 1,0 of the total pressure of the gas. Making 6 meters the limit for pure oxygen diving in commercial, recreational and technical diving. Military diving is somewhat of a law unto itself out of necessity. One cannot avoid a dive beyond this limit at the cost of assets or life. One of the reasons navy diving entry requirements are what they are. Spec ops will always push beyond what is acceptable to the rest of us because they must.

The limits above are for in-water application though and only mentioned to form a basis for comparison. In chamber application limits are very much higher because any seizure suffered is controllable in the safe environment inside a chamber compared to in water. Additionally, they are extremely rare with no reported occurrence since the 2008 amendment to HBOT rules in the UK.  It’s the reason commercial operations worldwide favour a procedure called surface decompression over in-water decompression. Surface decompression involves breathing pure oxygen at decompression depths. There are also air/oxy tables which provide instruction for in-water oxygen decompression. However, if a chamber is available, it would almost always be the choice in that it is much safer and easier to manage a diver from a practical standpoint, and to have a diver in the controllable environment of a chamber, rather than in water, if at all possible. [30] United States Navy Diving Manual - 2016

The original US Navy limits for CNS exposure was 2,8 ATA for in-water applications in the earlier revisions of the manual. As mentioned above the exceptional exposure table allows for relatively high ppO2 exposures in water.  With the USN Diving manual revision 7 stating that 2,4ATA is the threshold above which oxygen toxicity is possible in a dry environment and 1,3ATA in water. The USN Diving Manual is a fantastic resource of information and covers CNS toxicity extensively with mention of contributing factors such as exercise, carbon dioxide retention, thermal considerations and immersion in water (hydrostatic pressure response) among other such contributing factors to CNS toxicity susceptibly.

Hydrostatic pressure response is the one that supports the position taken with regard to HBOT. The action of immersing the human body in water has considerable effect on the physiological state of the body. It provides pressure which acts against the blood pressure. There are thermal considerations and it also causes a redistribution of fluid throughout the body and the body interprets this abundance of water as over hydration or some kind of oedema. This is why most people feel the need to urinate when immersed in water. It’s called immersion or hydrostatic diuresis and is the bodies effort to equalise what it perceives as over-hydration.

It’s this effect and rationale that bears on the safety of exposures to elevated oxygen partial pressures in a dry environment as opposed to those in water, and hence the higher tolerance limits. The body’s oxygen tolerance is far higher in a dry environment than a wet one. The USN manual also describes the use of air breaks as having a significant effect on prolonging the tolerance period at which high partial pressures of oxygen can be safely tolerated. [48] United States Navy Diving Manual – 7th Edition – Chapter 3 -12 Other Diving Medical Problems 3-12.1.1 – Hydrostatic Diuresis

For this reason, we dismiss in-water limits in HBOT as we will most certainly exceed them all. We do however observe the upper limit of 2,8 ATA, and generally speaking, recompression or HBOT treatments do not exceed this for any significant duration. With rare case studies reaching as high as 4ATA for brief periods but it is not the norm. In fact, most HBOT protocols are well inside this limit and generally a dosage of 2ATA to 2,4 ATA is observed for periods not normally exceeding 90 minutes. Mostly there is little established significant additional benefit above those pressures at this time. The volunteer managed, and de-regulated type 3 chambers in the UK generally do not exceed 2 ATA, with many favouring 1,75ATA as their preferred protocol. Additionally, the air breaks commonly accepted as standard, further protect against CNS O2 Toxicity and prevent occurrences of convulsion or tonic-clonic seizure.

Air breaks extend protection beyond CNS toxicity as well. They help protect the lungs from the other main form of toxicity, Pulmonary Toxicity.

Pulmonary Oxygen Toxicity:

Pulmonary oxygen toxicity refers to the damaging effect breathing pure oxygen, or gases enriched with oxygen, can have on the lungs in cases of long term exposure. It is said to result from inflammation, and ultimately fibrosis in the lung tissue following extended periods of “UNINTERUPTED” oxygen breathing. It is rarely encountered in diving owing to the fact that it is something that occurs over fairly long periods of time. Longer periods than even those encountered in standard HBOT treatment protocols. Ordinarily dive times and the above-mentioned exposure limits prevent a diver from coming anywhere within range of pulmonary toxicity or intolerance. It may become a consideration though in cases of extended decompression, or where chamber treatments or surface decompression procedures are adopted following a dive in which some exposure has already accrued.

Pulmonary toxicity presents as chest pain, wheezing, a dry cough and general respiratory pain and discomfort and can lead to tissue damage and fibrosis (scarring) in the lungs, if not managed properly. This tissue damage in many cases is reversible, especially with research into drugs which facilitate this protection, however in severe cases it can cause permanent damage. [30] United States Navy Diving Manual 7th Edition 2016

Pulmonary tolerance has historically been measured in “Oxygen Tolerance/Toxicity Units” or OTU’s. The word toxicity is again interchangeable with tolerance since it’s not so much a toxic response as an intolerance response when this does occur. It was also historically measure by the “UPTD”, the “unit pulmonary toxicity dose”. In cumulative measurements it is referred to as the “CPTD”, the “cumulative pulmonary toxicity dose”. Basically, they refer to ways of tracking OTU’s, the unit measure of exposure.

Exposure limits are based on the number of OTU’s a subject is exposed to.

One OTU is equal to breathing pure oxygen at sea level for one minute. [5] Tolerating Exposure to High Oxygen Levels – Repex and Other Methods Hamilton 1989

And by that I do mean pure 100% oxygen. It is unlikely that a free flow mask on a ward or ambulance will deliver anywhere near that purity. Only a tight fitting oral nasal mask can do that. So, when you’re told you’re breathing pure oxygen in the hospital, you aren’t. Your bed sheets are getting more oxygen than you are as it spills from your mask when you breathe out and is diluted by the vents when you breathe in. Even if 100% oxygen is delivered to the mask it is almost always diluted considerably on inspiration.

The number of allowable OTU’s for a 24-hour period varies with different analysis methods and is subject to several contributing factors.

These factors include things like, single exposures, multiple exposure, extended repetitive exposure, and compound residual build-up of the intolerance effect as well as of course, personal susceptibility.

Depending on which tracking method is subscribed to, a table of pre-determined exposure limits will likely be followed based on an upper limit on the number of OTU’s a person can tolerate in a single 24-hour period, or a table based on the cumulative effect of multiple exposures over many days. These tables are often tabulated into a single, dual purpose exposure limit table.

To make proper use of the tracking tables one must first calculate the number of OTU’s in each exposure. This is done by considering the partial pressure of the oxygen being breathed, (ppO2), and the duration of the exposure.

The following formula [5] Tolerating Exposure to High Oxygen Levels – Repex and Other Methods Hamilton 1989 is the standard OTU calculation formula:

Expressed as a spreadsheet friendly formula this translates to:

Where the values A1 & B1 refer to spreadsheet cell addresses and relate to t (time) and pO2 (pressure of oxygen). (As above)

The above formula and calculation comes from my favoured tracking method, the Repex Method. Any major search engine will find the PDF entitled

A recommended read for those interested in or engaged in hyperbaric medicine and activities where oxygen toxicity is a concern.

The Repex method follows a principal of whole body toxicity tracking as opposed to tracking CNS toxicity and pulmonary toxicity independently. It is a particularly useful method when tracking the cumulative effect of multiple exposure to lower partial pressure of oxygen over multiple days in diving or hyperbaric oxygen therapy. For single high ppO2 exposure it would still be advisable to follow a CNS tracking table as is the case with deep diving. However, for the purposes of HBOT and lower level exposure over longer durations and multiple days and cumulative effect, the Repex method is favoured.

The lung damage mechanism most agreed upon is that prolonged exposure to raised partial pressure of oxygen degrades the surfactant found lining the walls of the alveolar sacks, as previously discussed. This is described by some as exposing lung tissue to excessive oxidation and in the diving industry some refer to this as “burning” the lungs. This is not an entirely accurate description of the mechanism responsible for causing lung damage. Further belief is based upon the supposed presence of oxygen free radicals and a condition known as lung absorption collapse. [1] Oxygen and The Brain – The Journey of Our Lifetime – James 2014

The surfactant is affected, but rather causes a compromise in the blood/air barrier. As we mentioned above, surfactant in the lungs prevents blood and plasma leaking into the lungs. It also protects tissues from any leaked blood and fluid into tissue. This is evidently widely accepted when instructing life-guards in the art of life saving and awareness of dry drowning. A scenario in which a drowning victim exhibits dry lungs only later to drown in their own fluid which leaks into the lungs. This results in fatal oedema following a compromise of the surfactant and air/blood barrier caused by water ingress in the lungs which dilutes or completely washes away surfactant. Even though the lungs no longer contain water they will leak fluid across the barrier in the absence of surfactant. Surprisingly, it is less accepted as relevant when discussing pulmonary toxicity.

In his book, “Oxygen and the Brain – The Journey of our Lifetime” – 2014. Professor Philip B James [1] Oxygen and the Brain – The Journey of our Lifetime James 2014 explains this extremely well. Far better than I ever could. Basically, he suggests, and I subscribe to this, that:

“Despite a lack of evidence, it is a commonly held belief that the effects of oxygen on the lungs are due to the formation of the ever-fashionable free radicals and that they are produced directly by breathing a higher level of oxygen”.

He goes on to add that this is believed despite good evidence in recent years showing this to be untrue. He adds that despite divers breathing increased oxygen well in excess of what would be 100% at sea level, they do not suffer lung absorption collapse either.

Lung absorption collapse is described as a lowering of lung volume due to metabolism of oxygen in the lower reaches of the lower lobes of the lungs. Whilst breathing pure oxygen, the inert gas portion of air, nitrogen, is flushed out leaving only oxygen to keep the lungs inflated, which is then metabolised lowering its volume. This then causes those areas of the lung to partially collapse, attracting neutrophils and white blood cells to the area which themselves are designed to de-construct tissue resulting in tissue damage. This what they are designed to do in fighting what they perceive as injury or infection, resulting from the now hypoxic state of the surrounding tissues following any such collapse.

This only occurs however, after many hours of breathing pure oxygen. This is the other argument in favour of air breaks. By taking an air break, the lost inert nitrogen normally present in the lower reaches of the lungs is replaced. Without an air break, during oxygen breathing periods this nitrogen is displaced. As the body metabolises the now pure oxygen present, and the volume decreases in those alveoli, potentially leading to lung absorption collapse. This causes a reaction in now hypoxic tissue which signals the hypoxia inducible factor gene 1 alpha (HIF1A) which is the master regulator gene responsible for the upregulation of around 60 other genes upregulated when tissue hypoxia is detected. This includes the immune response and tissue repair response as well as inflammatory response. Remember that the body “thinks” there is an infection or injury because the tissues have become hypoxic following some measure of alveolar collapse. It’s this response that causes the damage. It’s at best, an indirect consequence of breathing pure oxygen and not a direct response, as is so often touted.

By replacing some of the nitrogen during an air break, the inert gas acts as a splint and keeps those areas of the lung inflated, preventing lung absorption collapse and any consequent misinterpreted immune response or hypoxia induced response.

Prof. James goes on to explain the mechanism of the air/blood barrier present in the alveoli and how it becomes compromised allowing plasma from the blood to leak into the lungs, eventually resulting in pulmonary oedema which can, if untreated, be fatal. By taking short air breaks this is avoided. Certainly, at the level and within the exposure time frames commonly found in HBOT.

He also establishes in his book that any damage that does occur, occurs because the air/blood barrier is compromised. This attracts neutrophils to the area, which stick to the capillary linings, and release free radicals into tissues on the blood side of the barrier as they are supposed to do. In effect this means that any damage that does occur, is not a result of direct poisoning of the lungs directly caused by oxygen breathing, but rather an immune response triggered on the blood side of the alveolar wall. Not direct toxicity at all but rather an “erroneous” physiological response to what is perceived as infection or damage owing to local hypoxia following alveolar collapse.

Returning to the Repex method, [5] Tolerating Exposure to High Oxygen Levels – Repex and Other Methods Hamilton 1989 and now that we can calculate the number of OTU’s attributable to a single or repetitive exposure/s, as speculated above, we can now refer to the limits suggested by the Repex curve table and the Repex OTU tables reproduced below:

These 2 tables tabulate the limits suggested as the upper most limits.

The first table shows that over a longer period, the permissible daily OTU limit comes down from as much as 850 units for a single one-day treatment to around 300 OTU’s per day over a 15-day period.

If memory serves, and as calculated using the Repex method, the standard US Navy table 6 for divers with decompression illness will incur an OTU penalty of about 600 units, and as such is within the tolerable limit for a single day. (Depending on extensions, this table may exceed 600 units but is still likely to remain within the tolerable 850 units mentioned below).

This was considered the original safe single exposure limit imposed by many diving agencies. This table is incidentally extendable, or it can be converted to other tables such as the table 4, as can be the Comex CX30 treatment table. In cases of extension or saturation intermittent oxygen breathing periods and air breaks help avoid toxicity response. The whole-body toxicity approach allows for an 850 unit upper limit as opposed to the original approximately 600 unit limit for pulmonary toxicity alone.

The second Repex limit table, on the previous page, is a table showing OTU’s per minute of duration of exposure. It saves one calculating for every depth. Once the ppO2 is known, cross the table to learn the OTU per minute penalty, and with that multiplied by the time of the exposure and total OTU count for that treatment/exposure can be calculated. For exposures over many days, refer to the first table for the daily limit allowed for the predicted number of days or repetitive treatments and cumulative effects. Inside these limits any dry cough, chest pain under the sternum, lung irritability etc will reverse readily following cessation of oxygen breathing.

Note: The lower limit, (and formula factor of 0,5ATA), is the accepted level of partial pressure of oxygen under which no significant damage will occur. This means that oxygen can be safely breathed indefinitely at a ppO2 of 0,5 ATA and less. [5] Tolerating Exposure to High Oxygen Levels – Repex and Other Methods Hamilton 1989

This is incidentally the pressure that was used in the early days of space exploration with the Apollo spacecraft being pressurised to just 5 psi, about a third of atmospheric pressure. [50] NASA History Online NASA routinely uses pure oxygen atmospheres, specifically in extra vehicular suits (spacesuits). Therefore, they too are pressurised to a pressure at or below the threshold of 0,5ATA under which no significant damage occurs to lungs breathing pure oxygen. It is more common nowadays however, as the duration of missions becomes longer and longer than the early missions, with astronauts taking up residence in the ISS for months at a time, and as much as a year or more, for atmospheres to be either enriched to a lesser degree or to be comprised of air and pressurised to the standard 14,7 psi which equates to 1 ATA. [51] The Space-Flight Environment: The International Space Station and Beyond Thirsk Et al 2009

Hyperbaric operations, diving, and specifically saturation chamber technology and saturation diving and treatment physics and physiology, make use of the same physics as those used in space exploration. The similarity between orbital habitat modules, or the proposed Mars or Lunar habitat modules, is uncanny. They even look like saturation complexes and hyperbaric chambers with the exception of being controlled by the occupants from the inside. Space shuttles, habitat modules, rovers, and even space suits are basically hyperbaric chambers using a pure oxygen or enriched air internal atmosphere. They are kept at lower than atmospheric pressure when using pure oxygen to avoid oxygen toxicity as well as to reduce the risk of fire to some degree. We shall visit that under the heading “risks” when we discuss chamber safety.

 The obvious question becomes, aren’t they then hypo-baric chambers? Chambers used to simulate lower than atmospheric pressure like vacuum or altitude chambers? In Earth’s atmosphere yes, they would be hypo-baric indeed. In space however, they contain a higher pressure than the outside pressure and would still be technically hyper-baric.

Accordingly, when considering the upper Repex OTU limits, breathing pure oxygen at sea level (1ATA) CANNOT be safely done indefinitely. If pure oxygen is administered via a tight fitting oral nasal mask at normal atmospheric pressure, and a patient does indeed receive undiluted 100% oxygen, OTU limits must be observed. As we can calculate: 1 ATA ppO2 incurs a 1-unit penalty per minute breathed. Since there are 1440 minutes in a day, a 24-hour period breathing un-diluted pure oxygen at 1 atmosphere of pressure, would incur an OTU penalty of 1440 OTUs. Well in excess of the recommended 850-unit upper limit for a single exposure, and certainly above the former limit of around 600 units. This why many hospitals may tell you you are breathing oxygen when you are actually breathing medical nitrox.

An argument often made by medical professionals is that anything more than baric oxygen will become toxic. In the case of breathing high concentrations for 24 hours at a time, and indeed days at a time in a spacecraft, this would be true. In the case of HBOT we routinely don’t treat for more than 2 hours at a time and go nowhere near the extended periods required for pulmonary toxicity rendering that argument flawed.

To continuously breathe mask supplied enriched medical air or nitrox for a full 24 hours, the maximum per minute allowable OTU would be 0,59 OTU’s per minute to achieve an 850 unit per day penalty. Less, if multiple days exposure duration is predicted. According to the second Repex table this would mean the oxygen fraction in the breathing mix should not exceed 75% at sea level, or expressed as a pressure, 0,75 ppO2. An important thing to know if you or a loved one ends up on pure oxygen administered by hospital staff in training or by those not fluent in diving medicine. Don’t kick off though, just sneak an air break now and then.

Incidentally, nitrox (diving) maximum depths (in terms of cerebral/CNS toxicity) can also be calculated by determining at which point the relative oxygen content as a fraction/pressure would reach 1,6ATA in the case of most diving standards, but as low as 1,4ATA for some agencies. This maximum tolerance level differs for HBOT and chambers as previously explained and can be substituted in the formula for the upper most level of 2,8 ATA (or even 3,0ATA at a push), mentioned for chamber calculations.

It’s worth noting that the most commonly used treatment tables for decompression illness (US Navy Rx tables 5 and 6) begin at 18 meters/60 feet breathing pure oxygen for 20 minutes. This is a recommended “go to” course of action taught in supervisor training and affords the supervisor the time to pull out tables, get his/her head in the right place, call for medical help and make appropriate decisions on how to proceed in an emergency. It is the depth at which the recommended upper limit of oxygen happens to be (2,8ATA), it is also the start point for many other therapeutic recompression tables enabling an acceptable crossover to most other tables from that point if required, as well as extensions and cross over to saturation treatment tables.

In fact, even the non-air table developed by Comex, the Cx30, which is a heliox mix of 50/50 (50% helium and 50% oxygen) treatment table can also be crossed to from this 18-meter start point. It only requires further compression to 30 meters and a gas switch. Then follow the table seeing as 20 minutes time was conveniently made available to send someone to go and find the table. It is also the extension that a diving doctor may order if the diver doesn’t improve after recompression. It is also the standard approach to DCI as defined by the US navy. Certainly, a good emergency starting point. It may seem less than relevant to discuss recompression tables for decompression illness however it is simply the case that weather clinical compression for HBOT, or diver recompression for decompression illness, both constitute HBOT.

In-Water Maximum Operating Depths (MOD) Calculated as follows:

Out of interest to divers I include the following:

The formula divides the absolute partial pressure of oxygen which can be tolerated, (1,6ata) (expressed in atmospheres or bar) by the fraction of oxygen in the breathing gas, (the percentage expressed as decimal fraction), to calculate the absolute/ambient pressure at which the mix can be breathed. Of this total pressure which can be tolerated by the diver, one atmosphere is due to surface pressure of the Earth's air, and the rest is due to the depth in water. So, the 1 atmosphere or bar contributed by the air is subtracted to give the pressure due to the depth of water on its own. The pressure produced by depth in water, is converted to pressure in feet sea water (fsw) or metres sea water (msw) by multiplying with the appropriate conversion factor, 33 fsw per atmosphere, or 10 msw per bar. Bar and atmosphere being interchangeable units in diving.

Formula below: Where MOD = Maximum Operation Depth, pO2 = partial pressure of oxygen and, msw = meters of sea water

Where: fsw = feet of sea water

Air (21% oxygen), for example, calculates as follows: 1,6ATA (max level of in-water tolerance) divided by 0,21 (fraction or % of oxygen in air) minus 1 for atmospheric pressure above the water, multiplied by 10. (To account 10 meters of depth for every bar or atmosphere of pressure in the result), i.e.: {(1.6/0.21) -1)} x 10 = 66.19 Meters of sea water. This, as discussed above is the maximum operating depth for air in the water when considering oxygen tolerance. In a chamber, or expressed as pressure absolute, that would equate to 7,619 ATA absolute since we are speaking in terms of ambient pressure in a chamber calculation and water pressure/depth only in a diving calculation.

The measurement known as “gauge pressure” will exclude the barometric pressure and reflect only the gauge pressure. This why when your car tyre shows 2 bar-gauge (2 Barg), it actually has 3 bar/atmospheres in it. One of those is offset by the actual atmosphere. Essentially 2 Barg is 2 additional bars above ambient pressure.

This calculation is mentioned because it is used to determine maximum safe pressure and maximum pressures and tolerance limits for in chamber pressurisation, by substituting a maximum tolerance of 2,8ATA or 3ATA as the case may be, demonstrating the safety of using hyperbaric oxygen when considering tolerance or toxicity.

As a measure of readiness, I carry a spreadsheet on my smart phone that works on a simple calculation of the Repex OTU tracking formula cited above. Also copies of the 2 tables above for easy reference should they ever be needed, or should I ever be confronted with an unfamiliar protocol or situation in which I may be required to offer some evidence to support my claims or protestations. I also carry the NOAA CNS exposure tracking table.

This however is not strictly necessary. It is fairly easy to commit to memory what protocols are acceptable. From this, I can calculate that even a 3ATA / 75-minute protocol could be tolerated for 5 consecutive days with little risk of incidence. It follows then that any lesser protocol would be well within limits especially considering that treatments are often delivered over 5 days with 2 days off between 5 day runs.

A standard 2 ATA / 90-minute protocol can be tolerated in excess of 15 consecutive days and probably more even. Although that is rarely done with days off every 5 or 6 days. Any mild symptoms which present will likely subside when staying well below the curve.

Hopefully the above considerations demonstrate adequately the safety of hyperbaric oxygenation as it pertains to oxygen toxicity, or at least raises the question and possibility that what have been hard held beliefs don’t necessarily apply to these intermediate levels of supplemental oxygen.  No one is arguing that oxygen can and does have a toxic effect in extreme exposures, what is being said is that these exposure levels are generally never exceeded in standard HBOT and even in recompression therapy for divers. There is no reason to deny a patient treatment based on the fear of toxicity. It simply isn’t the case.

..../ Part 2