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Maintaining Your Respiratory Reserve

Just like skeletal muscles, respiratory muscles have a limited ability to respond to respiratory loads, and when they can’t keep up underwater due to increased gas density at depth and the added load of your rebreather, you may be in for an “eventful” dive.

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JJ on his JJ.” Photo by Andreas Hagberg.

by John Clarke

This doesn’t work. Her respiratory muscles are not strong enough.  Illustration by Cameron Cottrill.

Just like skeletal muscles, respiratory muscles have a limited ability to respond to respiratory loads. An excellent example of this is a person’s inability to breathe through an overly long snorkel (Figure 1.) Our respiratory muscles simply aren’t strong enough to overcome the pressure difference between water depth and the surface.

The primary respiratory muscle is the diaphragm, (the brown organ lying below the lungs in Figure 2.) The diaphragm is designed for low-intensity work maintained 24/7 for the entirety of your life. Like the heart muscle, its speciality is endurance. When called upon to maximally perform, the diaphragm needs assistance. That assistance is provided by the accessory respiratory muscles, primarily the intercostal muscles linking the ribs within the rib cage.


The human diaphragm separating the lungs from the abdominal cavity. Graphic by John Clarke.

Unless you’re reading this while running on a treadmill, your body is probably idling. Your heart is beating rhythmically, your diaphragm is methodically contracting and relaxing. But, if some dire event were to happen, you would be primed for action. If you needed to react to an emergency, your heart and lungs would race at full speed.

The difference between idling and full-speed capability is called physiological reserve, which in turn is divided into its components; cardiac, muscular, and ventilatory reserve. As drivers, pilots, and boat captains will attest, it’s always good to have fuel reserves. Likewise, physiological reserve is good to have in abundance.

The Dive

The following is an imaginary tale of a young, blond-haired hipster drawn to the Red Sea for a deep dive. He chose to dive on the wall at Ras Mohammed on the Eastern Shore of the Sinai, which descends quickly down to a thousand feet and beyond. That was his target—1,000 feet.

The previous year he bought a rebreather so gas usage should not be a problem for his deep dive. He also sprang for the cost of helium-oxygen diluent. Trimix would have been cheaper, but he spared no expense. Nothing but the best. To that end, he used loose-fill, fine grain Sodalime in his scrubber canister. 

These were his thoughts as he descended. 

Free-falling at three hundred feet. Never been this deep before. The water’s getting cold, so the warm gas from the canister feels good.

800 feet. Wow, the gas is thicker now.

When he reached the bottom, he realized something wasn’t right. He sucked harder and harder, feeling his full face mask collapsing around his face with each inhalation. He was “sucking rubber,” feeling like he was running out of gas, but his diluent pressure gage still read 1800 psi. 

Unconsciously, he compensated for the respiratory load by slowing his breathing—easing his discomfort. Concerned, he briefly switched to open circuit bailout gas, but that didn’t feel any better. In fact, it was worse, so he switched back to the bag.

Surprisingly, he couldn’t get off the bottom. In fact, he was slipping further downslope. He needed to drop weights, but they were integrated. He fumbled with his vest, trying to remember how to release the weights, but he couldn’t work it out.

He found the pony bottle to inflate his integrated BC, but after a second’s spit of air, it stopped filling. He would have to swim off the bottom. As he struggled to swim upwards in the darkness, and without bubbles to guide him, he wasn’t sure which way was up.

His heart was beating at its maximum rate, trying to force blood through his lungs, but he couldn’t force enough gas in and out of his lungs to clear his bloodstream of its increasingly toxic CO2 load. The build-up of CO2 in the arterial blood was clouding his thinking. The CO2 was making him want to breathe harder, but he couldn’t. The feeling of breathlessness—and impending doom—was overwhelming. 


The accident investigation on the equipment was inconclusive. The dive computer had flooded, but that was irrelevant. Surface pre-dive checks were passed. The rebreather seemed to function normally when tested in a swimming pool. The investigators convinced a Navy laboratory to press the rebreather down to 1,000 feet, but nothing abnormal was found other than a slight elevation of controlled PO2

The Analysis

Normal human airways compared to airways during an asthma attack. Graphic by John Clarke.

An asthma attack can kill by narrowing the airways in the lung, making the person suffering the attack feel like they’re sucking air through a clogged straw. 

A healthy diver doesn’t have airways that constrict, but gas density increases with depth, causing the same effect as a narrowed airway. It becomes increasingly difficult to breathe as depth increases. A previous InDepth blog post on gas density discusses this subject.

If the strength of respiratory muscles is finite, just as it is for all muscles, then any load placed on those muscles will eat away a diver’s “respiratory reserve.” From the diaphragm’s perspective, the total loading it encounters is divided between that internal to the diver and that external to the diver. As gas density increases, internal loading increases. A rebreather is external to the body, so flow resistance through a rebreather adds to the total load placed on the respiratory muscles. If the internal resistance load increases a lot, as it does at great depth, there is very little reserve left for external resistance, like that of a rebreather. 

In this fictional tale of a hapless diver, he needlessly added respiratory resistance by using fine-grain Sodalime in his scrubber canister. Compared to large grain Sodalime, such as Sofnolime 408, fine-grain absorbent adds scrubber duration, but it also increases breathing resistance. It thus cut into the diver’s ventilatory reserve.

This fictional diver exceeded his physiological reserves by

1) not understanding the effect of dense gas on the “work of breathing,”

2) not understanding the limitation of his respiratory muscles, and

3) by not realizing the “best” Sodalime was not the best for breathing resistance. 

He also didn’t realize that a rebreather scrubber might remove all CO2 from the expired gas passing through it, but it is ventilation (breathing) that eliminates the body’s CO2 from the diver’s bloodstream. Once CO2 intoxication begins, cognitive and muscular ability quickly decline to the point where self-rescue may be impossible. 

Lessons From The U.S. Navy

Considering the seriousness of the topic, it is worthwhile to review the following figures prepared for the U.S. Navy. 

First, we define peak-to-peak mouth pressure, a measure of the pressure exerted by a working diver breathing through the external resistance of a rebreather. Total respiratory resistance for a diver comes in two parts: internal and external. In the following figures, those resistances in the upper airways are symbolized by a small opening, and in the external breathing apparatus, by a long, narrow opening representing a UBA attached to the diver’s mouth. 

High external resistance. In this case, the difference between mouth pressure and ambient water pressure is called ΔP1 Credit with modifcation: Direct measurement of pressures involved in vocal exercises using semi-occluded vocal tracts”.
Low external resistance. The difference between mouth pressure and ambient water pressure is called ΔP2. Credit with modification: “Direct measurement of pressures involved in vocal exercises using semi-occluded vocal tracts”.
Mouth pressure waveforms ΔP1 and ΔP2 during breathing with high (P1) and low (P2) external resistance.

This author reviewed over 250 dives by Navy divers at the Naval Medical Research Institute and the Navy Experimental Diving Unit. These were working dives involving strenuous exercise at simulated depths down to 1500 feet seawater, using gas mixtures ranging from air to nitrox and heliox. Gas densities ranged from about 1 gram per liter (g/L) (air at the surface) to over 8 g/L. Each dive was composed of a team of divers, so each plotted data point had more than one man-dive result included. An “eventful” dive was one where a diver stopped work due to loss of consciousness, or respiratory distress (“dyspnea” in medical terminology.) They were marked as red in the following figure. Uneventful dives were marked in black. 

Using a statistical technique called maximum likelihood, the data revealed a sloping line marking a boundary between eventful and uneventful dives. 

Peak-to-peak mouth pressure and gas density conspire to increase a diver’s risk of an “event” during a dive.

The fact that the zero-incidence line sloped downward illustrates the fact that the higher the gas density, the greater the respiratory load imposed on a diver by both internal and external (UBA) resistance. The higher that load, the lower the diver’s tolerance to high respiratory pressures. 

By measuring peak-to-peak mouth pressures, we are witnessing the effect of UBA flow resistance at high workloads. It does not reveal the flow resistance internal to the body. However, when gas density increases, internal resistance must also increase.

The interrupted lines in the figure illustrate lines of estimated equal probability of an event. The higher the peak-to-peak pressure for a given gas density, the higher the probability of an eventful dive.

Figure 7 suggests that at a gas density of over 8 grams per liter, practical work would be impossible. The only way to make it possible would be to reduce gas density by substituting helium for nitrogen, or substituting hydrogen for helium, and then doing as little work as possible to keep ΔP low.

For our fictional 1,000 foot diver, the gas density would have been between 6 and 7 grams per L. Using a rebreather, there would be virtually no physiological reserve at the bottom. Moderate work against the high breathing resistance at depth would be very likely to result in an “eventful” dive.

Image Citation for medical graphics: Robieux, Camille F, Christine Galant, Aude Lagier, Thierry Legou and Antoine Giovanni. “Direct measurement of pressures involved in vocal exercises using
semi-occluded vocal tracts.” Logopedics, phoniatrics, vocology 40 3 (2015):
106-12 .


John Clarke, also known as John R. Clarke, Ph.D., is a Navy diving researcher in physiology and physical science. Clarke was an early graduate of the Navy’s Scientist in the Sea Program. During his forty-year Navy career, he conducted physiological research on numerous experimental saturation dives. Two dives were to a pressure equivalent to 1500 fsw. For twenty-eight years he was the Scientific Director of the Navy Experimental Diving Unit in Panama City, FL. 

Clarke has authored a technothriller-science fiction series called the Jason Parker Trilogy. All three volumes, Middle Waters, Triangle, and Atmosphere, feature saturation diving from depths of 100 feet to 2,500 feet. The deepest dives involve hydreliox, a mixture of helium, hydrogen and oxygen. UFOs, aliens, and an uncaring cosmos lay the framework for political and human intrigue both on and off-planet.

Although recently retired, Clarke still works for NEDU as a Scientist Emeritus and contractor, when he isn’t writing about diving, aviation, and space. His websites are www.johnclarkeonline.com and www.jasonparkertrilogy.com. His thriller series is available at Amazon and Barnes & Noble. 

Additional Resources for Rebreather Divers

Fatal respiratory failure during a “technical” rebreather dive at extreme pressure

Education

Understanding Oxygen Toxicity: Part 1 – Looking Back

In this first of a two-part series, Diver Alert Network’s Reilly Fogarty examines the research that has led to our current working understanding of oxygen toxicity. He presents the history of oxygen toxicity research, our current toxicity models, the external risk factors we now understand, and what the future of this research will look like. Mind your PO2s!

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By Reilly Fogarty

Header photo courtesy of DAN

Oxygen toxicity is a controversial subject among researchers and an intimidating one for many divers. From the heyday of the “voodoo gas” debates in the early 1990s to the cursory introduction to oxygen-induced seizure evolution that most divers receive in dive courses, the manifestations of prolonged or severe hyperoxia can often seem like a mysterious source of danger. 

Although oxygen can do great harm, its appropriate use can extend divers’ limits and improve the treatment of injured divers. The limits of human exposure are tumultuous, often far greater than theorized, but occasionally–and unpredictably–far less.  

Discussions of oxygen toxicity refer primarily to two specific manifestations of symptoms: those affecting the central nervous system (CNS) and those affecting the pulmonary system. Both are correlated (by different models) to exposure to elevated partial pressure of oxygen (PO2). CNS toxicity causes symptoms such as vertigo, twitching, sensations of abnormality, visual or acoustic hallucinations, and convulsions. Pulmonary toxicity primarily results in irritation of the airway and lungs and decline in lung function that can lead to alveolar damage and, ultimately, loss of function. 

The multitude of reactions that takes place in the human body, combined with external risk factors, physiological differences, and differences in application, can make the type and severity of reactions to hyperoxia hugely variable. Combine this with a body of research that has not advanced much since 1986, a small cadre of researchers who study these effects as they pertain to diving, and an even smaller group who perform research available to the public, and efforts to get a better understanding of oxygen toxicity can become an exercise in frustration. 

Piecing together a working understanding involves recognizing where the research began, understanding oxygen toxicity (and model risk for it) now, and considering the factors that make modeling difficult and increase the risk. This article is the first in a two-part series. It will cover the history of oxygen toxicity research, our current models, the external risk factors we understand now, and what the future of this research will look like. 

Early Research

After oxygen was discovered by Carl Scheele in 1772, it took just under a century for researchers to discover that, while the gas is necessary for critical physiological functions, it can be lethal in some environments. The first recorded research on this dates back to 1865, when French physiologist Paul Bert noted that “oxygen at a certain elevation of pressure, becomes formidable, often deadly, for all animal life” (Shykoff, 2019). Just 34 years later, James Lorrain Smith was working with John Scott Haldane in Belfast, researching respiratory physiology, when he noted that oxygen at “up to 41 percent of an atmosphere” was well-tolerated by mice, but at twice that pressure mouse mortality reached 50 percent, and at three times that pressure it was uniformly fatal (Hedley-White, 2008). 

Interest in oxygen exposure up to this point was largely medical in nature. Researchers were physiologists and physicians working to understand the mechanics of oxygen metabolism and the treatment of various conditions. World War II and the advent of modern oxygen rebreathers brought the gas into the sights of the military, with both Allied and Axis forces researching the effects of oxygen on divers. Chris Lambertsen developed the Lambertsen Amphibious Respiratory Unit (LARU), a self-contained rebreather system using oxygen and a CO2 absorbent to extend the abilities of U.S. Army soldiers, and personally survived four recorded oxygen-induced seizures. 

Kenneth Donald, a British physician, began work in 1942 to investigate cases of loss of consciousness reported by British Royal Navy divers using similar devices. In approximately 2,000 trials, Donald experimented with PO2 exposures of 1.8 to 3.7 bar, noting that the dangers of oxygen toxicity were “far greater than was previously realized … making diving on pure oxygen below 25 feet of sea water a hazardous gamble” (Shykoff, 2019). While this marked the beginning of the body of research that resembles what we reference now, Donald also noted that “the variation of symptoms even in the same individual, and at times their complete absence before convulsions, constitute[d] a grave menace to the independent oxygen-diver” (Shykoff, 2019). He made note not just of the toxic nature of oxygen but also the enormous variability in symptom onset, even in the same diver from day to day. 

The U.S. Navy Experimental Diving Unit (NEDU), among other groups in the United States and elsewhere, worked to expand that understanding with multiple decades-long studies. These studies looked at CNS toxicity in: immersed subjects with a PO2 of less than 1.8 from 1947 to 1986; pulmonary toxicity (immersed, with a PO2 of 1.3 to 1.6 bar, and dry from 1.6 to 2 bar) from 2000 to 2015; and whole-body effects of long exposures at a PO2 of 1.3 from 2008 until this year. 

The Duke Center for Hyperbaric Medicine and Environmental Physiology, the University of Pennsylvania, and numerous other groups have performed concurrent studies on similar topics, with the trend being a focus on understanding how and why divers experience oxygen toxicity symptoms and what the safe limits of oxygen exposure are. Those limits have markedly decreased from their initial proposals, with Butler and Thalmann proposing a limit of 240 minutes on oxygen at or above 25 ft/8 m and 80 minutes at 30 ft/9 m, to the modern recommendation of no greater than 45 minutes at a PO2 of 1.6 (the PO2 of pure oxygen at 20 ft/6 m). 

Between 1935 and 1986, dozens of studies were performed looking at oxygen toxicity in various facets, with exposures both mild and moderate, in chambers both wet and dry. After 1986, these original hyperbaric studies almost universally ended, and the bulk of research we have to work with comes from before 1986. For the most part, research after this time has been extrapolated from previously recorded data, and, until very recently, lack of funding and industry direction coupled with risk and logistical concerns have hampered original studies from expanding our understanding of oxygen toxicity. 

Primary Toxicity Models

What we’re left with are three primary models to predict the effects of both CNS and pulmonary oxygen toxicity. Two models originate in papers published by researchers working out of the Naval Medical Research Institute in Bethesda, Maryland, in 1995 (Harabin et al., 1993, 1995), and one in 2003 from the Israel Naval Medical Institute in Haifa (Arieli, 2003). The Harabin papers propose two models, one of which fits the risk of oxygen toxicity to an exponential model that links the risk of symptom development to partial pressure, time of exposure, and depth (Harabin et al., 1993). The other uses an autocatalytic model to perform a similar risk estimate on a model that includes periodic exposure decreases (time spent at a lower PO2). The Arieli model focuses on many of the same variables but attempts to add the effects of metabolic rate and CO2 to the risk prediction. Each of these three models appears to fit the raw data well but fails when compared to data sets in which external factors were controlled.  


Comparison of predicted and recorded oxygen toxicity incidents by proposed model (Shykoff, 2019).

The culmination of all this work and modeling is that we now have a reasonable understanding of a few things. First, CNS toxicity is rare at low PO2, so modeling is difficult but risk is similarly low. Second, most current models overestimate risk above a PO2 of 1.7 (Shykoff, 2019). This does not mean that high partial pressures of oxygen are without risk (experience has shown that they do pose significant risk), but the models cannot accurately predict that risk. Finally, although we cannot directly estimate risk based on the data we currently have, most applications should limit PO2 to less than 1.7 bar (Shykoff, 2019).  

NOAA Oxygen Exposure Limits  (NOAA Diving Manual, 2001).

For the majority of divers, the National Oceanic and Atmospheric Administration’s (NOAA) oxygen exposure recommendations remain a conservative and well-respected choice for consideration of limitations. The research we do have appears to show that these exposure limits are safe in the majority of applications, and despite the controversy over risk modeling and variability in symptom evolution, planning dives using relatively conservative exposures such as those found in the NOAA table provides some measure of safety. 

The crux of the issue in understanding oxygen toxicity appears to be the lack of a definitive mechanism for the contributing factors that play into risk predictions. There is an enormous variability of response to hyperoxia among individuals–even between the same individuals on different days. There are multiple potential pathways for injury and distinct differences between moderate and high PO2 exposures, and the extent of injuries and changes in the body are both difficult to measure and not yet fully understood. 

Interested in the factors that play into oxygen toxicity risk and what the future of this research holds? We’ll cover that and more in the second part of this article in next month’s edition of InDepth.

Additional Resources:

  1. Shykoff, B. (2019). Oxygen Toxicity: Existing models, existing data. Presented during EUBS 2019 proceedings.
  2. Hedley-Whyte, John. (2008). Pulmonary Oxygen Toxicity: Investigation and Mentoring. The Ulster Medical Journal 77(1): 39-42.
  3. Harabin, A. L., Survanshi, S. S., & Homer, L. D. (1995, May). A model for predicting central nervous system oxygen toxicity from hyperbaric oxygen exposures in humans
  4. Harabin, A. L., Survanshi, S. S. (1993). A statistical analysis of recent naval experimental diving unit (NEDU) single-depth human exposures to 100% oxygen at pressure. Retrieved from https://apps.dtic.mil/dtic/tr/fulltext/u2/a273488.pdf
  5. Arieli, R. (2003, June). Model of CNS O2 toxicity in complex dives with varied metabolic rates and inspired CO2 levels
  6. NOAA Diving Manual. (2001). 

Two Fun (Math) Things:

CALCULATOR FOR ESTIMATING THE RISK OF PULMONARY OXYGEN TOXICITY by Dr. Barbara Shykoff

The Theoretical Diver: Calculating Oxygen CNS toxicity


Reilly Fogarty is a team leader for risk mitigation initiatives at Divers Alert Network (DAN). When not working on safety programs for DAN, he can be found running technical charters and teaching rebreather diving in Gloucester, MA. Reilly is a USCG licensed captain whose professional background includes surgical and wilderness emergency medicine as well as dive shop management.

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