Maintaining Your Respiratory Reserve

The following is a reprint from InDepth: Digital Scuba Diving Magazine by Global Underwater Explorers.

Published on September 6, 2019             By InDepth

by John Clarke

JJ on his JJ.” Photo by Andreas Hagberg.

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.

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

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 specialty 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 CO2 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

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.

Normal human airways compared to airways during an asthma attack. Graphic courtesy of Asthma and Allergy Foundation of America.

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 for dive duration 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 C, Galant C, Lagier A, Legou T, Giovanni A. Direct measurement of pressures involved in vocal exercises using semi-occluded vocal tracts. Logoped Phoniatr Vocol. 2015 Oct;40(3):106-12. doi: 10.3109/14015439.2014.902496. Epub 2014 May 21. PMID: 24850270.

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 government 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.

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 now retired, Clarke has worked for NEDU as a Scientist Emeritus. He now runs a consulting company, Clarke Life Support Consulting, LLC. He helps various companies, 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.

Related Blog Posts – Further Reading for Rebreather Divers

Hydrogen Diving: The Good, The Bad, the Ugly

In the preceding blog post, I reminded the reader that the Earth’s supply of helium is limited. It is not a renewable resource.

Being a diving professional, I am not concerned about the consequence of a helium shortage on party balloons. But I am thinking about the potential consequences on diving.

So, knowing that hydrogen has both good and bad traits, it would be prudent to begin thinking about whether or not there is a way to safely substitute hydrogen for helium in technical, scientific, commercial and military diving.

Perhaps the word “bad” is too much of an understatement. Perhaps “horrible” would be a better descriptor for something like the Hindenburg disaster.

With that sobering reminder of what can happen, we now cautiously move on to the science.

First, we begin with the explosion hazard of hydrogen in binary mixtures of hydrogen and oxygen.

For diving in the 10 to 20 bar range, 326 to 653 fsw range, the upper explosion limit is 94.2 molar percent. So that means that if a binary gas mixture contains 96% hydrogen and 4% oxygen, it should not explode when ignited.

Those underlined words are important. An explosive mixture of hydrogen and oxygen will not explode without an ignition source. Proof of that is exhibited in many college introductory chemistry lectures, and documented in the following YouTube video.

Arne Zetterström

As a forecast of our potential future, during World War II, Sweden was deprived of a ready source of helium coming from the U.S. and elsewhere. So, the clever and industrious Arne Zetterström conducted a series of experimental deep, hard hat dives from 1943 to 1945 using a mixture of 96% hydrogen and 4% oxygen on dives ranging from 12 to 17 bar.

Once at depth, Zetterström switched from a non-hydrox gas mixture to the “hydrox” gas mixture. His initial test dive was to 111 msw (362 fsw, 12 bar), progressing through six dives to a maximum depth of 160 msw (522 fsw, 17 bar).

That dive series was successful. Unfortunately, on the last dive on 7 August 1945, Zetterström died tragically when his dive tenders mistakenly pulled him directly to the surface from the bottom depth of 522 fsw. He died from fulminant decompression sickness.

From the above table we see that modern measurements confirm that Zetterström chose his gas mixes wisely. At a 96 mol% of hydrogen, he was above the upper explosion limit. If there had been an unexpected ignition event, his breathing gas mixture would not have exploded.

I have confirmed the oxygen partial pressure for Zetterström’s dives using PTC Mathcad Express 3.1 and will share the process.

First, I show pressure conversions familiar to Navy divers and diving scientists, but not known to most others.

For Zetterström’s 111 msw (362 fsw) dive, the partial pressure of oxygen (PO2) would have been 0.478 atm, at the top end of the target range (0.4 to 0.48) for U.S. Navy chamber oxygen atmosphere during saturation diving. A PO2 of 0.48 is believed to be the highest PO2 tolerated for extended periods. Saturation dives sometimes last over a month.

For Zetterström’s 6th and last dive, to 160 msw (522 fsw), the oxygen partial pressure was 0.7 ata, about half of what it normally is in modern electronic rebreathers with fixed PO2.

A far more detailed story of the Zetterström Hydrox dive series can be found in this book.

Arne Zetterström Memorial Dive

In 2012, the Swedish Historical Diving Society and the Royal Institute of Technology (KTH) Diving Club, Stockholm, conducted an Arne Zetterström Memorial dive to a relatively shallow depth of 40 msw or 131 fsw. The original 96% – 4% ratio of hydrogen and oxygen was maintained, resulting in a gas mixture with a PO2 of 0.20 atm.

As reported in the KTH Dive Club’s Dykloggen (dive log) report of July 2012, the team lead was Ola Lindh, Project Leader and Diver. Åke Larsson, another diver, contributed the following information about that dive.

The Hydrox divers used open circuit scuba, with back mounted air, and for decompression, bottles of hydrox and oxygen.

The Swedish divers did not go deeper than 131 feet because they were just above the mud at that depth in a quarry. Plus, they did not yet have details of Zetterström’s decompression plan for deeper diving.

Today, they do possess the wartime hydrogen decompression plan, so deeper hydrogen dives may be forthcoming.

Three gas mixtures – hydrogen, and air (nitrogen and oxygen)

When you mix an inert gas like nitrogen (or perhaps helium?) with hydrogen and oxygen mixtures, that greatly reduces the explosion hazard. But as this video shows, sooner or later the ratios might change enough to become explosive.

Naval Medical Research Institute

I spent 12 years working as a diving biomedical researcher at the Naval Medical Research Institute (NMRI) in Bethesda, MD.

Main entrance to the Albert R. Behnke Diving Medicine Research Center, at NMRI.

My laboratory was in the Behnke Diving Medicine Research Center building, but the hyperbaric hydrogen facility was situated a safe distance behind the main building. In the unlikely event of an explosion, the main Behnke facility and its hyperbaric chamber complex would be preserved.  

The hyperbaric hydrogen facility was used to test the effects of high-pressure hydrogen and biochemical decompression on pigs, rather than risk human divers. And all of that was done safely, thanks to the professionalism of Navy divers and scientists.

Dr. Susan Kayar checking on the hydrogen diving pigs.

Kayar, a member of the Women Divers Hall of Fame, used at 230 msw (751 fsw) a gas mixture of 88% hydrogen, 2% oxygen, balance helium with a slight amount of nitrogen. That 88% hydrogen mixture put the gas mixture well above the 71.3% upper explosion limit for three gas components at 24 bar pressure. The resulting PO2 was 0.5 ata.

Compagnie Maritime d’Expertises (COMEX)

COMEX and their human-rated hyperbaric chambers are located in Marseilles, France.

When it came to manned hydrogen diving, the effect of hydrogen narcosis forced COMEX to operate below the upper explosion limit during its long series of experimental hydrogen dives.

In 1985, COMEX’s Hydra V was the first manned hydrogen dive to 450 msw. Hydrogen fraction was 54%, helium fraction was 45%, and oxygen fraction 1%. PO2 was a nominal 0.45 atm, the same partial pressure used by the U.S. Navy for saturation dives.

In 1988 during Hydra VIII, the first open water hydrogen dive, the depth was 534 msw, or 1752 fsw. Hydrogen fraction was 49%, helium fraction was 50%, and oxygen fraction 1%. The resulting oxygen partial pressure was 0.54 atmospheres.

The following video documents the record-breaking Hydra VIII dive.

The 534 msw Hydra VIII depth record was broken by Hydra X, a 701 msw, 2300 fsw chamber dive. The gas mixture was the same as in Hydra VIII, hydrogen fraction 49%, helium 50%, and oxygen percentage 1%. Due to the increase in depth, PO2 rose to 0.7 atm, an oxygen partial pressure frequently used in older U.S. Navy rebreathers.

The head of the Diving Medicine Department at NMRI, CAPT Ed Flynn, M.D. (glasses and grey hair sitting on the right side of the console), was performing physiological studies on both Hydra VI and VIII. In essence he was the Patron Saint of the NMRI Hydrogen Research Facility.

Shallow Hydrogen Diving

What have the previous studies taught us? Well, for one thing, the Swedes showed in their Arne Zetterström Memorial dive that you can get away with oxygen concentrations close to normoxia, PO2~0.21 ata. The disadvantage of normal atmospheric partial pressures of oxygen, compared to higher pressures, is related to decompression time. There is a decompression advantage when breathing oxygen pressures of 1.3 to 1.45 ata. Virtually all modern electronic rebreathers use those oxygen pressures for that reason. But as the KTH Dive Club showed, hydrogen decompression can be safely handled at relatively shallow depths.

For recreational divers, there is an economic advantage for reducing helium usage by substituting nitrogen. We don’t yet know what the economic and safety comparison would be when using helium diluted hydrogen versus pure hydrogen.

Hydrogen, helium, and oxygen were the standard gases used by COMEX. But they were likely chosen to lessen hydrogen toxicity. Hydrogen toxicity would not be a problem at shallow depth. And in fact, the KTH Dive Club reported no toxicity problems.

Retrospection

As proud as I have been of the record-breaking COMEX hydrogen research program, and of the highly imaginative U.S. Navy hydrogen research program, it has not been lost on me that the first deep human hydrogen dives were conducted by an undoubtedly low-cost program led by a single Swedish Naval Officer, Arne Zetterström.

Now, I find it remarkable that the people testing hydrogen diving at relatively shallow depths, would also be Swedish. Unlike the COMEX and NMRI projects described above, I suspect the KTH Dive club was not sponsored by multimillion dollar programs.

You have to admire the Swedish chutzpah.

Disclaimer: The author is no longer employed by the Navy or Department of Defense. All opinions are my own, and not those of any government agency. This document is posted purely for historical and educational interest. At risk of violent death, under no circumstances should the reader be tempted to explore the production, storage, or use of hydrogen without thorough and certified safety training.

Autohemotherapy Saved My Brother

In 1940, my older brother, Albert, was born prematurely, with a severe case of ichthyosis (skin with scales like fish.)

Due to Albert’s prematurity, at birth his entire body fit in the palm of my father’s hand. Albert had no suckling reflex, and so the pediatrician said there was nothing that could be done to save him. The newborn was doomed.

Based on the above information, I would place the baby’s fetal development at roughly 2/3rds of the way through the second trimester, perhaps at 22 weeks, close to a pound in weight and at most eight inches from the top of his head to his rump. He would have been below the now standard 24 week “age of survivability.” Survival at that stage of prematurity was unlikely.

Dr. Albert S.J. Clarke, an orthopedic surgeon, was my Dad. The infant at risk was Dad’s first child, named after him (Albert Sidney Johnston Clarke III.) Being a physician, Dad was not going to give up on his son without a fight.

Due to Albert’s small size, and the condition of his skin, they were unable to start an I.V., which is the standard of care in today’s medical world. So, as my Mother explained it, as a last resort, Dad withdrew his own blood and injected it into the gluteal muscles of the baby. That blood carried nutrition and sustenance to Albert; e.g., water, minerals, protein, sugar.

That was not as crazy as it seems, since Autohemotherapy was used in the early 20th century to treat dermatological cases, starting in 1913. The following abstract is an example of a 1928 article after the method gained some medical acceptance.

Quoting from the abstract, “Autohemotherapy, first used in dermatologic conditions by Ravaut (1913), closely followed by Spiethoff (1913), consists in the withdrawal of blood … and its injection into the patient’s gluteal muscles, preferably.”

By the 1940’s, Dr. Clarke was no doubt aware of the questionable therapeutic efficacy of the old method, but as a means of delivering fluid and nutrition to an infant otherwise shut-off from the world, there was nothing to lose. Their blood types matched, so in theory, a blood injection would not hurt.

Although the Rh factor was just discovered that year (1940), Albert’s odds of survival were likely assured by the fact that most people are Rh positive.

At the beginning of the 20th century, there was virtually no standard of care for premature infants. Julius H. Hess (1876–1955) published the first book on the subject of medical care for the premature infant in 1922.

In that book, Hess described tube feeding, or gavage, as in the illustration below. However, in the following years, infants often died from aspiration pneumonia induced by early feeding after birth, and early-applied gavage fell out of favor.

A year after my father successfully salvaged my brother, Hess amended his guidance in his 1941 text, writing “Small premature babies (those weighing under 1200 g) were not fed for 24–48 h …. During this time the premature baby receives physiologic salt solution, subcutaneously in the thighs, one to three times daily.”

Obviously, physiological saline solution avoids the risk of incompatible blood reactions, but in the case of that baby and his father-physician, God had blessed them with fully compatible blood types.

I don’t know if Hess had been made aware of my Dad’s lifesaving treatment conducted a year before Hess made his latest recommendation, but that is certainly possible.

I never discussed with Dad the details of his saving intervention, but from what I’ve read about babies with ichthyosis, my brother’s survival and thriving until age 73 is a bit of a miracle. His pediatricians gave him zero chance of surviving his first days. They didn’t know just how determined my Father could be.

Due to my brother’s genetic skin disease, he shed skin in large flakes; his bed sheets were always covered in them. He had to be lathered in Vaseline to keep his brittle skin from cracking too deeply, and bleeding. He also had very poor tolerance to heat because he had few if any functioning sweat glands.

In spite of his disability, Albert was one of the nation’s first Respiratory Therapists. He trained other Respiratory Therapists in west coast colleges, and ran several Respiratory Therapy Departments in hospitals across the country.

With unlimited medical research libraries at his disposal, he discovered on his own that a drug used for treating psoriasis helped him control his own skin condition. As a result, his quality of life in his last decades greatly improved. He fulfilled a dream of remarrying, all made possible by a determined physician willing to take a chance when the “experts” had given up hope.

Dr. A.S.J. Clarke, M.D. in his later years.

Today, thanks to advances in the medical management of premature infants, autohemotherapy is medically unnecessary. In fact, many doubters question its efficacy. However, I have the physical scars from growing up with a rambunctious big brother to prove that, in at least one case, it was a lifesaver.

Pendelluft—The Beast Within

It was dark, the only light coming from the red glowing numerals of my digital alarm clock. I hadn’t set it to alarm—I needed to sleep as long as I could.

It was also quiet in my bedroom, quiet enough for me to hear my breathing as I lay still, trying to sleep. The breath sounds were rhythmic and calming, breathing in with a hiss, and out with a coarser and louder “huh,” endlessly repeated.

I had just been released from our local hospital after five days on oxygen, diagnosed with “respiratory failure” of unknown origin. The medical term for unknown origin is “idiopathic,” but that word added no clarity to what had happened.

What had happened has been described in a previous blog post, a post that correctly warned that if the illness that almost killed me was any indication, we should NOT expect COVID-19 to abate during the hot and humid months in the American South.

Whatever virus I picked up in Thailand in July, seemed to have a predilection for the hot and humid summer weather of Florida. In other words, it had made itself right at home in my lungs. The result was a puzzling but treacherous case of silent hypoxia, or as some have called it, happy hypoxia. In that regard, my respiratory failure was every bit as inexplicable and potentially deadly as COVID-19.

Thankfully, my viral infection had not yet reached the level of transmissibility of COVID-19. Otherwise, my wife of fifty years would certainly have been affected as she sat by my side for those long and frustrating days in the hospital.

But now, it was time for celebration. By sheer willpower and some tricks of the respiratory physiology trade, I had gotten myself discharged from the hospital. But that’s another story.

At home once again, my finger-tip pulse oximeter showed I was oxygenating reasonably well on air (in the low 90 percentile), but I was not back to normal (the high 90s). My lungs still had some healing to do before I could claim I was 100% normal.

As I now lay quietly as night enveloped me, entering almost a meditative state listening to my breathing, I noticed a strange sound. Alerted, I listened more intently. And what I heard scared the hell out of me.

There was something alien in my body. I couldn’t feel it, but I could hear it. When I breathed in, it breathed out. When I breathed out, it breathed in. It was clear as day, something was breathing in my chest, and it wasn’t me.

I had a monster in my chest.

At times like that, it is hard to be objective. But with years of training as a scientist, I forced myself to collect data and analyze the results before, well, FREAKING OUT!   

The first thing I noticed, was that the asynchrony between my breathing and the other’s breathing, was invariant. They were 180 degrees out of phase, and that never changed.

Professionally, I’ve dealt with probability my entire scientific career. So, if there were in fact some other living thing in my chest, the odds that it would never change its breathing rhythm seemed unlikely. Unless—it was waiting for my lungs to have a full “tidal” breath” before IT took a breath.

Of course! That is exactly what I would do if I was in some giant’s chest. I’d wait until their lungs were full before I’d steal air from them. After all, how else could I, as a little monster, breathe?

But wouldn’t X-rays at the hospital have shown its presence? Well, yes, and no. They didn’t do an MRI. If IT was soft bodied, and growing, it might not have been detected. And going an analytical step further, that could explain why my arterial oxygen saturation levels were not back to normal. IT was stealing oxygen from me.

My heart rate was increasing, which was the last thing I wanted it to do. The more blood I sent the thing, the faster IT would grow. I had to stay calm. But how?

I began thinking about physiology text books. That would put anybody to sleep. But that was also the magic moment. That was when I put a name on the creature in my chest.

I called it, Pendelluft.

Until that night, Pendelluft had been to me of little more than academic interest. I’d read about it, but I knew it is primarily found in patients with chronic obstructive pulmonary disease (COPD); which I do not have. I’ve also never been a smoker or asthmatic.

I knew of the diagrams which explain it, but I never thought that I would be able to hear it, in my body, and especially without a stethoscope.

An illustration of the mechanism of Pendelluft from a humorously named web site, Deranged Physiology.

After I explored the medical literature, I’m not sure anyone in the medical field thinks it possible for a patient to hear his own Pendelluft. But it must be true, since the monster never reared its ugly head, and my arterial oxygen level regained its expected normal value only after the “monster” faded away.

 According to a 1985 paper in the Journal of Applied Physiology, the experimental evidence and theoretical aspects of Pendelluft are attributable to varied pulmonary (lung) airway resistance and compliance (the opposite of stiffness), and were first described in a classic paper by Otis et al. in 1956.  

I was pleased when I read that one of my mentors, Dr. Arthur Otis, the one time Department Head of the Physiology Department at the University of Florida School of Medicine, had done the pioneering research on the subject.

However, I found no reference to breath sounds until I came across the 2012 article in the journal Pulmonary Medicine. That study used very complex instrumentation and statistical methodology to detect Pendelluft.

I have to admit that I smiled when I read that 2012 article. I was questioning how much money was spent on that very elaborate medical investigation. Arguably, it was fine work and contributed nicely to the field.

But, I wondered, did they try asking the patient, “Do you hear a monster in your chest?”

For what it’s worth, I did.

And it was scary as hell.

Warning Order

“Consider this a warning order.”

The voice on the other end was from the Pentagon. That was the last thing I’d expected to hear on Saturday morning, March 21st, 2020.

On October 1, 2018, I had happily retired after forty years of Federal service. I had remained engaged with the Naval Sea Systems Command and the Navy Experimental Diving Unit as their one and only Volunteer Scientist Emeritus, until I received that call.

Within 90 minutes, I had been reinstated with full security clearance and told to pack my bags.

The next day as I was flying on government orders in an almost empty plane to New Hampshire, I had no idea that the company I was sent to help would begin a ventilator design effort from scratch, that same day. I also couldn’t imagine that the resulting ventilator would receive FDA approval 41 days later. 

Wilcox Industries Hybrid Patriot 5510 Life Support System.

 The company, Wilcox Industries, in Newington, New Hampshire, has for twenty years built hybrid self-contained breathing apparatus (SCBA) for the military. In fact, twenty years ago, with full Navy support, I helped them design and test their first Scout (now Patriot), life-support system for Tier One operators. But when the COVID Task Force phoned me, Wilcox had no experience with medical devices, especially ventilators. But with the can-do attitude so typical of military support manufacturers, they were willing to learn. In fact, no one I met at Wilcox questioned that it could be done.

Jim Teetzel (center) and Gary Lemire showing me the latest Hybrid Patriot 5510 Life Support System.

 All it took was the drive and leadership of Jim W. Teetzel (center of the photo), a brilliant engineer, businessman and CEO who holds more patents than he can probably remember, young engineers who never considered failure being a possibility, a nimble supply system that provided needed parts within 24 hours, and the magic words which opened every door. Those words were, “COVID Task Force.”

Through the Wilcox network of friends and family, patient ventilation circuit parts almost magically appeared, as did the world’s best mechanical Test Lung.

Michigan Instruments Training Test Lung (TTL)

There was nothing I asked for that did not appear almost as soon as I requested it.

Most important for me was the opportunity to teach by showing, by taking pieces of patient tubing circuits and arranging them in a way that would work with a totally new ventilator concept, the Patriot SAVR (Synchronous Automatic Ventilating Resuscitator.)

The Mechanical Engineer, Nick Mercurio, who I call “The Magician,” is working his engineering magic.

Our tasking from the COVID Task Force was not to produce multiple copies of existing sophisticated ventilators that cost as much as a nice car, but to have all hands engaged in producing small, cheap ventilators built to exacting engineering and medical standards. The proof that Wilcox accomplished that goal was the hard won stamp of approval from the Federal Drug Administration (FDA.)

The Software Engineer, Jansen Habrial, or the “Wizard,” makes the SAVR do things I never could have imagined.

While we want Americans to have the finest medical care money can buy, to include BMW-priced ventilators if the need arises, the fact is that during a world pandemic there simply are not enough of those deluxe models to go around. In the most populous nations of the world where per capita income is low, the availability of hundreds of such ventilators are a luxury few if any outlying hospitals can afford. However, low-cost ventilators like the Patriot SAVR fill that need.

Colonel Dodge (ret) and I as I’m departing Wilcox Industries.

Wilcox is blessed with a retired Marine Corp Colonel, Kevin Dodge (on the left side of this photo), Jim Teetzel’s Chief Strategy Officer. Dodge not only has the experience of managing production and testing programs as complex as that for the V-22 Osprey, but has an understanding of the need for strategically placed world markets.

Together, Jim Teetzel, Kevin Dodge, the “wicked” smart Executive Director of International Programs and Lebanese-born Roula Assadi, and Jim’s senior engineers (Nic Goupil, Gary Lemire, Stan Carter) and their Maestro of Quality Assurance, Lorena Grol, have succeeded in turning a small but wealthy Arab nation into a manufacturing center for the Middle East and North African Region, as well as the huge Indo-Asian continent.

A photo of the first Patriot SAVR Q made overseas by the Barzan Industrial Group in Doha, Qatar. It is being held by John Bousquet, one of the young designers from Wilcox Industries.

Considering the tactical pedigree of this ventilator, and the company which built it, I foresee that eventually every U.S. military medic or independent duty corpsman will have one or more of the Patriot SAVR units available at their aid station, just in case any Patriots need saving.

Happy Hypoxia – A 2018 Warning

“Happy hypoxia,” or more properly, silent hypoxia, has been one of the most puzzling signs and symptoms of patients presenting to Emergency Rooms with COVID-19. The patient’s arterial oxygen saturation can be in the fifties instead of the normal values in the upper 90s, and yet the patient can be cheerful, fully coherent, and even chatty. Normally, with that low an oxygen concentration in the blood stream, a patient would be in severe respiratory distress.

I experienced silent hypoxia after a visit to Thailand in July of 2018, which makes me wonder: was there a coronavirus lurking in Southeast Asia in 2018 that later mutated to become the killer SARS CoV-2? Did I have SARS CoV-1.5? 

Summertime was everything you would expect in Thailand. It was warm and humid, but not uncomfortably so. I had twelve hours ahead of me in the Bangkok Airport waiting for my return flight to Taiwan, then the long leg across the Pacific to Los Angeles. Eventually, I would make my way back to my home in Panama City, Florida, which would also be hot and muggy. No surprises there. 

What was a surprise, was that a young lady wandering the airport asked if she could interview me for the Thai Ministry of Tourism. She had official looking IDs, and a load of interview questions. I wasn’t interested, and I was busy, I offered, already tired before the twelve hours of dead time even began.  

In truth, I wasn’t that busy, but felt it best not to mingle. I seemed to be the only person not speaking Thai, except for that young lady. Surprisingly,  she had no detectable accent and could pass for a Southern California blond.

After a couple of hours, she returned when I could no longer claim to be busy. She had a simple, youthful attractiveness and an unassuming manner. So, tiring of the boredom of waiting, I allowed her to sit beside me while she started running down her list of tourism related questions. 

She wanted to know why I came to Thailand. It was to give a talk at a medical and scientific conference on sports medicine. My subject was “Oxygen,” a fact that would soon become ironic. I discovered later that my travel, ostensibly paid for by the Thai Sports Authority, was bankrolled by Beijing. But I didn’t know that at the time. 

For 45 minutes the questions continued. They were business-like, the type of questions I would expect from a Tourist Bureau. But one thing caused me concern, her occasional hacky cough. She insisted it was nothing, and I was not alarmed. I thought no more about it as I finally boarded the plane for the first leg of my long journey home.

Eight hours after my arrival in Panama City, I felt ill as I lay in bed, trying to sleep after being exactly twelve hours time-shifted. I felt sicker by the minute. Jet lag doesn’t do that.

By morning, I had suffered chills and sweats, and my physician son insisted I be taken to the closest Emergency Room. As we neared the ER I felt I was going to vomit, and I leaned into a trash can that my wife brought for that purpose. 

The next thing I heard was her screaming at me.

I yelled back, completely confused and annoyed. “Why are you yelling at me?”

“I thought you’d died,” she said. “You sighed, threw your back into the seat, and your arms were stiff and shaking.”

Apparently I had passed out from a drop in blood pressure.  (I had not yet thought about hypoxemia.)

As I was being monitored in the ER, I felt OK. I conversed with my wife, and was half-joking and half-irritated at my unexpected welcome home event.

After awhile, I began to pay attention to the finger tip pulse-oximeter that was monitoring my arterial oxygen saturation. The reading was slipping lower than I had ever seen before, but neither the nursing staff nor the attending physician seemed the least bit concerned. My wife and I continued to chat. I was not in any discomfort, and ignored the monitors until I caught sight of the updated pulse-ox reading. It had plummeted down to a horrifically low 55%. 

I told my wife to alert the nurse. They finally started me on a nasal cannula with oxygen. (For those who know, that was an incredibly delayed reaction.) I also knew enough to realize I should be almost stuporous, yet I wasn’t. I was content, except for my circumstances.

Within a few minutes, an ambulance transported me to a real hospital. Being aware of my overseas travel, they assumed I had a pulmonary embolism, which if detected, would have required immediate surgery. But after a perfusion scan, nothing abnormal was revealed. 

After settling into a room, I had zero desire for any of the food they brought me. It was all tasteless, and remained that way for two days.

Initially they kept me on 3 liters of oxygen per minute by nasal cannula, which still wasn’t bringing my oxygen saturation above 84 percent. That was a problem.

At the urging of the CDC, the nursing staff came to my room fully gowned and face-shielded, and stuck that infamously long sampling swab up my nose. They tested me for the most recent viral illness in Southeast Asia at the time, the H7N9 Bird Flu virus of 2017. The results were negative.

In spite of my growing displeasure with being in the hospital, and not tolerating the taste, or lack thereof, of their food, I was happy and chatty with the nursing staff. But neither I, a respiratory physiologist, nor the medical staff could figure out what was wrong. My X-rays showed some consolidation in my lingula, a small lobe in the middle of my lungs, but that was not enough to cause hypoxia of the level I was experiencing. 

After a while, I began to get a few signs of pneumonia in my lower lung lobes, but not enough to cause any discomfort, or difficulty breathing. While physicians clobbered the growing infection with antibiotics and steroids, I remained happily hypoxic.

After five days in the hospital, and slowly watching my oxygen saturation rise, a respiratory therapist snuck behind me and turned off the oxygen. My saturation remained low, at 88%, but it didn’t drop further. 

That meant, I would remain on air until discharge. That encouraged me enough to call for a walking test, walking down the hospital corridor breathing nothing but air. Unfortunately, I failed that test, and was sent back to bed.

About that time, a pulmonologist came by and told me I had a good bit of atelectasis (collapsed alveoli or lung sacs) in my lower lobes. Finally, something I could fix. I knew what to do.

I wore out my incentive spirometer over the next couple of hours, and then called for another walking test. The Respiratory Therapist chided me…I would just fail again, she said. But I do love a challenge. With her by my side, I moved slowly down the hall, refusing to talk, and that time my oxygen saturation did not drop. 

Due to that walking test, I was discharged from the hospital with an oxygen saturation of 92% and returned home to fully recover. (That is in itself an interesting story which I’ll write about next.)

However, the point of this post is that as I read about COVID-19, I’m finding that physicians are puzzled about some of the same bizarre symptoms I experienced in 2018,  notably  a silent hypoxia. I was never “short of breath” as would be expected with an arterial saturation in the fifties. 

From my studies of respiratory physiology, I knew that what had happened to me in 2018 should not have happened, according to the text books. I did not have the SARS virus identified in 2017. But viruses mutate constantly. Could my symptoms have been the signs of a predecessor or cousin to COVID-19? Could it have been an unrecognized COVID-18?

When lungs are not filled with fluid from rampant pneumonia, the most likely way to become hypoxic breathing air is through something called ventilation-perfusion (V-Q) mismatch. A pulmonary embolus can cause massive V-Q mismatch, and can quickly kill if untreated.

However, a recent Science article suggested that COVID-19 might cause microemboli resulting in silent hypoxia. It seems reasonable that enough microemboli, if that’s what it was, could have caused my symptoms in the summer of 2018 without being detected on a pulmonary perfusion scan. 

And that worries me for the current pandemic. Summer heat and humidity might not kill this virus. It certainly didn’t kill the virus that I presumably caught from a pretty young girl with a “nothing” of a cough in late July of 2018. It may have been nothing for her, but it was sure something for me.

None of my friends at the medical conference got sick upon returning home. I was the only one spending 45 minutes less than a foot away from that coughing girl. I feel pretty confident where I got it. My only question is, did I pick up a version of coronavirus that was beginning to mutate towards the destructive potential of SARS CoV-2 which erupted just over a year later?

As for the statue at the beginning of this blog post? It is the Yaksha Guardian Giant at the Bangkok Suvarnabhumi airport. If you ask me, he failed completely at protecting me from a tiny little virus. The guardian was awfully big, but sometimes size does not matter.