Correlation is not Causation and Stop Judging Me!

One Halloween I went out in a wig with a name tag that read “Cora Lashun” and my t-shirt had the word “Causation” on it with a red circle around it and red line through it.

Correlation is not Causation.

Very few people got the joke. And ok, it wasn’t Halloween it was last Saturday for drag brunch. Stop judging me.

Anyway, everyone repeat after me: CORRELATION IS NOT CAUSATION!

This pithy little edict  is one to live by. And I know this contradicts my previous post about not living by pithy little edicts but this one is different. Stop judging me.

What happens when people assume causation from correlation is they tend to incorrectly reverse engineer a statistic associated with a therapy then blame, or avoid, that therapy. This is the kind of bad science that makes me ugly cry until my mascara runs. Stop judging me.

An example of this kind  I came across recently was with a severe refractory asthma attack that came into the ER. A fellow RT said casually “Studies show that mortality rates are really high with ventilated asthma patients. We should avoid intubating.”

The first half of this statement is true.

mortality rates in patients receiving intubation from 10% to 20% in this patient population” –

The second half is where the problem comes in. The “we should avoid intubating” part. This person took a dicey leap from “mortality rates are high in ventilated patients” to “ventilating patients causes a high mortality.”

You know what else has a really high mortality rate? Avoiding therapy because of feared statistical outcome, like not ventilating patients who can’t breathe. And yes, I just indirectly claimed that mechanical ventilation is therapy. Stop judging me.

This is known as a ‘post hoc ergo propter hoc’ fallacy often simplified to just  ‘post hoc’ fallacy. This fallacy comes in the form of A occurred then B occurred therefore A caused B. Then to add insult to injury, it was combined with the false logical inverse that assumes avoiding A will prevent B. This makes Cora Lashun very, very angry. Hoc iudicate me. That means “stop judging me” in Latin.

These kinds of fallacies are easy traps to fall in. There is a correlation in ARDS patients that shows the higher the FiO2 requirement, the higher the mortality rate. But you aren’t going to save the patient by willy-nilly reducing their oxygen. Their O2 needs must be met regardless of the statistical association with death. Lurking somewhere between the post and the hoc that makes one assume A then B therefore A caused B, is that devious little letter C. C stands for Confounding Variable which influences the dependent and independent variables (A and B) giving rise to spurious associations between the two and the incorrect elimination of the null hypothesis and then science fails us and suddenly bigfoot is real because I’m a Libra and I don’t want to live on this planet anymore.

In this case C is the disease state. The worse the disease state (C), the higher the oxygen requirements (A). The worse the disease state (C), the higher the mortality (B). So yes, the higher the oxygen requirements (A), the higher the mortality (B). Correlation. Not Causation.

Perhaps instead of hypocritically contradicting my previous diatribe against axiomatic absolutes I should soften the blow of this maxim and say “Correlation does not imply Causation.” Because correlation can also be causation. If we had started with “The worse the disease state the higher the mortality rate” we’re left with A then B and – also, not therefore – A caused B.

The crux of the fallacy lies in the ‘therefore’. So when faced with statistics and you find yourself thinking “therefore”, think of me in my wig and my Cora Lashun name tag in my NOT CAUSATION t-shirt, cringe a little, and be cautious. I’ll always be therefore you.

See what I did there. ‘Therefore you’. I can’t help it. Stop judging me.


Ventilators are Not Therapy! Or they are! Whatever! Who Cares!

During rounds in the ICU, crowded around an intubated, ventilated patient, the attending perused his platoon of intimidated interns and said “Repeat after me: Ventilators are not Therapy”

This particular attending, a plucky, pontificating pulmonologist, was short, both of stature and temper, and I nicknamed him Nappie. This sobriquet served up the delightfully duel indignities of being both, redolent of whiny babies in diapers, and also cleverly ‘short’ for Napoleon.  

“Ventilators are not Therapy” droned the flock.

“Respiratory Therapist,” nipped Nappie, “why didn’t you chime in?”

I do have a name. It’s there on the badge in fine print underneath the giant capitalized “RESPIRATORY THERAPIST.” But that’s not important. We’re just there to smile and push buttons.

“I’m sorry, I couldn’t speak because all my energy was focused on not rolling my eyes at you,” I smiled. “Did I succeed?”

Button. Pushed.

The only person in the room that laughed was the patient. I couldn’t hear him of course. Intubated. But his peak pressures shot up for a moment. So I took that as a sign of approval.

“Ventilators are not Therapy!”

Medicine is chock full of these kinds of axiomatic absolutes. Maxims meted out mindlessly generation after generation and regurgitated time and again as indisputable truths.

Sound and fury, signifying nothing.

The fundamental point being made by this particular dictum is actually a solid one. What Nappie means when he says that ventilators are not therapy is that ventilators do not cure the underlying illness that makes ventilation necessary. They only support the patient until the pathology resolves. I’m totally on board with this idea. Also, giant DUH. You mean my tidal volume and PEEP settings didn’t cure the sarcoidosis?? No way!! But, anyhow, reducing concepts to these pithy little precepts does exactly that, it reduces the concepts. It reduces them into something unchallengeable, leaving the student at an educational dead end where further thought or analysis is not only dispensable, but discouraged.

“This is box that pushes air into patient. It is not therapy. I is edumacated now. I be doctor.”

It all boils down to semantics. It is a definitional argument. If the delineating factor between “therapy” and “support” is that therapy battles the disease while support helps the patient survive the disease, well then 99% of what we do isn’t therapy. We’re left with surgery and antibiotics. We might as well shout out “Medicine is not therapy!”

So, fine. Let’s say ventilators are not therapy. But, there’s yet another common soundbyte one hears in respiratory care:  “Oxygen is a drug!” So I guess you can call the ventilator ‘pharmaceutical support’ if you’re in the “not therapy” camp or call it “drug therapy” if you’ve joined the “Oxygen = Drug” cult or call it “Skynet” and wait for it to become self-aware so it can push its own buttons. The point is, it doesn’t matter what you call it as long as you know how to use it to benefit the patient. And ventilators absolutely benefit the patient. I think on this point, although he was not nearly as amused as the patient,  Nappie and I agree.

“The art of medicine consists of amusing the patient while nature cures the disease.” – Voltaire


The ABC’s on ABG’s and VBG’s

Arterial Blood Gases are the gold standard in measuring pH, PaO2, PaCO2 and bicarbonate as indicators of overall respiratory and metabolic health. People seem to make a big deal out of getting an arterial blood gas. You find a pulse you put a needle in it. It’s not rocket science.

Tangent: Rocket science isn’t even really, idiomatically, rocket science. It’s simple trajectory and angles and trigonometry. It is firmly rooted in Newtonian physics. You want real “Rocket Science” in a metaphorical sense go for quantum physics. I now declare the phrase “It’s not rocket science” obsoleted and to be permanently replaced with the phrase “It’s not quantum physics”

Double Tangent: In rocket science if you go off on a tangent, you fall out of orbit and fly eternally into deep space. Which is the perfect metaphor for where this article has gone.

Anyhoo… back to ABGs. Different hospitals have different care protocols and cultures. In some places ABGs are as common as MRSA in others, they are a rare order. In places like the latter, VBGs are often used as proxy. But how exactly does VBG information correlate to ABG information?

First lets start with  the basics of ABGs. They are easy to interpret. It’s not rocke…er… quantum physics.

Normal values are:
pH: 7.35 to 7.45
PaCO2: 35 to 45 mmHg
PaO2: 80 to 100 mmHg
SaO2: 93 to 100%
HCO3: 22 to 28 mEq/L

Fun Fact:  Some people use mmHg and torr interchangeably as units. They are not exactly the same. However the margin of difference is so tiny, less than 0.000015%, that this indulgence can be forgiven with a simple haughty eyeroll.

Fun Fact 2: mEq, milliequivalents, are the atomic weight of each of the atoms in a compound divided by the valence. The valence is the combining power of the compound based on the absolute value of the number of extra or missing electrons in the molecules outermost valence shell which dictates acidity or alkalinity. Por ejemplo, HCO3has a valence of 1. Negative and positive represent extra or missing electrons and anions and cations respectively. And that’s more than you ever need to actually know. It’s not exactly quantum physics, but easily as difficult as rocket science. But if you are curious, here’s a great tutorial:

Starting with oxygenation, if the PaO2 is low, you need to get more oxygen to the patient. Giant Duh. For a mechanically ventilated patient, this means two things: Increasing the PEEP or increasing the FiO2.

PaO2 can also be too high implying over-oxygenation. Breathing 100% O2 at sea level (760 mmHg),  then your Alveolar partial pressure of O2, PAO2, is 760 mmHg. At 100% humidity water vapor has a partial pressure of 47. So subtract that out and we are left with the gas pressure of 713. The partial pressure of O2 in the blood is always lower than the partial pressure of O2 in the alveoli, otherwise it would flow in the wrong direction. The difference between these pressures is called the A-a gradient, and normal values depend on age. The equation to approximate this gradient is ((age/4) + 4)). Therefore an adult at age 40 has a gradient of 14. At 100% oxygen at sea level, his PaO2 would max out at 713-14, or 699 mmHg. My philosophy in life is “Math not Meth”.

If your patient has a PaO2 of 699, you are doing something very, very wrong. Oxygen toxicity. It’s a thing. Look it up.  Actually I already looked it up for you. I’m nice that way.  Horse to water. Here, take a drink:

Now onto ventilation which is slightly more complicated than oxygenation but still not quantum physics. Ventilation is about the removal of CO2 from the blood which affects the pH. An abnormal pH is either the result of a respiratory problem, meaning the patient is retaining or exhaling too much CO2, or it is a metabolic problem.

Differentiation between respiratory and metabolic derangements can be accomplished by simply comparing the PaCO2 with the pH. With respiratory issues, the pH and PaCO2 move in opposite directions.  With metabolic issues, they move in the same direction. Easy as pie. Not irrational like pi.

If the problem is metabolic there is often respiratory compensation and, conversely, if the problem is respiratory, there is often metabolic compensation. Compensation can bring the pH back into the normal range. But generally the body does not overcompensate. So if your HCO3 and PaCO2 are both out of the normal range, whichever side of 7.40 the pH lands tells you if we are compensating from acidosis or alkalosis and whether or not the problem is primarily respiratory or metabolic. It CAN be both. But one will usually be dominant.

Here’s a nifty chart I made just for you. I’m a giver. I give and I give and I give.

Clinical Diagnosis pH PaCO2 HCO3
Respiratory Alkalosis Normal
Respiratory Acidosis Normal
Respiratory Alkalosis with metabolic compensation
Respiratory Acidosis with metabolic compensation
Metabolic Alkalosis Normal
Metabolic Acidosis Normal
Metabolic Alkalosis with respiratory compensation
Metabolic Acidosis with respiratory compensation


So that’s the nitty-gritty, the lowdown, the brass tacks, the ABCs of ABGs. If you’re an RT none of this should have been new to you. However, if your education was like mine, a lot of time was dedicated to the interpretation of ABGs and VBGs were overlooked like an unwanted stepchild on Christmas morning.  Santa loved ABG. VBG wept quietly in the corner, neglectedly nibbling on a shriveled fig that fell from the crowded plate of a drunken uncle.

VBG’s, not surprisingly, also have a set of normal values:

pH: 7.31 to 7.41
PaCO2: 41 to 51 mmHg
PaO2: 30 to 40 mmHg
SaO2: ~75%
HCO3: 23 to 29 mEq/L

When it comes to correlation between VBGs and ABGs there have been quite a few studies.


Studies show is that there is a strong reliable correlation between arterial and venous pH. That difference being ~.035, venous being obviously more acidotic due to the exchange of O2 for CO2 at the capillaries.


It gets more complicated when dealing with PaCO2. The correlation is good with normocapnia. PvCO2 is 100% specific in ruling out arterial hypercapnia with the cutoff being < 45 mmHg and 100% sensitive for detecting hypercapnia if > 45 mmHg. However, above 45 mmHg the correlation becomes less and less predictable so an actual measurement of PaCO2 cannot be calculated in a hypercapnic patient.

PaCO2 and PvCO2 are non-correlative in severe shock and in hypocapnic patients.


Good correlation. Arterial HCO3 can be reliably calculated by simply subtracting ~1.5 from the venous HCO3


Here’s where VBG’s fail us. These values have poor correlation. However, with SpO2’s handy everywhere we can still assess for adequate oxygenation. We cannot however, determine the PaCO2 which in many patients, is helpful to know. Notably, ARDS patients for who the PaO2/FiO2 ratio is both a diagnostic tool, and a helpful marker to trend for treatment success or failure.

In summary, we may need ABGs a lot less often than we tend to think. They are essential for patients in severe shock and patients with ARDS, both populations commonly already having an arterial line in place. And also to determine the specific PaCO2 in patients who are hypercapnic.

Maybe we’ve spent too long needling VBG’s when VBG’s can make a fine point. Stop groaning. That’s how I amuse myself.

Sans Everything

I am currently in the waiting room in the ambulatory surgery department waiting for Greg who is having cataract / lens replacement surgery because oxidation, despite weeks of prone positioning designed to prevent it, clouded his vision after multiple retinal tears and vitrectomies. This procedure should be the end of it, the last step in a nearly decade long process we’ve titled “Ageing sucks but it beats being dead.”

At least for now that seems true. But we’re getting old. And as we age, the gap between the pain of existing and the joy of being alive grows narrower procedure by procedure, prescription by prescription, diagnosis by diagnosis, injury by injury and limitation by limitation, until we are left in a second childhood facing oblivion sans teeth, sans eyes, sans taste, sans everything. Shakespeare. So cheery. And that is from one of his “comedies.”

Lung function peaks around age 20. This is commonly measured by what we call the A-a gradient, the partial pressure of alveolar oxygen minus the partial pressure of the arterial oxygen. Because O2 moves in one direction across the alveolar membrane to the capillaries, the alveolar pressure is always higher. How _much_ higher is a reflection of alveolar integrity or the diffusion capacity of the lungs. And that integrity and diffusion capacity, no matter how we might fight it, no matter what good of shape we are in, decreases with age.  Now I sound as morbidly depressed as Jacques in As You Like It. This is distinctly NOT as I like it.

An estimation or expected A-a gradient is calculated using the equation G = (age/4) + 4. So at age 20, an average gradient would be 9 torr. At age 80 it would be 24 torr.

PaO2, arterial O2, requires a blood draw. This is common, and sometimes super easy if a patient has an ART line in and one has direct access to their arterial blood without the need for another needle stick. PAO2, alveolar O2, however, requires math. No one in medicine seems to like math but me. So the A-a isn’t often a topic of discussion or a measure of therapeutic impact.

We do have a simpler derived option. The P/F ration. In this equation P = PaO2, and F = FiO2 or Fraction of inspired O2. For people breathing room air, this is .21. But the majority of patients for which such numbers would even be of interest are being mechanically ventilated either invasively or non-invasively.

If you remember from previous posts, and you probably don’t because no one reads this blog and you’re probably not even reading this, the FiO2 is a major variable in the Alveolar Air Equation used to calculate PAO2. The other variable of note is PaCO2 but its impact is far less than that of FiO2 on the PAO2, so we can simply choose to ignore the requisite math and use FiO2 in its place and the ratio of PaO2/FiO2 as a measure for overall lung health. And tracking this ratio actually is a used and useful measure of therapeutic impact. So much so that this ratio is one of the main diagnostic measurements in the Berlin Definition of ARDS. Along with timing, chest imaging, and origin of edema, the P/F ration dictates the severity of the disease as shown below.


Tracking this ratio can indicate the progress of the disease and let us know if the patient is about to shuffle off this mortal coil or shuffle off to buffalo.

OK, Greg is out of surgery and I have to take him home now where we will drink and eat. Because he may be temporarily sans eyes, he is not sans teeth nor sans taste. Jacques was such a drama queen.

Wetsuit Yourself.

Three miles off the coast of Placencia, Belize on a boat, suiting up for a dive, the conversation turned to the second most common dive conversation after “All things Turtles”, and that conversation is about ‘Pee’.

When you dive, you pee. It’s such a consistently observed phenomenon that even without empirical study, one could upgrade it past theory and right into physical law. Just like I know that when i jump out a window I will splat on the pavement, I know that when I jump off a dive boat, no matter how empty my bladder at the time, I will pee. It’s like the 5th law of thermodynamics: When you dive, entropy increases as you pee. Of course, this would be labeled the 4th law because stupidly, they zero-based numbered them and there is actually a Zeroth Law of Thermodynamics. So yeah, that oft-quoted Second Law of Thermodynamics? It’s actually third on the list. Mind = Blown. Which increases entropy and hence, obeys the third… i mean second law of thermodynamics.

So yes, you pee. It’s fine. Wetsuits trap water, but there is still a steady exchange across the membrane of the wetsuit that flushes it out.

However, this is why I have never, and will never, dive in a “dry” suit. Cuz no, ick, ew. While I would never kink-shame anyone for what they do in the privacy of their own bathtubs, I don’t need to commingle my hour under the sea observing the awe-striking beauty of nature with some kind of adult diaper fetish. That kind of multitasking diminishes both experiences.

Anyhoo, one particularly meticulous man in a pricey Blueseventy couture cerulean wetsuit with matching headpiece adorned with marine-themed accouterments chimed in:

“I don’t pee in my wetsuit,” he said.

“Yes, you do,” I responded.

“No. I don’t”

“Yes. You do.”

We went back and forth on this til we jumped off the boat. Later, at 80 feet, I wrote on my white board “Yes you do” and flashed it at him. Although I think I was suffering from nitrogen narcosis at the time because after the dive I looked at the board and it said “Turtle!”

Anyschmoo, I decided to investigate this issue, find proof that this is a real physiological phenomenon, and rub his face in it. The evidence, not the pee. Or both if he asked nicely. My research led me to something I had read about before called ADH, Antidiuretic Hormone.

ADH, also called arginine vasopressin, because naming things is hard I guess, is secreted by the hypothalmus AND the posterior pituitary gland, because redundancy is redundant. ADH regulates the amount of water in your circulatory system and it’s release from whichever of the two glands decides to step up first, is triggered by osmotic sensors and baroreceptors monitoring electrolytic concentration and blood pressure respectively.

Antidiuretic means ‘prevent diuresis’, obviously, so ADH _prevents_ urination. So when elctrolytic concentrations are low and BP is high, the hypothalmus or the posterior pituitary _stop_ producing ADH to allow for diuresis. ADH prevents dehydration, it does not prevent you from volumetric explosion.

When we dive two things happen. Cold water causes peripheral vasocompression sending more blood to the body core. Also, when we are buoyant in water, gravity no longer is dragging our blood toward our feet, also increasing the volume of blood in the body core. This central blood volume spike triggers osmotic receptors and baroreceptors to inform those two glands to stop producing ADH. Then the kidneys just start producing urine willy-nilly and an irresistible flow comes out of your willy-nilly into your wetsuit. Even if its a rental. Yes, that wetsuit you are renting has been peed in.

Back on land, warm, re-victimized by gravity, ADH is again produced and we get thirsty. We rehydrate. We start the process over and over again.

Take THAT cerulean wetsuit dude who probably watched The Devil Wears Prada too many times and hence bought a cerulean wetsuit!




The Big C(OPD)

Smoking causes COPD. There I said it. I said it because it’s true. Despite the billions of dollars invested in quashing evidence, silencing researchers, and in buying senators at their low,  low, bargain prices, smoking does indeed cause COPD. And also a nefarious arsenal of other conditions like bad breath and cancer. But today let’s talk COPD.

COPD is the 3rd leading cause of death in the USA after the Big C and heart disease. The Big C is cancer, and also a bit of a cheat because “cancer” comes in a variety of forms with a variety of pathophysiological processes and a variety of causes and are really a variety of different diseases. But let’s not go down that disturbing, winding path toward understanding the taxonomical practice that names diseases. It’s about as logical as a Escher drawing. All I’m sayin’ is, COPD is a specific disease state, where cancer is not. Nor is “heart disease” really, so… my point is, and I do have one, is that if diseases were named in a more specific manner that defines the disease itself instead of the general process of the disease, COPD would have been titled “The Big C” not cancer.

COPD is understandably bitter about this. Cancer is like the Kanye of diseases and COPD is Taylor Swift.

Anyway, stuck in third (not win, not place, but *show*) COPD is the only one of the top three that is decidedly, explicitly preventable.


Without smoking, COPD would still exist but it would be a rare condition limited to occupational hazards and a genetic condition called alpha-1 antitrypsin deficiency. Without smoking, COPD wouldn’t even make top 20. In causes of death it would rank somewhere down there between being eaten by your exotic pet and spontaneous combustion.

While not everyone who smokes gets COPD, the vast majority of patients with COPD have smoked. The numbers quoted are somewhere around 25% of smokers with a 20 packyear history or more show symptoms of COPD. The guess is that there is a genetic predisposition and research is currently being done to pinpoint exactly where that flaw lies. But as far as I know and have read, nothing has been genetically specified yet. Unlike say Cystic Fibrosis, which has clear, hereditary, testable markers.

Of course the ability to test for a genetic predisposition to COPD isn’t a pathway toward rationalizing smoking. There are other things you can get. Like lung cancer. The Big C. But lets not talk about that because it makes COPD jealous. It’s OK COPD. You’re a deadly, deadly disease. Yes you are. *pat pat pat*.

So what exactly is COPD? In school we learned the almost-acronym, more of an initialism, yes there is a difference,  CBABE to describe the 5 diseases that define COPD: Cystic Fibrosis, Bronchiectasis, Asthma, Bronchitis (chronic), and Emphysema.

Yes yes, I know this contradicts what I said earlier about COPD being a *specific* disease. Unbunch your secretly lacy panties, we’re getting to it.

More recently, CF, and it’s common counterpart Bronchiectasis, have been extracted from the general discourse and study of COPD. While they are indeed obstructive diseases, they are unique in their development and require their own realm of study. The same goes for Asthma, which has always been done a disservice by lumping it under the COPD umbrella. Asthma is such a complex and common domain of respiratory disasters itself, that it requires it’s own special category and specialists.

Essentially, if you make a foundation for it, it should be a separate disease. For example, many forms of cancer have their own separate foundations, and yet they are all called cancer, usurping the spotlight from COPD and reveling in the ‘Big C’ moniker. Which is just unfair. Disease gerrymandering. It’s a thing.

So in COPD we are left with Emphysema and Chronic Bronchitis. And while you may call them separate ‘diseases’, they are inextricably linked, always appear in some combination, and could be classified as symptoms of the same disease state known as COPD. So there. Take that.

The Chronic Bronchitis disease…er.. I mean symptom of COPD affects the non-cartilaginous airways, or bronchioles, that begin 4-5 generations of airway division into the lung. It involves increased mucus production, inflammation, chronic cough and decreases airway cilia.

Emphysema is a disease/symptom of the alveoli which destroys elastin fibers in the walls of the alveoli, increasing the lung compliance, and essentially turning your little happy alveolar balloons into saggy plastic bags easy to fill but impossible to empty. As the walls around the alveoli disintegrate like my integrity at an all-you-can-eat chocolate buffet, bullae, large air pockets that replace lung tissue, develop.

This may encourage you to joke with patients and make quips like, “I may be full of bull, but you’re full of bullae.”



COPD is first considered in patients with dyspnea, chronic cough, excess sputum production and/or a history of exposure to risk factors, mainly tobacco smoke. Once suspected, the diagnosis is confirmed through spirometry, specifically the forced vital capacity (FVC).

FVC is the amount of air one can exhale after maximum inhalation. FVC1 is the volume of that air that comes out in the first second of the FVC. Since obstructive disease interfere with expiration, the FVC1/FVC gives us a measurement of the level of obstruction.

An FVC1/FVC < 70% is a confirmation of existing obstruction.

The FVC1 itself is also compared to expected values based on age, height, gender and ethnicity. Once the existing obstruction is confirmed, the severity of the obstruction is based on the FVC1 / Expected FVC1. The details are on the chart below.


However, if one has a restrictive disease as a comorbidity to the obstructive disease, the severity of the COPD itself may need to be calibrated to the overall volumes of the restrictive disease. Pulmonologists I have discussed this with disagree. So I will die agnostic about it. Get it” “Die agnostic”? Yeah, I’m that good.


Treatment is also based on the severity of the disease. SABAs, LABAs, LAMAs, LABA + LAMAs, ICS, but I will save all that for another post. There’s only so much you can read in a day. I don’t want to burden you. Plus I have two episodes of Star Trek Discovery to catch up on. Priorities. Last episode Michael Burnham figured out how to use a giant multidimensional space Tardigrade to navigate the ship anywhere in the cosmos: The other “Big C”

Speaking of Cosmos. Neil deGrasse Tyson’s reboot of Carl Sagan’s Cosmos got one season. Duck Dynasty is now on season 8.

Oh America, you are dying of the Big I, Ignorance.


Into Thick Air

A couple of months ago, I validated my collapse while climbing a 5200 foot peak by using the alveolar air equation to prove that I was indeed a victim of acute altitude sickness!

Now we are experience the opposite extreme. We are on a dive trip in Placencia, Belize and diving twice daily to a depth of 60-70 feet.

Unlike the atmosphere, where the pressure slowly decreases as you climb, the inverse under water happens much more rapidly. The pressure increases 1 ATM or 760 Torr every 33 feet. Interestingly enough, gravitational acceleration is 33 ft/s^2. Is the linear increase of water pressure of 1 ATM per 33 feet related to gravitational acceleration which is 33 feet/s^2? Or is this just a peculiar coincidence.

We have a theo22540134_10157226263087925_7711134980624509568_nretical physicist on our trip so I asked him about this numerical peculiarity between dives. His first knee-jerk response was “Just a coincidence, as evidenced by the change of medium one dives in. If you were going down in mercury, which has a higher molecular weight, the pressure would climb much faster.”

“Ah,” I said smugly the way ‘ah’ usually is said, “but we build a lot of our units of measure off of the molecular weight of H2O, therefore, while other mediums may increase pressure with depths at different rates, water could be the base medium from which we originally derived those pressures, and therefore, ergo and so forth, it may still not be a coincidence.”

“Hmm I’ll have to think about that,” he said as he jumped off the boat.

After the dive I approached him, “So, any insights?”

“No. There were turtles.”

Damn turtles. Everyone loves them. But as much as we love to anthropomorphize them, they have brains the size of a pea and probably have more in common with a walnut than a human. So I still don’t know cuz turtles. #ThanksTurtles

So lets table that question for a while, because to truly answer it requires some deep digging into unit factoring and I am in Belize with a rum hangover and unit factoring is not a vacation sport.

Another question to ponder: Is there a limit to how high ones PaO2 can go.

At 66 feet, a common dive depth for 30 minutes or so, pressure goes up to 3 atm or 2280 torr. The air we breathe from a tank is completely dry, and the regulators go in the mouth, circumventing the conchae and mucosa of the nasal cavity that create turbulence and moisture respectively.

if we plug that into our Alveolar Air Equation: PAO2 = ( FiO2 * (PB- PH2O)) – (PaCO2 / RQ)

we get PAO2 = (.21 * (2280 – 0)) – (40/ .8) = 428 torr.

This is similar to what you would see if someone were breathing 70% O2 at sea level. The difference being that, at sea level as FiO2 goes up, there is less and less nitrogen in the mix, and the A-a gradient increases. While diving, it is the pressure that goes up, the gas mixture remains relative, and therefore I can assume the A-a gradient stays constant. Could this be an argument to use barometric chambers on people with severely compromised respiration that isn’t CO based?

Also, people who dive frequently don’t dive on air usually. they dive on Nitrox. Nitrox is essentially any mixture of O2 and N2 where the O2 is not the standard 20.9% as it is in regular air. Nitrox divers tend to dive at a 31% O2 to 69% N2 ratio.

we get PAO2 = (.31 * (2280 – 0)) – (40/ .8) = 656 torr.

This is more similar to breathing 100% O2 at 1 atm. However the A-a gradient would increase slightly due to the change in gas mixture.

The point of diving on Nitrox is less absorbed N2 in the blood and hence less chance of the bends, aka decompression sickness aka caisson disease. This allows longer dive times in the 50-100 foot range of depths because of the reduction in nitrogen. I hear a lot of divers say things like “Well I just feel better when I dive on Nitrox.” No you don’t. You’re not gluten intolerant either. You just get longer bottom times. And when the dive master is limiting your dives to 45 minutes anyway, you’re paying 10 bucks extra per tank for nothing.

However, on the flip side, the divers opens himself up to the potential for oxygen toxicity. There are two kinds of oxygen toxicity: Central Nervous System and Pulmonary.

CNS toxicity occurs when breathing O2 at a partial pressure of greater than 1.6 ata or 1216 torr. Diving on nitrox to a depth beyond 120 feet would put you right on that edge hence the recreational guidelines limit you to 100 feet.

Pulmonary Toxicity is not generally a problem with recreational divers as it is the result of extended exposure to high O2 contents. It can, however, be a problem with long term mechanically ventilated patients on high FiO2.

Ok enough. I’m going diving to look at turtles and forget that I still haven’t answered that other question.