From Air to Trimix at depth

[LiteHedded]

I'm not an expert ... I can only report on what I have experienced, and that is as follows ...

- In one of my tech classes (I forget which one, actually), my instructor invited me to try the nitrox-to-trimix experiment at about 110 feet. I was using EAN32 ... he was using 25/25. When he handed me his reg I did notice a slight difference, but not very significant. After about two minutes, I switched back from his reg to mine ... and I noticed a rather stark difference almost immediately. I'll leave it to the "experts" to speculate why.

- In numerous deeper dives using air or EAN28 (aka "slightrox") ... I've never noticed any significant difference in narcosis symptoms between the two.

- I've noticed two significant symptoms of CO2 retention ... a feeling of "I can't get enough air", and sometimes a moderate headache. During those times when those symptoms were noticeable, I've never felt like I was narc'ed ...

... Bob (Grateful Diver)

going to the nitrox is where you notice it more in my experience as well

 

[Michael Guerrero]

I have looked at the data on CO2 retention with hyperoxia and wondered if we all operate just a little bit on hypoxic drive, and that's why we see a bit of hypercapnia when normal people are exposed to high ppO2s. That's not what is generally taught, but the data make one wonder.

Could it be the constriction of the vascular system due to the high ppO2 that prevents us from getting the CO2 out of our bodies as efficiently?

From pg 119 of Deeper Into Diving, "Interestingly, some experiments show that nitrogen washout may actually be reduced by increasing the concentration of oxygen too greatly, probably due to the cardiovascular changes such as the reduced perfusion, heart rate, and cardiac output that may accompany increased inspired oxygen concentrations."

Could removal of CO2 be affected the same way?

The study they cite is: Anderson, D, Nagasawa G, Norfleet W, Olszowka, Lundgren C. "O2 pressures between 0.12 and 2.5 atm abs, circulatory function, and N2 elimination", Undersea Biomed Res 1991; 18(4):279-92.

 

[DiverRtNY]

Could it be the constriction of the vascular system due to the high ppO2 that prevents us from getting the CO2 out of our bodies as efficiently?

From pg 119 of Deeper Into Diving, "Interestingly, some experiments show that nitrogen washout may actually be reduced by increasing the concentration of oxygen too greatly, probably due to the cardiovascular changes such as the reduced perfusion, heart rate, and cardiac output that may accompany increased inspired oxygen concentrations."

Could removal of CO2 be affected the same way?

The study they cite is: Anderson, D, Nagasawa G, Norfleet W, Olszowka, Lundgren C. "O2 pressures between 0.12 and 2.5 atm abs, circulatory function, and N2 elimination", Undersea Biomed Res 1991; 18(4):279-92.

CO2 elimination is ventilation. Oxygen is perfusion. Someone not breathing can be fully oxygenated and someone breathing normal can have poor oxygenation. Think of carbon monoxide poisoning. Still blow off co2 but hemoglobin can't bind to oxygen.Try not to get the two confused or associate the two with being interactive in the normal settings. Nitrogen washout is a medical term associated with breathing high levels of oxygen and is used intentionally to treat a pneumo that is under 10% of lung volume. Theory is oxygen, being a smaller molecule, will alleviate the air (nitrogen being about 78% of air) out of the pleural space and replace the space with oxygen. This oxygen being less dense will decrease the volume of the pleural space and alleviate the pneumo over time. High concentration of oxygen also leads to atelectasis (collapse of alveoli, or the space where air takes place) for same reason. Nitrogen being denser helps to keep airways open. It's not exactly a vasoconstricter in the cardiac sense. Blood still pumps through the permeable membrane (where co2 is eliminated and oxygen is perfused) but the alveoli (where the blood vessels are surrounded) are collapsed so the exchange doesn't take place. I don't foresee this having a direct influence on perfusion or ventilation in a healthy individual but causes impediment on individuals with poor elasticity and compliance. The potential change is very minor and not a direct influence on co2 retention alone. I feel any CO2 retention is more of an effect on the neuro side than anything. Hypoventilation.
What does have a direct influence on veinous return and cardiac output is having too much positive pressure in the lungs. Think of those alveoli I mentioned earlier having too much pressure causing the alveoli to be overinflated and that can constrict the blood flow going through the permeable membrane of co2/oxygen exchange. Air is there, but blood isn't.

 

[Michael Guerrero]

If CO2 elimination is dependent on venous blood flow, whether as bicarbonate, bound to hemoglobin, or simply as dissolved gas, then how would cardiovascular changes which reduce blood flow not have an affect on CO2 elimination? Wouldn't there necessarily be less CO2 delivered to the lungs to be eliminated?

Here's a link to an abstract of a study that explains what I'm thinking a bit better.

Systemic vasoconstrictor effects of oxygen admi... [Am J Cardiol. 1986] - PubMed - NCBI

So if you produce X amount of CO2, and you reduce blood flow--and I think therefore elimination--then you would expect to see an increase in CO2 retention and a concomitant increase in ventilation to compensate for it. Maybe the increase is very small though.

Have I gone off topic yet?

 

[DiverRtNY]

The normal healthy heart would be able to overcome these impeding venous return by pumping stronger. Not saying there wouldn't be any restriction but not to the point where it would be of any significance. Someone who is already dealing with right sided heart failure and has a reduced ejection fraction than they would have more complications.
From your article: In that instance where the individual already has a significant issue with OPVD (pulmonary arterial hypertension), which qualifies them of having unique and rare disorder seemingly not much different than other forms of pulmonary hypertension but not as easily treatable (as medications like Viagra or Flolan could correct) then it shows an instance where this could create an issue. But like someone mentioned earlier, this person probably wouldn't be able to dive as dyspnea on exertion and SOB doing simple tasks would impede their lifestyles. I dig the sources! And we've gone a little off topic but it's good stuff! Maybe patients with pulmonary hypertension could benefit from some Viagra during scuba diving. Might get a couple double takes but whatever works! Perhaps we can get a grant from Duke University and find a niche into getting our careers and hobbies to coincide! What a wonderful world this would be...

 

[TONY CHANEY]

I hear mentioning of hypercapnea being related to hypoxia (hypoxemia). But the other twist would be hyperoxemia... getting too much oxygen. Outside of talking about oxygen toxemia, let's talk about individuals that are more prone to being hypercapneic: COPD emphysema patients, patients with hypoventilatory syndrome (morbid obesity, diaharagmatic paralysis, etc...)
Indivduals who fall in these catagories are also prone to having lower levels of PaO2 in their blood... oxygen. These individuals have sensors in their noggins that are prone to trigger based on oxygen levels as opposed to co2 levels. If these individuals are abosrbing a higher level of oxygen, hyperoxemia, there central system will depress their systems to ventilate less to compenste for the high levels of oxygen. This resulting in a build up of CO2.
As a respiratory therapist, we see patients in the hospital that go into hypercapneic respiratory failure due to being exposed to too much oxygen in the inpatient setting. Hyperoxemia, not hypoxemia, will lead to hypercapnea and thus leading to lethargy, altered mental status and impending respiratory failure. Hypoxic patients, initially, will increase their ventilation and blow off too much CO2 and will be Alkalotic... not acidotic.

Don't let this confuse you with oxygen toxicity... that is a whole other ball of wax as we know due to very high oxygen levels and absorption due to increased positive pressure that can't realistically be obtained on the surface by oxygen alone. Hence why diving it IS realistic.

Someone that is a co2 retainer (COPDers) have a lot to consider with deep diving. Coming from my pulmonary background, best option would be to get serial Arterial Blood Gasses on individual divers at different depths to specifically tune what each individuals should be breathing to keep themselves in a nice safety zone when pertaining to oxygen requirements, and lack there of.

This post went off the OP but rolling with it.:meeting:



An individual can be hypercapneic and hypoxic but that's a chicken or the egg question. There were events that led to hypercapnea that led to respiratory failure and THEN led to hypoxemia (cause you aren't breathing!). Not the other way around. Unless they were hypoxic and exhausted ones respiratory drive by breathing very heavy and fatiguing themselves into respiratory failure

It was just a matter of time that somebody would post this belief. It really has very little merit pertaining to this post and also very little merit even pertaining to respiratory care. Care to debate it I will gladly play.

 

[dreamdive]

The normal healthy heart would be able to overcome these impeding venous return by pumping stronger. Not saying there wouldn't be any restriction but not to the point where it would be of any significance. Someone who is already dealing with right sided heart failure and has a reduced ejection fraction than they would have more complications.
From your article: In that instance where the individual already has a significant issue with OPVD (pulmonary arterial hypertension), which qualifies them of having unique and rare disorder seemingly not much different than other forms of pulmonary hypertension but not as easily treatable (as medications like Viagra or Flolan could correct) then it shows an instance where this could create an issue. But like someone mentioned earlier, this person probably wouldn't be able to dive as dyspnea on exertion and SOB doing simple tasks would impede their lifestyles. I dig the sources! And we've gone a little off topic but it's good stuff! Maybe patients with pulmonary hypertension could benefit from some Viagra during scuba diving. Might get a couple double takes but whatever works! Perhaps we can get a grant from Duke University and find a niche into getting our careers and hobbies to coincide! What a wonderful world this would be...

Be careful with Viagra and scuba!
First off, people with known PulHTN are at increased risk developing Immersion Pulmonary Edema - since the development of IPE is independent of depth, those individuals with Pulm Hyptertension should think twice about diving!

Second, Blatteau, Brubakk, Gempp, Castagna et al published April 2013 in PLOS ONE, Volume 8, issue 4 the paper that demonstrates that "Sidenafil Pre-Treatment Promotes Decompression Sickness in Rats" (Sidenafil is generic for Viagra. This study could be expanded to all phosphodiesterase-5 blockers.

Third, Richard Moon, MD from Duke University already studies the use of Viagra in IPE. That was at least 2 years ago and I am not sure if those studies are closed.

Overall, CO2 elimination is a function of ventilation as DiverRtNY already specified. The problem in diving is when your ability to eliminate CO2 (via ventilation) is overwhelmed by the amount of CO2 produced (i.e. work-load).

 

[TSandM]

The only way you are going to get elevated ARTERIAL levels of CO2 (which is hypercapnia) is if you don't adequately ventilate the lungs. CO2 diffuses very easily, so no matter what the load is that is delivered to the alveolar capillaries, it WILL be reduced to normal if ventilation is adequate. The body has to be that way, because CO2 is intimately involved in the maintenance of normal pH, and the body tolerates only an extremely small window of change in pH.

Discussions of the pathophysiology of CO2 retainers and pulmonary hypertension are really not very relevant to scuba, as such patients are rarely in any condition to dive.

 

[dumpsterDiver]

CO2 elimination is ventilation. Oxygen is perfusion. Someone not breathing can be fully oxygenated and someone breathing normal can have poor oxygenation. Think of carbon monoxide poisoning. Still blow off co2 but hemoglobin can't bind to oxygen.Try not to get the two confused or associate the two with being interactive in the normal settings. Nitrogen washout is a medical term associated with breathing high levels of oxygen and is used intentionally to treat a pneumo that is under 10% of lung volume. Theory is oxygen, being a smaller molecule, will alleviate the air (nitrogen being about 78% of air) out of the pleural space and replace the space with oxygen. This oxygen being less dense will decrease the volume of the pleural space and alleviate the pneumo over time. High concentration of oxygen also leads to atelectasis (collapse of alveoli, or the space where air takes place) for same reason. Nitrogen being denser helps to keep airways open. It's not exactly a vasoconstricter in the cardiac sense. Blood still pumps through the permeable membrane (where co2 is eliminated and oxygen is perfused) but the alveoli (where the blood vessels are surrounded) are collapsed so the exchange doesn't take place. I don't foresee this having a direct influence on perfusion or ventilation in a healthy individual but causes impediment on individuals with poor elasticity and compliance. The potential change is very minor and not a direct influence on co2 retention alone. I feel any CO2 retention is more of an effect on the neuro side than anything. Hypoventilation.
What does have a direct influence on veinous return and cardiac output is having too much positive pressure in the lungs. Think of those alveoli I mentioned earlier having too much pressure causing the alveoli to be overinflated and that can constrict the blood flow going through the permeable membrane of co2/oxygen exchange. Air is there, but blood isn't.

Oxgen has a higher molecular weight and a higher density than nitrogen?

 

[DiverRtNY]

Oxgen has a higher molecular weight and a higher density than nitrogen?

opposite

---------- Post added October 25th, 2014 at 09:39 AM ----------

It was just a matter of time that somebody would post this belief. It really has very little merit pertaining to this post and also very little merit even pertaining to respiratory care. Care to debate it I will gladly play.

What belief are you pertaining to? Debate away...