Deep dive and user adjustment knob

[Angelo Farina]

You are completely right!

I prefer a reg that breathes like sh** over one that starts free-flowing.

When I learned to dive I was taught to breathe slowly and deeply and my regs got adjusted for ice diving and while they are "a little bit" hard to breathe, I got used to that.

Well, I am not so extreme as @Subcooled , but I understand his point, and, at least in part, I do the same. I am still using very old Scubapro MK5+109 (converted to BA, of course).
I keep the IP around 9 bar, as if I tune them too "hot", the second stage, albeit being balanced, becomes "less progressive", it breaks opens too suddenly for my taste.
Regarding the second stage, I usually tune them with a cracking effort around 1.1"-1.2", with the knob all out. These regs do not have yet the VIVA system, so no Venturi "injecting effect", the pressure must be maintained slightly negative (around 0.3" ) during the whole inspiratory phase. I do not like the strong Venturi effect that many modern regulators provide, where, after cracking the valve open, they inject air in your lungs with a positive pressure.
Said all that, I usually start diving with the knob all out, for minimal cracking effort.
The nice thing of these vintage beauties is that they actually work better at depth than at the surface, so going deep, the cracking effort reduces and I breath with very small effort (of course as I was trained: very slow, very deep, and with a short inspiratory pause). If, for any reason (as swimming against current or working face-down inside a cavity) the reg starts to free flow slightly, then I close the knob of one turn, or more if required. The knob, for me, means the safety that I can control the free flow if needed.
Starting with the knob all in makes the reg really hard to breath, and this is not healthy for your lungs: having to suck air with strong negative pressure can trigger IPE, a very dangerous thing. On the other air, for preventing IPE, it is not good to use a reg with almost no expiratory effort, such as the SP D-series. Actually I think that for beìng "healthy" a reg should have, on average over the whole cycle, more positive pressure during exhale than negative pressure during the inhale. On average over many cycles this maintains your lungs in a positive pressure state, preventing IPE.
The small exhausts valve (and its position) of these brass-chrome vintage regs ensures that expiration always requires at least 0.5" of positive pressure, or more if you exhale quickly. This ensures that this positive pressure will "push away" the blood from your lungs, preventing IPE.
IPE was unknown with those vintage regs. It started to be a problem with rebreathers (which often require to suck the mixture with significant negative pressure, particularity those with back-mounted counter-lungs) and with modern regs with minimal or zero flow resistance during exhalation.

 

[lexvil]

Ok, well now I’ve heard everything.

 

[John C. Ratliff]

Angelo, I'm not at all sure your explanation for prevention of IPE is backed by DAN.

Immersion Pulmonary Edema | The Heart & Diving - DAN Health & Diving

Divers Alert Network, Immersion pulmonary edema (IPE)

Please, if you have some technical papers or references, could you provide them?

SeaRat

 

[rsingler]

Well, before you jump all over @Angelo Farina , whether or not there are any studies, what he's suggesting has theoretical merit. The rebreather community has given us good anecdotal data on the IPE risk of back mounted counterlungs, so there is no reason why negative static lung loading wouldn't be a problem with open circuit.
However, double hose regs aside, I'm not sure that actual negative static loading can actually occur. But what can occur is just what he's cited: the negative inspiratory pressure required to trigger a poorly tuned reg breath after breath, especially at depth with high gas density.
I'm not sure that I want my expiratory effort to be high, for CO2 retention reasons, but his argument for having a reg tuned for easy breathing is spot on, and it relates to exactly the same principal that causes IPE, whether or not we have any case reports.

 

[GJC]

Angelo, I'm not at all sure your explanation for prevention of IPE is backed by DAN.

Immersion Pulmonary Edema | The Heart & Diving - DAN Health & Diving

Divers Alert Network, Immersion pulmonary edema (IPE)

Please, if you have some technical papers or references, could you provide them?

SeaRat

In your first citation, I read that increased negative pressure in the alveoli is a contributing factor to IPE.

I can also add that a standard treatment used on ambulances and in ERs for pulmonary edema caused by congestive heart failure is CPAP (continuous positive airway pressure starting at a pressure of 5 cm of water) applied by a mask. The increase in airway pressure helps hold back fluid that is being pushed into alveoli.

So I agree with Angelo that having a little exhalation resistance is probably a good thing. Minimizing inhalation resistance is definitely a good thing.

 

[John C. Ratliff]

I have used some of the hardest breathing regulators ever designed. These include the U.S. Divers Company DA Aqualung, with no Venturi at all, and the Dacor R-2 regulator; the outlets of both these regulators pushed air into the side of the case. Other than the work of breathing (WOB) I experienced no real effects to my lungs from these regulators. Cousteau' divers used these regulators in the 1950s to very deep depths, without Immersion Pulmonary Edema showing (they experienced many other problems though).

I have also used, and own, some of the easiest Breathing regulators ever developed. These include the Scubapro Pilot and A.I.R. I regulators, and while most of my diving has been shallow, sometimes under high workloads (fighting river currents in a dam tailrace, for instance). Again, no problems. The U.S. Navy selected the Scubapro Pilot for chamber diver, sometimes under high workloads, at 2000 feet depths, without IPE showing (at least, not reported). One reason for the extreme ease of exhalation on these two regulators is that the LP diaphragm is also the exhalation valve. The Pilot regulator has a variable Venturi, which can be set for both positive pressure or less positive breathing, depending on the orientation of the Venturi opening.

These are my reasons for questioning Angelo's description of increased negative pressures on both the inhalation and exhalation cycle for prevention of IPE. I understand the reasoning of extrapolating the negative pressure Breathing in rebreathers with back-mounted breathing bags, but this is negative breathing of a somewhat different sort. So what I am looking for is actual reswpearch studies to back up what Angelo is saying. Why? Because it goes against both my own experience and the other studies I have seen.

Now, what DAN was talking about was a shift in blood from the extremities to the central system's of the body, thereby increasing arterial pressures in the alveoli, which with some other conditions (negative breathing pressures being one) could lead to leakage of fluid into the alveoli, which results in IPE.

Immersion pulmonary edema (IPE) is a form of pulmonary edema — an accumulation of fluid in the tissues of the lungs — that specifically affects divers and swimmers. Immersion at depth is a key factor in the development of IPE. That's because immersion in an upright position causes a significant shift of fluid from the peripheral to the central circulatory system, resulting in higher pressure in the capillaries of the pulmonary system. Elements of the diving milieu that contribute to IPE's occurrence include the fact that divers breathe gases that are denser than air at sea level, which means more negative pressure within chest is needed to inhale; the likelihood of gas bubbles becoming trapped in the vasculature of the lungs; the cold underwater environment; and the potential in underwater settings for exertion or panic, which can exacerbate elevated capillary pressure.
https://www.diversalertnetwork.org/health/heart/immersion-pulmonary-edema

The factors that they then list in the article include negative air pressure in the alveoli (air sac) of the lungs.

So I ask again for research reports that support detuning regulators and increasing exhaust resistance as preventative measures for IPE.

SeaRat

PS, here's one study that indicates underlying cardiac conditions as a main contributing factor for IPE.
Immersion Pulmonary Edema: Case Reports From Oceania - PubMed

 

[Angelo Farina]

What I wrote is not based on medical evidence based on diving cases, but to what reported to me by friend whos is a MD working as a lung specialist in Mantua hospital, one of the cities most affected by Covid 19.
They had hundreths of death due to pulmonary edema. The therapy working better was CPAP, ensuring to keep a pulmonary over pressure.
When they finished the CPAP helmets, they had to invent something. The simple solution was to have patients using a full face snorkeling mask' fed with pure oxygen, and with frontal exhaust valve obstructed. This way the patient was forced to exhale through a significant resistance, and this pushes away fluid from lungs...

 

[John C. Ratliff]

Angelo,

Thank you for the explanation. Please realize that CPAP (Continuous Positive Airway Pressure) is a treatment, not a prevention.
Continuous positive airway pressure - Wikipedia

My wife is a hospital pharmacist (retired, but she still works part time), who has looked up COVID-19 extensively, and the pulmonary edema produced by this disease is much different than the that of Immersion Pulmonary Edema. Apparently (and I'll have to check with her to make sure) the COVID-19 virus infects the cells of the air sacs (alveoli) and the blood vessels around them. This causes a huge increase in the pressure inside the blood vessels, which then "leak" plasma through the cell walls into the alveoli. There is very little space (one cell's worth) between the airspace and the blood vessel, and this facilitates the exchange of oxygen (I know you, as a biologist already know this, but I wanted to explain it for others who may be reading). What kills people is the filling of the lungs with fluid, and other than CPAP, the further treatment when the CPAP doesn't work anymore is to bypass the lungs with a heart/lung bypass machine. Here's an example of that being used:
COVID-19 was killing him. How a last-resort intervention brought this Toronto man back from the brink
This therapy is very risky, as the patient must sometimes stay on the machine a long time, and the risk of infection is pretty high.

IPE has a different run-up, and the causes are multiple according to what I've now read. Some have a previous heart condition, which other conditions (depth, shunting of blood to the core of the body, regative pressure breathing, etc.) can exacerbate.

I really appreciate what you said about the doctors using a full-face snorkeling mask as a makeshift CPAP machine. When the existing machines are all in use, this is a great alternative. They may be needed for an extended time.

SeaRat

 

[GJC]

We probably know less about predicting IPE than we know about predicting DCS.

The following mentions that IPE may very well be the most common cause of death in recreational scuba divers. It may have been missed in many cases attributed to drowning.

Immersion Pulmonary Oedema - UKDMC

This whole discussion makes me want to dive more with my Sea Hornet second stage. Cracking pressure tuned to 0.5 inch. It also has a venturi I can turn on or off.

 

[Angelo Farina]

Angelo, I'm not at all sure your explanation for prevention of IPE is backed by DAN.

Immersion Pulmonary Edema | The Heart & Diving - DAN Health & Diving

Divers Alert Network, Immersion pulmonary edema (IPE)

Please, if you have some technical papers or references, could you provide them?

SeaRat

In reality you already linked to the same sources from which I derived the information I have on the causes triggering IPE.
Here from the first of your links:
"Pulmonary edema is caused by <...> and negative pressure in the alveoli due to resistance from breathing through a faulty regulator."

And from the second one:
"Development of IPE may be from this effect in concert with a multitude of other contributing factors including <...> and high breathing resistance (particularly on inhalation). "