SAC - RB vs OC

[Janos]

Shtop!

I think it's a perfectly good question.

1) Firstly ignore depth
2) This is MCCR, so we do know how much O2 we metabolise when we are at rest as we tweak the flow by adjusting the IP.
3) Nick has measured his O2 consumption to be around 1 l / min.
4) Every schoolboy knows that the %O2 in expired air is around 16% to 17%
5) This implies that metabolised O2 is around 4%
6) Nick's OC SAC is 12l/min

Put all that together and you have an inconsistency - Nick is metabolising around 1/2 a litre of O2 when on OC (assuming his SAC is the same when on the surface) but metabolising 1 litre a minute on his RB.

Now. Either something funny (unconcious skip breathing?) is going on when he's diving on OC. Or one of assumptions (1) to (6) is wrong.

Which is it and why?

Janos

[MattS]

Originally Posted by Janos

Shtop!

I think it's a perfectly good question.

1) Firstly ignore depth
2) This is MCCR, so we do know how much O2 we metabolise when we are at rest as we tweak the flow by adjusting the IP.
3) Nick has measured his O2 consumption to be around 1 l / min.
4) Every schoolboy knows that the %O2 in expired air is around 16% to 17%
5) This implies that metabolised O2 is around 4%
6) Nick's OC SAC is 12l/min

Put all that together and you have an inconsistency - Nick is metabolising around 1/2 a litre of O2 when on OC (assuming his SAC is the same when on the surface) but metabolising 1 litre a minute on his RB.

Now. Either something funny (unconcious skip breathing?) is going on when he's diving on OC. Or one of assumptions (1) to (6) is wrong.

1. is wrong. You can not ignore depth on OC.
4. is wrong. On the surface expired air contains .16 to .14 BAR O2. What does it contain at 20m?

You forgot 7.
7. On the surface breathing normoxic air your Haemoglobin is roughly 1/2 saturated. What do you think happens to the Haemoglobin when the inspired PPO reaches about .70?

[ibbo]

good this, i like it but the maths fails. what's your sac if you use 1l o2 at 100m. if you use oc formula that you are trying to you get a different sac at every depth. lol.

[NotDeadYet]

Originally Posted by Janos

4) Every schoolboy knows that the %O2 in expired air is around 16% to 17%
5) This implies that metabolised O2 is around 4%

Doesn't 5 imply that the exhaled gas is binary? Exhaled gas is the same volume of nitrogen, a reduced fraction of O2 and a new volume of CO2. The figure in 5 doesn't seem to account for CO2.

[gobfish1]

im going alpine so i dont give a sh**t

[nigelH]

3 is wrong but 4 is the problem.

Originally Posted by MattS

7. On the surface breathing normoxic air your Haemoglobin is roughly 1/2 saturated. What do you think happens to the Haemoglobin when the inspired PPO reaches about .70?

Huh?
I have a nice HG saturation meter and it matches the readings I get from the big hospital ones quite well.
Instrumentation engineers with heart conditions worry about these sort of things.

I'm currently idling along at 98%

[David Pye]

Originally Posted by Janos

Shtop!
<snip>
4) Every schoolboy knows that the %O2 in expired air is around 16% to 17%

<snip>

Janos

Part of this is because you breathe in essentially dry air, but you exhale a considerable amount of water vapour so you're diluting the oxygen that way, rather than consuming it all.

David

[MattS]

Originally Posted by nigelH

I have a nice HG saturation meter and it matches the readings I get from the big hospital ones quite well.
Instrumentation engineers with heart conditions worry about these sort of things.

I'm currently idling along at 98%

Huh? Let me guess, that is 98% of normal. That or you are very, very ill!

Ok let's try a more expansive answer.

Summary

When you breathe off a rebreather O2 is consumed mainly by metabolism.

When you breathe off O/C, O2 is mainly wasted to the atmosphere and is not consumed by metabolism.

Comparing inspired ppO2 to expired ppO2 only reveals ppO2 diffusion through the lungs during the period of the breath.

O2 consumed during metabolism is transported by Hemoglobin. O2 that is not bound to Hemoglobin is dissolved in blood plasma and is not directly available for metabolism.

You can not ignore depth when using open circuit scuba equipment as haemoglobin saturation is dependant on inspired ppO2, hence dependant on depth. On CCR you can ignore depth as the inspired ppO2 is fixed and so the hemoglobin saturation is constant. CCR surface set points typically cause much higher hemoglobin saturation at the surface than is experienced breathing normoxic air through open circuit scuba equipment.

Hemoglobin provides a buffer between inspired O2 and O2 that is available for metabolism. The capacity of the buffer is dependant on Hemoglobin saturation. Hence the capacity of the buffer is variable on OC and fixed on CCR.

SAC simply is not relevant to metabolism other than by virtue of the act of breathing, which increases metabolic rate and so O2 consumption and CO2 production. CO2 production during metabolism is highly variable and is extremely difficult to calculate instantaneously.


Blood chemistry 101
Blood is a suspension. When it is separated by a centrifuge it forms 3 distinct layers.
1. A straw coloured liquid plasma, ~55%
2. A thin white layer of buff, < 1%
3. The red cells ~45%

Free gas molecules are dissolved in the plasma. The plasma exerts the blood's gas pressure. The free gas molecules carried in plasma are not used directly during metabolism.

The red cells contain hemoglobin molecules. Hemoglobin molecules transport Oxygen molecules that are metabolised directly. Each hemoglobin molecule comprises 4 heme sites. Each heme site allows one O2 molecule to bind to hemoglobin to form oxyhemoglobin. Once an O2 molecule has bound to a heme it is no longer a free gas and exerts no gas pressure.

Each hemoglobin molecule carries up to four Oxygen molecules and it is these molecules which are consumed by metabolism. Oxygen molecules that bind to hemoglobin do not exert a gas pressure, however the partial pressure of Oxygen dissolved in the plasma associates Oxygen molecules to hemoglobin. The higher the partial pressure of Oxygen of arterial blood (PaO2) the more heme sites become occupied by Oxygen molecules (SaO2). The relationship of Oxygen gas pressure to the number of Oxygen molecules which will bind to hemoglobin is described by the Oxygen Disassociation curve.

The oxygen disassociation curve is a very steep S shape with ppO2 on the X axis and % Hemoglobin Saturation on the Y access. The curve shifts left or right depending on health.

Carbon Monoxide poisoning shifts the curve to the right. The CO binds easily to heme sites and a much larger ppO2 is required to bind O2 to the remaining heme sites. Although the volume of CO is relatively small it causes rapid hypoxia as the heme sites are not available for O2 and hence the O2 remains in the plasma and can not be metabolised.

Emphysema shifts the curve left. Emphysema causes a permanent state of hypoxia which eventually alters the hemoglobin causing O2 to bind to heme sites more readily. With the hemes already occupied, acute Oxygen toxicity may occur when Emphysema sufferers inspire gasses with ppO2 as low as ~0.6 bar. The hemoglobin has no capacity to buffer the ppO2 shift, causing the plasma to saturate rapidly, leading to Oxtox by whatever mechanism causes Oxtox when healthy people breathe very high ppOs (typically >2 bar).

The figures in my earlier post were very rough. Commonly a healthy adult breathing normoxic air with a ppO2 of 0.21 Bar is at the bottom of the disassociation curve's slope, with about 20% of heme sites occupied with Oxygen molecules. At the top of the slope the % saturation figure rises to about 80% when the inspired ppO2 is 0.65 bar. The ppO2 of Arterial blood is not quite that of inspired gas as the inspired gas mixes with water vapour in the trachea and CO2 in the alveoli which contribute to the total of partial pressures within the lungs.

We end up with hemoglobin providing a buffer between inspired Oxygen pressure and Oxygen molecules which are available for metabolism. The inspired ppO2 is the pressure exerted by plasma. The Oxygen which is metabolised exerts no pressure. The capacity of the buffer is directly related to the inspired ppO2.

Metabolism 101
Metabolism is the burning (oxidisation) of Oxygen and Hydro Carbons (Sugars) catalysed by Adrenaline, which changes chemical energy to mechanical and heat energy and produces CO2. If it were the fire triangle, Sugar would be the fuel, Adrenaline the heat and CO2 the smoke and ash.

The volume of CO2 produced per O2 molecule consumed during metabolism is known as the respiratory quotient (RQ). The RQ depends on the nature of the fuel. Simple sugars like carbohydrates have RQs of about 1. Fats have lower RQs around .7, proteins .8 - .9 and enzymes (which form and break down protein) high RQs. Net RQ is a function of health, diet and exercise. An adult with a healthy mixed diet at rest has an RQ of roughly 0.8 RQ may rise above 1 during moderate exercise which burns carbohydrates. The process of metabolism itself can cause RQ to rise above 1, such as when carbohydrates are burnt to produce fats.


As best I understand it.

[nigelH]

Originally Posted by MattS

Huh? Let me guess, that is 98% of normal. That or you are very, very ill!

That's the ratio of oxy-hemoglobin to anoxy-hemoglobin.
That is a quite meaningful meaning for saturation in this context.
Jacking the ppO2 up isn't going to put many more mols of O2 in the system because the bulk carrier is fully loaded.

O2 consumed during metabolism is transported by Hemoglobin. O2 that is not bound to Hemoglobin is dissolved in blood plasma and is not directly available for metabolism.

Basic Physics: the red blood cells only transfer oxygen to and from the plasma.
It is the plasma that is fed by the lungs and feeds the tissues.

I'm not going to pick details on the rest or it will get silly.

[Rydive]

Hi, I've read all this with interest, and more than a bit of confusion. I don't dive CCR but can you answer what is probably a very simple question?

It was stated above that PP is irrelevant when considering the amount of O2 that is metabolised. So, if you only metabolise a constant amount of O2 regardless of depth why is ppo2 so important in terms of oxygen toxicity? Is it the effect of pressure forcing more of the gas in to suspension or an inability to use it all causing a build up of O2? I should probably know this, shouldn't I!

Edit: I just read Matt's post again and I think that explains it.