Breathing is Confusing Me

[Seabear70]

What I do not get is that in certain circumstances, or so I'm told, due to decresed CO2 levels you will stop breathing (I have seen that part repeatedly) but at the same time your O2 levels can drop to lethal levels.

 

[Laurence Stein DDS]

Go Gators! :11:

Oops, Hi Jim,

Good explanation. The last time I took any real physiology was 30 years ago...at least I can still remember some of it...just not all of it.

OK, a little curiosity question here. When referring to ppO2 or ppCO2, are the partial pressures referring ONLY to the respective gases dissolved in the mediums OR is this an "averaging" statement meaning both the real pp of the respective gases and the "equivalent" pp of those gases as carried by the transporting agent like hemoglobin for O2 or bicarbonate for CO2? Damn, that question even confused me!

Er...what I'm having a hard time saying is pp refers to the pressure of one gas of a mixture of gases. O2 bound to hemoglobin is not really a gas. The same for CO2. There is the ppCO2 of the dissolved gas in the plasma but there is also bicarbonate which is transporting components of the CO2 in a non-gasious form...later to be released in a gasious form into the lungs for removal.

So....is the pp notation one of convention and convience for the total gas loads or does it only refer to the true dissolved gas?

There, I said it!

Thanks for your great previous reply.

Larry Stein

 

[Laurence Stein DDS]

What I do not get is that in certain circumstances, or so I'm told, due to decresed CO2 levels you will stop breathing (I have seen that part repeatedly) but at the same time your O2 levels can drop to lethal levels.

Hi Seabear,

This is the shallow water blackout scenerio again.

I'm gonna make up some number now...just to help think.

Suppose a person will black out whenever the partial pressure of oxygen is, say, 50. Now suppose you are doing a breath hold dive to 33 fsw and have managed to overcome you urge to breathe due to CO2 drive OR as you believe you have read, you HYPERVENTILATED prior to this dive and "blew off" extra CO2. This has the effect of reducing your CO2 drive because you haven't reached that threshold that would make you "want" to take a breath.

At 33 feet the ambient pressure is double the surface pressure. If your ppO2 is let's say 80 at depth and you then surface, somewhere before you reach the surface, the ppO2 falls below the magical number of 50 and you black out....see...easy.

Hope that helped.

Larry Stein

 

[Ryukyu-diver]

What you are seeing here is when someone purges themselve (hyperventilates) of the CO2 prior to doing a breath hold dive. The CO2 is the primary stimulus to ventilation, and since the diver has chosen to rid his/her body of it: by the time that the diver has built up enought CO2 during the dive, the O2 has been depleted and this leads to shallow water black out.

 

[Sideband]

This is why you need to take full breaths, to totally flush out all of the CO2 in your lungs.

It isn't your lungs so much that the deep breaths are clearing. It is the dead air spaces, i.e. your regulator or snorkle and the air passages leading to the lungs. If you breath shallow then you are exhaling stale air into these dead air spaces then pulling it right back in on the next shallow breath with very little fresh air. Long slow breaths will maximize the amount of fresh air reaching the lungs on each breath.

Joe

 

[Ryukyu-diver]

Good input Sideband, but I have took it a bit farther by telling most of my friends to exhale as much as possible in order to rid the CO2 in all of the dead air spaces. OBTW, no need to worry about lung collaspe because the surfactant will prevent this from happening.

 

[GoBlue!]

So....is the pp notation one of convention and convience for the total gas loads or does it only refer to the true dissolved gas?

pCO2, pO2, etc. only refers to the dissolved portion; it does not take any of the bound (or buffered) gases into account. In fact, blood gas analyzers will use the concept to give you a calculated bicarbonate value (they measure pCO2 & pH, and calculate HCO3- using the Henderson-Hasselbach equation).

Jim

 

[eponym]

Great post, Jim--thanks for the detail, and for the corrections.

Interestingly, the carotid & aortic chemoreceptors are NOT affected by anemia, as the blood flow to these receptors is so incredibly large they actually get all their oxygen needs from the dissolved oxygen in the blood; they don't rely on hemoglobin-bound oxygen at all, and therefore don't respond to it.

Don't you just love those sublime engineering solutions we carry around with us. They work so well we don't even have to know they're there.

Go Darwinians!

 

[Mako Mark]

Either drive to breathe can be partially overcome with practice. This is one way free divers can stay down longer. Unfortunately, learning to ignore the urge to breathe imparts no immunity to passing out due to low ppO2. This is the reason for "shallow water blackout" The diver resists the urge to breath at depth and upon ascending, the lower ambient pressure results in a ppO2 that cannot sustain consciousness.

here is a diagram I use to explain this process.

 

[Mako Mark]

Now, as to the USUAL regulation of breathing. Breathing is controlled by the brainstem, The chemical signals that lead to increased ventilation are: (1) rise in blood pCO2 (this is the DISSOLVED CO2 in the blood stream); (2) rise in blood or CSF H+ concentration (i.e., reduced pH); and (3) reduction in blood pO2 (dissolved O2).

Blood pH, pCO2, and pO2 are sensed by clusters of cells at the branching of the carotid arteries & at the root of the aorta. The primary overall driving force is the dissolved CO2 in the blood.

OK got it, CO2 is sensed by the brainstem not the lungs and disolved CO2 is the driving force in involuntary breathing

Bicarbonate, however, has no impact on ventilatory drive. Hydrogen ion does have some impact on the chemoreceptors, but this is actually separate from the effect of dissolved pCO2.

Dissolved pCO2 can rapidly cross the blood-brain barrier, diffusing into the interstitial fluid of the brain & the cerebrospinal fluid (CSF). H+ & HCO3- in the blood, however, cannot cross this barrier. pCO2 in the CSF then combines with water once again, and it is the resultant new H+ ion formed that has a profound effect on the medullary chemoreceptors. In fact, in experimental models where the pCO2 of the CSF was varied while holding H+ constant, there was little effect on ventilation. Any change of the H+ concentration, however, profoundly affected ventilatory drive.
Jim

Woah, Im getting speed wobbles here, this seems to contradict the first bit. Let me get this straight, it is not the levels of bicarbonate nor the levels of pCO2 disolved in the bloodstream, rather the creation of bicarbonate in the CSF, realeasing a free hydrogen ion that the receptors respond to.
.

[ since CO2 is simply the metabolic waste product of aerobic metabolism; so, your production of CO2 at depth is the same as it would be on the surface should you do the same amount of work.

so as blood CO2 is disolved and is measured as gas tension rather than partial pressure, there is no effect on it due to changing ambient pressure except at the change of gas phase on the blood/alviolar boundary because of the effects on the difuusion gas gradient.

And you body makes it at the same rate anyhow..

So, corrections (as I see them) to the previous posts are: (1) there aren't "CO2 sensors" in the lungs; (2) the "relative" amount of CO2 doesn't matter; (3) while the majority of CO2 is actually circulated in the form of bicarbonate, it is actually dissolved CO2 (& hydrogen ion) that have the impact on ventilation.

Jim

Thanks Jim and Laurence, this is the first time in my diving career, that anyone has been able to explain the bicarbonate process in real terms. It makes me wish I hadnt dropped out of biochem.

(note to self: remember you dropped out of biochem because of Krebs citric acid cycle. Damn you Kreb, Damn you)