Breathing is Confusing Me

[dlwalke]

As I understand it, the desire to breathe comes from an excess of CO2. Is this free CO2 in the circulatory system? I am trying to understand how depth influences, if at all, the impulse to breathe. At 60 ft, for example, you have a lot more oxygen in your lungs and, presumably, a lot more CO2. But you don't need to breathe any more frequently. Perhaps it is CO2 levels in the blood and maybe this remains constant irrespective of depth, the rate-limiting factor for oxygen uptake into the circulatory system being effort expended. Just trying to figure this out.

Thanks
Dave

 

[GrierHPharmD]

Think in terms of partial pressures. If the partial pressure of the CO2 in your circulatory system is too low to require you to breathe, and the partial pressure of O2 is too low to support consciousness (yes, I know I'm oversimplifying and not discussing hemoglobin, dissociation curves, etc.), then you don't breathe when you body needs to and you pass out and drown. It's called shallow water blackout and it kills freedivers who hyperventilate and supress the urge to take a breath.

Hope that helps,
Grier

 

[Ontario Diver]

It shouldn't be confusing. The urge to breathe is driven by CO2 sensors in your lungs. When there is an "abundance" of CO2 gas, you get the desire to breathe. I do not believe it has much to do with the disolved CO2 in your blood stream.

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

 

[eponym]

Yes, I believe there's a small level of CO2 in your blood and tissues at all times.
From my reading in decompression theory, the normal CO2 levels are roughly 2% of total gasses in lungs, blood, and body tissues.

It's apparently the percentage concentration of CO2 in the lungs that triggers the breathing reflex--at least as far as I understand it. I don't know what the percentage of total gasses CO2 has to exceed to get that response.

-Bryan

 

[eponym]

Oh, note that since the breathing response is triggered by the relative amount of CO2 (percent of total gas), diving's compression of gas in your lungs, resulting in more actual atoms of gasses present, doesn't (as far as I know) affect the mechanism. Pretty smart on the part of our bodies or else diving would be a whole other ball game.

 

[dlwalke]

note that since the breathing response is triggered by the relative amount of CO2 (percent of total gas)...

OK. Well, if that's true, then that is the missing piece of the puzzle that clears things up. Thanks.

 

[miketsp]

Excellent description of process here:
http://www.madsci.com/manu/gas_gas.htm

 

[Laurence Stein DDS]

We talk of CO2 being the driving force stimulating the urge to breathe. If memory serves me correctly, CO2 is carred in the blood as bicarbonate (H2CO3). It is released into the lungs by dissociating into H2O +CO2.

It is not the gas, CO2 in your blood stream. Instead, it is dissolved bicarbonate. Bicarbonate affects the pH of the blood and through chemo-receptors, this pH is monitored by your body and as bicarbonate rises, the pH also changes. The result is the urge to breathe.

There is also a less powerful urge to breathe created by low ppO2.

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.

It is also interesting that the majority of oxygen carried in the blood is NOT in the form of O2. Instead, it is carried by the heme molcule of hemoglobin (oxyhemoglobin). A small amount of oxygen is carried in the plasma as dissolved gas.

Nitrogen is dissolved in body tissue fluids, and plasma and removed by diffusion into the lungs.

I might be wrong about the bicarbonate but I don't think so. Your blood is not the same as a carbonated drink.

Larry Stein

 

[eponym]

It is also interesting that the majority of oxygen carried in the blood is NOT in the form of O2. Instead, it is carried by the heme molcule of hemoglobin (oxyhemoglobin).

Great point, Doctor Larry. Which is why (do I have this right?) carbon monoxide is so poisonous. Hemoglobin binds to CO a hundred times more easily than O2, and holds onto it more tenaciously. The blood ends up without any way to transport oxygen to the tissues.

I might be wrong about the bicarbonate but I don't think so. Your blood is not the same as a carbonated drink.

Well, let's hope so--sounds like a dive gone very very wrong.

-Bryan

 

[GoBlue!]

Some good info here, but quite a bit that I hope I can clarify a bit. Warning that this may get to be a long post. Please let me know if something doesn't sound right & I'll dig up references if need be. Always happy to stand corrected.

First, it's important to note that there are two separate controls of breathing at the brain level...(1) voluntary (this is you attempting to hold your breath, actively think about breathing, etc.) which is controlled by the cerebral cortex; and (2) automatic (the usual daily grind of "breathe in-breathe out" that most of us thankfully don't have to think about) which is controlled by the brainstem (pons/medulla).

I bring this up first, because the extremes of pCO2 rising & pO2 falling ("shallow water blackout") are the products of voluntary breathing (i.e., breath-holding) to the "breaking point" - i.e., when you just can't hold it anymore.

Now, as to the USUAL regulation of breathing. Breathing is controlled by the brainstem, which is influenced by chemical & nonchemical stimuli. Let's just stick w/ the chemical, because that's what we're mostly interested in. 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. This has been shown in studies of carotid chemoreceptor denervation, that essentially abolishes the ventilatory response to pH & pO2, but leaves the response to pCO2 intact (only 30-35% affected). Obviously, pCO2 is influencing other systems...which I'll get to in a second.

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

Now, Larry pointed out that the bicarbonate buffer system is the primary system in the body for dealing with CO2 & attempting to keep pH stable. In short, CO2 + water combined to form bicarbonate (HCO3-) & a hydrogen ion (H+). 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.

To address pO2 briefly.... pO2 can fall to the point of stimulating ventilation, but this usually occurs at a level < 60mmHg, which is quite low (especially at depth!). There is actually increased firing of the chemoreceptors when pO2 falls < 100mmHg, but ventilation is not stimulated until < 60mmHg for reasons that I'd be happy to explain if anyone actually wants more.

Bottom line, however, is that none of this really matters all that much at depth, 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. Since CO2 is so rapidly diffusable, you just blow it off at depth, just as you do on the surface. If CO2 was in your breathing mix, it's a whole different story....in that case, when partial pressure of inhaled CO2 approaches that of the partial pressure of alveolar CO2, elimination becomes difficult & you are left with CO2 blackout. As long as CO2 isn't in your breathing mix, depth should not affect your breathing.

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