Low O2 or High CO2 as trigger for blackout?

You have some odd theory instructors. For sure, black out is normally associated with low O2. Its possible to pass out from excessive hyperventilation causing low co2 which results in restricted coronary arteries, but this is far less common than low 02 related blackouts. No freediver should be hyperventilating near enough to pass out, because of the more likely result of a low 02 blackout because the diver dropped his co2 level so low that he/she ran out of 02 before the rising co2 level triggered a high need to breath.

What certification organization is this school associated with?

This does sound to me as though it's an odd thing for freedive instructors to assert so strongly.
(If I heard this while on a course then I'd be interested to discover their references...)


I'm certainly not a medical expert, but here's my own understanding, from the reading that I've done, of how these things might work...

Blackout happens when the brain doesn't get the oxygen it needs. This is (cerebral) hypoxia. One reason for this, particularly from apnea, would be low O2 in the blood. This is known as hypoxemia, which is not quite the same thing as hypoxia (which is low O2 in body tissues, muscles, brain, etc.)

It is possible to have a reasonable level of O2 in the blood (i.e. not actually be hypoxemic), yet not enough of this blood getting to the brain - for example, due to vasoconstriction (as can happen when hyperventilating a lot), or due to some kind of cardiovascular problem (e.g. the heart not behaving in the right way to send that oxygen-rich blood around the body). So you can then suffer from some form of hypoxia without actually being hypoxemic.


OK, so with that basic terminology and overview out of the way, let's put this into more of the context of apnea & diving...

Freedivers talk a lot about hypoxia while probably actually thinking mostly of low O2 in the blood, i.e. hypoxemia - though that would typically lead to hypoxia, particularly in the context of apnea.

However, there are a couple of other things that don't get mentioned so much by freedivers that happen towards the end of, and for a while after, a strong breathhold. These are:

• reduction in cerebral blood-flow autoregulation (I'll shorten this to just "reduction of CBA")
• brady-arrhythmias (slow, irregular heartbeats)

I've left some links to a few refs at the end of the post (and it's easy to search for more), but here's an overview of these two things:

• CBA is what keeps the blood distributed & flowing evenly around your head/brain, despite rapid changes in blood pressure as the heart beats (diastolic vs systolic), and despite you moving your head around (i.e. inertial forces acting on the blood in the head/brain). An example of what happens when CBA doesn't quite do its job would be that light-headedness you might occasionally feel when you stand up quickly.
• Brady-arrhythmias can happen during and for a while after breathhold and are related to the bradycardia part of the diving response. (You might be aware of feeling such strong slow beats yourself sometimes after a long BH?) But the key thing is that these strong & slow heart beats mean that the blood is flowing even less uniformly than usual, with larger pressure changes.

The result of this combination of brady-arrhythmias along with the reduction in CBA means the danger of light-headedness and even blackout is further increased beyond what you would have just from hypoxemia itself – I suspect these two things may well be among the main reasons that a freediver can blackout even after several seconds of recovery breaths on the surface when you would expect that O2 should already be increasing back to normal.


So what are the causes of reduced CBA and brady-arrhythmias?

• Reduction of CBA can occur as a result of falling O2, both in the blood (i.e. hypoxemia) as well as in various tissues/muscles (i.e. hypoxia). But it is also affected by high CO2 (i.e. hypercapnia) even without that much hypoxemia/hypoxia.
• Bradycardia, which can lead to brady-arrhythmias, often occurs as part of the dive reflex simply from hypercapnia as well as from hypoxia/hypoxemia - though even more from both together. Brady-arrhythmias can be even stronger from dynamic apnea due to the tension between the dive response that wants to slow cardiac rate/output vs the use of muscles (finning/swimming) that wants to increase it. (This is a conflict between the sympathetic and parasympathetic nervous systems.)

Consequently, I think reduced CBA plus brady-arrhythmias do mean there could be an increase in the potential for BO from high CO2 by itself, without O2 being that low in the blood (i.e. being hypercapnic without being hypoxemic). Furthermore, I suspect the reduced CBA could mean that the rapid change in ambient pressure while ascending from depth might more easily lead to blood-flow problems in the brain.


However, as mentioned at the beginning, I think this all still fundamentally comes down to a lack of O2 supplied to the brain, i.e. cerebral hypoxia - it's just that the reason for this hypoxia isn't purely from being hypoxemic.

In conclusion, then, it seems like a surfacing freediver is subjected to the 'perfect storm' of potential hypoxemia, hypercapnia, reduced CBA, plus fluctuating blood-flow/pressure from arrhythmias and rapid pressure changes. Together these increase the chance that the probably already somewhat hypoxemic blood (esp. from rapid drop in partial pressure of O2 in the lungs lowering its diffusion into the blood) will not reach some critical part of the brain, causing cerebral hypoxia, and potentially leading to blackout.

Hopefully that makes sense!
(Maybe someone with a proper medical background in these kinds of areas can verify that my understanding of this is reasonably correct...)


Check out these refs to find out more about CBA (second one below is particularly related to apnea):

For information about brady-arrhythmias from apnea, see the following:

Leander said:

After many years in the water I finally decided to get the certifications as nearby a freediving school opened.

In theory class today, I was told that the blackout and samba are part of the body's response to high CO2 levels and have little to do with the level of O2, just like the urge to breathe and contractions.

I asked for more clarification but it still confuses me; it would be like a car with a full tank but a faulty fuel gauge stalling because the dial says 'out of fuel'.

Can anyone explain this to me?

Click to expand...

Didn't see the earlier posts, this just repeats them:
I learned that the blackout occurs because of low O2. The low O2 can happen because the breathing urge is triggered by CO2 and is apparently not much linked to low O2, if at all. If you hyperventilate, you purge CO2 much more than you boost O2 (which is usually already close to 100% saturation), so you blackout from low O2 before CO2 levels cause the breathing urge to kick in, or because you force yourself to resist it. Can't say about the spasms, but it seems to fit that they are also CO2 driven.

Just to add to what I wrote above about arrhythmias & BOs, here's a fascinating case study I came across showing variations in heart-rate during STA for four competitors. Three of them completed theirs successfully, whilst the fourth showed an unusual cardiac arrhythmia, and subsequently blacked out after a little over 5mins:

Case Studies in Physiology: Is blackout in breath-hold diving related to cardiac arrhythmias?​

What makes it really interesting is that the arrhythmia develops after only ~2.5mins into the STA - and I'd assume he would still have a decent level of O2 in the blood by then (i.e. not yet hypoxemic). But I do wish they'd also shown a plot of spO2 during the apnea itself (rather than giving only the lowest value, presumably just after end of apnea, as often happens during recovery), so we could tell blood O2 levels at the different stages...

One other thing they mention, which I'd not considered before, was the potential role of contractions (or IBMs, as they call them -"involuntary breathing movements") in causing sudden changes in intrathoracic pressure, which can subsequently produce yet more beat-to-beat variation in heart-rate. -So maybe add that to the list of things that a freediver's cardiovascular system has to cope with near/at the end of a dive!

I think it shows there's still some decent research could be done to create a clearer link between heart-rate variations (esp. arrhythmias), contractions (IBMs), impaired cerebral autoregulation, levels of blood gases (both CO2 & O2), and blackouts/LMCs during and after apnea - as well as that the situation can be a touch more nuanced than simply "running low on O2"...

adrian.u said:

Just to add to what I wrote above about arrhythmias & BOs, here's a fascinating case study I came across showing variations in heart-rate during STA for four competitors. Three of them completed theirs successfully, whilst the fourth showed an unusual cardiac arrhythmia, and subsequently blacked out after a little over 5mins:

Case Studies in Physiology: Is blackout in breath-hold diving related to cardiac arrhythmias?​

https://journals.physiology.org/doi/full/10.1152/japplphysiol.00708.2022

What makes it really interesting is that the arrhythmia develops after only ~2.5mins into the STA - and I'd assume he would still have a decent level of O2 in the blood by then (i.e. not yet hypoxemic). But I do wish they'd also shown a plot of spO2 during the apnea itself (rather than giving only the lowest value, presumably just after end of apnea, as often happens during recovery), so we could tell blood O2 levels at the different stages...

One other thing they mention, which I'd not considered before, was the potential role of contractions (or IBMs, as they call them -"involuntary breathing movements") in causing sudden changes in intrathoracic pressure, which can subsequently produce yet more beat-to-beat variation in heart-rate. -So maybe add that to the list of things that a freediver's cardiovascular system has to cope with near/at the end of a dive!

I think it shows there's still some decent research could be done to create a clearer link between heart-rate variations (esp. arrhythmias), contractions (IBMs), impaired cerebral autoregulation, levels of blood gases (both CO2 & O2), and blackouts/LMCs during and after apnea - as well as that the situation can be a touch more nuanced than simply "running low on O2"...

Click to expand...

Thanks Adrian, the subject has indeed much more "nuance" than I had any idea of.

To add a bit of nuance to the discussion:

Black out is directly caused by not enough O2 in the brain. It can be brought on by extremely low co2 levels ( extreme hyperventilation) causing the carotid arteries to contract so much that blood flow(and 02) to the brain is almost cut off. I suspect this is what Leanders instructor is reffering too. It is caused much more commonly by a generally low 02 level causing low 02 in the brain, despite the body trying to adapt (bohr shift, expanding carotid arteries,etc). If the instructor does not know that, find another instructor.

Blackout are not always without warning, just often enough that we should treat them as ALL having no warning. I know many divers that have expereinced seeing stars, losing color vision and other symptoms of low 02 in the brain(me included). Thats spitting distance from BO and the only reason(probably) that we remember is the fact that we got some 02 into the brain before we could BO. A really knowledgable instructor will know that.

One thing I have found to be a real problem in freediving instruction is belief in the infalability of "received knowledge." Some instructors, especially those with limited backgrounds, incorrectly believe that they have received perfect knowledge from their instructors, that what they have been taught is THE WAY. It even afflict some very good instructors. It leads to harmless errors like telling a coffee addict (me) that he must immediately stop caffiene during the course if he wants to maximize his technique or that all blackouts have no warning, to dangerous stupidity like teaching hyperventilation as a safe technique to extend breath hold (I once read an early PADI publication that actually taught this. That has long since changed, of course)

Short and simple non-medical explanation: you can feel the high CO2, but it's the low O2 which causes the blackout. From the start of your dive your CO2 levels will increase and your O2 levels will decrease. Hyperventilating, i.e., reducing the starting point of CO2 so that it is only high enough to feel later in the dive, is problematic because you can feel fine but have low O2, and so you can black out without any warning.

It's worth remembering that your blood will typically be close to 100% saturated at any given time, so there is little you can do to increase your O2 level at the start of the dive. The breathe-up is (usually) more about relaxing so that your O2 consumption is lower.

There are some relevant nuances about depth, but I'll leave it at that for now. Any questions, please feel free to ask.