Hey Kevin,

You're correct, the body and brain do have homeostatic mechanisms that control vasoactivity, respiration rate, heartbeat, and arterial pH.  However, it's carbon dioxide (CO2) levels and not oxygen (O2) levels that acts as the primary stimulus for these homeostatic mechanisms. 

For example, if you do jumping jacks for 30 seconds or climb a couple flights of stairs at a fast pace, you start breathing faster and your heart also starts beating faster.  What you can't see is your arteries dilate as well.  All this happens due to the build up of CO2 in the venous and arterial blood as a result of the increased physical activity. 

As CO2 takes the form of carbonic acid in the blood, this increase in acidity results in a lower pH. There's also a build up of lactic acid that's generated when muscle tissue is stressed without enough oxygen. (If you're a jock, you know this is called anaerobic glycolysis.)  This build up in lactic acid drops the pH of the venous and arterial blood even further.

When the chemo sensors in the brain detect an elevation in CO2 levels and drop in arterial pH, an acid-base homeostatic mechanism kicks in and the brain signals the heart to beat faster, the lungs to breath faster and the arteries to dilate.  It does all this to pump more blood to the lungs where the excess carbonic acid can be cast off or downloaded from blood hemoglobin as CO2 and oxygen in uploaded. 

This increased respiration rate and heartbeat will continue until the excess CO2 is cast off to allow CO2 levels to fall back in the normal range and the arterial pH to rise back into the normal range.  At that point the brain signals the heart to slow to a normal rhythm and respiration to slow to a normal rate.  It also signals the dilated arteries to constrict back to a normal lumen (diameter).

Understanding this acid-base homeostatic mechanism and knowing that it works in both directions to maintain an acid-base balance in an arterial pH range of 7.35 to 7.45 is the key to understanding how to use oxygen therapy more effectively and why higher flow rates that support hyperventilation are needed.

When we breathe 100% oxygen at normal respiration rates, we elevate the partial pressure of oxygen in the blood above normal.  This is defined as hyperoxia and this condition is a component of the cluster headache abort mechanism with oxygen therapy. 

The exact mechanism(s) remain(s) unclear, but hyperoxia from breathing 100% oxygen stimulates vasoconstriction and as vasodilation is part of the pathophysiology of the cluster headache, stimulating vasoconstriction helps stop the pain and abort the cluster headache.  This leaves us with the following physiological equation:

   hyperoxia = vasodilation = CH abort

Now here's where CO2 levels play a role in the cluster headache abort mechanism during oxygen therapy.  We already know from the discussion above on acid-base homeostasis that an increase in carbonic acid (CO2) levels in the blood stream above normal (hypercapnia) will trigger vasodilation. 

It also turns out that when carbonic acid (CO2) levels in the blood stream drop below normal (hypocapnia), acid-base homeostasis kicks in to trigger a decrease in heartbeat, a slowing of the respiration rate and vasoconstriction.  This is done to slow the loss of carbonic acid (CO2) from the lungs and allow it to build back up to normal levels. 

That means if we can lower the carbonic acid (CO2) levels in the blood stream below normal (hypocapnia), we can stimulate vasoconstriction. 

How do we do this?  Simple...  We intentionally hyperventilate long enough to raise arterial pH above the normal range of 7.35 - 7.45.  This results in respiratory alkalosis.

That leaves us with the following physiological equations with respect to oxygen therapy at flow rates that support hyperventilation:

If
  hyperoxia = vasoconstriction
and
  hypocapnia = vasoconstriction
then 
  hyperoxia + hypocapnia = greater vasoconstriction = faster CH abort

Now here is where things can get complicated.  From the study that Ricardo cited where they added 5% CO2 to the oxygen breathed by the children, they observed no vasoconstriction.  That leaves us with the following physiological equation with respect to the relative vasoactive strengths of hyperoxia and hypercapnia:

  hypercapnia > hyperoxia

In other words, excess carbon dioxide in the bloodstream is a more powerful vasodilator than excess oxygen is as a vasoconstrictor.

Let's see how that plays out when we're trying to abort a cluster headache with oxygen therapy...

If we breath 100% oxygen at a flow rate of 15 liters/minute and remain motionless with a low level of physical activity, we should be able to bring about an abort of the cluster headache as long an the cluster headache pain is low enough to allow us to remain at a low level of physical activity.

However, if the cluster headache pain starts us rocking back and forth or dancing in circles and the level of lung ventilation provided by an oxygen flow rate of 15 liters/minute is insufficient to cast off the excess CO2 resulting from the increased physical activity, an abort with oxygen therapy may not be possible or it will take much longer than normal.  That leaves us with the following physiological equation:

   hyperoxia + hypercapnia = vasodilation ≠ CH abort

This is why we say that oxygen therapy at flow rates that support hyperventilation is more effective with shorter abort times than oxygen therapy at flow rates ≤15 liters/minute.

This discussion assumes that through the act of intentionally hyperventilating with 100% oxygen, we are able to bias the acid-base homeostasis mechanism to achieve a greater level of vasoconstriction regardless of the level of physical activity and this will result in a fast abort of the cluster headache pain and triggering mechanism. 

Is this the only mechanism in play?  No.

Another related mechanism occurs when we hyperventilate with 100% oxygen.  It's called the Bohr effect.  Under normal conditions when the blood pH is low as it is in the body and brain tissues, hemoglobin offloads oxygen and uploads carbon dioxide.  When the blood pH is high as it is in the lungs, hemoglobin offloads carbon dioxide and uploads oxygen.  This is the normal oxygen and carbon dioxide transport mechanism between the body and lungs.

However when we artificially elevate arterial pH in the lungs even further through the act of intentionally hyperventilating with 100% oxygen, hemoglobin increases its affinity for oxygen and uploads more oxygen than normal.  This results in a super-oxygenated flow of blood to the brain greater than the hyperoxia from breathing 100% oxygen at normal respiration rates and that results in an increased level of vasoconstriction.

Clearly, there are other mechanisms involved in the cluster headache abort process with oxygen therapy and that's what Ricardo wants to learn.  That leads us to a possible question as to which is the predominant mechanism in play, acid-base homeostasis, or a cocktail of hormones, enzymes, and chemical messengers triggered by hyperoxia?

I don't know...  The neurochemistry involved is well above my pay-grade. 

What I do know from personal experience, and from the results of an informal pilot study we conducted with 7 other participants, is that oxygen therapy at flow rates that support hyperventilation is far superior with greater efficacy as a cluster headache abortive than is possible with oxygen therapy at a flow rate of ≤15 liters/minute.  Moreover this method of oxygen therapy has significantly shorter abort times.

Take care,

V/R, Batch