Title: Re: Went to NP today
Post by Batch on Feb 5th, 2012 at 3:17pm
Hey BB,
Sorry for the delay in responding… You're correct. We all have equal billing here at CH.com when it comes to helping fellow CH'ers in need. Please forgive my comments about your oxygen system if they came across like a turd in a punch bowl… Poor choice of wording on my part… must have been a senior moment… My comments were not intended as a put down to the way you use oxygen therapy… I know it works for you or you wouldn't have made the post.
As old hands living with CH, we all want the same thing… to help fellow CH'ers in need find the best and most effective methods of controlling their CH… It's hard enough to get CH'ers to try oxygen therapy so the last thing we want to do is confuse them.
The focus of my comments on the flexible breathing tube is based on the results of the pilot study of oxygen therapy with hyperventilation that Michael Berger, a.k.a. "Wildhaus" and I conducted in 2008 with assistance from Royce Fishman and the folks at LifeGas.
During that study, we collected data on over 600 aborts with oxygen therapy, 366 of them at oxygen flow rates that support hyperventilation. The results were amazing. All 7 participants were able to use this method of oxygen therapy effectively with either an oxygen demand valve or a 0-60 liter/minute InGage™ oxygen regulator made by Flotec and O2PTIMASK™ kit. There were no adverse events…
The overall efficacy of this method of oxygen therapy was 95% with an average abort time of 8 minutes across CH pain levels 6 through 9 on the 10-Point Headache Pain Scale. The relationship between average abort time and CH pain level was also linear with higher pain levels having longer abort times. For example, a CH at pain level-3 aborted in an average of 4 minutes and a CH at pain level-9 aborted in an average of 11 minutes with this method of oxygen therapy…
Out of 366 logged attempts to abort a CH with this method of oxygen therapy, 364 met the success criteria of 25 minutes or less to abort. Two had a starting pain level of 10 and both attempts ended at 30 minutes with an imitrex injection. In both cases the study subject was trapped away from oxygen therapy equipment for several minuets after the CH began and was unable to start this method of oxygen therapy until the pain had already reached level-10.
We included these two failures in the overall efficacy of this method of oxygen therapy using the "Crap Happens" principle just to make the point that it's essential to start any method oxygen therapy as early as possible… preferably at the first indication of an impending CH.
In short, the longer you wait before starting oxygen therapy, the higher the pain will climb, and that means longer abort times with any method of oxygen therapy. If a CH reaches pain level 9 to 10, you're in for some heavy sledding and you're just along for the ride… Even an imitrex injection is going to take longer to take effect.
I should point out that the abort times used in this study were measured to a pain free state and that the pain levels recorded were the maximum encountered during each session using this method of oxygen therapy. The pain level at start of therapy was up to one pain level less in some cases.
What was equally amazing is this method of oxygen therapy produced aborts in less than a third the time of aborts with oxygen therapy at a flow rate of 15 liters/minute at each pain level… Overall, aborts using a flow rate of 15 liters/minute averaged 30 minutes to an abort across pain levels 6 through 9…
In the process of preparing the protocol and procedures for this study, we sorted through hundreds of clinical studies related to oxygen therapy at various flow rates, respiratory physiology, side effects, safety and the physiological effects of carbon dioxide and oxygen as well as their role in controlling vasoactivity…
Some of the best information, with respect to improving the efficacy of oxygen therapy to abort CH, came from studies of the cerebral vascular response to a reduction in the concentration of arterial carbon dioxide. In the end, we collected a lot of information from these studies and in particular from the two I'll discuss below.
We used this same information in preparing the patent we submitted to the USPTO in June of 2008, for the Demand Valve Method Of Oxygen Therapy For Rapid Aborts Of Cluster Headache. I ran our evidence of proof section by a senior Navy Flight Surgeon and an Aviation Physiologist at the Naval Aerospace Medical Institute… It got an up-check from both of them, and so far, I'm not aware of any challenge filed against this patent since the USPTO published it in Jan 2010.
Getting back to my original comments… The End Tidal CO2 (ETCO2) is the partial pressure or maximum concentration of carbon dioxide (CO2) at the end of an exhaled breath. It's usually expressed as a percentage of CO2 or mmHg. The normal values at normal respiration rates and tidal volumes are 5% to 6% CO2, which is equivalent to 35-45 mmHg.
I estimated the volume of dead space in the 22 mm flexible breathing tube, mouthpiece and O2PTIMASK™ manifold at 116 cc. At 6% ETCO2, that works out to 7 cc of CO2. Divide the 7 cc CO2 by the 3 liters, (3000 cc) of oxygen from the O2PTIMASK™ reservoir bag if it's fully inflated and totally collapsed at the end of the inhalation cycle, and you end up with 0.2% of the inhaled mix being CO2.
However, at a flow rate of 15 liters/minute, the O2PTIMASK™ reservoir bag rarely fully inflates between breaths so the volume of oxygen inhaled with each breath is roughly 1.5 liters making the CO2 concentration around 0.4% of the inhaled mix. In either case, that may not sound like much CO2…
Unfortunately, the insidious part of all this is the CO2 from the dead space in the flexible breathing tube prevents a complete release of CO2 from the lungs due to the decreased concentration differential. This means the arterial blood flowing from the lungs carries a higher concentration of CO2 and repeated inhalation of this mix eventually comes back full cycle to the lungs as higher concentrations of CO2 in the venous blood. This cycle can easily increase the arterial concentration of CO2 with each breath.
Moreover, CO2 takes the form of carbonic acid (H2CO3) when dissolved in blood. When there's a higher concentration of arterial CO2 than normal, the condition is called hypercapnia and the arterial blood becomes more acidic with a resulting decrease in arterial pH.
If you follow the accepted findings that the cluster headache syndrome includes a rapid dilation of the cerebrovascular structures in and around the trigeminal nerve, and you couple that with the accepted fact that a depressed arterial pH triggers vasodilation, the slightest increase of arterial CO2 concentration will trigger a greater level of vasodilation that counteracts and overrides the vasoconstrictive properties of the oxygen we use to abort our CH.
In short, inhaling even a little CO2 during oxygen therapy can impact the effectiveness of oxygen as a CH abortive.
I'd also like to point out that this condition can and will occur if lung ventilation is restricted by low oxygen flow rates up to and including 15 liters/minute when using a non-rebreathing oxygen mask that prevents room air from entering during inhalation. The problem is further compounded if there's any physical activity above remaining motionless as this generates more CO2. Rocking back and forth in a fetal position or doing the cluster two-step around the oxygen cylinder only serve to increase the metabolic rate at which the body produces CO2.
This problem gets worse as the pain level rises and the level of physical activity increases. We also found from our study that the relationship between abort times and pain levels was nearly linear… In short, the higher the pain level, the longer it took to abort with either method of oxygen therapy… except there were several instances where an oxygen flow rate of 15 liters/minute took well over 30 minutes to abort an attack.
This is exactly why we suggest the most effective method of oxygen therapy that results in greatest efficacy and shortest abort times, involves the use of oxygen flow rates that support hyperventilation… 25 to 40 liters/minute if you want to hang numbers on the required flow rates…
As the increased lung ventilation during hyperventilation casts off CO2 faster than the body generates it through normal metabolism, this condition is called hypocapnia. Moreover, as the concentration of CO2 in the arterial blood is lower than normal during extended periods of hyperventilation, there's less acid so the arterial pH is higher and more alkaline… hence the term respiratory alkalosis.
The important thing to remember here is hypercapnia (an elevated CO2 concentration above normal), induces cerebral vasodilation with increased cerebral blood flow (CBF) and velocity. This tends to make a CH last longer and more painful, where hypocapnia, (lower than normal CO2 concentrations), induces cerebral vasoconstriction that decreases CBF resulting in less painful CH of shorter duration and frequency. It also results more rapid aborts when accomplished with 100% oxygen.
Hint… vasoconstriction is one of the CH abortive mechanisms achieved when taking sumatriptan succinate (imitrex) or one of the other triptans. The big difference is this method of oxygen therapy accomplishes the same vasoconstriction with its abortive effect on CH without the high cost or risks associated with repeated doses of sumatriptan succinate.
The following set of images and table from two different studies graphically illustrate the above discussion why we want to avoid breathing any CO2 during oxygen therapy and more importantly, why we want to keep CO2 levels below normal by hyperventilating with 100% oxygen to abort our CH more reliably and as fast as possible.
The first set of images comes from an article by Hiroshi Ito, et al, published in the Journal of Cerebral Blood Flow & Metabolism titled: Changes in Human Cerebral Blood Flow and Cerebral Blood Volume During Hypercapnia and Hypocapnia Measured by Positron Emission Tomography.
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During this study they employed a PET imaging technique that uses colors to display and measure the rate of microvascular cerebral blood flow (CBF) and cerebral blood volume (CBV).
The three respiratory conditions measured during this study included: Baseline - breathing air, Hypercapnia - breathing a mixture of oxygen with 4% CO2, and Hypocapnia - hyperventilating for one minute to cast off more CO2 than normal.
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The red color in the CBF column, top image titled "Baseline" illustrates a normal velocity arterial CBF when breathing air. The second set of images titled "Hypercapnia" (higher than normal level of arterial CO2) illustrates increased regions of higher CBF during hypercapnia brought about by breathing oxygen with 4% CO2. As you can see from the increase in regions of red, hypercapnia results in increased vasodilation throughout the brain.
The lower set of images titled "Hypocapnia" (lower than normal level of arterial CO2) illustrate a significant decrease in CBF throughout the brain indicating vasoconstriction due to hypocapnia brought about by hyperventilation for one minute. CBV remained relatively constant for all three cases.
The following table comes from a similar study by J.M. Clark et al, published in the Journal of Cerebral Blood Flow & Metabolism in 1996 titled: Relationship of 133Xe Cerebral Blood Flow to Middle Cerebral Arterial Flow Velocity in Men at Rest.
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During this study they measured cerebral blood flow with Xenon-133, a synthetic isotope of Xenon and radionuclide with a half-life of 5 days. They measured blood flow velocity with Transcranial Doppler (ultrasound). Throughout the study they collected data on arterial oxygenation, acid-base state, and hemodynamic responses as test subjects breathed air, 100% oxygen, a mixture of oxygen with 4% CO2, a mixture of oxygen with 6% CO2, and finally, hyperventilating with 100% oxygen. The following table illustrates the results:
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I've circled the 2nd and 3rd row test conditions for breathing 100% O2 and O2/4% CO2 in red and the 5th test condition, O2 with hyperventilation, in green. I've also linked these two test conditions with their corresponding hemodynamic response in the lower half of this chart.
Take a look at the 2nd and 3rd row from the top and the changes that take place when CO2 is inhaled with the oxygen. The partial pressure of CO2 (PCO2) goes up and arterial pH drops, yet the partial pressure of arterial O2, (PO2) remains essentially the same…
Now look at the corresponding hemodynamic response to the addition of CO2 to the inhaled oxygen in the lower second half of the chart. You'll notice that as the PCO2 increases and the arterial pH drops indicating a higher acid content, the velocity of blood flowing through the middle cerebral artery (MCA) increases and the CBF jumps nearly 30% from 32.1 to 42.3 ml/100g/minute.
This is a clear indication of vasodilation. To a CH'er hoping for an abort of a CH with oxygen therapy… this means… fat chance! This is a no-brainer… No abort for this CH'er under these conditions if he inhales that volume of CO2 during oxygen therapy…
If the CO2 content is much less during oxygen inhalation therapy at the lower flow rates, the pain level is low, and the CH'er remains motionless, he might just get an abort, but it will take much longer
Now let's take a look at the 5th and final test condition where the subjects intentionally hyperventilated with 100% oxygen… The first thing to note is the 30% drop in PCO2 from 38.5 mmHg to 27.2 mmHg. This is a clear indication the test subjects were casting off CO2 faster than it was being generating through normal metabolism…
This drop in PCO2 means less carbonic acid in the blood so the arterial pH climbs from 7.432 while breathing O2 at normal respiration rates to a pH of 7.584 when hyperventilating with 100% oxygen. This makes the arterial blood more alkaline – hence the condition called respiratory alkalosis…
What's even more impressive is the PO2 jumps from 570.8 mmHg while breathing 100% oxygen at a normal respiration rate to 585.8 mmHg when hyperventilating with 100% oxygen. In short, during this test condition while hyperventilating on 100% oxygen, the test subjects were super-oxygenating the arterial blood flow to their brain.
As 100% oxygen acts as a CH abortive through vasoconstriction, sending more oxygen to the brain by hyperventilating actually increases vasoconstriction to produce a more rapid CH abortive effect… and that's exactly what happens…
If you compare the relative hemodynamic responses between breathing 100% oxygen at a normal respiration rate and breathing 100% oxygen with hyperventilation, you'll see the velocity of blood passing through the MCA decreases by over 26% from 58 cm/sec down to 42.8 cm/sec and the volume of CBF decreases by over 15% from 31.1 ml/100g/minute down to 27.2 ml/100g/minute... That is a clear indication of increased vasoconstriction.
I realize this is a tedious and protracted explanation of the rationale I used in my initial comment on the use of the flexible breathing extension tube with an O2PTIMASK™ as being " the wrong way to go for effective oxygen therapy…" but there you have it.
This missive also provides the medical evidence and respiratory physiology supporting the statement that oxygen therapy with hyperventilation is safe, effective, and superior to oxygen therapy at normal respiration rates with greater efficacy and shorter abort times…
Now for the $64,000 question some CH'ers may be thinking... as asked by Sir Laurence Olivier in the 1976 film classic Marathon Man, as he drills holes Dustin Hoffman's teeth without anesthesia... Is it safe?
The simple answer is yes... You bet… Very safe… It's far safer in fact than repeated doses of sumatriptan succinate (imitrex) or any of the other triptans. Moreover, unlike the triptans, you can use oxygen therapy as many times a day or night as needed without fear of overuse.
Hope this helps.
Take care,
V/R, Batch
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