Chris,
Aviation experts and concerned pilots recognized the problem of hypoxia as early as 1917 when advances in aircraft engines pushed aircraft operating ceilings well above 10,000 feet. The first use of supplemental oxygen by pilots occurred about that time. It involved heavy iron cylinders filled with compressed oxygen and the method of delivery was a simple cylinder valve connected to a rubber tube fitted with a pipe stem the pilot held between his teeth.
A lot of innovative advances followed in short order after that most notably with the advent of the oxygen mask with inhalation and exhalation check valves. However, all of the early oxygen masks were fed from constant flow regulators until 1942 when Navy and Army Air Corp aircraft were fitted with demand type oxygen regulators.
I’ve done some research on history of the oxygen demand valve regulators you might find interesting. The Auer Company developed the first demand type oxygen regulator in Germany in 1936.
Coincidently, The first documented use of oxygen as an abortive for severe "migraine" attacks (read cluster headaches) as they were originally diagnosed, dates back to 1939 with work done by the Linde Air Products Co and the Mayo Clinic in Rochester, MN. Yes, the Linde Air Products was a spinoff from the Linde Co in Germany and it’s known today as Linde LifeGas.
By 1941, the US observers had had ample opportunity to recover functioning examples of the new German Demand oxygen breathing regulators and masks from downed Luftwaffe aircraft.
The apparent advantages the German system offered over the older continuous flow systems were immediately evident and the captured technology was quickly removed to the Wright Aeromedical and Engineering Labs for analysis in June of 1941. By 1942 most US Navy, Marine Corps and Army Air Corps aviators were using derivations of the German design.
There were always a few cases over the years since then when idiots eager to exit the gene pool neglected to wear their oxygen masks when flying above 10,000 feet, but the initial requirements for supplemental oxygen were well established by 1920.
OPNAVINST 3710, also known as the Naval Air Training and Operating Procedure Standardization (NATOPS) Program that mandates the use of oxygen from takeoff to landing went into effect in 1964. It superseded the Navy’s Bureau of Aeronautics instruction that dated back to 1917 and essentially stated the same requirement for supplemental oxygen on all flights above 10,000.
The use of diluter demand oxygen regulators began during WW II with the requirement for extended missions escorting bombers. The compressed oxygen cylinders could not hold enough oxygen for these prolonged missions using 100% oxygen flow rates so they made a compromise using diluter demand mode from 10,000 to 20,000 feet when they would switch to 100% oxygen. The liquid oxygen (LOX) system design also lifted from captured Luftwaffe Me-109s began entering service in US fighter and attack aircraft around 1945.
The initial requirement to use oxygen masks from takeoff to landing began when the first Jets entering service in 1945. These fighter and attack aircraft used bleed air from the compressor section of the jet engines to pressurize the cockpit. As the early jet engines utilized centrifugal flow compressors, they tended to leak engine oil from the bearings and suck in hydraulic fluid from small leaks in the plenum chamber. As a result, the bleed air coming from the compressor sections frequently contained toxic fumes.
The single seat F-9F8 Cougars I flew in 1967 still had compressed oxygen cylinders and diluter demand oxygen regulators. We were required to remove our oxygen masks during engine run-up to full power prior to takeoff to do a “Sniff Check” for fumes as part of the Take Off Check List. All the other aircraft I flew after that including the TF-9F8, the T-2A/B/C, TA-4 Skyhawk, F-8 H/J Crusader and F-4B/N/J/S Phantoms were all configured with the standard 5 liter LOX dewars with converters and demand flow regulators that delivered 100% oxygen.
Answers to the questions about oxygen flow rates and the requirement for prescriptions for same would be humorous if the consequences weren’t so costly in terms of increased out of pocket costs, all to frequent delays, and suffering.
It was cost avoidance that drove the medical insurance companies to lobby Congress and the FDA to make USP Oxygen a prescription item. The only problem is it has backfired as more than 30% of the home oxygen costs can be directly attributed not to its purity testing or handling procedures, but to the regulatory expenses involve in patient compliance testing for oxygen saturation levels and the huge bureaucracy involved in administering it’s use.
I’ve spoken with top Navy Flight Surgeons and Aviation Physiologists at the Naval Aerospace Medical Institute (NAMI) in Pensacola, FL about the use of oxygen flow rates greater than 15 liters/minute. They claim that most primary care physicians and neurologists are not trained in aviation physiology or aerospace medicine so are basically clueless when it comes to the use of oxygen other than as a supplement during surgery or for COPD sufferers.
Consequently, most US physicians/neurologists consider any flow rate above 7 to 9 liters/minute “High” so are hesitant to prescribe any higher flow rates. They also look at you in surprise and disbelief when you ask for your oxygen therapy prescription to be written for a flow rate 15 to 25 liters/minute.
The need to treat most medical conditions conservatively and lack of any gold standard (randomized, double-blind, placebo-controlled) clinical studies on oxygen flow rates greater than 12 liters/minute (see Goadsby’s 2006 study of oxygen therapy at 12 liters/minute published last January) also makes it difficult for PCPs or neurologists to justify prescribing oxygen flow rates of 15 liters/minute and higher.
Having said that, the most current standard of care for the acute treatment of cluster headache with 100% oxygen at a flow rate of 15 liters/minute as compiled and validated by the European Federation of Neurological Societies (EFNS), can be found at the following link: Multimedia File Viewing and Clickable Links are available for Registered Members only!! You need to
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I've met with Dr, Peter Sandor on several occasions regarding the use of oxygen therapy at flow rates that support hyperventilation for cluster headaches, and in July of this year with Dr. Arne May at UKE Hamburg on the same topic. Both are convinced that when Dr. Todd Rozen completes his study of this method of oxygen therapy and publishes the results, it will make a substantial change in the way neurologists treat this disorder and in the research into the pathophysiology of the attack and abort mechanisms.
I've also met with Dr. Peter Goadsby who conducted the most recent study of oxygen therapy as an abortive for cluster headache to the gold standard. It with the first major randomized double-blind placebo-controlled crossover trial comparing oxygen therapy versus placebo (forced air) for patients with cluster headache. A summary of his study results can be found at the following link: Multimedia File Viewing and Clickable Links are available for Registered Members only!! You need to
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When you look at the success rate or efficacy of oxygen therapy at flow rates of 7 to 9 and up to 12 liters/minute as an abortive for cluster headaches, you usually see the 70% figure. What you don’t see is why the efficacy is not higher than 70% or the relationship between headache pain levels and time to abort.
What we found in our informal proof of concept study of oxygen therapy at flow rates that support hyperventilation was a 99% efficacy (success rate) by all 7 participants (I didn’t count myself at 100%) and average abort times 2 to 3 times less than at a flow rate of 15 liters/minute. We also found a very clear and direct correlation between pain levels and time to abort. In short, a Kip-3 to Kip-4 cluster headache aborted in 3 to 4 minutes, and a Kip7 to Kip-8 cluster headache aborted in 8 to 12 minutes at flow rates that support hyperventilation.
In a side-by-side comparison, we found the average time to abort to a pain free state for pain levels 6 through 9 on the same 10-Point numerical pain scale using flow rates that support hyperventilation was 9 minutes with 100% effectiveness. For a flow rate of 15 liters/minute the average abort time was 31 minutes with 52% effectiveness.
At this point I probably need to address why we need hyperventilation during oxygen therapy if we want fast and reliable aborts. Hyperventilation is defined as ventilating the lungs with a greater volume of normal air or oxygen than needed.
For reference, the method of oxygen therapy many of us use involves voluntarily hyperventilating with 100% oxygen to attain respiratory alkalosis with symptoms of paresthesia and sustain it until the abort with complete cessation of cluster headache pain.
The goal of this method of oxygen therapy is to abort both the excruciating pain and the triggering mechanism of a cluster headache as rapidly as safely as possible with a very high efficacy. The mechanisms involved include hyperoxia, hypocapnia, and an elevated arterial pH as all three conditions stimulate the vasoconstriction associated with pathophysiology of an effective acute therapy in aborting the cluster headache.
The elevated arterial pH carries the added benefit of the Bohr Effect, increasing hemoglobin's affinity for oxygen thereby super oxygenating blood flow to the brain, specifically to the affected vascular structures in and around the trigeminal nerves dilated by the cluster headache triggering mechanism.
If the level of physical activity increases such as doing the cluster dance, rocking back and forth, or banging your head against the wall or floor, you are working harder than sitting motionless. Under these levels of increased physical activity the level of CO2 production goes up… and so does the respiration rate in order to maintain normal CO2 and arterial pH levels.
To put things in perspective, just because your respiration rate and tidal volume is higher during physical activity, it doesn’t mean you’re hyperventilating. For example if you did jumping jacks for 30 seconds or ran up three to four flights of stairs, you would likely have a minute volume of lung ventilation equal to 50 liters.
A minute volume of respiration is equal to the amount of air or oxygen inhaled in one minute. Even with this level of physical activity and a minute volume of 50 liters you wouldn’t be hyperventilating as this level of lung ventilation is “NORMAL” for that level of physical activity. You would need a minute volume of 60 liters (an oxygen flow rate of 60 liters/minute) to be considered hyperventilating…
The direct relationship between increasing headache pain levels and increased time to abort to a pain free state suggests a possible quantitative relationship between cluster headache pain levels and the amount of CO2 removed from the bloodstream to achieve an abort.
In other words, we suspect higher cluster headache pain levels are associated with progressively greater levels of vasodilation caused by the lower levels of arterial pH (higher levels of acid) and it takes progressively longer hyperventilating to pump out enough CO2 (carbonic acid) to elevate the arterial pH enough to trigger the vasoconstriction needed to abort a cluster headache and its triggering mechanism.
The dramatic drop in time to abort at each pain level when hyperventilating with an oxygen flow rate that supports hyperventilation suggests the lowering of PaCO2 levels made possible by this method of oxygen therapy plays a significant role in the efficacy and rapid nature of this abort mechanism.
We also suspect the reverse or opposite effect may be true if PaCO2 levels are too high due to restricted lung ventilation (too low an oxygen flow rate) and increased physical activity. In other words, an abort with oxygen therapy may be prolonged or it may not be possible to abort the cluster headache with oxygen therapy if the flow rate is too low, the pain level is too high, and there is any physical activity during the oxygen therapy. This could easily answer the question why the traditionally prescribed oxygen flow rate of 7 to 9 liters/minute and even up to 12 liters/minute is only 70% effective.
Hope this helps or at least provides some food for though…
Take care,
V/R, Batch
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