In years past I discovered and then used EERS[a][1] to help with the “loop gain”[3] issues brought into my life through the stress added thereto by a traumatic attack. I have used it every year since I found it late 2009 near the anniversary of the attack.

And so I now use it this year. But with a slight modification. I added a little leak at the “normal” lossy mask vent point. My thinking is simply this, if I am breathing at the very modest rates that are appropriate for asleep at rest in bed then I want fresh air only. This should keep my breathing volume lower processing carbon dioxide needs more efficiently using less air (and so keeping me further away from the respiratory effort related arousal issues[3] which would result if a a higher volume of air was being used to keep the carbon dioxide rates down). And in that state the small leak near the usual vent point should clear the last bit of carbon dioxide ladened air left during the pause at the end of exhale before inhale begins. But if the volume of the air used or the breathing rate increases there will be a bit of air left in the mask to be re-breathed and which should lessen the possibility of coming near the too little carbon dioxide “apneic threshold” or otherwise reducing circulation and metabolism in the body but especially the brain[4] due to carbon dioxide maintenance issues related to the higher breathing levels.

Frankly it works better than expected. More energy, better feel, more getting done. And so nice to wake up with near normal breathing rates, good mouth moisture, and warm feet. Definitely a keeper.

[1]: Gilmartin G, McGeehan B, Vigneault K, Daly RW, Manento M, Weiss JW, Thomas RJ. Treatment of positive airway pressure treatment-associated respiratory instability with enhanced expiratory rebreathing space (EERS). Source: J Clin Sleep Med. 2010 Dec 15;6(6):529-38. Division of Pulmonary, Critical Care and Sleep Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.


[2]: Yoseph Mebrate, Keith Willson, Charlotte H. Manisty, Resham Baruah, Jamil Mayet, Alun D. Hughes, Kim H. Parker and Darrel P. Francis Dynamic CO2 therapy in periodic breathing: a modeling study to determine optimal timing and dosage regimes. J Appl Physiol 107:696-706, 2009. First published 23 July 2009; doi: 10.1152/japplphysiol.90308.2008


[3] Danny J. Eckert, David P. White, Amy S. Jordan, Atul Malhotra, and Andrew Wellman “Defining Phenotypic Causes of Obstructive Sleep Apnea. Identification of Novel Therapeutic Targets”, American Journal of Respiratory and Critical Care Medicine, Vol. 188, No. 8 (2013), pp. 996-1004. doi: 10.1164/rccm.201303-0448OC

[4] Philip N. Ainslie , James Duffin , Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation. American Journal of Physiology – Regulatory, Integrative and Comparative PhysiologyPublished 1 May 2009Vol. 296no. 5, R1473-R1495DOI: 10.1152/ajpregu.91008.2008

[a] Late 2002 undiagnosed severe obstructive sleep apnea with extreme hypoxia landed me in shelter. No doctor found this. Actually it was my shelter bunk mates who were the ones who told me what was going on and got me to the doctor with enough information for them to eventually diagnose it (AHI=52 (90 supine) SpO2 nadir 55%).

CPAP helped. But the effectiveness of CPAP seemed to lessen when I was under pressure. If I had several stressful days in a row the lack of effectiveness became quite noticeable.

Then late 2005 I was robbed, stabbed, and beaten. A severe traumatic attack. We were stuffing the stab wounds for eight weeks. They tell me my eye swelled up to about the size of the rest of my head. They thought I had lost that eye. I am very very lucky nothing critical was hit.

The stress of being near the anniversary time of the attack brought me to the emergency room each of two years following the attack. I would find my heart racing and high respiratory rates for days before and after the date. I would loose days of sleep. I was simply hyper-vigilant with no way to slow things down.

Trying to sleep with CPAP became difficult. I often woke up breathing hard with my heart beating out if my chest. Lots of dry mouth. For the first time aerophagia entered the picture. It became much harder to sleep with CPAP starting about six weeks before the anniversary date.

Then in late 2009 (if memory serves) I was listening to a Sleep Apnea related web interview where Bytuko Breathing was being discussed. I tried the “nose clearing” exercise (without the hold your nose and bob up and down part – I was taking notes) and found that not only did my nose clear but my heart rate (constantly tending to race that time of year) reduced notably. This got me thinking and it made sense to me that the heart rate would be the lowest when metabolism was best facilitated by the breathing level. So I started using my pulse/oximiter to find that lowest level and while doing so discovered that SpO2 could be used to tell me if I were near that quite constantly. This made my days during the time of year near the time of the attack go much better.

But what to do at night. As I looked into the medical literature concering ventilatory stability and CPAP use I ran across the use of enhanced expiratory rebreathing space (EERS)[1] as well as how they were looking into dynamic CO2 therapy[2]. To facilitate EERS one needs to simply move the “lossy mask system” vent point downstream a hundred milliliters or so. For me not hard to do.

And the results were immediate and good. Not waking up with my heart beating out of my chest. No aerophagia. Mouth moistness much better. It was not perfect but it helped greatly.