The Oxygen Myth: What Doctors May Not Know About Breathing

One of my biggest frustrations while performing surgery is having to work with certain anesthesia staff that don’t realize that the patient is not breathing. The problem is that they are focused too much on their instruments, not realizing what’s really happening until things start to go wrong. 
During sleep, your muscles are relatively more relaxed. For modern humans, due to a combination of narrowed jaws, soft tissue crowding, inflammation and gravity, the airway becomes more narrow and more prone to obstructed breathing. This is the main theme in my book, Sleep Interrupted: A physician reveals the #1 reason why so many of us are sick and tired
Once in the operating room last week, I performed a drug-induced sleep endoscopy (DISE) procedure. This is when I look at the airway with a camera while the patient is in deep sleep using intravenous propofol, but still breathing regularly. If you give too much propofol, breathing stops entirely since there’s no signal from the brain to breathe. This is called a central apnea. What I typically see is called an obstructive apnea, where the blockage occurs at different areas of the throat, while the patient is trying to inhale. However, if the patient has 100% oxygen running, then it takes longer for the levels on the monitor to drop when the patient stops breathing, whether from central or obstructive apneas. 
However, once in a while, I see that the patient is clearly obstructing and straining to breathe, but since the oxygen level on the monitor is in the high 90s, and there’s some carbon dioxide (CO2) coming out the the lungs, the anesthesiologist thinks that everything seems fine. However, if this goes on for too long, the oxygen level will drop quickly since the patient is struggling to breathe through an opening the size of a small straw. Having a little bit of CO2 coming out is not ideal. Once the oxygen level begins to drop to dangerous levels, only then does the anesthesiologist quickly take measures to have the patient breathe better again. 
You can even see only partial degrees of breathing blockage with the patient straining to breathe, but the oxygen level will be fine. This is equivalent to what’s called flow limitation in sleep studies, where you have flattening of the typical rounded nasal airflow tracings that are not severe enough to be called apneas or hypopneas. Flow limitation can oftentimes lead to brain wave arousals from deep top lighter stages of sleep. This is what’s shown in Dr. Guilleminault’s classic article on upper airway resistance syndrome (UARS).
What I do to prevent this situation is to carefully watch the patient’s breathing patterns, rather than look at the monitors. I will thrust the jaw forward, like what a mandibular advancement device does for sleep apnea, but much more aggressively. Rarely, even this doesn’t work and we have to ventilate with a face mask using positive pressure. 
I don’t blame anesthesiologists since they are not used to keeping patients in a relatively lighter state of anesthesia compared to what they’re normally used to doing. With good education, communication and teamwork, these procedures a very safe. If you’re not obstructing, there’s no reason to give 100% oxygen; even room air will work fine. If you’re obstructed, no air will get through at all. 
What’s I’ve learned from doing hundreds of these sleep endoscopies recently is that almost everyone with upper airway resistance syndrome will have significant (and sometimes severe) obstruction at one or more levels. You can read my publication here describing sleep endoscopy findings in people who don’t officially have sleep apnea (AHI < 5). 
The main gist of this article is that sometimes, thinking that oxygen will help you to breathe better is a myth. There are a number of other factors to consider when trying to breathe optimally. However, the most important consideration to good breathing is to have completely unobstructed breathing, during the daytime and especially when you’re sleeping. Once this is accomplished, then you can address the quality of the air (including the oxygen content), and what your body does with the oxygen once it’s received into the lungs.

Please note: I reserve the right to delete comments that are offensive or off-topic.

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6 thoughts on “The Oxygen Myth: What Doctors May Not Know About Breathing

  1. I use a full face mask with my CPAP. The bottom of the mask rests against my chin, which forces my jaw backwards. Any suggestions?

  2. The link for your article on sleep endoscopy findings on normal people seems to be missing. Can you add it?

    Just a data point for you, my sleep endoscopy showed clear obstruction but my sleep studies were all negative for sleep apnea. Until the pressure sensor was added, when the AHI jumped to 30. It should have been easier to score my events considering what I saw in the endoscopy so I conclude that it must not be an accurate representation of what actually happens in practice. I’m curious if my experience can be corroborated with research on the procedure.

  3. You can go back to a nasal mask but use a chin strap to keep your mouth closed. There are many other different mask options. Good luck.

  4. You made a great point in this article Steven. Something that can be easily missed when performing operation and it’s pretty much horrifying from a patient point of view to know that not all anesthesiologist keep attention to this important detail. I hope that because of your article this changes for better. I also learned that it’s more important to have completely unobstructed breathing than more oxygen thanks to you Steven. Thanks for sharing this.

  5. In numerous articles I have written and posted to my website, I suggest that the daytime “awake” manifestation of an event while asleep is triggering the “fight or flight” or “Stress” response, which facilitates compensations which open the airway and concurrently increase BP, heart beat (rhythm & tempo (include force) and breathing (rate: rapid & shallow) to manage airflow through a narrower oral-pharyngeal airway. This is from secreted norepinepherine. When balance is reestablished, residual norepinepherine is felt in it’s cardiovascular effect on the heart beat, the rhythm & tempo of which feels different as it relates to the awake distraction to the senses, including thoughts. Ones sensation of this shows up in our description of the this sensation, which ranges from boredom to anger to fear to surprise, even shock all of which have a distinguishing heart beat rhythm & tempo and are confused with actual “Stress”.
    Because we are awake, relaxation does not usually ( except, possibly, when the effect is a sensation we describe as boredom) disrupt airway stability except when we snort while laughing (relaxation), loss of oral-pharyngeal muscle control does. I suggest that that while awake , we are subject to almost constant disruptions in airway stability followed by recovery. The absence of this is what we experience as being in the zone, a moment of “Grace” “in the “Groove” and we are not thinking as “thoughts are distractors and disruptors of airway muscle balance. That is why meditation helps reduce “Stress”. While awake, deep breathing also helps in another way, which, I suggest may tie into you observations you discuss in the above article. Here, I believe the oxygen or air reserve in the lungs desensitizes the triggering of the stress response and secretion of the norepinepherine, which, I believe shows up in change of sleep stage to a lighter one with increased muscle tone. The question about this trigger is whether it is oxygen level induced or airflow or airway caliper induced or both.
    I believe that as long as the Medical Community remains “Trapped in Sleep” in considering an anatomical condition , which is present round-the-clock we are not going to meaningfully resolve these issues. I believe it is not scientific practice to ignore this rather to enthusiastically explore this.
    The last paragraph in your article appears to address breathing during the daytime, so I suspect you are more aware of what I am describing than you delve into.
    Perhaps, this may be because of lack of published literature on this, which has to do with the structure of medicine, medical school , even medical/dental associations, their identities and perceived financial security that impacts and is impacted by all decisions made regarding research and publications that may disrupt or shake-up the status quo. Perhaps it is not.
    My discussion of the experience of sensations attributed to “stress” and the sensation of ones heart beating caused by residual norepinepherine is based upon my own observations, and I challenge you to test it out and let me know what you find. One can trigger this by mimicking the descriptions by saying aloud and acting out being “sad”, “angry”, “bored’, “afraid”. Consider, the distraction, loss of airway stability and correction of this before one “feels” these particular “sensations”. A useful question is how is this Psychology, anatomy, Physiology and Biochemistry integrating.
    I invite further discussion of this!
    I am not proof reading this so, please, be easy on critique of grammar.