RosemaryB wrote:split_city wrote: 2) Obstructive events results in a lot of changes in muscle structure and function. Increased hypoxia (low oxygen episodes) during obstructive events remodels muscles and also parts of the brain. These changes might be permanent and consequently affect the upper airway even when an individual loses weight
Speaking of the brain, what's going on with the brain and sleep architecture? There are some atypical sleep patterns amongst the members of this forum.
For instance, one person whose sleep study shows very little, if any, stages 3&4 sleep. My atypical feature is a lot of unexplained "spontaneous arousals" not accounted for by snoring or PLMs and there is another member with these as well. I do have a larger proportion of delta, too, around 30%. In my case, I don't have much hypoxia, just a dip or two below 90 in my sleep study.
I'm wondering if there's something going on in the brain, not necessarily the result of hypoxia, or the breathing mechanism, but perhaps something to do with the reticular activating system, melatonin production, or anything like that.
Since you work in a sleep lab, perhaps you see these kinds of atypical sleep studies. Are there thoughts about these other phenomena.
Patients who come in for sleep studies generally have disturbed sleep architecture due to equipment, the bed, pillow, having to sleep on their back, the absence of their partner. It's hard to pinpoint the reason why the patient you mentioned had a lack of stage 3 & 4 sleep. What I said above might explain this. Did this person have much REM? What was their AHI?
There is an area of sleep studies which is looking at the "arousal threshold." Some people have a low arousal threshold (perhaps in your case) or a high threshold. There are several factors which influence the arousal threshold including:
1) sleep stage
2) drug use
3) alcohol use
4) sleep deprivation
Studies have looked at what induces an arousal. These include:
1) CO2 levels
2) Oxygen levels
3) Upper airway resistance
4) Respiratory drive i.e. how hard you're breathing
5) Respiratory muscle activity
4) Fatigue of respiratory muscles
Interestingly, it was shown by our group that hypoxia impacts upon this arousal threshold. Furthermore, another group showed that despite different chemical stimuli i.e. CO2 and hypoxia, subjects aroused at the same respiratory drive (measured by oesophageal pressure). While a different group concluded that arousal was triggered at a certain point at which the diaphragm became fatigued.
Our lab has looked at whether arousal is good or bad. It's good because it allowed restoration of airflow and also prepares us for the "fight or flight response." How is it bad though?
1) Breathing rate is generally regulated by CO2 levels in the blood
2) You stop breathing when CO2 in your blood falls below a certain level (apnoea threshold).
3) When you arouse, you hyperventilate due to increased CO2 in the blood.
4) Typically, you blow off so much CO2, the CO2 levels fall below the apnoea threshold and then you begin to hypoventilate
5) At the same time, your upper airway muscles are switched off due to low CO2 levels
6) When falling back asleep, a number of people develop a central apnoea.
7) CO2 builds so breathing starts again, but the muscles are still turned off --> allowing for upper airway collapse.
Arousal is triggered, followed by hyperventilation etc...and cycle begins again
Kind of got off the track but I thought it would be good to discuss. Sleep architecture is controlled by a number of systems. It all comes down to which side the seesaw is tilted i.e. hormones which control sleep versus those which control wakefulness. A lot of work has been done in this area. However, this isn't something I have studied in any great detail
