Hi avi123!avi123 wrote:IMO, we don't need to deal with arousals, not only b/c we can't measure them, but we can't do much about them.
(Sleep Docs like to mentioned them probably to charge some more money, or to raise their respect)
Check this:
Arousal is believed to be needed for upper airway opening in obstructive hypopneas–apneas, without compelling evidence to support this notion. The association may be incidental. I studied the temporal relation between arousal and opening and impact of arousal on flow response at opening in 82 patients (apnea–hypopnea index, 46 ± 35/hour). Obstructive apneas–hypopneas were induced by dial-down of continuous positive airway pressure. Obstructions and hypopneas occurred in 44 and 56% of dial-downs, respectively. When arousal occurred (83% of dial-downs), the temporal relation between arousal and opening was inconsistent between and within patients. Frequency of opening without or before arousal increased with milder obstructions (p < 10−9) and with delta power of EEG (p < 10−6). Time of opening was unaffected by whether arousal occurred before or after opening (18.0 ± 9.8 vs. 18.1 ± 10.5 seconds). Flow response was already excessive when opening occurred without or before arousal (180 ± 148% of initial flow decline) and was considerably higher when arousal occurred (267 ± 154%, p < 10−10). Flow undershoot after first ventilatory response was greater if arousal occurred (p < 0.01). It is concluded that arousals are incidental events that occur when thresholds for arousal and for arousal-independent opening are close. They are not needed to initiate opening or to obtain adequate flow and they likely increase the severity of the disorder by promoting greater ventilatory instability.
Source: http://ajrccm.atsjournals.org/content/1 ... l.pdf+html
I would dearly love to be able to "see" when arousals occure in my data. Anything that fractures my sleep I do consider important.
Perhaps we can. SleepyHead apparently has a graph of the pulse data that contains enough of the perfusion information to extrapolate an inferred arousal. When cross checked with the other data this might work. I will get back to you later after I attempt to make this work (so much to do, so little time).
As well, the iBrain is coming down the pike and development is being done with sleep studies in mind. Available to the common man?? - No idea.
I think that breathing is based in developed reflexes contained in varous parts of the nervous system which can recieve consious control if available. I am rather facinated by "Flow undershoot after first ventilatory response was greater if arousal occurred (p < 0.01)" as I am suspicious that a hypocapnic state preceeds apneas or hypopneas and that a better correction is facilitated by a more awake brain. As for the statement "It is concluded that arousals are incidental events that occur when thresholds for arousal and for arousal-independent opening are close. They are not needed to initiate opening or to obtain adequate flow and they likely increase the severity of the disorder by promoting greater ventilatory instability" I have come to believe that there are many "micro-apneas" that occure through the night - do not initiate an arousal - do initiate a sympathetic nervous system response. Perhaps the author is correct, that arousal - I think from greather sympathetic nervous system response - links to greater ventalatory instability however I think the concious brain does a better job controlling the system physiologically (breathing reflexes) otherwise.
I also very much believe that if AHI - AND - Breathing Stability (effort only as needed to maintain healthy blood gas levels) are brought under control, unfractured sleep results, and better health and performance result.
Have a lot of fun!
Todzo