avi123 wrote:I myself don't pay attention to them (hyponeas) b/c I suffer strictly from OSA without underlying medical conditions such as heart failure issues, neuromuscular, COPD, etc
As to avi's idea that hypopneas don't matter and shouldn't be counted: Well, the sleep docs diagnosing us with OSA all believe hyponeas should be counted---or at least some hypopneas should be counted. Which ones should count still seems to be a bone of contention which is why we've got the confusing mess of the AASM Recommended Standard for hypopneas and the AASM Alternative Standard for hypopneas. See
http://www.ncbi.nlm.nih.gov/pubmed/19238801 and
http://www.journalsleep.org/ViewAbstract.aspx?pid=27368 for a scholarly discussion of how and when these two standards affect a patient's diagnosis of OSA as well as the formal definitions of the two standards:
AASM Recommend: A hypopnea requires at least a 30% reduction in airflow for at least 10 seconds AND a corresponding O2 desaturation of at least 4%. Such a hypopnea does NOT require an EEG arousal.
AASM Alternative: A hypopnea requires at least a 50% reduction in airflow for at least 10 seconds AND
one or both of the following conditions: A EEG arousal OR an O2 desat of at least 3%.
And of course, under both standards, the disordered breathing has to occur during an epoch when the patient is ASLEEP according to the EEG evidence.
Note that under the AASM Alternate rules, if there's a reduction in airflow of at least 50% for at least 10 seconds that ends with an EEG arousal, then a hyponea with arousal CAN and SHOULD be scored---even if there is NO drop in O2 at all. And the whole reason that the Alternative standard has been adopted as a
valid way to score hyponeas is that there is evidence that an excessive number of
arousals from sleep disordered breathing can be just as harmful to the body as O2 desats are: The EEG arousals are associated with a number of physiological changes in the body that can loosely be described in layman's terms as "flight or fight". At this point, many (but not all) sleep doctors believe that these respiratory arousals (be they hyponeas with arousal or RERAs) need to be addressed by PAP therapy in the same way that OAs need to be addressed. But Medicare still insists on having a deep 4% O2 desat to be present for scoring a hypopnea. Hence one standard has to be used for Medicare and one standard can be used by docs who believe it is in their patients' best medical interests to deal with the "arousal" problem
before their OSA progresses to the point where it is causing desats as well as arousals.
However the chosen sleep lab chooses to score the hypopneas, the associated sleep docs do believe the scored hypopneas should be counted in the definition that's used to diagnose a patient with OSA. And hence, those docs also believe eliminating or minimizing those hypopneas should be part of the strategy of xPAP therapy: Standard PSG protocol calls for the tech to attempt to eliminate
all hypopneas as well as apneas; and the titration algorithm does tell the tech to increase the pressure when something like 3 hypopneas occur in a short period of time. And the manufacturers of other auto CPAP machines tend to agree with the sleep docs since their machines do respond (although sometimes slowly) to machine scored hypopneas.
Now the notion that hypops come in both central and obstructive varieties is indeed an issue that seems to not be well understood. But most labs are NOT set up to determine whether a given hypop is or is not obstructive in nature. Indeed, my understanding of the AASM standards is that unless labs have some specialized equipment, they are NOT supposed to try to classify hypops as central or standard. And my patient-level understanding of what I've read is that hypops are typically assumed to be obstructive simply because the patient is continuing to breath, albeit not very well, during a hypopnea. And in a lab PSG
central apneas are scored only when there is
no effort to breath as measured by the belts around the chest and abdomen. So in a PSG, patency of the airway is not determined solely from the flow data the way our xPAP machines do: In the lab, they use the belts---if there's effort to breath, then the airway is assumed to be obstructed; if there's no effort to breath, it doesn't matter if the airway is open or closed since the problem is
central in nature---i.e. the brain is not
sending the order to breath and that's the main reason there's no air going in/out of the lungs. On our xPAPs, determining an "closed" versus "open" airway apnea through FOT or PP is just a proxy measure for whether we're making an effort to breath or not.