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Hi, I've been on CPAP for the last two months but just managed to get my sleep studies. I only had an Apn/Hypn Idx of 1.1 but Arousal Index of 33.6.
The Calculation of Respiratory Disturbance Index listed: #RERAs: 137, TOTAL SLEEP TIME 282.5,
RERA INDEX: 29.10, AHI 1.1, RDI: 30.20.
At the beginning it states there was no desaturation below 90%, but under Calculation of Oxygen Desaturation Index is listed # of Oxygen Desaturations: 4 and Desaturation Index: 0.85. Without cpap the min is listed as SaO2 Min:90; with cpap the SaO2 Min is 93. That doesn't seem enough to justify treatment.
For my second study with CPAP the results states "CPAP improved RDI but increased arousals at all pressures." Pressure at 5 with AHI: 0 Arousal Index: 41.3, Pressure at 7 with AHI: 0 Arousal Index: 74.9, Pressure at 9 with AHI: 1.2 Arousal Index: 66.4, Pressure at 11 with AHI: 0 Arousal Index:86.4.
I showed the study to my GP...who is not a pulmonologist...and she said she would just drop the therapy, so I'm really confused as to whether the 137 RERAs are breathing related or just another problem. Would love to have feedback from those experienced in therapy.
The Calculation of Respiratory Disturbance Index listed: #RERAs: 137, TOTAL SLEEP TIME 282.5,
RERA INDEX: 29.10, AHI 1.1, RDI: 30.20.
At the beginning it states there was no desaturation below 90%, but under Calculation of Oxygen Desaturation Index is listed # of Oxygen Desaturations: 4 and Desaturation Index: 0.85. Without cpap the min is listed as SaO2 Min:90; with cpap the SaO2 Min is 93. That doesn't seem enough to justify treatment.
For my second study with CPAP the results states "CPAP improved RDI but increased arousals at all pressures." Pressure at 5 with AHI: 0 Arousal Index: 41.3, Pressure at 7 with AHI: 0 Arousal Index: 74.9, Pressure at 9 with AHI: 1.2 Arousal Index: 66.4, Pressure at 11 with AHI: 0 Arousal Index:86.4.
I showed the study to my GP...who is not a pulmonologist...and she said she would just drop the therapy, so I'm really confused as to whether the 137 RERAs are breathing related or just another problem. Would love to have feedback from those experienced in therapy.
Views: 241
Replies to This Discussion
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Permalink Reply by Steven Y. Park, MD on
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You don't have much apneas or hypopneas, but you do stop breathing 29 times every hour. RERAs are respiratory event related arousals, and if the breathing pause doesn't last longer than 10 seconds, it won't get counted as an apnea or hypopnea. So you don't have any significant oxygen desaturation issues, but you to have significant breathing pauses that prevents you from staying in deep sleep. It's treated the same way as OSA since it's an anatomic breathing problem. This is along the lines of what's called upper airway resistance syndrome. Symptoms include poor quality sleep, daytime fatigue, depression, anxiety, blood pressure fluctuations, headaches, and many others.
If you can tolerate CPAP, I would continue for a while longer, making sure that your compliance numbers are good. Unfortunately, your effective AHI won't help, since it's so low to begin with. Another option is to use a mandibular advancement device, but only if your oral cavity anatomy makes you a good candidate.
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Permalink Reply by Dale Jackson on
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Thank you so much for your response. You have answered the question I was unsure of...that the RERAs are breathing related. I will continue the therapy until I'm sure that it is indeed helping and not hurting. I have myasthenia gravis and cardiomyopathy so I know either can be affected by problems with respiration.
My AHI is actually worse on CPAP than during my sleep study. Perhaps some of the RERAs are being recorded as apneas or hypopneas? I have a data capable machine and regularly check my sleep status. I do seem to feel more alert with the machine but I still have the every one to two hour awakenings throughout the night...not bathroom trips...I never get up during the night.
I'm still having problems with the correct pressure for optimum benefit. I know a lower pressure is better for me and I thought the variable was best but sometimes I feel the machine starts chasing an apnea and goes wild. My DME sets the pressure by doctor's orders but I don't think it is optimum yet. I started on 9, then 5 to 20, then 7, and now 5 to 15.
I mentioned the mandibular advancement device to my dentist but he indicated he didn't think it would help me.
Any new ideas for better results would be appreciated. Thank you!
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Permalink Reply by RockRpsgt on
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Your arousals are a learned defense to your sleep related breathng disorder. This is your body's way of fixing the problem. Your arousals could be worse due to a neurologic reverberation that happens from the sleep/arousal loop of OSA or any sleep related breathing problem.
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Can this "learned defense" be unlearned as therapy progresses and the body does not feel threatened? Is this as good as it gets? I have a feeling that the arousals occur more often as I go into REM sleep. I awaken with vivid recollection of dreams and have read that dreams are recalled more vividly if awakened during dream. My sleep studies indicated reduced REM sleep. My goal for sleep would be to awaken and say "Hey, I slept through the night!".
Rock Hinkle said:Your arousals are a learned defense to your sleep related breathng disorder. This is your body's way of fixing the problem. Your arousals could be worse due to a neurologic reverberation that happens from the sleep/arousal loop of OSA or any sleep related breathing problem.
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Yes it will get better. How long will it take? Who knows. There have been studies that have shown people with apnea related arousal have continued to have them 6 months after PAP therapy was started. When an activity of the brain becomes a survival method it is sometimes hard for the brain to discontinue this potentially life saving action. Fight or Flight.
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Some good studies on the subject.
http://www.journalsleep.org/ViewAbstract.aspx?pid=25869
http://www.journalsleep.org/ViewAbstract.aspx?pid=24678
View the Full Text to get some more detailed information.
Study Objectives: The following hypotheses were investigated: 1) severe obstructive sleep apnea (OSA) can mask concurrent periodic limb movement (PLM) disorder (PLMD), which becomes evident or worsens after treatment with continuous positive airway pressure (CPAP); 2) in patients with mild OSA, PLMs are not masked but may be triggered by subclinical hypopneas or respiratory effort-related arousals and improve after CPAP.
Design: Retrospective analysis was performed on 2 polysomnographic studies per patient—1 baseline, the second with CPAP titration. The apnea-hypopnea index (AHI) and PLM index (PLMI) under the 2 conditions were statistically analyzed.
Setting: University hospital sleep disorders center.
Patients: Patients were selected if they had a baseline AHI of 5 or greater and CPAP titration resulted in reduced AHI. Also, each needed to have either a PLMI of 5 or greater on baseline PSG or during CPAP titration. Patients who started or discontinued a medication that could affect PLMs after the baseline PSG were excluded. Interventions: As clinically indicated, CPAP for OSA.
Measurements and Results: Eighty-six patients qualified and were divided into 3 groups based on OSA severity. Significant correlations (P<0.05) were found between AHI and PLMI on the baseline PSG (-0.50), between AHI on baseline PSG and PLMI on CPAP titration (0.49), and between PLMI on baseline PSG and on CPAP titration (-0.21). The increase in PLMI during CPAP titration in patients with severe OSA was statistically significant (P<0.001). The PLMI decreased with CPAP in 20 of 86 patients, mostly in the mild OSA subgroup. Regression of post-CPAP reduction of AHI and change in PLMI yielded a significant logarithmic relationship (R2=0.3042).
Conclusions: Severity of OSA may determine the effect of CPAP on PLMs. The PLMs may increase in moderate to severe OSA due mainly to “unmasking” of underlying PLMD. The PLMs may decrease in mild OSA post-CPAP due to resolution of PLMs associated with respiratory effort-related arousals. This suggests that PLMs may have more than 1 etiology and may be categorized as spontaneous (as in PLMD) and induced (when secondary to respiratory effort-related arousals).
Citation: Baran AS; Richert AC; Douglass AB et al. Change in periodic limb movement index during treatment of obstructive sleep apnea with continuous positive airway pressure. SLEEP 2003;26(6):717-20.
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Isn't there a specific xPAP device that best treats UARS? Since I don't have UARS I haven't followed in the info on it closely and most of what I did read passed out the other ear since it wasn't info I was using and I needed room to hold on to the info pertinent to my situation.
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Dr Park, I would have been inclined to send this person to you or to Dr Barry Krakow as two I thought I'd read post information on UARS and treating UARS.
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Very interesting articles, but I'm not sure I am understanding the meaning. If OSA is mild to moderate CPAP may resolve it?...but if severe can unmask and increase PLM?
Both sleep studies indicated 0 for PLMS, but I notice in my copy of the sleep study that TECH REVIEW OF STUDY states "very mild snore, Leg movements but not significant". Under PHYSICIAN REVIEW it states "leg jerks appear to be RERA's". So, I'm more confused when I read over my study. As I am having RERAs could this be causing leg jerks that I am not aware of and cause the arousals? And why was PLMS indicated as 0 on the study?
However I do have mild RLS. This only bothers me occasionally and is oddly enough, relieved by taking an aspirin and within 20 to 30 minutes symtoms go away. (I have two daughters who get the same relief with aspirin).
Thanks, Rock! I really appreciate the time involved in researching this for me.
Rock Hinkle said:Some good studies on the subject.
http://www.journalsleep.org/ViewAbstract.aspx?pid=25869
http://www.journalsleep.org/ViewAbstract.aspx?pid=24678
View the Full Text to get some more detailed information.
Study Objectives: The following hypotheses were investigated: 1) severe obstructive sleep apnea (OSA) can mask concurrent periodic limb movement (PLM) disorder (PLMD), which becomes evident or worsens after treatment with continuous positive airway pressure (CPAP); 2) in patients with mild OSA, PLMs are not masked but may be triggered by subclinical hypopneas or respiratory effort-related arousals and improve after CPAP.
Design: Retrospective analysis was performed on 2 polysomnographic studies per patient—1 baseline, the second with CPAP titration. The apnea-hypopnea index (AHI) and PLM index (PLMI) under the 2 conditions were statistically analyzed.
Setting: University hospital sleep disorders center.
Patients: Patients were selected if they had a baseline AHI of 5 or greater and CPAP titration resulted in reduced AHI. Also, each needed to have either a PLMI of 5 or greater on baseline PSG or during CPAP titration. Patients who started or discontinued a medication that could affect PLMs after the baseline PSG were excluded. Interventions: As clinically indicated, CPAP for OSA.
Measurements and Results: Eighty-six patients qualified and were divided into 3 groups based on OSA severity. Significant correlations (P<0.05) were found between AHI and PLMI on the baseline PSG (-0.50), between AHI on baseline PSG and PLMI on CPAP titration (0.49), and between PLMI on baseline PSG and on CPAP titration (-0.21). The increase in PLMI during CPAP titration in patients with severe OSA was statistically significant (P<0.001). The PLMI decreased with CPAP in 20 of 86 patients, mostly in the mild OSA subgroup. Regression of post-CPAP reduction of AHI and change in PLMI yielded a significant logarithmic relationship (R2=0.3042).
Conclusions: Severity of OSA may determine the effect of CPAP on PLMs. The PLMs may increase in moderate to severe OSA due mainly to “unmasking” of underlying PLMD. The PLMs may decrease in mild OSA post-CPAP due to resolution of PLMs associated with respiratory effort-related arousals. This suggests that PLMs may have more than 1 etiology and may be categorized as spontaneous (as in PLMD) and induced (when secondary to respiratory effort-related arousals).
Citation: Baran AS; Richert AC; Douglass AB et al. Change in periodic limb movement index during treatment of obstructive sleep apnea with continuous positive airway pressure. SLEEP 2003;26(6):717-20.
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Ok this is my understanding of it. A periodic limb movement (PLM) is different from an isolated leg movement or RERAs. PLM is a completely different disorder with no common generator to apnea.
http://www.ncbi.nlm.nih.gov/pubmed/10476008?dopt=Abstract.
A leg movement is classified as .5 to 10 second movement that leads to an amplitude increase in the leg signal.
A leg movement by itself is just a leg movement.
A PLM is 4 leg movements within 90 seconds. PLMs are usually seen as trains of limb movements seen throughout NREM sleep. Leg movements such as these are usually seen in people with Kidney, neurological problems, or an iron defficiency.
A leg movement or arousal connected to any type of flow limitation is an event with an arousal ie OSA with arousal, Central with arousal, hypopnea with arousal or a RERA. These events are very well defined and easy to pick out on a psg. These types of event typically have o2 desats. Arousals connected to these types of sleep related breathing events are a learned behavoir.
RERAs are a little different. A RERA is a sequence of breaths lasting 10 seconds in duration that results in a decrease of oral nasal breathing with an increase in lung effort that ends or leads to an arousal(LM). The arousals involved with RERAs are a learned reaction in keeping you breathing. Without them your RERAs would probably be apneas.
If You have a severe breathing disorder with arousels over a mild to moderate one this can greatly influence how long it takes your mind to stop doing it. Severe apnea in a great many cases will cover a PLM disorder. Arousals related to your sleep relateed breathing disorder will clear up with PAP therapy. Periodic Limb Movement disorder is not related to a breathing problem so it may or may not.
I hope that was not to much info, and that I explained it right.
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Thank you very much! That was not too much information and the referenced article helped. As my study indicated no PLM's, I feel there's the chance that sleep arousals can be unlearned and that the CPAP therapy is beneficial. After my GP said she would just drop it, I tried one night without and toward morning decided I felt worse and more congested so put on the mask for the last hour and a half! I also have to consider the compliance thing too.
For a little while I dreamed of just chucking the CPAP! As everyone on this forum knows, learning to live with CPAP is no picnic and to think it has no benefit and may be making things worse is very distressing.
Thank you again!
Rock Hinkle said:Ok this is my understanding of it. A periodic limb movement (PLM) is different from an isolated leg movement or RERAs. PLM is a completely different disorder with no common generator to apnea.
http://www.ncbi.nlm.nih.gov/pubmed/10476008?dopt=Abstract.
A leg movement is classified as .5 to 10 second movement that leads to an amplitude increase in the leg signal.
A leg movement by itself is just a leg movement.
A PLM is 4 leg movements within 90 seconds. PLMs are usually seen as trains of limb movements seen throughout NREM sleep. Leg movements such as these are usually seen in people with Kidney, neurological problems, or an iron defficiency.
A leg movement or arousal connected to any type of flow limitation is an event with an arousal ie OSA with arousal, Central with arousal, hypopnea with arousal or a RERA. These events are very well defined and easy to pick out on a psg. These types of event typically have o2 desats. Arousals connected to these types of sleep related breathing events are a learned behavoir.
RERAs are a little different. A RERA is a sequence of breaths lasting 10 seconds in duration that results in a decrease of oral nasal breathing with an increase in lung effort that ends or leads to an arousal(LM). The arousals involved with RERAs are a learned reaction in keeping you breathing. Without them your RERAs would probably be apneas.
If You have a severe breathing disorder with arousels over a mild to moderate one this can greatly influence how long it takes your mind to stop doing it. Severe apnea in a great many cases will cover a PLM disorder. Arousals related to your sleep relateed breathing disorder will clear up with PAP therapy. Periodic Limb Movement disorder is not related to a breathing problem so it may or may not.
I hope that was not to much info, and that I explained it right.
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Judy, I had wondered if I needed the xPAP as I have myasthenia gravis which can affect the breathing muscles. I am taking prednisone which has relieved severe double vision lasting five years and ptosis of shorter duration. I have been on prednisone for a year now. I don't seem to have a problem with exhaling but in sleep who can be sure. My MG neurologist is not aware of the CPAP therapy as my next appointment is in December. I am not even sure the apnea is related. Thanks for the input.
Judy said:Isn't there a specific xPAP device that best treats UARS? Since I don't have UARS I haven't followed in the info on it closely and most of what I did read passed out the other ear since it wasn't info I was using and I needed room to hold on to the info pertinent to my situation.
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