I found this article which I thought was very interesting. Since this is something that may be happening to me, it was especially interesting. Thought you might find it so, too. If I am reading this correctly, it could be used as a mean to treat hypoxemia in people with low AHI's for whom, for whatever reason, CPAP is not a viable treatment method. In my case, it seems to keep me up more than help me.
Am J Rhinol 2001 Sep-Oct;15(5):311-3
Treatment of hypoxemia in obstructive sleep apnea.
Friedman M, Landsberg R, Ascher-Landsberg J.
Department of Otolaryngology, Illinois Masonic Medical Center, Chicago,USA.
Many patients suffering from obstructive sleep apnea (OSA) have intermittent oxygen desaturation associated with periods of apnea or hypopnea. Oxygen saturation levels below 90% are considered harmful. Usually, treatment is directed at correcting the apnea, which will in turn prevent hypoxemia. Unfortunately, many patients fail or are not candidates for nasal continuous positive airway pressure (CPAP) or surgical correction of their OSA. Forty-three patients with persistent OSA and nocturnal hypoxemia below 90% who were not candidates for additional surgical or CPAP therapy were treated with nocturnal oxygen supplementation. Standard symptoms associated with OSA and the Epworth Sleepiness Scale (ESS) were recorded before treatment and 30 days after the start of the treatment. In 21 patients, polysomnography studies were performed to compare the Respiratory Disturbance Index (RDI) score and minimum oxygen saturation levels when the patients were breathing room air or breathing 4 L/minute of oxygen by nasal cannula. Subjective symptoms of obstructive sleep apnea improved, and the ESS score significantly decreased after a 30-night treatment with oxygen. Split-night polysomnography showed a significant increase in minimum oxygen saturation during oxygen administration. The RDI did not significantly change with treatment. Oxygen administration for the correction of OSA-related nocturnal hypoxemia was both safe and effective in alleviation of OSA-related symptoms. It also appeared to have a beneficial effect on minimum oxygen saturation levels. Thus, oxygen therapy may be considered a treatment option in patients who fail to comply with CPAP and are not candidates for a surgical procedure.
Oxygen Supplementation vs CPAP
-
Sleepless on LI
- Posts: 3997
- Joined: Mon May 30, 2005 6:46 pm
- Location: Long Island, New York
Oxygen Supplementation vs CPAP
L o R i
-
Guest
I found this interesting also.
Treatment Complications
H.3 Sleep Disorders
Nocturnal oxygen desaturation in COPD patients is fairly common and often unrecognized. It is not usually caused by sleep apnea. Instead, sleep-related hypoxemia has been attributed to ventil-ation-perfusion abnormalities and transient hypo-ventilation during rapid eye movement, (REM), sleep. Nonobese patients with COPD who have daytime normoxemia and transient nocturnal hypoxemia during sleep rarely develop coexisting upper airway obstruc-tion or “obstructive sleep apnea.” But in some obese individuals with COPD an “overlap syndrome” occurs, adding an obstructive component to the typical mechanisms of transient hypoxemia.
Sleep-related hypoxemia is suggested by the presence of an expanded red cell mass as reflected by an increased hematocrit, along with a patient’s reports of morning headaches and daytime somnolence. Often, the patient's spouse is aware of intense snoring and even chooses to sleep in a separate room because of it. The spouse may also notice pauses in breathing followed by loud bursts of snoring when breathing resumes. These reports strongly suggest obstructive sleep apnea.
Diagnosis
Sleep-related hypoxemia and its mechanisms can be diagnosed via overnight home monitoring with a pulse oximeter. The pulse oximeter should be equipped with a memory system and a device to observe whether chest motion ceases during episodes of hypoxemia. Such pauses indicate that a coexisting obstructive component is present. Home sleep studies must be ordered and interpreted by a qualified specialist. Formal polysom-nography can provide additional information about the mechanisms associated with nocturnal hypoxemia, but such studies are expensive and must be conducted in a sleep lab, an unusual sleeping environment.
Treatment
Whether or not nocturnal hypoxemia should be treated with oxygen supplementation has been the subject of numerous studies. Two controlled clinical trials in patients with daytime normoxemia (PaO2 >60 mm Hg) showed a better survival rate in those who did not experience nocturnal desaturation compared with those who did. These studies also showed a trend toward increased survival in oxygen-treated desaturators, compared with desaturators who breathed room air. In fact, one double-blind trial of nocturnal oxygen supplementation for sleep desaturation in patients with daytime normoxemia showed an approximate 4 mm Hg reduction in pulmonary arterial pressures in those treated with oxygen. In contrast, patients who breathed only room air had an increase in their mean pulmonary arterial pressure of approximately 4 mm Hg.
At the present time, experts plan to conduct additional controlled clinical trials to determine whether or not mortality in COPD can be reduced when nocturnal desaturation is treated with oxygen. The outcomes of these studies will answer remaining questions about prescribing nocturnal oxygen. In light of our current knowledge in this area, what should primary care physicians do if nocturnal desaturation is suspected? If home monitoring with a pulse oximeter identifies nocturnal hypoxemia (SaO2 < 88%), and if symptoms of headache, fatigue, and poor exercise tolerance are present, it would be wise for the physician to prescribe home oxygen at a liter-flow rate sufficient to correct the hypoxemia. The oxygen “dose” can be determined by studying pulse oximeter readouts taken over several nights while the patient breathes supplemental oxygen. The physician should also ask the patient to report any symptom improvements. In the case of overlap syndrome, providing continuous positive airway pressure, (CPAP), via a well-fitting nasal mask can also be beneficial.
Caution should be used in prescribing sedative agents for insomnia in COPD patients, and patients should be warned against excessive alcohol consumption. Some of these agents may cause disordered sleep patterns and, in extreme cases, might depress respiration, thus augmenting nocturnal hypoventilation.
Treatment Complications
H.3 Sleep Disorders
Nocturnal oxygen desaturation in COPD patients is fairly common and often unrecognized. It is not usually caused by sleep apnea. Instead, sleep-related hypoxemia has been attributed to ventil-ation-perfusion abnormalities and transient hypo-ventilation during rapid eye movement, (REM), sleep. Nonobese patients with COPD who have daytime normoxemia and transient nocturnal hypoxemia during sleep rarely develop coexisting upper airway obstruc-tion or “obstructive sleep apnea.” But in some obese individuals with COPD an “overlap syndrome” occurs, adding an obstructive component to the typical mechanisms of transient hypoxemia.
Sleep-related hypoxemia is suggested by the presence of an expanded red cell mass as reflected by an increased hematocrit, along with a patient’s reports of morning headaches and daytime somnolence. Often, the patient's spouse is aware of intense snoring and even chooses to sleep in a separate room because of it. The spouse may also notice pauses in breathing followed by loud bursts of snoring when breathing resumes. These reports strongly suggest obstructive sleep apnea.
Diagnosis
Sleep-related hypoxemia and its mechanisms can be diagnosed via overnight home monitoring with a pulse oximeter. The pulse oximeter should be equipped with a memory system and a device to observe whether chest motion ceases during episodes of hypoxemia. Such pauses indicate that a coexisting obstructive component is present. Home sleep studies must be ordered and interpreted by a qualified specialist. Formal polysom-nography can provide additional information about the mechanisms associated with nocturnal hypoxemia, but such studies are expensive and must be conducted in a sleep lab, an unusual sleeping environment.
Treatment
Whether or not nocturnal hypoxemia should be treated with oxygen supplementation has been the subject of numerous studies. Two controlled clinical trials in patients with daytime normoxemia (PaO2 >60 mm Hg) showed a better survival rate in those who did not experience nocturnal desaturation compared with those who did. These studies also showed a trend toward increased survival in oxygen-treated desaturators, compared with desaturators who breathed room air. In fact, one double-blind trial of nocturnal oxygen supplementation for sleep desaturation in patients with daytime normoxemia showed an approximate 4 mm Hg reduction in pulmonary arterial pressures in those treated with oxygen. In contrast, patients who breathed only room air had an increase in their mean pulmonary arterial pressure of approximately 4 mm Hg.
At the present time, experts plan to conduct additional controlled clinical trials to determine whether or not mortality in COPD can be reduced when nocturnal desaturation is treated with oxygen. The outcomes of these studies will answer remaining questions about prescribing nocturnal oxygen. In light of our current knowledge in this area, what should primary care physicians do if nocturnal desaturation is suspected? If home monitoring with a pulse oximeter identifies nocturnal hypoxemia (SaO2 < 88%), and if symptoms of headache, fatigue, and poor exercise tolerance are present, it would be wise for the physician to prescribe home oxygen at a liter-flow rate sufficient to correct the hypoxemia. The oxygen “dose” can be determined by studying pulse oximeter readouts taken over several nights while the patient breathes supplemental oxygen. The physician should also ask the patient to report any symptom improvements. In the case of overlap syndrome, providing continuous positive airway pressure, (CPAP), via a well-fitting nasal mask can also be beneficial.
Caution should be used in prescribing sedative agents for insomnia in COPD patients, and patients should be warned against excessive alcohol consumption. Some of these agents may cause disordered sleep patterns and, in extreme cases, might depress respiration, thus augmenting nocturnal hypoventilation.
-
Sleepless on LI
- Posts: 3997
- Joined: Mon May 30, 2005 6:46 pm
- Location: Long Island, New York
SLEEPYHED,
You were singing my tune. I was morning headaches every day, snored like a machine and had the daytime somnolence they spoke of. My desats ONLY occurred in REM sleep. Boy, do I fit that category. Plus, I couldn't be further from obese. I thought my borderline high BP was due to the oxygen desats, but five months of being on CPAP only to fix the BP problem with a water pill proved that not to be the case.
Does this sound just like you, too? And I am seeing that patients did better on O2 therapy rather than room air/CPAP. I have a feeling I may be heading down this road very shortly. I am now, more than ever, very anxious to see my results. If they show desats still, I still won't think I need the CPAP, but rather O2 treatment. Why did they put me (and you) on this to begin with?
You were singing my tune. I was morning headaches every day, snored like a machine and had the daytime somnolence they spoke of. My desats ONLY occurred in REM sleep. Boy, do I fit that category. Plus, I couldn't be further from obese. I thought my borderline high BP was due to the oxygen desats, but five months of being on CPAP only to fix the BP problem with a water pill proved that not to be the case.
Does this sound just like you, too? And I am seeing that patients did better on O2 therapy rather than room air/CPAP. I have a feeling I may be heading down this road very shortly. I am now, more than ever, very anxious to see my results. If they show desats still, I still won't think I need the CPAP, but rather O2 treatment. Why did they put me (and you) on this to begin with?
L o R i
Why did they? It was just easy and the standard approach to our symptoms.
I changed sleep docs a while back and saw a new doctor. When I went to his office (at a major facility in Milwaukee) I was greeted in the room by 3 doctors. My doctor a Neurologists sleep doc, a Pulmunologists sleep doc and an ENT specializing in sleep medicine and nationally known. This blew me away that 3 specialist all evaluated me just to come up with a very simple diagnosis.
Deviated septum and clogged turbinates. Why could my G.P and original sleep doc not diagnosis this? I have no clue.
This explains the obstructive part of my problem, but does not entirely explain the desat during REM.
Like you I am not obese, but would like to drop the 15 lbs i had mentioned on an earlier post. This is really got me thinking today maybe after my nose plumbing I could possibly be done with this whole hosehead thing.
I understand that only a sleep study would tell for sure, but this time I will have them use oxygen for part of the test.
If anyone needs a great Sleep Doc in Milwaukee, let me know.
Kirk
I changed sleep docs a while back and saw a new doctor. When I went to his office (at a major facility in Milwaukee) I was greeted in the room by 3 doctors. My doctor a Neurologists sleep doc, a Pulmunologists sleep doc and an ENT specializing in sleep medicine and nationally known. This blew me away that 3 specialist all evaluated me just to come up with a very simple diagnosis.
Deviated septum and clogged turbinates. Why could my G.P and original sleep doc not diagnosis this? I have no clue.
This explains the obstructive part of my problem, but does not entirely explain the desat during REM.
Like you I am not obese, but would like to drop the 15 lbs i had mentioned on an earlier post. This is really got me thinking today maybe after my nose plumbing I could possibly be done with this whole hosehead thing.
I understand that only a sleep study would tell for sure, but this time I will have them use oxygen for part of the test.
If anyone needs a great Sleep Doc in Milwaukee, let me know.
Kirk
-
Sleepless on LI
- Posts: 3997
- Joined: Mon May 30, 2005 6:46 pm
- Location: Long Island, New York
COPD=Chronic Obstructive Pulmonary Disease
O.
O.
_________________
| Mask: AirFit™ P10 Nasal Pillow CPAP Mask with Headgear |
| Additional Comments: Machine: Resmed AirSense10 for Her with Climateline heated hose ; alternating masks. |
-
Sleepless on LI
- Posts: 3997
- Joined: Mon May 30, 2005 6:46 pm
- Location: Long Island, New York
O,
Thanks for the thought, but I do not fit the bill in any way as far as what I just read the symtpoms are. Plus, I don't smoke. Whenever I've had surgery, they laugh when they give me that plastic thing with the little balls in it that you're supposed to work at to be able to pull them up with your breath? First try, it's a joke. My lung power is incredible, I don't cough, suffer from bronchitis or emphysema, or spit up spewtum, or any of thse horrible symptoms associated with this. Unless you know more about it than what I just read, and I would be interested to hear it, I don't think that is the problem.
My son is concerned that is cardiac-related. He sais an x-ray, believe it or not, will show if there is fluid in the chest which will show if the heart is not pumping up to capacity, which is a possible cause for oxygen desaturation. Being I had 40+ years of heart trouble until being corrected four years ago, maybe my heart was compromised and is not pumping up to its capacity.
I am going to wait out to see the results of this test and then possibly go for a cardiology follow-up, which I haven't done since 2001 thinking I was fine now. This could be the cause of why I'm going through what I've been going through.
Thank you for the thought.
Thanks for the thought, but I do not fit the bill in any way as far as what I just read the symtpoms are. Plus, I don't smoke. Whenever I've had surgery, they laugh when they give me that plastic thing with the little balls in it that you're supposed to work at to be able to pull them up with your breath? First try, it's a joke. My lung power is incredible, I don't cough, suffer from bronchitis or emphysema, or spit up spewtum, or any of thse horrible symptoms associated with this. Unless you know more about it than what I just read, and I would be interested to hear it, I don't think that is the problem.
My son is concerned that is cardiac-related. He sais an x-ray, believe it or not, will show if there is fluid in the chest which will show if the heart is not pumping up to capacity, which is a possible cause for oxygen desaturation. Being I had 40+ years of heart trouble until being corrected four years ago, maybe my heart was compromised and is not pumping up to its capacity.
I am going to wait out to see the results of this test and then possibly go for a cardiology follow-up, which I haven't done since 2001 thinking I was fine now. This could be the cause of why I'm going through what I've been going through.
Thank you for the thought.
L o R i
-
Sleepless on LI
- Posts: 3997
- Joined: Mon May 30, 2005 6:46 pm
- Location: Long Island, New York
Re: 02 SAT
Those of you who know me know I will. Trust me, it's hard to keep me quiet...DEANC wrote:Lori, am very interested to hear what your o2 sat is, as this could be very enlightning and helpful. Please keep us posted. Thanks, Dean
L o R i
-
Guest
Lori,
you have got me thinking now. Maybe when I go back to my sleep doc I shoudl ask abotu this. My o2 levels dropped to 80% during my sleep study. and last time I was there for a reg appt they always take my bp and weight and yada yada, and they do the pulse ox thing and she had it on me and it was like 98 or 99% then I bent over to get something out the floor and she was like sit up! cause my o2 just me leaning over went down to like 90% I am wondering if they shoudl do the at home pulse ox thing overnight on me too just to make sure my o2 levels are staying good. Yes I do feel better on cpap by far but I do wake up a LOT (prob 5 or 6 times)during the night. Hmmm....
you have got me thinking now. Maybe when I go back to my sleep doc I shoudl ask abotu this. My o2 levels dropped to 80% during my sleep study. and last time I was there for a reg appt they always take my bp and weight and yada yada, and they do the pulse ox thing and she had it on me and it was like 98 or 99% then I bent over to get something out the floor and she was like sit up! cause my o2 just me leaning over went down to like 90% I am wondering if they shoudl do the at home pulse ox thing overnight on me too just to make sure my o2 levels are staying good. Yes I do feel better on cpap by far but I do wake up a LOT (prob 5 or 6 times)during the night. Hmmm....
-
Guest
-
Sleepless on LI
- Posts: 3997
- Joined: Mon May 30, 2005 6:46 pm
- Location: Long Island, New York
-
Guest
I do believe that it MAY be an option - nocturnal O2 - but not a substitute for CPAP. CPAP should always be tried first! As mentioned, O2 does not change the RDI or AHI - thus you are not getting proper sleep, even with the O2 - it does not change the fact that you are having obstructed breathing. It only changes the sats. I did not have any major desats during my sleep study - the lowest I went was to 90-91% - not bad at all as far as OSA goes - BUT my AHI was in the 26 range and my arousals were 26 per hour on top of that - so I was "arousing" 50 times an hour or so wither due to obstructions that caused apnea, or obstructions that my brain was trying to correct before apnea occurred. So you can only imagine that with an AHI of 26 - you are still going to be tired regardless of your O2 sat.