Description (a quote from first linked article): Patients with complex sleep apnea at first appear to have obstructive sleep apnea and stop breathing 20 to 30 times per hour each night. But unlike typical obstructive sleep apnea patients, their breathing problem is not completely alleviated by a CPAP (continuous airway pressure) machine, which functions like a pneumatic splint to open a patient's airway. Instead, once the CPAP is applied to complex sleep apnea patients, the obstruction seems to dissipate, but still they do not breathe properly. Symptoms of central sleep apnea then appear and fragmented sleep results, due to frequent pauses in breathing.
Prevalence:
Abstracts of several studies are posted separately below. In the Mayo study, the prevalence of complex sleep apnea syndrome, OSAHS, and CSA (in 223 adults consecutively rerferred over 1 month) was 15%, 84%, and 0.4%.
In the Australian study, the prevalence of 'CSA-CPAP' was found to be 13%.
Following are several links to information about Complex Sleep Apnea (CompSA).
Complex Sleep Apnea Article at MedPage Today
By Neil Osterweil, Senior Associate Editor, MedPage Today
Reviewed by Robert Jasmer, MD; Assistant Professor of Medicine, University of California, San Francisco
September 01, 2006
http://www.medpagetoday.com/Pulmonary/SleepDisorders/tb/4034
(It is my understanding that ResMed may introduce an upgraded/newer version of above device sometime in early 2008).
Respironics
BiPAP® Auto SV™ Sleep Therapy System [...] "it's clinically proven to treat obstructive, central and complex apneas and hypopneas, as well as periodic breathing."
Also from the Respironics site:
"Complex Sleep Apnea
Complex sleep apnea is a condition that occurs when a patient is identified as having OSA, but with the application of Continuous Positive Airway Pressure (CPAP) to eliminate the OSA, the patient develops Central Sleep Apnea. The cause of complex sleep apnea is not known at this time".
Link: http://bipapautosv.respironics.eu/
(I am not sure when the Respironics device will be available in the US market. It was FDA approved March 2007.)
Last edited by Guest MJ on Sat Feb 09, 2008 8:34 pm; edited 6 times in total
Complex Sleep Apnea Syndrome (CompSAS) was first described in 2006. At the beginning of 2008, it seems that there are many professionals who are unaware of its existence, which is a problem for those patients who may have it. The following are good articles for patients to show to their health care providers:
Trained to identify typical obstructive and central sleep apnea phenotypes of sleep disordered breathing (SDB), many sleep lab clinicians and technicians remain unfamiliar with complex sleep apnea syndrome (complex SAS). This syndrome can be considered the simultaneous presence of upper airway obstruction and chemoreflex-driven respiratory oscillations during sleep. Complex SAS is often encountered in the clinical sleep laboratory. The complex-pattern breathing of predominantly mixed apneas and obstructed periodic breathing in some patients or obstructive apneas that resolve with continuous positive airway pressure (CPAP) only to reveal central apnea or the Cheyne-Stokes breathing pattern is not classified as a distinct breathing disorder.1,2,3 Their prevalence ranges from 15% 1 to as high as 48%4 in clinical practice, based on study population characteristics. The difficulty in recognition may be directly related to the standard practice in sleep labs of not scoring mixed apneas and hypopneas and limitations of viewing the polysomnography (PSG) in 30 second epochs and the scoring guidelines governing it.5 Moreover, the International Classification of Sleep Disorders–2 explicitly states that mixed apneas should be considered obstructive. The purpose of this review is to enhance the knowledge base of SDB phenotypes, to create greater awareness of complex SAS among sleep lab clinicians and technicians, and to define complex SAS in objective terms that are extracted from the current literature.
Last edited by Guest MJ on Mon Feb 18, 2008 1:57 pm; edited 8 times in total
Complex sleep apnea syndrome: is it a unique clinical syndrome? Sleep. 2006 Sep 1;29(9):1203-9.
Morgenthaler TI, Kagramanov V, Hanak V, Decker PA.Mayo Clinic Sleep Disorders Center, Division of Pulmonary and Critical Care Medicine, 200 First Street SW, Rochester, MN 55905, USA.
STUDY OBJECTIVES: Some patients with apparent obstructive sleep apnea hypopnea syndrome (OSAHS) have elimination of obstructive events but emergence of problematic central apneas or Cheyne-Stokes breathing pattern. Patients with this sleep-disordered breathing problem, which for the sake of study we call the "complex sleep apnea syndrome," are not well characterized. We sought to determine the prevalence of complex sleep apnea syndrome and hypothesized that the clinical characteristics of patients with complex sleep apnea syndrome would more nearly resemble those of patients with central sleep apnea syndrome (CSA) than with those of patients with OSAHS. DESIGN: Retrospective review SETTING: Sleep disorders center. PATIENTS OR PARTICIPANTS: Two hundred twenty-three adults consecutively referred over 1 month plus 20 consecutive patients diagnosed with CSA. INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: Prevalence of complex sleep apnea syndrome, OSAHS, and CSA in the 1-month sample was 15%, 84%, and 0.4%, respectively. Patients with complex sleep apnea syndrome differed in gender from patients with OSAHS (81% vs 60% men, p < .05) but were otherwise similar in sleep and cardiovascular history. Patients with complex sleep apnea syndrome had fewer maintenance-insomnia complaints (32% vs 79%; p < .05) than patients with CSA but were otherwise not significantly different clinically. Diagnostic apnea-hypopnea index for patients with complex sleep apnea syndrome, OSAHS, and CSA was 32.3 +/- 26.8, 20.6 +/- 23.7, and 38.3 +/- 36.2, respectively (p = .005). Continuous positive airway pressure suppressed obstructive breathing, but residual apnea-hypopnea index, mostly from central apneas, remained high in patients with complex sleep apnea syndrome and CSA (21.7 +/- 18.6 in complex sleep apnea syndrome, 32.9 +/- 30.8 in CSA vs 2.14 +/- 3.14 in OSAHS; p < .001). CONCLUSIONS: Patients with complex sleep apnea syndrome are mostly similar to those with OSAHS until one applies continuous positive airway pressure. They are left with very disrupted breathing and sleep on continuous positive airway pressure. Clinical risk factors don't predict the emergence of complex sleep apnea syndrome, and best treatment is not known.
Central sleep apnea on commencement of continuous positive airway pressure in patients with a primary diagnosis of obstructive sleep apnea-hypopnea. J Clin Sleep Med. 2007 Aug 15;3(5):462-6
Lehman S, Antic NA, Thompson C, Catcheside PG, Mercer J, McEvoy RD.
Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, South Australia, Australia.
INTRODUCTION: Central sleep apnea (CSA) may occur in patients with snoring and obstructive sleep apnea-hypopnea (OSAH) during commencement of continuous positive airway pressure (CPAP) therapy. The presence of CSA may limit the effectiveness of CPAP therapy. The aims of this study were to assess the prevalence of CSA amongst patients starting CPAP for OSAH and to identify possible predictors of this condition. METHODS: We reviewed the polysomnograms (PSGs) and clinical records of 99 consecutive patients with a primary diagnosis of OSAH who were referred for an in-laboratory CPAP titration study. Patients with a CSA Index of > or =5 per hour at or near (+/-1 cm H2O) prescribed CPAP level formed the CSA-CPAP group. The remaining patients made up the noCSA-CPAP group. Demographic, baseline and CPAP titration PSG variables were compared between the 2 two groups. RESULTS: 13 subjects (13.1%) had CSA-CPAP. Patients with and without CSA-CPAP did not differ with respect to age or body mass index. 46% of patients with CSA-CPAP had CSA on their baseline PSGs compared with 8% in the noCSA-CPAP group (p <0.01). CSA-CPAP patients also had a higher apnea-hypopnea index (72.1 vs. 52.7 p = 0.02), a higher arousal index (43.3 vs. 29.2 p <0.01), and a higher mixed apnea index (6.8 vs. 1.3 p = 0.03), on their baseline PSGs. Therapeutic CPAP could not be determined in 2 CSA-CPAP patients due to a very high frequency (of severe) central apneas. In the remaining 11, the CPAP prescription to eliminate obstructive events was higher than in the noCSA-CPAP group (11.0 vs. 9.3 p = 0.08). AHI was greater both at or near prescribed CPAP (48.8 vs. 6.7 p <0.01) and overall (47.4 vs. 14.9 p <0.01). A history of ischemic heart disease or heart failure was more frequent amongst patients with CSA-CPAP than those without (p = 0.03). CONCLUSION: A significant minority of patients with a primary diagnosis of OSAH have either emergence or persistence of CSA on CPAP. Risk factors include male sex, history of cardiac disease, and CSA on baseline PSG.
That was done because this Interesting Links section doesn't get seen as often or by as many people. Your questions might get a better and quicker response in that section. My apologies for not seeing your post until now. Hopefully you've gotten your issue resolved by now, but if not, you might post again in the Help Sleep Apnea section.
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