Diagnosing Complex Sleep Apnea

[Sam888]

Have any guidelines been established, and if so, what are they in diagnosing Comp SA?  What markers before and during the PSG must be present when physicians suspect this newly defined Sleep disordered breathing?

[Sam888]

Thank you!. I I also understand that Complex SA can be present with or without CPAP as indicated in the article by Geoffrey S Gilmartin; Robert W Daly; Robert J Thomas on "Recognition and Management of Complex Sleep-Disordered Breathing (see below).

Also, how does the recently published information (October 22, 2007 Biology Journal) implicating the amyglada in working "overtime" in sleep deprived patients,  suggesting a link between sleep interruption/disruption and anxiety? How has this affected the medical community in  diagnosing or treating patients who have poor sleep and mood disorders?  Are they still typically focusing  on treating the mood disorder first with medication(s) in those patients who have sleep apnea but who don't respond to well to CPAP without further exploring the plausibilty of Complex Sleep Disordered Breathing?

Recognition and Management of Complex Sleep-Disordered Breathing
Geoffrey S Gilmartin; Robert W Daly; Robert J Thomas
Curr Opin Pulm Med. 2005;11(6):485-493. ©2005 Lippincott Williams & Wilkins
Posted 10/27/2005

Summary: Complex sleep-disordered breathing is a distinct form of sleep apnea. It has recognizable characteristics that are present without, and often worsened during, positive airway pressure treatment. Both sleep state stability and the behavior of the respiratory control system contribute to this complexity. It is only with a clear understanding of the factors contributing to complex sleep-disordered breathing that implementation of truly effective clinical therapy can be achieved for this disorder, which to date is poorly controlled.

[Enoch Choi, MD]

This is a pretty newly defined disorder.  The following recently released study highlights the need for prospective trials to determine the best treatment since CPAP isn't appropriate for all complicated sleep apnea patients.

There is even confusion over the definition.  The most common sleep apne is obstructive (OSA), due to floppy tissues that block airflow, and typically improves with CPAP.  Central sleep apnea (CSA) is due to the brain not sending the signa to breathe to the lungs, such as wth heart failure or strokes.  Complex sleep apnea is a mix of the 2.  

Although complex sleep apnea can be suspected in patients with CHF or strokes, it's not diganosed until a PSG diagnoses the OSA and an individual is found not to respond well to CPAP.  Adaptive servo ventilation (ASV or VPAP) can be helpful for some patients.

Dr. Enoch Choi, MD
Palo Alto, CA


Tomasz J. Kuzniar1, Snigdha Pusalavidyasagar2, Peter C. Gay2 and Timothy I. Morgenthaler2, 3

(1) Division of Pulmonary and Critical Care, Evanston Northwestern Healthcare, Evanston, IL, USA
(2) Sleep Disorders Center, Mayo Clinic, Rochester, MN, USA
(3) Sleep Disorders Center, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
Published online: 15 September 2007

Abstract  Patients with complex sleep apnea syndrome (CompSAS) have obstructive sleep apnea but develop troublesome central sleep apnea activity or Cheyne–Stokes breathing when provided continuous positive airway pressure (CPAP) therapy. We examined whether CompSAS activity persists with long-term CPAP treatment. We retrospectively identified all patients with CompSAS who underwent two therapeutic polysomnograms (PSGs) separated by at least 1 month during 2003–2005. We compared PSG findings between the initial and follow-up study and noted clinical responses to therapy. We identified 13 CompSAS patients meeting criteria. Most follow-up PSGs were ordered after an abnormal overnight oximetry on CPAP or because of CPAP intolerance after 195 (49–562) days. The residual apnea–hypopnea index (AHI) on CPAP decreased from 26 (23–40) on the first PSG to 7 (3–21.5) on the follow-up PSG. Only seven patients reached AHI < 10 and 6 had AHI ≥ 10 (“CPAP nonresponders”) at follow-up. “CPAP nonresponders” were sleepier (Epworth Sleepiness Score 13 [12.5–14] vs 9 [6–9.5], p = 0.03) and trended toward lower body mass index (29.7 [28.6–31.6] vs 34.3 [32.5–35.1], p = 0.06). Both groups were equally compliant with CPAP therapy. Although the AHI tends to improve over time in CompSAS patients treated with CPAP, in this retrospective study nearly half-maintained a persistently elevated AHI. A prospective trial is merited to determine the optimal treatment for these patients.
Keywords  Continuous positive airway pressure - Sleep apnea - Complex sleep apnea


Timothy I. Morgenthaler
Email: tmorgenthaler @ mayo.edu