Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Central Sleep Apnea Syndromes Treatment & Management

  • Author: Kendra Becker, MD, MPH; Chief Editor: Ryland P Byrd, Jr, MD  more...
 
Updated: Mar 16, 2015
 

Medical Care

No clear guidelines are available on when or whether to treat central sleep apnea in the absence of symptoms, particularly when central sleep apnea is discovered after polysomnography (PSG) is performed for another reason. Clearly, when the symptoms are present, treatment is warranted. The decision to treat should be made on an individual basis.

Up to 20% of central sleep apnea cases resolve spontaneously. If the patient is not symptomatic, observation may be the only appropriate step. This may be the case in patients who have central sleep apnea during sleep-wake transition, patients without significant oxygen desaturation, or in those who experience central sleep apnea during continuous positive airway pressure (CPAP) treatment of obstructive sleep apnea.

If present, treatment of the underlying disorder often improves central sleep apnea. For example, descending to a low altitude is effective in treating high-altitude periodic breathing. Similarly, instituting nocturnal dialysis and optimizing medical treatment are often effective for Cheyne-Stokes breathing-central sleep apnea (CSB-CSA) due to renal failure and heart failure, respectively. Heart transplantation has also been reported either to resolve CSB-CSA or to decrease the cycle length of CSB-CSA breathing. Interestingly, a small study indicates that exercise training lessens the severity of obstructive sleep apnea but does not affect central sleep apnea in patients with heart failure and sleep disordered breathing.[25] These findings provide compelling evidence for prescribing exercise training in the treatment of patients with heart failure with sleep apnea, particularly in those with obstructive sleep apnea, but larger studies are needed to verify this finding.

Several different treatments aimed at central sleep apnea include positive airway pressure, adaptive servo ventilation (ASV), oxygen, added dead space, carbon dioxide inhalation, and overdrive atrial pacing.

Continuous positive airway pressure

CPAP improves cardiac function in patients with congestive heart failure and CSB-CSA.

A study published in 2000 suggesting that CPAP may reduce the combined rate of mortality and cardiac transplantation in heart failure patients with CSB-CSA.[26] This observation raised substantial interest and resulted in the institution of a large prospective study, the Canadian Prospective Continuous Positive Airway Pressure (CANPAP) trial for congestive heart failure trial. While this latter study failed to confirm a mortality benefit, CPAP was associated with attenuation of central sleep apnea, improvement of nocturnal oxygenation, lowering of norepinephrine levels, improvement in ejection fraction, and the increased distance walked in six minutes.[27]

Another study demonstrated that despite lowering of the AHI, CPAP had no significant effect on the frequency of arousals, sleep efficiency, or the amounts of total, slow wave, or rapid eye movement (REM) sleep in heart failure patients with central sleep apnea.[28]

Bilevel positive airway pressure

Bilevel positive airway pressure (BIPAP) is effective for treating patients with hypercapnic central sleep apnea (associated with hypoventilation). The inspiratory positive airway pressure (IPAP) is higher than the expiratory positive airway pressure (EPAP). A high IPAP-to-EPAP differential provides breath-by-breath pressure support to augment ventilation. In addition to reinforcing the spontaneous breaths, patients with central sleep apnea may require additional breaths set as a back-up rate, especially when the central apneas are long. Patients with high-pressure requirements may benefit by elevation of the head end to 45-60°, which often dramatically decreases their pressure requirements.

Pressure-cycled BIPAP is usually adequate. Volume-cycled ventilators are rarely necessary and have their own limitations in terms of inability to adjust for high leaks, humidification, and expense.

Some patients with nonhypercapnic central sleep apnea, such as CSB-CSA, and primary central sleep apnea have been shown to benefit from BIPAP. Because BIPAP can be used with a back-up rate, it is beneficial in patients with long apneas. However, BIPAP, especially when used with a high IPAP-to-EPAP differential, has the potential to worsen central sleep apnea by lowering the PaCO2. BIPAP has been used to treat patients with heart failure and CSB-CSA with variable results and further studies are needed to better assess the role of BIPAP treatment in this group of patients.

Added dead space or inhaled carbon dioxide

Added dead space by attaching a plastic cylinder of variable volume (400-800 mL) to a tightly fitting mask can act as a source of increased carbon dioxide concentration in the inspired air and can increase the carbon dioxide reserves above the apneic threshold. Such a treatment in an experimental setting was effective against both primary central sleep apnea and CSB-CSA. The increase in PaCO2 is miniscule (approximately 1.5-2 mm Hg) but can be effective in stabilizing the breathing pattern.

Minimizing hypocapnia, by adding 100-150 mL enhanced expiratory rebreathing space (EERS), was documented to improve CSA and is a potentially useful adjunctive therapy for positive pressure–associated respiratory instability and salvage of some CPAP treatment failures.[29]

Similar results have been obtained by adding supplemental carbon dioxide (5%), but safety and accuracy of carbon dioxide delivery devices remains a concern.

Another potential problem of added dead space or inhaled carbon dioxide is worsening of obstructive sleep apnea by the increased mechanical load. Hypercarbia stimulates sympathetic discharge with potential deleterious effects on the heart.

Adaptive servo ventilation

ASV is used for treatment for CSA, especially CSB-CSA.

ASV provides positive expiratory airway pressure (EPAP) and inspiratory pressure support (IPAP), which is servocontrolled based on the detection of CSA. The device provides a fixed EPAP determined to eliminate obstructive sleep apnea. The ASV device changes the inspiratory pressure above the expiratory pressure as required to normalize patients’ ventilation. Pressure support may be set to a minimum of 0 and maximum pressure minus the EPAP (the MaxPS should equal MaxPressure – MinEPAP). With normal breathing, the device acts like fixed CPAP by providing minimal pressure support. When the device detects CSA, the device increases the pressure support above the expiratory pressure up to a maximum pressure, which can be set by the user. Additionally, an automatic, timed backup up rate is available.

Studies demonstrate that ASV is superior to conventional positive airway pressure therapy for controlling the number of central sleep apneas,[30, 31] improving sleep architecture and daytime hypersomnolence, particularly for CSB-CSA, central sleep apnea syndrome, and complex sleep apnea. In one study, both ASV and CPAP decreased the AHI, but, noticeably, only ASV completely corrected CSA-CSA by attaining a AHI below 10/h.[30] ASV may also effectively reduced central apneas and the overall AHI in patients on long-term opiates.[32]

The acute use of ASV is effective on CSA by increasing oxygen saturation and reducing heart rate and heart rate variability.[33] In a long-term 12-month study, ASV improved CSA-CSR and brain natriuretic peptide more effectively than CPAP in patients with heart failure.[34]

The benefit of ASV in treating patients with heart failure and CSB-CSA is dependent on the suppression of the periodic breathing.[35] Therefore, ASV should be prescribed with the guidance of PSG that documents suppression of CSB-CSA.

Oxygen

Supplemental oxygen may be effective in some patients with CSB-CSA due to heart failure and has also been shown to improve ejection fraction.[36] It is thought to work by decreasing the hypoxic drive and thus attenuating the hyperventilatory response to a change in PaCO2. When comparing oxygen therapy to ASV, CSA-CSR is reduced to a greater extent by ASV than oxygen therapy over 8 weeks but oxygen therapy is better accepted.[37] Oxygen is effective against high-altitude periodic breathing and improves the sleep architecture. Any patient with central sleep apnea and significant hypoxemia is a potential candidate for a trial with supplemental oxygen. The optimal flow rate can be titrated during PSG until central sleep apnea resolves.

Overdrive atrial pacing

Overdrive atrial pacing has been shown to reduce both obstructive and central apneas in patients with sleep-disordered breathing who have dual-chamber pacemakers. One study demonstrated a reduction in AHI of approximately 60% in patients who received pacemakers for symptomatic sinus bradycardia.[38] Obstructive apneas fell from 6 to 3 per hour, central apneas from 13 to 6 per hour, and the overall AHI from 28 to 11 events per hour. The mechanism behind this phenomenon has not been definitively characterized, although stabilization of autonomic tone has been suggested to play a role. Other researchers, however, failed to reproduce these results.[39]

 
 
Contributor Information and Disclosures
Author

Kendra Becker, MD, MPH Sleep Medicine Department, Kaiser Permanente Fontana Medical Center

Kendra Becker, MD, MPH is a member of the following medical societies: American College of Physicians, American Medical Association, American Academy of Sleep Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Jeanne M Wallace, MD, MPH Professor of Clinical Medicine, University of California at Los Angeles School of Medicine

Jeanne M Wallace, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Chair of the Clinical Competency Committee, Pulmonary and Critical Care Fellowship Program, Senior Staff and Attending Physician, Division of Pulmonary and Critical Care Medicine, Henry Ford Health System; Chair, Guideline Oversight Committee, American College of Chest Physicians

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, Society of Critical Care Medicine, American Thoracic Society

Disclosure: Nothing to disclose.

Chief Editor

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, World Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Rahul K Kakkar, MD, FCCP, FAASM, to the development and writing of this article.

References
  1. Panossian LA, Avidan AY. Review of sleep disorders. Med Clin North Am. 2009 Mar. 93(2):407-25, ix. [Medline].

  2. American Academy of Sleep Medicine. International Classification of Sleep Disorders. 2nd ed. Westchester, Ill: American Academy of Sleep Medicine; 2005.

  3. White DP. Pathogenesis of obstructive and central sleep apnea. Am J Respir Crit Care Med. 2005 Dec 1. 172(11):1363-70. [Medline].

  4. Arzt M, Harth M, Luchner A, et al. Enhanced ventilatory response to exercise in patients with chronic heart failure and central sleep apnea. Circulation. 2003 Apr 22. 107(15):1998-2003. [Medline].

  5. Teichtahl H, Wang D, Cunnington D, et al. Ventilatory responses to hypoxia and hypercapnia in stable methadone maintenance treatment patients. Chest. 2005 Sep. 128(3):1339-47. [Medline].

  6. Wang D, Teichtahl H, Drummer O, et al. Central sleep apnea in stable methadone maintenance treatment patients. Chest. 2005 Sep. 128(3):1348-56. [Medline].

  7. Walker JM, Farney RJ, Rhondeau SM, et al. Chronic opioid use is a risk factor for the development of central sleep apnea and ataxic breathing. J Clin Sleep Med. 2007 Aug 15. 3(5):455-61. [Medline].

  8. Verbraecken JA, De Backer WA. Upper airway mechanics. Respiration. 2009. 78(2):121-33. [Medline]. [Full Text].

  9. Bixler EO, Vgontzas AN, Ten Have T, Tyson K, Kales A. Effects of age on sleep apnea in men: I. Prevalence and severity. Am J Respir Crit Care Med. 1998 Jan. 157(1):144-8. [Medline].

  10. Hanly PJ, Zuberi-Khokhar NS. Increased mortality associated with Cheyne-Stokes respiration in patients with congestive heart failure. Am J Respir Crit Care Med. 1996 Jan. 153(1):272-6. [Medline].

  11. Luo Q, Zhang HL, Tao XC, Zhao ZH, Yang YJ, Liu ZH. Impact of untreated sleep apnea on prognosis of patients with congestive heart failure. Int J Cardiol. 2009 Apr 2. [Medline].

  12. Mehra R, Stone KL, Varosy PD, et al. Nocturnal Arrhythmias across a spectrum of obstructive and central sleep-disordered breathing in older men: outcomes of sleep disorders in older men (MrOS sleep) study. Arch Intern Med. 2009 Jun 22. 169(12):1147-55. [Medline]. [Full Text].

  13. Johansson P, Alehagen U, Svanborg E, Dahlstrom U, Brostrom A. Sleep disordered breathing in an elderly community-living population: Relationship to cardiac function, insomnia symptoms and daytime sleepiness. Sleep Med. 2009 Oct. 10(9):1005-11. [Medline].

  14. Eckert DJ, Jordan AS, Merchia P, Malhotra A. Central sleep apnea: Pathophysiology and treatment. Chest. 2007 Feb. 131(2):595-607. [Medline]. [Full Text].

  15. Javaheri S. Central sleep apnea in congestive heart failure: prevalence, mechanisms, impact, and therapeutic options. Semin Respir Crit Care Med. 2005 Feb. 26(1):44-55. [Medline].

  16. Leung RS, Huber MA, Rogge T, Maimon N, Chiu KL, Bradley TD. Association between atrial fibrillation and central sleep apnea. Sleep. 2005 Dec 1. 28(12):1543-6. [Medline].

  17. Malhotra A, Bertisch S, Wellman A. Complex sleep apnea: it isn''t really a disease. J Clin Sleep Med. 2008 Oct 15. 4(5):406-8. [Medline]. [Full Text].

  18. Javaheri S, Smith J, Chung E. The prevalence and natural history of complex sleep apnea. J Clin Sleep Med. 2009 Jun 15. 5(3):205-11. [Medline]. [Full Text].

  19. Guilleminault C, Simmons FB, Motta J, et al. Obstructive sleep apnea syndrome and tracheostomy. Long-term follow-up experience. Arch Intern Med. 1981 Jul. 141(8):985-8. [Medline].

  20. Anderson P. New guideline for sleep apnea diagnosis. Medscape Medical News. Available at http://www.medscape.com/viewarticle/829717. Accessed: August 11, 2014.

  21. Qaseem A, Dallas P, Owens DK, Starkey M, Holty JE, Shekelle P. Diagnosis of obstructive sleep apnea in adults: a clinical practice guideline from the american college of physicians. Ann Intern Med. 2014 Aug 5. 161(3):210-20. [Medline].

  22. Collop NA, Anderson WM, Boehlecke B, et al. Clinical guidelines for the use of unattended portable monitors in the diagnosis of obstructive sleep apnea in adult patients. Portable Monitoring Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2007 Dec 15. 3(7):737-47. [Medline]. [Full Text].

  23. Tonelli de Oliveira AC, Martinez D, et al. Diagnosis of obstructive sleep apnea syndrome and its outcomes with home portable monitoring. Chest. 2009 Feb. 135(2):330-6. [Medline].

  24. Santos-Silva R, Sartori DE, Truksinas V, et al. Validation of a portable monitoring system for the diagnosis of obstructive sleep apnea syndrome. Sleep. 2009 May 1. 32(5):629-36. [Medline]. [Full Text].

  25. Ueno LM, Drager LF, Rodrigues AC, et al. Effects of exercise training in patients with chronic heart failure and sleep apnea. Sleep. 2009 May 1. 32(5):637-47. [Medline]. [Full Text].

  26. Sin DD, Logan AG, Fitzgerald FS, Liu PP, Bradley TD. Effects of continuous positive airway pressure on cardiovascular outcomes in heart failure patients with and without Cheyne-Stokes respiration. Circulation. 2000 Jul 4. 102(1):61-6. [Medline].

  27. Bradley TD, Logan AG, Kimoff RJ, et al. Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med. 2005 Nov 10. 353(19):2025-33. [Medline].

  28. Ruttanaumpawan P, Logan AG, Floras JS, Bradley TD. Effect of continuous positive airway pressure on sleep structure in heart failure patients with central sleep apnea. Sleep. 2009 Jan 1. 32(1):91-8. [Medline]. [Full Text].

  29. Gilmartin G, McGeehan B, Vigneault K, Daly RW, Manento M, Weiss JW, et al. Treatment of positive airway pressure treatment-associated respiratory instability with enhanced expiratory rebreathing space (EERS). J Clin Sleep Med. 2010 Dec 15. 6(6):529-38. [Medline]. [Full Text].

  30. Philippe C, Stoïca-Herman M, Drouot X, et al. Compliance with and effectiveness of adaptive servoventilation versus continuous positive airway pressure in the treatment of Cheyne-Stokes respiration in heart failure over a six month period. Heart. 2006 Mar. 92(3):337-42. [Medline].

  31. Allam JS, Olson EJ, Gay PC, Morgenthaler TI. Efficacy of adaptive servoventilation in treatment of complex and central sleep apnea syndromes. Chest. 2007 Dec. 132(6):1839-46. [Medline].

  32. Javaheri S, Malik A, Smith J, Chung E. Adaptive pressure support servoventilation: a novel treatment for sleep apnea associated with use of opioids. J Clin Sleep Med. 2008 Aug 15. 4(4):305-10. [Medline]. [Full Text].

  33. D'Elia E, Vanoli E, La Rovere MT, Fanfulla F, Maggioni A, Casali V, et al. Adaptive servo ventilation reduces central sleep apnea in chronic heart failure patients: beneficial effects on autonomic modulation of heart rate. J Cardiovasc Med (Hagerstown). 2012 Apr 11. [Medline].

  34. Randerath WJ, Nothofer G, Priegnitz C, Anduleit N, Treml M, Kehl V, et al. Long-term auto servo-ventilation or constant positive pressure in heart failure and co-existing central with obstructive sleep apnea. Chest. 2012 Jan 26. [Medline].

  35. Brown LK. Filling in the gaps: the role of noninvasive adaptive servoventilation for heart failure-related central sleep apnea. Chest. 2008 Jul. 134(1):4-7. [Medline].

  36. Sasayama S, Izumi T, Matsuzaki M, et al. Improvement of quality of life with nocturnal oxygen therapy in heart failure patients with central sleep apnea. Circ J. 2009 Jul. 73(7):1255-62. [Medline].

  37. Campbell AJ, Ferrier K, Neill AM. The effect of oxygen versus adaptive pressure support servo-ventilation in patients with Central Sleep Apnoea-Cheyne Stokes Respiration and Congestive Heart Failure. Intern Med J. 2011 Oct 27. [Medline].

  38. Garrigue S, Bordier P, Jais P, et al. Benefit of atrial pacing in sleep apnea syndrome. N Engl J Med. 2002 Feb 7. 346(6):404-12. [Medline].

  39. Luthje L, Unterberg-Buchwald C, Dajani D, Vollmann D, Hasenfuss G, Andreas S. Atrial overdrive pacing in patients with sleep apnea with implanted pacemaker. Am J Respir Crit Care Med. 2005 Jul 1. 172(1):118-22. [Medline].

  40. Javaheri S, Parker TJ, Wexler L, Liming JD, Lindower P, Roselle GA. Effect of theophylline on sleep-disordered breathing in heart failure. N Engl J Med. 1996 Aug 22. 335(8):562-7. [Medline].

  41. Quadri S, Drake C, Hudgel DW. Improvement of idiopathic central sleep apnea with zolpidem. J Clin Sleep Med. 2009 Apr 15. 5(2):122-9. [Medline]. [Full Text].

 
Previous
Next
 
The role of loop gain in determining respiratory instability. A) When loop gain is less than 1, the tendency for an overshoot of the corrective response to an apnea or hypopnea is lessened, and ventilation returns to a steady pattern. B) When loop gain is greater than or equal to 1, the vigorous responses to respiratory disturbances result in continuous oscillation between the events and the corrections, resulting in an unstable periodic breathing pattern. Adapted from White DP Pathogenesis of obstructive and central sleep apnea. Am J Respir Crit Care Med. Dec 1 2005;172(11):1363-70.
This polysomnogram demonstrates central sleep apnea and Biot respiration in a patient receiving long-term morphine for chronic pain. The Biot pattern may be irregular without any type of periodicity, or it can consist of runs of similar-sized breaths alternating with central apneas.
Obstructive sleep apnea (OSA): This polysomnogram demonstrates typical hypopneas occurring in OSA prior to continuous positive airway pressure titration. In OSA, airflow is absent or reduced, but ventilatory effort persists.
Cheyne Stokes: This polysomnogram represents Cheyne Stokes breathing and occurred subsequent to continuous positive airway pressure titration for OSA in the same patient in the previous media file. Cheyne Stokes breathing has a classic crescendo-decrescendo breathing pattern.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.