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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.


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

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.


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.


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.

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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.
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