Central Sleep Apnea Treatment & Management

  • Author: Kendra Becker, MD, MPH; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: Jan 22, 2010
 

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 have been suggested to 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 by Ueno and colleagues 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.[23] 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 further evaluate.

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 by Sin and colleagues[24] published in 2000 suggesting that CPAP may reduce the combined rate of mortality and cardiac transplantation in heart failure patients with CSB-CSA raised substantial interest that supported the institution of a large prospective study, the Canadian Prospective Continuous Positive Airway Pressure (CANPAP) trial for congestive heart failure. While this study failed to show 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 6 minutes.[25]
    • 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.[26]
  • 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 has been shown to be 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. 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 represents a relatively novel way of approaching treatment for central sleep apnea, especially CSB-CSA.
    • The device provides a fixed CPAP of 5 cm water. Superimposed on this CPAP are pressure swings that vary from a minimum setting of 4-10 cm water. The variation in the pressure swings is controlled by a high-gain integral controller. When the ASV is at its minimum support, a maximum support of 9 cm water and a minimum support of 5 cm water (CPAP) is provided during the pressure swings. If the patient’s breathing decreases, the servo-controlled mechanism increases the pressure swings to achieve a target ventilation of 90% of the patient’s baseline ventilation. A maximum pressure swing of 10 cm water (ie, a maximum pressure of 15 cm water and a minimum of 5 cm water) can be achieved.
    • Studies show that ASV is superior to conventional positive airway pressure therapy for controlling the number of central sleep apneas,[27, 28] improving sleep architecture and daytime hypersomnolence, particularly for CSB-CSA, central sleep apnea syndrome, and complex sleep apnea. In one study,[27] both ASV and CPAP decreased the AHI, but, noticeably, only ASV completely corrected CSA-CSA, with AHI below 10/h. A small study by Javaheri et al[29] demonstrated ASV more effectively reduced central apneas and the overall AHI in patients on long-term opiates.
    • The benefit of ASV in treating patients with heart failure and CSB-CSA is dependent on the suppression of the periodic breathing.[30] 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.[31] It is thought to work by decreasing the hypoxic drive and thus attenuating the hyperventilatory response to a change in PaCO2. 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. Garrigue and coworkers[32] reported a reduction in AHI of approximately 60% in patients who received pacemakers for symptomatic sinus bradycardia. Obstructive apneas fell from 6 to 3/h, central apneas from 13 to 6/h, and the overall AHI from 28 to 11 events/h. The mechanism behind this phenomenon has not been definitively characterized, although stabilization of autonomic tone has been suggested to play a role. Lüthje and his colleagues,[33] however, failed to reproduce these results.
Proceed to Medication
 
 
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 Academy of Sleep Medicine, American College of Physicians, and American Medical Association

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, and American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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, and World Medical Association

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

Daniel R Ouellette, MD, FCCP  Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System

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

Disclosure: Boehringer Ingleheim Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Astra Zeneca Honoraria Speaking and teaching

Timothy D Rice, MD  Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, St Louis University School of Medicine

Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine 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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