Central Sleep Apnea Clinical Presentation

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

History

Like obstructive sleep apnea, central sleep apnea frequently presents with nighttime awakenings, nocturnal hypoxia, and excessive daytime sleepiness.[14] Sometimes, bed partners report witnessed apneas and mild snoring. Patients also report nonrestorative sleep, choking, and shortness of breath.

The most common reported symptoms are insomnia and excessive daytime sleepiness or fatigue. In general, the degree of daytime hypersomnolence is less than that observed with obstructive sleep apnea, and insomnia is more prominent. The presence of insomnia may actually put these patients at increased risk of central apneas because a greater number of sleep-wake transitions provide more opportunities for an unstable breathing pattern.

Patients also may have symptoms pertaining to the underlying cause (eg, symptoms of heart failure, stroke, renal failure, Parkinson disease, or multiple system atrophy). Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and other heart failure symptoms can be seen with CSB-CSA.

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Physical

In contrast to obstructive sleep apnea, no physical findings predict the presence or absence of central sleep apnea. The patients usually have a normal body habitus. Because CSB-CSA is highly prevalent in patients with congestive heart failure, signs of heart failure may be sought.[15] Sleep-disordered breathing is associated with nocturnal cardiac arrhythmias.[12] One study[16] has implicated central sleep apnea in the development of atrial fibrillation, but the methods used to differentiate central and obstructive events were not satisfactory. Patients with CSB-CSA may exhibit a periodic breathing pattern even while awake.

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Causes

This discussion includes the differentiation of various central sleep apnea syndromes from one another. Central sleep apnea in various forms can be seen in the following conditions or events:

  • Cheyne Stokes breathing-central sleep apnea: CSB-CSA is characterized by classic a crescendo-decrescendo pattern that typically occurs with a periodicity of 45 second or greater cycles (see image below). The ICSD-2[2] specifies that at least 10 central apneas and hypopneas per hour of sleep should occur, accompanied by arousals and derangement of sleep structure. The arousals occur at the peak of the hyperpnea phase. Patients usually have predisposing factors such as heart failure, stroke, or renal failure, as well as a lower resting PaCO2 than normal.
    • Heart failure
    • Stroke
    • Renal failureCheyne Stokes: This polysomnogram represents CheynCheyne 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.
  • Central sleep apnea due to a medical condition: The patient has a history of an underlying disorder other than heart failure or renal failure. Patients with stroke can have either classic CSB-CSA or central apneas without a crescendo-decrescendo pattern.
    • Stroke
    • Diabetes mellitus
    • Hypothyroidism
    • Parkinson disease
    • Multiple system atrophy or Shy-Dragger syndrome
    • Familial dysautonomia
    • Postpolio syndrome
    • Damage to medullary respiratory centers by tumor, infarction, or infection
    • Arnold-Chiari malformation types I-III
    • Cervical cordotomy
    • Muscular dystrophy
    • Myasthenia gravis
    • Prader-Willi syndrome
    • Idiopathic cardiomyopathy
    • Acromegaly
  • High-altitude periodic breathing: The single most important feature is that high-altitude periodic breathing occurs only with recent ascent to high altitudes. Many patients develop this at an altitude of 5000 meters or greater, while almost everyone develops it at an elevation of 7600 meters. The cycle length is shorter than in CSB-CSA, 12-34 seconds.
  • Use of opiates and other CNS depressants: This is most easily recognized by a history of opiate use. Wang et al[6] demonstrated that 30% of participants in a stable methadone maintenance program had a central apnea index (CAI) of greater than 5 and 20% had a CAI of greater than 10. Methadone blood concentration was significantly associated with the severity of central sleep apnea.
  • Primary central sleep apnea: This is an uncommon condition in which 5 or more central apneas, lasting 10 seconds or more, occur per hour of sleep. Patients have a low-normal PaCO2. The central apneas terminate abruptly with a large breath and without associated hypoxemia. They do not have a crescendo-decrescendo pattern of breathing
  • Complex sleep apnea: Central sleep apnea may emerge during titration of CPAP in patients previously diagnosed with obstructive sleep apnea. This syndrome, termed complex sleep apnea, has become a controversial topic in the sleep literature[17] and has been raised as a possible type of difficult-to-treat obstructive sleep apnea. As many as 6.5% of patients with obstructive sleep apnea may develop emergent or persistent central sleep apnea with CPAP treatment. CPAP emergent central sleep apnea is generally transitory and is eliminated after 8 weeks of CPAP therapy. Persistent CPAP-related central sleep apnea has been observed in approximately 1.5% of treated patients.[18] Similarly, complex sleep apnea can occur following a tracheostomy for obstructive sleep apnea. Central apneas have been found initially after a tracheostomy, but after an extended period, central sleep apnea decreased on repeat PSG.[19]
  • Physiologically normal apneic events
    • Central sleep apnea during sleep-wake transition: Up to 40% of healthy individuals may exhibit central apneas during sleep-wake transition. The central apneas occur during the period that chemoreceptors are resetting and instability of ventilation control occurs. They are usually brief and not associated with significant oxygen desaturation. The clinical significance of this entity is unknown. Once stable sleep is reached, normal individuals should not have more than 5 central apneas per hour of sleep.
    • Postarousal central apnea or postsigh central apnea: During a PSG review, central apneas are commonly seen following an arousal or after a sigh and are usually inconsequential. They are thought to be a result of Herring-Breuer reflex or hypocapnia induced by hyperventilation caused by a sigh or arousal.
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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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