Central Sleep Apnea Workup

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

Laboratory Studies

The laboratory findings in persons with central sleep apnea syndromes are not helpful except for a finding of respiratory alkalosis (PaCO2 < 40 mm Hg while awake) in patients with primary central sleep apnea, high-altitude periodic breathing, and CSB. Patients with heart failure and high-altitude periodic breathing may also have relative or absolute hypoxia shown with arterial blood gas analysis.

Underlying causes should be sought if clinically relevant. For example, fasting blood glucose levels should be checked because central sleep apnea is more common in patients with diabetes, serum creatinine levels can be measured to assess for renal failure, or antibodies to acetylcholine receptors can be evaluated in patients with suspected myasthenia gravis.

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Imaging Studies

Imaging study finding are also nonspecific and are characteristic of the underlying cause rather than helpful in diagnosing a specific central sleep apnea syndrome. Patients with stroke, CNS tumor, and Arnold-Chiari malformation may have characteristic findings on brain CT scan or MRI examination. However, routine imaging studies are not warranted in the diagnosis of central sleep apnea.

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Other Tests

  • Polysomnography: Most diagnoses of central sleep apnea are made on the basis of PSG studies.
    • In primary central sleep apnea, more than 5 central apneas occur per hour of sleep, each lasting 10 seconds or longer with more than 50% of the events determined to be central rather than obstructive. They appear to be more common during sleep stages 1 and 2. Severe fragmentation caused by apnea may preclude the patient from going into deep sleep (delta sleep). The events are less common during REM sleep for the reasons explained above. The length of the apneic-ventilatory cycle is less than 45 seconds.
    • The CSB-CSA cycle in heart failure is usually triggered by an arousal resulting in large tidal volume and the consequent lowering of PaCO2. As the patient falls asleep, the apneic threshold is elevated, and ventilation tends to oscillate around the apneic threshold, propagated by slow circulation time. The cycle length of apnea-hyperpnea is usually greater than 45 seconds, is directly proportional to circulation time, and is inversely proportional to cardiac output. Shortening of the cycle length has been reported following cardiac transplantation. The arousals typically occur at the peak of the hyperpneic phase. ICSD-2[2] criteria require the presence of at least 10 central events per hour of sleep in the crescendo-decrescendo pattern to diagnose CSB.
    • For the diagnosis of high-altitude periodic breathing, a central apnea-hypopnea index (AHI) of greater than 5 is required at a high altitude. The usual cycle length is from 12-34 seconds. This condition also gives rise to fragmented sleep, increased stage 1 and 2 sleep, and decreased delta sleep. It is only seen during non–rapid eye movement (NREM) sleep and improves over the course of a few days.
    • Central sleep apnea due to drugs or substance abuse is more common during NREM sleep than REM sleep.[6] Both periodic and nonperiodic breathing patterns can be seen, the cycle length typically being short. An AHI of greater than 5 in the absence of periodic breathing and an AHI of greater than 10 in the presence of periodic breathing is required to make a diagnosis of central sleep apnea due to drugs or substance abuse. Sometimes, ataxic or a Biot breathing pattern is also seen with narcotics use.
  • Esophageal pressure monitoring with a balloon catheter: Sometimes, distinguishing central sleep apnea from obstructive sleep apnea may be difficult. Esophageal pressure monitoring with a balloon catheter is helpful in distinguishing central from obstructive events, by revealing the substantial reduction in intrapleural pressure that occurs with the obstructive events.
  • Home monitoring: No studies have evaluated the accuracy of portable monitoring devices for the detection of central apneas.[20] However, data show portable monitoring can be an effective diagnostic tool to diagnose obstructive sleep apnea syndrome in suspected moderate-to-severe obstructive sleep apnea.[21, 22]
  • Echocardiography: Patients with CSB-CSA and heart failure commonly have an ejection fraction of less than 0.40, but it can also be seen in conjunction with diastolic dysfunction. Some cases of CSB-CSA in association with pulmonary artery hypertension have also been reported. Usually, patients have a known history of heart failure, and echocardiography is not recommended as a routine test for the evaluation of central sleep apnea in the absence of risk factors or signs and symptoms of heart failure.
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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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