Approach
Patients with central sleep apnea (CSA) of all types may present with symptoms of disrupted sleep. These are shared with other causes of disrupted sleep including obstructive sleep apnea (OSA), and diagnostic testing is required to make the distinction.
Symptoms
Excessive fatigue, poor concentration, poor attention span, poor perceived quality of sleep, and insomnia are classic presenting symptoms. Complaints of both sleep-onset and sleep-maintenance insomnia are common. Although in congestive heart failure (CHF) patients with sleep-disordered breathing specific symptoms are apparent, sleep questionnaire score results (e.g., Epworth Sleepiness Scale) are not sufficiently sensitive or specific to predict sleep-disordered breathing.[22]
It is useful to obtain a sequential history of the patient's sleep experience:[1]
Description of usual sleep-wake schedule
Any perceived difficulty in falling asleep
Unusual number or duration of awakenings after initial sleep onset
Sleep partners observing periodic breathing or cessation of breathing; snoring is common
Any experience of transient dyspnea that awakens from sleep or prevents sleep onset
Any pattern of headaches upon waking
Sleepiness is best assessed by inquiring about specific situations such as reading, watching television, and driving, and the propensity of the patient to fall asleep during those activities. An Epworth Sleepiness Scale may be used as a guide to assess sleepiness, with scores of ≥10 considered to indicate abnormal sleepiness.
With high-altitude periodic breathing, symptoms will consist of frequent awakenings, poor quality of sleep, and a feeling of suffocation
Some patients are relatively asymptomatic, and the abnormal breathing pattern is noted either by serendipitous observation or through screening with oximetry.
History suggesting alternative cause
Because symptoms are nonspecific and may be ascribed to comorbid, age-related, or other causes, a careful history is necessary to develop the differential diagnosis. In patients presenting with these symptoms, the presence of risk factors such as male sex, heart failure, atrial fibrillation, and age ≥60 years should prompt consideration of CSA in addition to OSA. Complicating the relationship between OSA and CSA, OSA may be an independent risk factor for and predate events such as stroke or myocardial infarction that subsequently predispose to CSA physiology.
In addition to positive historical factors, other causes of the primary complaints of poorly restorative sleep, insomnia, and fatigue or sleepiness must be sought.
Poor sleep habits
Presence or absence of restless leg syndrome
Depression: because sleep and depression symptoms overlap, it is sometimes helpful to use standardized questionnaires such as the Beck Depression Inventory or the Patient Health Questionnaire-9 as an aid in assessing likelihood of depression
Inadequately treated heart or renal failure may lead to sleep disruption due to orthopnea, paroxysmal nocturnal dyspnea, and anxiety with or without CSA
Other causes of nocturnal dyspnea, such as panic attacks, nocturnal gastroesophageal reflux, or asthma, should be considered
In patients classified as New York Heart Association class II through IV, with heart failure and suspicion of sleep-disordered breathing or excessive daytime sleepiness, a formal sleep assessment is needed to distinguish OSA from CSA.[7][22]
Patients with secondary CSA will also present with signs and symptoms of the underlying disorder. CSA symptom onset may or may not be associated with progression of underlying disease.
History of predisposing conditions
Cheyne-Stokes breathing (CSB) has been described in patients with systolic as well as diastolic heart failure.
In a large case series of patients with CHF referred to a sleep disorders laboratory, risk factors for CSA included male sex, atrial fibrillation, age ≥60 years, and hypocapnia (partial pressure of carbon dioxide <38 mmHg during wakefulness).[9]
A high prevalence of CSA has also been reported in patients with Arnold-Chiari malformations, brainstem neoplasm, acute cerebrovascular accident, and multiple system atrophy. In addition, endocrine disorders such as acromegaly and hypothyroidism have been associated with CSA.
Although patients with treatment-emergent CSA tend to be older (age ≥60 years), have a high prevalence of coronary artery disease, and have fragmented sleep, these clinical predictors are not sufficient to differentiate them from those without CSA.
Medications
Frequency and doses of any opioid medication are important in assessing possible sleep apnea. Ataxic breathing is more frequent at a morphine equivalent daily dose of 200 mg/day or higher.[34] Many other medications are associated with insomnia or somnolence, including beta-blockers and many antidepressants. An assessment of the relationship between initiation or dosage adjustments and symptom onset is important.
Physical examination
There are no specific physical examination clues that lead to the diagnosis of CSA. The presence of periodic breathing during wakefulness would certainly be suggestive, but would rarely be seen. Instead, the examination can offer clues to underlying conditions that would constitute a risk factor for CSA or clues suggesting alternative diagnoses:
Crowded oropharynx, big tongue, high neck circumference, or all, are suggestive of OSA risk
Abnormal heart rhythm or the presence of third or fourth heart sounds indicating CHF
Abnormal chest wall and diaphragm excursions suggesting a restrictive physiology or diaphragmatic paralysis, which would be atypical for CSA
Focal neurologic deficits indicative of a cortical or subcortical disorder (e.g., stroke, Chiari malformation, brain neoplasm)
Neuromuscular weakness suggestive of central or peripheral neuropathy or myopathy, which would be more suggestive of a sleep-related hypoventilation disorder than CSA
Diagnostic tests
It is important to note that the diagnosis is difficult to make based on history and examination, and therefore physiologic testing is essential. CSB is sufficiently prevalent in patients with CHF that even in the absence of symptoms, many advocate screening this population with overnight oximetry to detect sleep-disordered breathing.[35]
Home overnight oximetry can be useful to screen for the presence of sleep-disordered breathing in a high-risk population but it does not differentiate between central and obstructive events.[35] Therefore, polysomnography is required, and patients should be referred to a facility with polysomnographic testing and interpretation expertise.[36] The polysomnogram consists of close observation and recording of several channels of data during an entire night of sleep in a specialized facility. Measures include air flow, chest and abdominal movements, electroencephalogram, ECG, submental and anterior tibialis electromyogram, oxygen saturation, and eye movements.[Figure caption and citation for the preceding image starts]: Cheyne-Stokes breathing: polysomnography demonstrating the characteristic waxing and waning of ventilation separated by central apneas (seen best in the nasal pressure transducer signal [Nasal P] and the abdominal [Abd], chest [Chest], and Sum respiratory impedance traces), resulting in almost sinusoidal desaturations in oxyhemoglobin saturation. Cycle duration between events is 75 seconds; ECG demonstrates atrial fibrillation, both characteristic of a patient with advanced heart failureSleep-related breathing disorders. In: Krahn L, Silber M, Morgenthaler T. Atlas of sleep medicine. New York. Informa Healthcare, 2011. By permission of Mayo Foundation for Medical Education and Research. All rights reserved [Citation ends].
Other investigations for predisposing conditions may be performed including serum thyroid-stimulating hormone, serum creatinine, ECG, and echocardiogram. Patients suspected of having acromegaly should have serum insulin-like growth factor 1 measured.
Use of this content is subject to our disclaimer