History and exam
Key diagnostic factors
common
presence of risk factors
Key risk factors include age ≥60 years, male sex, heart failure, end-stage renal disease, opioid use, atrial fibrillation, stroke, and brainstem lesions.
insomnia, especially sleep-maintenance insomnia
In men, sleep-maintenance insomnia (difficulty remaining asleep or returning to sleep after mid-nocturnal awakenings) is less common in obstructive sleep apnoea (49%) but is relatively common in CSA (79%).[37]
poor concentration and attention span
Another reflection of sleep deprivation.
observed periodic breathing or cessation of breathing or snoring during sleep (by partner)
Sleep partners may observe periodic breathing or cessation of breathing; snoring is common.
transient dyspnoea that awakens from sleep or prevents sleep onset
Should be elicited on history-taking.
headaches upon waking
Common complaint.
uncommon
complaints of poorly restorative sleep and/or daytime sleepiness
Most patients with CSA syndrome complain of poorly restorative sleep (waking up tired, frequent night-time awakenings, waking up short of breath) and/or excessive daytime sleepiness (specifically, tendency to fall asleep during boring and monotonous activities such as reading or watching television).
In extreme cases, some patients may be visibly somnolent during the examination, or complain of difficulty staying awake while operating a vehicle. Those patients are severely impaired, should be counselled to avoid driving, and should be referred for a polysomnogram as soon as possible.
periodic breathing during wakefulness
Some patients exhibit a periodic breathing pattern while awake, during the physical examination. They have periods of increased rate and depth of breathing alternating with periods of depressed rate and depth of breathing. This is more likely to happen in patients with underlying heart failure and is indicative of the presence of CSA with Cheyne-Stokes breathing.[5]
Other diagnostic factors
uncommon
abnormal heart rhythm or the presence of third or fourth heart sounds
Indicates congestive heart failure.
focal abnormality on neurological examination
Physical examination showing deficits in cortical or subcortical areas, such as cranial nerves.
neuromuscular weakness
Muscular weakness on physical examination can point to an underlying central nervous system involvement or to a peripheral neuropathy or myopathy leading to respiratory muscle depression and hypoventilation during sleep.
history of endocrine disorders
Acromegaly and hypothyroidism have both been associated with CSA.
Risk factors
strong
congestive heart failure
In patients with congestive heart failure (CHF), CSA is estimated to occur in 25% to 40% of those with low left ventricular ejection fraction.[1][8][9]
Severity might correlate with that of the CHF and could negatively affect prognosis of CHF.[6][20][21] In patients classified as New York Heart Association class II to 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]
stroke
Prevalence following stroke has been reported to be 1.4% to 19.0%.[11][12][13]
Has been reported to occur in strokes involving autonomic and respiratory networks, but is also seen independent of the anatomical location of the stroke.[13][23]
Incidence also appears to be higher in patients with concomitant stroke and cardiac dysfunction, as well as stroke and nocturnal hypocapnia.[13]
renal failure
Sleep disordered breathing has been reported in more than 50% of haemodialysis patients.[24][25] Central sleep apnoea has a reported point prevalence of approximately 10% in patients with chronic kidney disease (range 0% to 75%).[26]
Proposed pathophysiological mechanisms include possible direct effects of uraemia on the central nervous system or respiratory musculature, and low partial pressure of carbon dioxide resulting from chronic metabolic acidosis with resultant ventilatory control instability.
male sex
Men are far more likely than women to develop CSA as reported in a prospective study of the general population, with a relative risk for women of 0.04 (95% CI 0 to 0.05).[27]
Another study looking at patients with heart failure found men to be at risk for CSA with an odds ratio of 3.50 (95% CI 1.39 to 8.84).[9]
Males were also shown to develop a higher frequency of central events at lower altitude than females, requiring weaker hypobaric and/or hypoxic stimulations than females.[17]
atrial fibrillation
There is probably a bi-directional link between arrhythmias and sleep disordered breathing (SDB).[28] CSA appears to be associated with a 2‐ to 3‐fold increased odds of developing atrial fibrillation (AF), with increased odds in older people.[28][29][30] However, the majority of studies suffer from a lack of clarity regarding the precise pathophysiological subtype of SDB represented in their cohorts, i.e., obstructive sleep apnoea (OSA) versus CSA, as well as an absence of objective cardiac function measures limiting the ability to assess causality.[28]
age ≥60 years
More prevalent in older people. This may be a reflection of the increased prevalence of comorbid conditions or of an inherent change in sleep stability that increases the likelihood of CSA.[31]
opioid use
Chronic opioid use is a well-known risk factor with a prevalence of 30% reported in patients taking chronic opioids.[14]
Opioids affect the central respiratory centres by binding to the mu-receptors on the ventral part of the medulla.
brainstem lesions
Can result in CSA due to effect on respiratory control in the central nervous system.
A high prevalence of CSA has been reported in patients with Arnold-Chiari malformations.
weak
neuromuscular weakness
May suggest central or peripheral neuropathy or myopathy leading to respiratory muscle depression and hypoventilation during sleep.
acromegaly
The presence of CSA in acromegaly is associated with increased levels of disease activity markers and is thought to result from an increased respiratory chemoresponsiveness.[32]
hypothyroidism
There is higher than expected prevalence of CSA in patients with hypothyroidism, although the mechanism is poorly understood.
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