Central Sleep Apnea: Symptoms, Causes, Diagnosis, and Evidence-Based Treatments

Central sleep apnea (CSA) is a sleep-related breathing disorder in which the brain intermittently fails to send the proper signals to the muscles that control breathing during sleep. Unlike obstructive sleep apnea (OSA), where the airway is physically blocked by collapsed soft tissue, central sleep apnea involves a neurological disruption — the respiratory drive itself temporarily shuts down. The sleeper literally stops making any effort to breathe for periods of ten seconds or longer, sometimes much longer, leading to drops in blood oxygen levels and repeated micro-arousals throughout the night.

The International Classification of Sleep Disorders, Third Edition (ICSD-3) recognizes several subtypes of central sleep apnea, including primary (idiopathic) central sleep apnea, Cheyne-Stokes breathing pattern, central sleep apnea due to a medical condition, central sleep apnea due to high-altitude periodic breathing, and treatment-emergent central sleep apnea (also called complex sleep apnea). Each subtype has a somewhat different underlying mechanism, but all share the core feature of absent or diminished respiratory effort during sleep.

Central sleep apnea is considerably less common than obstructive sleep apnea. Estimates suggest that CSA accounts for roughly 5–10% of all sleep apnea cases referred to sleep laboratories. However, prevalence is significantly higher in specific populations: research indicates that 30–50% of patients with heart failure (particularly those with reduced ejection fraction) exhibit central sleep apnea or Cheyne-Stokes respiration. CSA also appears more frequently in older adults, in individuals who have experienced a stroke, and in those using chronic opioid medications. Because CSA often occurs alongside other serious medical conditions, it is frequently underdiagnosed or misattributed to the primary illness.

The symptoms of central sleep apnea can overlap substantially with those of obstructive sleep apnea and other sleep disorders, which sometimes makes clinical recognition challenging. However, several hallmark features distinguish CSA or suggest that a central component is present:

• Witnessed apneas without apparent effort: A bed partner may observe that the sleeper stops breathing entirely — with no chest or abdominal movement — before suddenly gasping or resuming respiration. This absence of respiratory effort is the cardinal distinction from obstructive events.
• Excessive daytime sleepiness: Fragmented sleep caused by repeated arousals leads to significant fatigue, difficulty concentrating, and an overwhelming urge to sleep during the day.
• Frequent nighttime awakenings: People with CSA often wake multiple times during the night, sometimes with a sensation of breathlessness or air hunger. These awakenings can be abrupt and distressing.
• Insomnia and difficulty maintaining sleep: Unlike OSA, where patients often fall back asleep quickly after arousals, individuals with central sleep apnea frequently report sustained difficulty returning to sleep, making insomnia complaints more prominent.
• Morning headaches: Repeated drops in oxygen and elevations in carbon dioxide during the night can cause dull, persistent headaches upon waking.
• Mood disturbances: Chronic sleep disruption from CSA is associated with irritability, depressed mood, anxiety, and cognitive difficulties including impaired memory and reduced executive function.
• Shortness of breath at night: Some individuals experience paroxysmal nocturnal dyspnea — awakening suddenly with a sense of suffocation — particularly those with Cheyne-Stokes breathing associated with heart failure.

Notably, snoring is less prominent in central sleep apnea than in obstructive sleep apnea, though it can still be present, especially when both conditions coexist. The relative absence of loud, habitual snoring in someone who has witnessed apneas and excessive daytime sleepiness should raise clinical suspicion for a central rather than purely obstructive process.

Central sleep apnea arises from instability in the brain's respiratory control system — specifically, the ventilatory feedback loop that regulates breathing based on levels of carbon dioxide (CO₂) and oxygen (O₂) in the blood. When this feedback mechanism becomes overly sensitive or is disrupted, breathing can oscillate between hyperventilation and apnea. The specific causes and risk factors differ by CSA subtype:

Heart Failure and Cheyne-Stokes Respiration

Heart failure is the most common medical condition associated with central sleep apnea. In this context, CSA typically manifests as Cheyne-Stokes breathing (CSB) — a characteristic crescendo-decrescendo pattern of tidal volume alternating with central apneas or hypopneas. Prolonged circulatory time (the delay between changes in blood gas levels in the lungs and their detection by chemoreceptors in the brain) causes the respiratory control system to overcorrect, creating rhythmic oscillations. Research suggests that 30–50% of patients with systolic heart failure (ejection fraction ≤45%) exhibit this pattern.

Neurological Conditions

Conditions that damage the brainstem — where the respiratory centers (medullary respiratory groups) are located — can directly impair automatic breathing control during sleep. These include:

• Stroke, particularly brainstem strokes
• Brain tumors affecting the posterior fossa
• Neurodegenerative diseases such as multiple system atrophy, Parkinson's disease, and amyotrophic lateral sclerosis (ALS)
• Arnold-Chiari malformation
• Encephalitis and other central nervous system infections

Opioid-Induced Central Sleep Apnea

Chronic use of opioid medications is a well-established cause of central sleep apnea. Opioids depress the brainstem's respiratory centers, reduce hypercapnic ventilatory response (the normal increase in breathing when CO₂ rises), and cause irregular, ataxic breathing patterns during sleep. Studies have found that approximately 24–30% of patients on chronic opioid therapy demonstrate significant central sleep apnea on polysomnography.

Treatment-Emergent Central Sleep Apnea (Complex Sleep Apnea)

Some patients initially diagnosed with obstructive sleep apnea develop central apneas after beginning continuous positive airway pressure (CPAP) therapy. This phenomenon, termed treatment-emergent CSA or complex sleep apnea, occurs in an estimated 5–15% of patients started on CPAP. In many cases, it resolves spontaneously within weeks to months of continued therapy, but in a subset of patients, it persists.

High-Altitude Periodic Breathing

Ascent to altitudes above approximately 2,500 meters (8,200 feet) triggers hyperventilation due to low oxygen levels. This drives CO₂ below the apneic threshold — the level below which the brain temporarily ceases respiratory drive — resulting in cyclical central apneas during sleep. This is a normal physiological response and typically resolves with acclimatization or descent.

Additional Risk Factors

• Age: CSA is more prevalent in adults over 65, likely reflecting age-related changes in ventilatory control stability.
• Male sex: Men are affected more frequently than women, possibly due to hormonal influences on ventilatory control (progesterone is a respiratory stimulant).
• Atrial fibrillation: Independent of heart failure, atrial fibrillation has been associated with increased risk of central sleep apnea.
• Renal failure: End-stage renal disease is associated with altered chemoreceptor sensitivity and metabolic disturbances that promote central apneas.

The definitive diagnostic tool for central sleep apnea is an in-laboratory, attended polysomnography (PSG) — an overnight sleep study that simultaneously records brain activity (EEG), eye movements (EOG), muscle tone (EMG), airflow, respiratory effort, blood oxygen saturation, heart rhythm, and body position. This comprehensive recording is essential because distinguishing central from obstructive apneas requires confirmation that respiratory effort is absent during the breathing pauses.

Diagnostic Criteria

According to the ICSD-3, central sleep apnea is diagnosed when polysomnography demonstrates:

• Five or more central apneas or central hypopneas per hour of sleep (a central apnea-hypopnea index, or central AHI, ≥ 5/hour)
• Central apneas and hypopneas constitute more than 50% of the total respiratory events
• The pattern is not better explained by another sleep disorder, medication use, or substance use (unless the specific subtype, such as opioid-induced CSA, is being diagnosed)

Key Diagnostic Distinctions

During a central apnea, the polysomnogram shows simultaneous cessation of airflow and cessation of thoracic and abdominal respiratory effort. This contrasts with obstructive apneas, where airflow stops but the chest and abdomen continue making increasingly vigorous efforts against a closed airway. Mixed apneas — events that begin as central and end as obstructive — are also common and may indicate overlap between the two conditions.

Additional Diagnostic Workup

Because CSA is frequently secondary to other medical conditions, diagnosis typically prompts a broader evaluation:

• Echocardiography to assess cardiac function, particularly left ventricular ejection fraction
• Brain MRI if a neurological cause is suspected
• Blood gas analysis to evaluate baseline CO₂ levels (hypocapnic vs. hypercapnic CSA have different treatment implications)
• Medication review with specific attention to opioids, benzodiazepines, and other CNS depressants
• Renal function tests in appropriate clinical contexts

Home sleep apnea testing (HSAT), which is commonly used to diagnose obstructive sleep apnea, is not recommended for diagnosing central sleep apnea. Most home testing devices do not adequately measure respiratory effort, making it impossible to reliably distinguish central from obstructive events. When central sleep apnea is suspected, in-laboratory polysomnography remains the standard of care.

Treatment of central sleep apnea is more complex and less standardized than treatment of obstructive sleep apnea. The approach depends heavily on the underlying cause, the specific CSA subtype, and the patient's overall medical status. The primary evidence-based strategies include:

1. Treating the Underlying Condition

Because CSA is frequently secondary to another medical disorder, optimizing treatment of the root cause is the first and most important intervention. For patients with heart failure-related CSA, guideline-directed medical therapy (including beta-blockers, ACE inhibitors or ARBs, diuretics, and in appropriate candidates, cardiac resynchronization therapy) has been shown to reduce central apnea severity. Addressing opioid-induced CSA may involve opioid dose reduction or rotation under careful medical supervision. Treating atrial fibrillation, managing renal failure, and addressing neurological conditions can all contribute to improvement in central apnea.

2. Positive Airway Pressure Therapies

• CPAP (Continuous Positive Airway Pressure): Although primarily designed for obstructive sleep apnea, CPAP can effectively treat CSA in some patients, particularly those with heart failure. By increasing intrathoracic pressure and improving cardiac output, CPAP can stabilize ventilatory control. It is often considered a first-line PAP therapy for CSA associated with heart failure.
• Adaptive Servo-Ventilation (ASV): ASV is a sophisticated form of positive pressure ventilation that continuously adjusts inspiratory pressure support on a breath-by-breath basis, providing more support during apneas and less during normal breathing. ASV is highly effective at eliminating central apneas. However, the landmark SERVE-HF trial (2015) demonstrated that ASV was associated with increased cardiovascular mortality in patients with heart failure and reduced ejection fraction (EF ≤ 45%). As a result, ASV is contraindicated in patients with symptomatic heart failure with reduced ejection fraction. It remains a viable option for other CSA subtypes, including idiopathic CSA and treatment-emergent CSA.
• Bilevel PAP (BiPAP) with a Backup Rate: BiPAP with a timed backup respiratory rate ensures a minimum number of breaths per minute, preventing prolonged central apneas. This modality is sometimes used for opioid-induced CSA and CSA due to neurological conditions.

3. Supplemental Oxygen

Nocturnal supplemental oxygen can reduce the frequency and severity of central apneas, particularly in heart failure-related CSA and high-altitude periodic breathing. Oxygen supplementation raises blood oxygen levels, reducing hypoxic ventilatory drive and stabilizing the feedback loop. While it may not fully normalize the apnea-hypopnea index, it can meaningfully improve oxygenation and reduce arousals.

4. Pharmacological Approaches

• Acetazolamide: This carbonic anhydrase inhibitor induces a mild metabolic acidosis, which stimulates ventilation and raises baseline CO₂ levels above the apneic threshold. It has demonstrated efficacy in high-altitude periodic breathing and has shown benefit in some cases of idiopathic and heart failure-related CSA. Side effects include paresthesias, altered taste, and metabolic disturbances.
• Theophylline: This respiratory stimulant has shown modest benefit in some studies of CSA related to heart failure by stimulating the central respiratory drive. However, its narrow therapeutic window and potential for cardiac side effects limit its clinical use.

5. Phrenic Nerve Stimulation

The remedē System, an implantable device that delivers transvenous phrenic nerve stimulation, was approved by the FDA in 2017 for the treatment of moderate to severe central sleep apnea. The device stimulates the phrenic nerve during sleep, causing the diaphragm to contract and restoring breathing. Clinical trial data demonstrated significant reductions in central AHI, improvements in oxygen saturation, and reductions in arousals. This option is considered for patients who do not tolerate or respond to positive airway pressure therapy.

The prognosis for central sleep apnea varies considerably depending on the underlying cause, the severity of the apnea, the success of treatment, and the patient's overall health status.

Heart Failure-Related CSA: The presence of Cheyne-Stokes respiration in heart failure is an independent predictor of increased morbidity and mortality. It reflects the severity of the underlying cardiac dysfunction. However, this does not necessarily mean that CSA itself worsens cardiac outcomes independent of heart failure severity — this remains an area of active research and debate, particularly following the SERVE-HF trial results. When heart failure is optimally managed, central apnea often improves substantially, and in some cases resolves.

Treatment-Emergent CSA: The prognosis for this subtype is generally favorable. Research indicates that in approximately 50–60% of cases, treatment-emergent central apneas resolve spontaneously within the first few months of continued CPAP use. For persistent cases, switching to ASV (in patients without contraindications) or bilevel PAP with a backup rate can be effective.

Idiopathic CSA: Primary central sleep apnea without an identifiable underlying cause tends to be a chronic condition that requires ongoing management. With appropriate treatment — typically positive airway pressure therapy — symptoms can be well controlled, and patients can achieve meaningful improvements in sleep quality, daytime alertness, and quality of life.

Opioid-Induced CSA: If opioid medications can be safely discontinued or significantly reduced, central sleep apnea often improves or resolves. When opioid therapy must be continued (as in chronic pain management or opioid agonist therapy for addiction), CSA typically persists and requires targeted respiratory support during sleep.

Untreated central sleep apnea, regardless of subtype, carries significant health risks. Chronic intermittent hypoxemia and sleep fragmentation are associated with cardiovascular complications (hypertension, arrhythmias, worsening heart failure), neurocognitive deficits (impaired attention, memory, and executive function), mood disorders (depression and anxiety), and reduced quality of life. There is also evidence suggesting increased risk of motor vehicle accidents due to excessive daytime sleepiness.

Central sleep apnea rarely exists in isolation. It is closely linked to a web of medical and psychiatric comorbidities that influence its presentation, management, and prognosis:

• Obstructive Sleep Apnea (OSA): The two conditions frequently coexist. Many patients have a combination of obstructive and central events, and treatment-emergent CSA is by definition a condition that arises in the context of OSA treatment. Clinicians must evaluate for both types of events on polysomnography.
• Congestive Heart Failure: As discussed, this is the most common medical condition associated with CSA. The relationship is bidirectional — heart failure promotes CSA, and CSA may further stress the cardiovascular system through sympathetic activation and intermittent hypoxemia.
• Atrial Fibrillation and Other Arrhythmias: Central apneas can trigger or exacerbate cardiac arrhythmias through swings in intrathoracic pressure, sympathetic nervous system activation, and hypoxemia. Atrial fibrillation is both a risk factor for and a consequence of CSA.
• Stroke: Stroke can cause CSA (particularly brainstem strokes), and sleep-disordered breathing in the post-stroke period is associated with worse neurological recovery and increased mortality.
• Depression and Anxiety: Chronic sleep disruption from CSA is strongly associated with depressive symptoms, anxiety, and reduced psychological well-being. These mood disturbances can, in turn, worsen sleep quality, creating a reinforcing cycle.
• Insomnia: Central sleep apnea can produce a clinical picture that closely resembles chronic insomnia, with difficulty maintaining sleep and non-restorative sleep. This comorbid insomnia may require targeted behavioral interventions (such as cognitive behavioral therapy for insomnia, or CBT-I) in addition to CSA-specific treatment.
• Chronic Kidney Disease: End-stage renal disease is associated with both central and obstructive sleep apnea. Fluid shifts, metabolic acidosis, and uremic toxins may all contribute to ventilatory instability.
• Chronic Opioid Use Disorders: Opioid use disorder and chronic pain conditions requiring long-term opioid therapy are significant risk factors. The intersection of substance use, pain management, and sleep-disordered breathing requires coordinated multidisciplinary care.

While central sleep apnea is fundamentally a respiratory and neurological condition, its consequences extend deeply into psychological and cognitive functioning. Clinicians and patients alike should understand these impacts, as they are often the symptoms that most directly affect daily quality of life.

Cognitive Effects

Chronic sleep fragmentation and intermittent hypoxemia impair multiple cognitive domains. Research consistently shows that individuals with untreated sleep apnea — both central and obstructive — demonstrate deficits in sustained attention, working memory, verbal fluency, and executive function (planning, decision-making, and impulse control). These cognitive effects can be subtle but cumulative, affecting work performance, academic functioning, and interpersonal relationships. In older adults, untreated sleep-disordered breathing has been associated with accelerated cognitive decline, though the causal relationship remains under investigation.

Mood and Emotional Regulation

Sleep deprivation from any cause degrades emotional regulation, but the chronic, insidious nature of CSA-related sleep disruption poses particular challenges. Many individuals develop depressive symptoms, irritability, emotional lability, and anxiety that they may not connect to a sleep disorder. Research suggests that effective treatment of sleep apnea — when it normalizes sleep architecture and oxygenation — can significantly improve mood symptoms, though coexisting mood disorders may require independent treatment.

Impact on Relationships

The daytime sleepiness, irritability, and personality changes associated with chronic sleep disruption can strain intimate and family relationships. Bed partners may also experience disrupted sleep from witnessing apneic episodes, which can be frightening. Educating both the patient and their support system about the nature of CSA is an important component of comprehensive care.

Central sleep apnea is a serious medical condition with significant cardiovascular, neurological, and psychological consequences when left untreated. Prompt evaluation is recommended in the following circumstances:

• A bed partner witnesses pauses in breathing during sleep — particularly if these pauses appear to involve a complete absence of breathing effort (no chest or abdominal movement), rather than snoring and gasping.
• You experience excessive daytime sleepiness that interferes with work, driving, or daily activities, especially if this sleepiness occurs despite seemingly adequate time in bed.
• You wake frequently during the night with breathlessness or a choking sensation, particularly if you have a known diagnosis of heart failure or a neurological condition.
• You are on chronic opioid therapy and experience symptoms of sleep-disordered breathing, including unrefreshing sleep, morning headaches, and daytime fatigue.
• You have been diagnosed with heart failure, atrial fibrillation, or have had a stroke and notice worsening sleep quality, daytime function, or mood disturbance.
• You are using CPAP for obstructive sleep apnea but continue to experience symptoms or your machine data show persistent central apnea events.

The appropriate starting point is typically your primary care physician or a board-certified sleep medicine specialist. Given the strong association between CSA and cardiovascular disease, a cardiology consultation is often warranted. If mood or cognitive symptoms are prominent, referral to a mental health professional — such as a clinical psychologist or psychiatrist with expertise in sleep-related disorders — should also be considered.

Do not attempt to self-diagnose or self-treat central sleep apnea. The condition requires objective polysomnographic confirmation, and the treatment approach depends on accurate identification of the underlying cause and subtype. Inappropriate treatment — such as using adaptive servo-ventilation in a patient with reduced ejection fraction heart failure — can have life-threatening consequences.