Central Sleep Apnea: Symptoms, Types, Causes and Treatment

Central Sleep Apnea (CSA) is a complex sleep disorder that disrupts normal breathing patterns during sleep. Unlike obstructive sleep apnea, which results from physical blockage of the airway, CSA is defined by a lack of respiratory effort due to impaired signaling from the brain. This article will explore the symptoms, types, causes, and treatments of CSA, providing an evidence-based and reader-friendly overview for patients, caregivers, and clinicians.

Symptoms of Central Sleep Apnea

Central Sleep Apnea often goes unnoticed, but its impact on sleep quality and overall health can be significant. Recognizing the symptoms is crucial for early diagnosis and effective management. While some symptoms are shared with other forms of sleep-disordered breathing, CSA can also present unique challenges.

Symptom	Description	Frequency	Source(s)
Insomnia	Trouble falling or staying asleep	Common	7
Depression	Mood changes, low energy	Reported	7
Daytime Sleepiness	Unrefreshing sleep, fatigue during the day	Less frequent than OSA	1, 7
Snoring	Noise during sleep	Infrequent in CSA	10
Nocturnal Awakenings	Waking up during the night	Sometimes present	10
Sleep Fragmentation	Repeated arousals, poor sleep continuity	Common	1, 3
Poor Concentration	Difficulty focusing during the day	May occur	3, 7

Table 1: Key Symptoms of Central Sleep Apnea

Understanding the Symptoms

CSA is often more subtle in its presentation than obstructive sleep apnea (OSA), making it harder to spot. Many patients may not report classic symptoms like loud snoring or dramatic pauses in breathing witnessed by others.

Insomnia and Sleep Fragmentation

Patients with CSA commonly experience insomnia, reporting difficulty falling asleep or staying asleep. Sleep is often fragmented due to repeated arousals caused by breathing interruptions and oxygen desaturations during the night 1, 7. This can leave individuals feeling unrested even after a full night in bed.

Daytime Sleepiness and Fatigue

Unlike OSA, frank hypersomnolence—meaning overwhelming daytime sleepiness—is less frequently reported in CSA. However, many patients still describe persistent fatigue, poor concentration, and reduced alertness, especially as the condition progresses or becomes severe 1, 7.

Mood and Cognitive Symptoms

Depression and irritability are not uncommon in patients with CSA, likely due to the chronic disruption of restorative sleep. Memory problems and trouble focusing can also occur, further impacting daily functioning 7.

Absence of Typical OSA Symptoms

Interestingly, many patients with CSA do not snore or have witnessed apneas, which are hallmark symptoms of OSA. This lack of obvious symptoms can delay recognition and diagnosis 2, 7.

Comorbidities and Symptom Overlap

CSA is frequently identified in older adults and those with heart failure or neurologic conditions, but it can also exist without any obvious comorbidities. Unlike OSA, the direct association between CSA and common sleep-disordered breathing symptoms is less pronounced 2.

Types of Central Sleep Apnea

Central Sleep Apnea is not a single disease but a syndrome with several distinct types, each with its own underlying mechanism, triggers, and clinical relevance. Understanding these types helps tailor diagnosis and treatment.

Type	Main Features/Triggers	Common Setting	Source(s)
Idiopathic/Primary	No identifiable cause	Rare, often young/middle-aged	1, 4
Cheyne-Stokes Respiration	Crescendo-decrescendo breathing with apneas	Heart failure, stroke	1, 3, 9
High Altitude Periodic Breathing	Apneas at high altitude due to hypoxia	>4,000m elevation	1, 4
Drug/Substance-Induced	Caused by opioids or sedatives	Opioid therapy, substance use	1, 9
Medical/Neurological Condition	Secondary to brainstem or neuromuscular disease	Brain injury, neuromuscular disease	1, 4, 7
Primary Sleep Apnea of Infancy	Present in infants, congenital	Newborns, rare	1

Table 2: Types of Central Sleep Apnea

Key Subtypes Explained

Idiopathic (Primary) CSA

This rare form of CSA occurs without any apparent cause or underlying disease. It is thought to involve abnormalities in ventilatory control, such as increased sensitivity to carbon dioxide (CO2) or unstable respiratory drive during sleep 1, 4.

Cheyne-Stokes Respiration

Cheyne-Stokes respiration is a distinctive pattern of CSA, characterized by cycles of gradually increasing and then decreasing breathing effort, interspersed with central apneas. It is most commonly seen in patients with congestive heart failure and sometimes after stroke. This type is associated with poorer prognosis in heart failure patients 1, 3, 9.

High Altitude Periodic Breathing

At elevations above 4,000 meters (about 13,000 feet), reduced oxygen levels trigger a pattern of rapid breathing followed by central apneas. This form is reversible with acclimatization or descent to lower altitude 1, 4.

Drug or Substance-Induced CSA

Central apneas can occur in people who use certain medications—especially opioids or sedatives—that depress respiratory centers in the brain. The prevalence of CSA is particularly high among chronic opioid users 1, 9.

Medical or Neurological Condition-Related CSA

Various neurological disorders (e.g., brainstem lesions, neuromuscular diseases) and some medical conditions can impair the neural control of breathing, resulting in CSA 1, 4, 7.

Primary Sleep Apnea of Infancy

This rare variant occurs in newborns and is usually due to congenital abnormalities in the neural control of breathing 1.

Causes of Central Sleep Apnea

The development of CSA is rooted in a failure of the brain to consistently signal the breathing muscles during sleep. Multiple physiological and pathological processes can trigger this failure.

Cause	Pathophysiology/Trigger	Typical Population/Setting	Source(s)
Instability in Ventilatory Control	High loop gain (overreaction to CO2 changes)	Adults, especially with CHF	4, 8
Heart Failure	Circulatory delay, sensitive CO2 response	CHF patients	3, 1, 9
High Altitude	Hypoxia-induced hyperventilation, hypocapnia	Travelers, climbers	1, 4
Opioid Use	Depressed respiratory drive	Chronic opioid users	9, 1
Neurological Disorders	Damage to brainstem, impaired chemosensitivity	Brain injury, congenital disorders	7, 1
Idiopathic	Unknown, possible genetic or control instability	Rare	1, 4

Table 3: Common Causes of Central Sleep Apnea

Mechanisms Underlying CSA

Instability in Ventilatory Control

The most common physiological underpinning of CSA is an unstable ventilatory control system, often referred to as "high loop gain." This means the brain’s response to changes in blood CO2 is exaggerated, causing cycles of over-breathing (hyperventilation) followed by periods where breathing stops entirely (central apnea) 4, 8.

• Controller gain: High sensitivity to CO2 changes
• Plant gain: Enhanced response in some patients, especially those who retain CO2

Heart Failure and Cheyne-Stokes Respiration

In heart failure, poor cardiac function leads to a delay in blood circulation between the lungs and the brain. This delay impairs the normal feedback loop that regulates breathing, often resulting in the characteristic Cheyne-Stokes breathing pattern 3, 1, 9.

High Altitude

At high altitudes, hypoxia (low oxygen) leads to increased breathing (hyperventilation). This, in turn, reduces CO2 levels too much (hypocapnia), suppressing the drive to breathe and triggering central apneas 1, 4.

Drug-Induced CSA

Opioids and certain sedatives can directly suppress the brain's respiratory centers, leading to a diminished or absent drive to breathe during sleep 9, 1.

Neurological Disorders

Damage to the brainstem—whether from trauma, stroke, tumors, or congenital conditions—can disrupt the neural signals that control breathing, resulting in CSA 7, 1.

Idiopathic and Genetic Causes

In rare cases, CSA occurs without any obvious trigger. Genetic factors, such as mutations affecting respiratory control pathways (e.g., PHOX2B gene in congenital central hypoventilation syndrome), may play a role 1, 9.

Treatment of Central Sleep Apnea

Managing CSA requires addressing both the underlying cause (if possible) and the breathing disorder itself. Treatment options have evolved as our understanding of CSA pathophysiology has grown, but some forms remain challenging to manage.

Therapy	Main Indication/Use	Notes/Effectiveness	Source(s)
CPAP (Continuous Positive Airway Pressure)	First-line for CSA, especially in CHF	Reduces apneas in many CSA forms	6, 1
ASV (Adaptive Servo-Ventilation)	CSA, CompSAS, Cheyne-Stokes; not for CHF with LVEF ≤45%	Highly effective but caution in some CHF	11, 12, 9
Supplemental Oxygen	CSA with hypoxemia, high altitude, CHF	Reduces central apneas	1, 10
Acetazolamide	High altitude, idiopathic CSA	Carbonic anhydrase inhibitor, reduces apneas	1, 6, 7
Treat Underlying Disease	CHF, neurological disease, medication review	Essential first step	1, 6
BPAP with Backup Rate	If CPAP/ASV not effective	Consider for CHF-related CSA	6, 11
Medication Change	Opioid/sedative reduction	If drug-induced	1, 9

Table 4: Main Treatments for Central Sleep Apnea

Approaches to Management

General Principles

• Treat the underlying condition: Optimizing heart failure management, addressing brain injury, or reviewing medications is crucial before considering direct CSA therapies 1, 6.
• Select therapy based on CSA type and comorbidities.

Positive Airway Pressure Therapies

• CPAP: Often first-line, especially in CSA related to heart failure. CPAP stabilizes breathing by maintaining airway pressure and improving oxygenation. It is effective for many, but not all, forms of CSA 6, 1.
• ASV: Adaptive servo-ventilation is highly effective for many patients with CSA or complex sleep apnea syndromes. However, it should NOT be used in patients with heart failure and a reduced ejection fraction (LVEF ≤45%), as it is associated with increased cardiac mortality in this group 11, 12, 9.
• BPAP with backup rate: Considered when CPAP and ASV are ineffective or not tolerated, particularly in CHF-associated CSA 6, 11.

Supplemental Oxygen

Oxygen therapy can significantly reduce the frequency of central apneas, especially in people with Cheyne-Stokes respiration, high-altitude CSA, or idiopathic forms 1, 10. It also helps improve sleep quality by reducing arousals associated with apneas.

Pharmacologic Approaches

• Acetazolamide: A carbonic anhydrase inhibitor that induces mild metabolic acidosis, stimulating breathing and reducing central apneas. Particularly useful at high altitude and sometimes in idiopathic CSA 1, 6, 7.
• Sedative-hypnotics: Zolpidem and triazolam may be considered in select idiopathic cases, but only if there are no risk factors for respiratory depression 6.

Addressing Drug-Induced CSA

If CSA is caused by opioids or sedatives, reducing or discontinuing the offending drug is the most effective intervention. In some cases, ASV may be used for persistent symptoms 9, 1.

Other/Adjunct Treatments

• Nocturnal dialysis or bicarbonate buffer: For CSA associated with end-stage renal disease 6.
• Lifestyle modifications: Weight management, sleep hygiene, and avoidance of alcohol or sedatives may also help.

Conclusion

Central Sleep Apnea is a multifaceted disorder that can quietly undermine sleep quality and health, particularly in individuals with heart failure, neurologic disease, or those exposed to certain medications or high altitudes. While diagnosis can be challenging due to subtle symptoms, advances in understanding have led to more effective, individualized treatments. Early recognition, targeted therapy, and careful management of underlying conditions remain the foundation of care.

Key Points Covered:

• CSA often presents with insomnia, fragmented sleep, and subtle daytime symptoms; loud snoring is uncommon.
• There are several types of CSA, including idiopathic, Cheyne-Stokes respiration, high altitude-related, drug-induced, and those secondary to medical or neurological disorders.
• Causes include unstable ventilatory control, heart failure, opioid use, high altitude, neurological injury, and rare genetic syndromes.
• Treatments range from positive airway pressure (CPAP, ASV), supplemental oxygen, medications like acetazolamide, to managing underlying diseases and medication adjustments.
• Therapy must be tailored to the CSA type and underlying comorbidities; ASV is contraindicated in some heart failure patients.

By understanding the nuances of CSA, patients and clinicians can work together to restore healthy sleep and improve quality of life.