What is central sleep apnea (CSA), how is it diagnosed, and what are the differences between CSA and obstructive sleep apnea (OSA) in patients with a history of cardiovascular disease or neurological disorders?

Central Sleep Apnea: Definition, Diagnosis, and Differentiation from Obstructive Sleep Apnea

What is Central Sleep Apnea?

Central sleep apnea (CSA) is a sleep-disordered breathing condition characterized by recurrent cessations of airflow during sleep with absent or diminished respiratory effort, fundamentally distinguishing it from obstructive sleep apnea where respiratory effort continues despite airway obstruction. 1, 2

Pathophysiology

• CSA results from instability in chemical control of breathing, occurring primarily during light sleep (stages N1 and N2) when breathing is under CO₂-dependent chemical control rather than voluntary control 1
• The condition involves the "apnea threshold" concept: when PaCO₂ falls below a critical level, breathing cessations occur 2
• Loss of the "wakefulness drive to breathe" at sleep onset contributes to CSA, particularly in patients with already diminished central respiratory drive 2

Primary Etiologies

CSA encompasses diverse conditions with different underlying causes 1, 3:

• Heart failure is the most common cause, typically presenting with Cheyne-Stokes respiration pattern and long cycle length (45-75 seconds) 1, 4
• Neurological disorders (particularly stroke) disrupt respiratory control centers 1
• Atrial fibrillation causes CSA with shorter cycle length (<45 seconds) compared to heart failure 1
• Pulmonary hypertension independent of heart failure 1
• Renal failure through metabolic derangements affecting respiratory drive 1
• Medication-induced CSA, particularly from opioids and benzodiazepines 1, 4
• Treatment-emergent CSA occurs in approximately 1% of patients starting CPAP for OSA, typically resolving within 1-3 months 1

How to Diagnose Central Sleep Apnea

Polysomnography (PSG) is essential and mandatory for CSA diagnosis, as clinical tools, questionnaires, or prediction algorithms alone are inadequate and should not be used without objective testing. 1

Required Polysomnographic Parameters

PSG must include 1:

• Oxygen saturation measurement
• Rib cage and abdominal movement monitoring (to assess respiratory effort)
• Nasal and oral airflow measurement
• Sleep staging via electroencephalography, electrooculography, and electromyography
• Electrocardiogram

Diagnostic Criteria

• CSA is diagnosed when the apnea-hypopnea index (AHI) is ≥5 events/hour with central events predominating (central events > 50% of total respiratory events or central apnea index > obstructive apnea index) 5, 1
• Severity classification follows standard AHI thresholds: mild (5-14), moderate (15-29), severe (≥30) 5

Clinical Assessment Prior to PSG

Before objective testing, obtain 1:

• Detailed sleep history including witnessed apneas, gasping, nonrefreshing sleep, nocturia, and excessive daytime sleepiness
• Comprehensive medication review, specifically identifying sedative-hypnotics and opiate analgesics 1
• Alcohol use assessment 1
• Cardiovascular and neurological history, as heart failure, stroke, atrial fibrillation, and renal disease are major risk factors 1, 6

Cycle Length Assessment

Measuring cycle length during PSG helps distinguish CSA etiologies 1:

• Long cycle length (45-75 seconds): suggests heart failure-associated CSA with Cheyne-Stokes respiration
• Short cycle length (<45 seconds): associated with atrial fibrillation, narcotics, pulmonary hypertension, renal failure, high altitude, or stroke

Key Differences Between Central and Obstructive Sleep Apnea

Fundamental Pathophysiologic Distinction

The critical difference is the presence or absence of respiratory effort during apneic events: OSA shows continued respiratory effort against an obstructed airway, while CSA demonstrates absent or diminished respiratory effort. 1, 2

Polysomnographic Differentiation

Feature	Obstructive Sleep Apnea	Central Sleep Apnea
Respiratory effort	Present and ongoing during apneas [1,2]	Absent or diminished during apneas [1,2]
Rib cage/abdominal movement	Paradoxical movement continues [1]	Absent movement [1]
Upper airway	Anatomical obstruction present [5]	Patent airway [2]
Cycle pattern	Variable [5]	Often periodic (Cheyne-Stokes in heart failure) [1]

Clinical Presentation Differences

OSA patients 5:

• More likely to be obese with anatomical upper airway abnormalities
• Prominent snoring and witnessed choking episodes
• Retrognathia, macroglossia, tonsillar hypertrophy, narrow pharynx
• Mallampati score 3-4

CSA patients 1, 6:

• Often older and thinner than OSA patients
• Higher prevalence of cardiovascular comorbidities (heart failure, arrhythmias, coronary disease)
• May present with orthopnea and paroxysmal nocturnal dyspnea (in heart failure-associated CSA)
• More severe hypoxemia (higher oxygen desaturation index)
• Less prominent snoring

Risk Factor Profiles

Independent risk factors for CSA (versus OSA) include 6:

• Older age
• Comorbid arrhythmia or heart failure
• Elevated oxygen desaturation index
• Lower body mass index

Complex and Mixed Presentations

Important caveat: CSA and OSA frequently coexist rather than occurring in isolation 7, 6:

• In severe sleep apnea patients, 72% with CSA also exhibit other apnea subtypes 6
• Complex sleep apnea (CompSA) describes emergence of CSA upon treatment of OSA 7
• Pure or dominant CSA represents only 5% of all sleep apnea patients 6

Treatment Implications

Treatment differs fundamentally based on apnea type 1, 3:

For OSA 5:

• CPAP is first-line therapy
• Oral appliances, positional therapy, upper airway surgery

For CSA 1, 3:

• Treatment of underlying condition is primary (optimize heart failure management, address neurological disorders)
• Adaptive servo-ventilation (ASV) for normocapnic CSA with ventilatory instability
• Critical contraindication: ASV is contraindicated in heart failure patients with reduced ejection fraction due to increased mortality risk 1
• Non-invasive ventilation with backup rate for hypercapnic CSA or REM hypoventilation
• Avoid benzodiazepines and opioids that worsen CSA 4

Common Diagnostic Pitfalls

Never assume all apneas are the same type without polysomnography assessing respiratory effort 1:

• Older patients may have CSA without obesity, leading to missed diagnoses if only OSA is considered 8
• Patients with cardiovascular or neurological disease require high suspicion for CSA 1
• Home sleep testing (portable monitors) may not adequately distinguish CSA from OSA, as they often lack comprehensive respiratory effort monitoring 5
• In patients with suspected CSA or significant comorbidities (heart failure, stroke, pulmonary disease), in-laboratory PSG is preferred over portable monitoring 5