The Challenges of Differentiating between Central vs. Obstructive Hypopneas -

Why is it important to differentiate obstructive and central hypopnoea events you may ask?

Accurate differentiation and reporting of central and obstructive hypopnoeas is essential for proper diagnosis and treatment planning decisions in people with Obstructive and Central Sleep Apnoea. The current AASM hypopnoeas scoring rules recommend distinguishing central vs obstructive hypopnoeas, and is also recommended by the European Respiratory society and the French Sleep Society (1-3). Sleep disorders, particularly sleep apnea, present a degree of complexity for clinicians and researchers alike. The challenge lies in accurately identifying the underlying cause, which requires careful analysis of respiratory signals.

Here’s an in-depth guide:

What Are Hypopnoeas?

Hypopnoeas are episodes characterised by a 30% reduction in airflow during sleep, often accompanied by a oxygen desaturation (3% or 4%) or arousal. They are a key component in diagnosing sleep-disordered breathing. However, not all hypopnoeas are the same, and distinguishing their types is vital.

Central verses Obstructive Hypopnoeas: What’s the Difference?

Central Hypopnoeas: These happen when the brain temporarily reduces sending appropriate signals to the muscles responsible for breathing. In essence, there is a decrease in respiratory effort, resulting in reduced airflow without any physical airway obstruction.

Key Features:

– Significant airflow reduction (≥30%) lasting at least 10 seconds.

– Marked reduction of thoracoabdominal breathing effort during the event.

– No evidence of upper airway obstruction (e.g., no snoring, no airway flattening, no paradoxical breathing).

– Typically accompanied by stable or absent airflow efforts that mirror the effort reduction.

– May be associated with EEG arousals (arousal that comes later at maximum cycle in comparison to OH where the arousal arrives at the end of the event) but lack signs of airway collapse.

(4) Apnea and hypopnoea characterisation using esophageal pressure, respiratory inductance plethysmography, and suprasternal pressure: a comparative study | Sleep and Breathing

Obstructive Hypopnoeas: Conversely, these occur when the airway narrows or collapses physically, even though the brain continues to send signals to breathe. As a result, airflow is impeded by an airway obstruction despite ongoing respiratory effort.

Key Features:

– Airflow reduction (≥30%) lasting ≥10 seconds.

– Continued or paradoxical thoracoabdominal effort, indicating active respiratory muscle effort to breathe.

– Often linked with snoring, paradoxical breathing, or increased upper airway resistance.

– Desaturation often occurs (≥3-4%), paired with EEG arousals.

– Presence of airway collapse signs, such as increased resistance or vibratory sounds (snoring).

The Diagnostic Challenge

Distinguishing between these two types of hypopnoeas can be challenging, as both may exhibit similar reductions in airflow and oxygen levels, yet they stem from fundamentally different mechanisms—factors that significantly impact treatment approaches.

According to guidelines from leading sleep medicine societies—namely, the American Academy of Sleep Medicine (AASM) and the European Sleep Research Society (ESRS)—careful analysis is essential

Expert Consensus and Recommendations

Both the AASM and ESRS acknowledge that:

Accurate differentiation hinges on comprehensive respiratory monitoring during sleep studies.
Recognising the limitations—such as signal quality and patient-specific factors—is essential.
Experienced interpretation is important to avoid misclassification of events, which can impact treatment choices like CPAP therapy or other interventions.

While technology and guidelines have advanced our ability to distinguish between central and obstructive hypopneas remains challenging. Careful analysis and expert interpretation are critical, and sometimes, additional testing is necessary. Awareness of these nuances helps clinicians tailor more effective, personalised treatment strategies with the ultimate aim of improving patient outcomes.

Treating residual CSA and Central Hypopnoeas – what are the options

Treatment of Central Sleep Apnoea in Adults: An American Academy of Sleep Medicine Clinical Practice Guideline was published in draft form in February 2025 (5). This is what the guidelines recommend:

Key Principles – (Good Practice recommendations):

Treatment must be tailored to the patient’s clinical features, co-morbidities, and sleep study results.

The priority is optimising therapy for conditions causing CSA and improving patient symptoms/quality of life.

If central events persist after starting treatment, re-evaluate underlying factors and consider alternatives treatments.

Treatment Recommendations (All Conditional – Weak Evidence):

CPAP: Suggested for most CSA types (Primary, Heart Failure, Medication/Substance, Treatment-Emergent, Medical Condition). May reduce breathing events and mortality.

NIV with Backup Rate: Suggested for Primary, Medication/Substance, Treatment-Emergent, Medical Condition CSA. Avoid NIV without Backup Rate (can worsen CSA).

Adaptive Servo-Ventilation (ASV): Suggested for most CSA types. Caution: Different devices have different algorithms; safety data varies. One specific device (now discontinued) was linked to increased mortality in severe heart failure.

Low-Flow Oxygen:

May be recommended for CSA due to Heart Failure.

Suggested for CSA at High Altitude (>2500m). Mild/transient symptoms may not need treatment.

Acetazolamide (Oral):

May be suggested for most CSA types (Primary, Heart Failure, Medication/Substance, Treatment-Emergent, Medical Condition).

May be suggested for CSA at High Altitude. Common mild side effects (tingling, taste changes, diuresis).

Transvenous Phrenic Nerve Stimulation (TPNS): Suggested only for Primary CSA or CSA due to Heart Failure in patients who failed other therapies.

Key Limitations of these guidelines:

Evidence supporting treatments is generally low or very low certainty.

Significant knowledge gaps remain in CSA mechanisms and optimal treatments.

Long-term outcome data (e.g., mortality, quality of life) is scarce

This guideline provides conditional, evidence-limited suggestions for various CSA treatments, stressing the need for personalised care focused on underlying causes and patient symptoms. CPAP, specific BPAP, ASV (with caution), oxygen (for heart failure/high altitude), and acetazolamide are potential options. TPNS is a last-resort invasive option. Significant research gaps persist.

When it comes to treating residual CSA and Central hypopnoeas and particularly Treatment Emergent CSA – (TECSA) there are differences in CPAP device algorithms ability to be able differentiate between Obstructive and Central Hypopnoeas and report these events. Clinicians should be made aware of these differences.

In a recent large real world study by Pepin et al 2024, the prevalence of central sleep apnoea when central hypopnoeas were included was 20% and they concluded that not differentiating between central and obstructive hypopneas will underestimate the severity of central sleep disordered breathing abnormalities that mislead therapeutic decisions (9). Several recent publications highlight this potential to miss TECSA and particularly Central Hypopnoeas and this may impact on patient care and treatment outcomes and if these events are under reported patients may not receive appropriate therapy (6-8).

A recent study by Vidal et al 2025 highlights inconsistencies in residual AHI calculations among CPAP manufacturers, raising concerns and suggests that there are potential patient care issues related to inconsistencies in reporting residual AHI_flow calculations across different devices. They suggest a need for a scientific consensus to establish a standard way of calculating residual AHI_flow to promote safer care for patients undergoing CPAP telemonitoring (8). Central apnoeas and hypopneas are linked to significant health risks, including cardiovascular complications and excessive daytime fatigue as well as significant multimorbidity and symptom burden. Identifying these events can play a pivotal role in reducing these risks.