0534 Systematic Evaluation of Respiratory Arousal Latency in Sleep Apnea

Abstract Introduction Sleep apnea is characterized by episodes of apneas and hypopneas, often triggering cortical arousals associated with the resumption of breathing. The timing of these arousals has not been rigorously studied, leading to inconsistencies in the characterization of sleep disordered breathing and its impact on sleep continuity and clinical outcomes. Our objective was to characterize respiratory arousal latency within a well-defined sleep apnea research cohort. Methods Patients with a history of moderate to severe sleep apnea participated in two research sleep studies: one polysomnography (PSG) while on CPAP and the other after a three-night CPAP withdrawal, in a randomized order. The analysis included data from 127 participants (mean age: 53.1±11.4, male:female: 86:41, mean AHI: 57.9±31.0) on the last night of their CPAP withdrawal. The dataset included 20,510 apneas, 21,227 hypopneas, and 27,578 EEG arousals. Respiratory arousal latency (RAL) was defined as the time interval, from (A) the end of an apnea or hypopnea to, (B) the onset of the subsequent EEG arousal. We identified A and B time markers utilizing a moving analysis window spanning 10 seconds prior to the end of each event and extending 20 seconds post-event termination. The influence of respiratory event types, sleep stage, and event severity (SpO2 % desaturation, event length) was examined using linear mixed effects models. Results RAL following hypopneas have modeled Beta estimates of 2.23s [1.94,2.52] after the event (mean [CI]; p< 0.001). Central and obstructive apneas were significantly prolonged compared to hypopneas, 2.91s [2.36,3.45] and 2.42s [2.02,2.82], respectively (p< 0.001). Mixed apneas and central hypopneas were significantly prolonged by 2.31s [1.82,2.8] and 2.74s [1.84,3.65], respectively (p< 0.001). More severe hypoxia or longer SDB events had shortened latencies (p< 0.001). RAL for stage N2 estimated to be 2.23s [1.94,2.52] after the events (p< 0.001). Stage N1 had a shortened latencies compared to N2, 2.00s [1.61,2.39] (p< 0.001), while N3 and REM had prolonged latencies of 2.69s [2.11,3.27] and 2.56s [2.12,3.01] (p< 0.01), respectively. Conclusion RAL differs between event types, sleep stage, event duration and severity of SpO2 desaturation. Support (if any) R01HL135483

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Journal
SLEEP
Published
2026-05-01
DOI
https://doi.org/10.1093/sleep/zsag091.0533
Primary Topic
Obstructive Sleep Apnea Research
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article
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article

0534 Systematic Evaluation of Respiratory Arousal Latency in Sleep Apnea

Jonathan Jun, Francis Sgambati, Luu Pham
SLEEP
Obstructive Sleep Apnea Research
article

0534 Systematic Evaluation of Respiratory Arousal Latency in Sleep Apnea

Jonathan Jun, Francis Sgambati, Luu Pham
article en

Abstract

Abstract Introduction Sleep apnea is characterized by episodes of apneas and hypopneas, often triggering cortical arousals associated with the resumption of breathing. The timing of these arousals has not been rigorously studied, leading to inconsistencies in the characterization of sleep disordered breathing and its impact on sleep continuity and clinical outcomes. Our objective was to characterize respiratory arousal latency within a well-defined sleep apnea research cohort. Methods Patients with a history of moderate to severe sleep apnea participated in two research sleep studies: one polysomnography (PSG) while on CPAP and the other after a three-night CPAP withdrawal, in a randomized order. The analysis included data from 127 participants (mean age: 53.1±11.4, male:female: 86:41, mean AHI: 57.9±31.0) on the last night of their CPAP withdrawal. The dataset included 20,510 apneas, 21,227 hypopneas, and 27,578 EEG arousals. Respiratory arousal latency (RAL) was defined as the time interval, from (A) the end of an apnea or hypopnea to, (B) the onset of the subsequent EEG arousal. We identified A and B time markers utilizing a moving analysis window spanning 10 seconds prior to the end of each event and extending 20 seconds post-event termination. The influence of respiratory event types, sleep stage, and event severity (SpO2 % desaturation, event length) was examined using linear mixed effects models. Results RAL following hypopneas have modeled Beta estimates of 2.23s [1.94,2.52] after the event (mean [CI]; p< 0.001). Central and obstructive apneas were significantly prolonged compared to hypopneas, 2.91s [2.36,3.45] and 2.42s [2.02,2.82], respectively (p< 0.001). Mixed apneas and central hypopneas were significantly prolonged by 2.31s [1.82,2.8] and 2.74s [1.84,3.65], respectively (p< 0.001). More severe hypoxia or longer SDB events had shortened latencies (p< 0.001). RAL for stage N2 estimated to be 2.23s [1.94,2.52] after the events (p< 0.001). Stage N1 had a shortened latencies compared to N2, 2.00s [1.61,2.39] (p< 0.001), while N3 and REM had prolonged latencies of 2.69s [2.11,3.27] and 2.56s [2.12,3.01] (p< 0.01), respectively. Conclusion RAL differs between event types, sleep stage, event duration and severity of SpO2 desaturation. Support (if any) R01HL135483

SLEEPVol. 49(Supplement_1)
Johns Hopkins University (US), Johns Hopkins Medicine (US)
Openalex Percentile: Top 7%
Obstructive Sleep Apnea Research
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