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Updated: Jun 20, 2026

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Published on: December 6, 2016
Upper airway collapsibility during REM sleep in children with the obstructive sleep apnea syndrome
Jingtao Huang1, Laurie R Karamessinis, Michelle E Pepe
1Sleep Center, Children s Hospital of Philadelphia, University of Pennsylvania School ofMedicine, Philadelphia, PA, USA.
Insights
Children with obstructive sleep apnea syndrome (OSAS) experience reduced airflow during REM sleep due to a more collapsible airway. However, they can maintain breathing by increasing respiratory rate.
Area of Science:
- Pediatric Pulmonology
- Sleep Medicine
- Respiratory Physiology
Background:
- Obstructive events in children predominantly occur during rapid eye movement (REM) sleep.
- Understanding upper airway dynamics during sleep is crucial for diagnosing and managing obstructive sleep apnea syndrome (OSAS).
Purpose of the Study:
- To investigate the hypothesis that children with OSAS exhibit impaired upper airway stability during REM sleep compared to controls.
- To compare airflow maintenance during inspiratory pressure drops in REM and slow wave sleep (SWS) between children with OSAS and healthy controls.
Main Methods:
- Utilized a sleep laboratory setting to monitor 14 children with OSAS and 23 age-matched control subjects.
- Measured airflow, respiratory rate, tidal volume, and ventilation during SWS and REM sleep under varying inspiratory pressures.
- Assessed airflow limitation by comparing measurements at a holding pressure and at 5 cm H2O below the holding pressure.
Main Results:
- Children with OSAS demonstrated a significant decrease in airflow during REM sleep when faced with inspiratory pressure drops, unlike control subjects.
- While tidal volume decreased, minute ventilation was maintained in OSAS patients through increased respiratory rate.
- Increased inspiratory time and inspiratory time to total respiratory cycle time ratio were observed in children with OSAS during REM sleep.
Conclusions:
- Children with OSAS exhibit a more collapsible upper airway during REM sleep, leading to airflow instability.
- Compensatory mechanisms, including increased respiratory rate, help maintain adequate minute ventilation despite upper airway collapse.
- Further research into local reflexes and central control mechanisms is needed to elucidate the pathophysiology and compensation strategies in pediatric OSAS.
Study Objectives:
In children, most obstructive events occur during rapid eye movement (REM) sleep. We hypothesized that children with the obstructive sleep apnea syndrome (OSAS), in contrast to age-matched control subjects, would not maintain airflow in the face of an upper airway inspiratory pressure drop during REM sleep.
Design:
During slow wave sleep (SWS) and REM sleep, we measured airflow, inspiratory time, inspiratory time/total respiratory cycle time, respiratory rate, tidal volume, and minute ventilation at a holding pressure at which flow limitation occurred and at 5 cm H2O below the holding pressure in children with OSAS and in control subjects.
Setting:
Sleep laboratory.
Participants:
Fourteen children with OSAS and 23 normal control subjects.
Results:
In both sleep states, control subjects were able to maintain airflow, whereas subjects with OSAS preserved airflow in SWS but had a significant decrease in airflow during REM sleep (change in airflow of 18.58 +/- 12.41 mL/s for control subjects vs -44.33 +/- 14.09 mL/s for children with OSAS, P = 0.002). Although tidal volume decreased, patients with OSAS were able to maintain minute ventilation by increasing the respiratory rate and also had an increase in inspiratory time and inspiratory time per total respiratory cycle time
Conclusion:
Children with OSAS do not maintain airflow in the face of upper-airway inspiratory-pressure drops during REM sleep, indicating a more collapsible upper airway, compared with that of control subjects during REM sleep. However, compensatory mechanisms exist to maintain minute ventilation. Local reflexes, central control mechanisms, or both reflexes and control mechanisms need to be further explored to better understand the pathophysiology of this abnormality and the compensation mechanism.
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