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Alteration in obstructive apnea pattern induced by changes in oxygen- and carbon-dioxide-inspired concentrations
D W Hudgel1, C Hendricks, A Dadley
1Department of Medicine, Case Western Reserve University, Cleveland, Ohio.
The American Review of Respiratory Disease
|July 1, 1988
Summary
Breathing carbon dioxide (CO2) during sleep increased upper airway muscle activity and reduced obstructive sleep apnea events. Oxygen (O2) had the opposite effect, worsening apnea. This highlights the role of respiratory control in sleep apnea.
Area of Science:
- Respiratory Physiology
- Sleep Medicine
- Neuromuscular Control
Background:
- Obstructive sleep apnea (OSA) is characterized by upper airway collapse during sleep.
- The role of ventilatory control and pharyngeal muscle activity in OSA pathophysiology is not fully understood.
Purpose of the Study:
- To investigate the effects of hypercapnia (elevated CO2) and hyperoxia (elevated O2) on upper airway muscle activity and apnea events in patients with OSA.
- To determine if manipulating respiratory drive can alter the pattern of upper airway collapse during sleep.
Main Methods:
- Seven patients with symptomatic OSA were studied.
- Inhalation of 3-6% CO2 and 50% O2 during sleep.
- Measurement of pharyngeal and chest wall inspiratory muscle electrical activity.
- Quantification of apnea time and periodic breathing.
Main Results:
- CO2 inhalation preferentially stimulated upper airway inspiratory muscles, decreased apnea time from 60% to 12% of sleep time, and diminished periodic breathing.
- O2 inhalation decreased inspiratory muscle activity and increased apnea time to 75% of sleep time.
- Significant changes in upper airway inspiratory collapse patterns were observed with CO2 and O2 manipulation.
Conclusions:
- Manipulation of respiratory drive via CO2 and O2 significantly alters upper airway muscle activity and breathing patterns during sleep in OSA patients.
- Physiologic variables controlling upper airway inspiratory muscles are crucial in OSA pathophysiology.
- Targeting respiratory control mechanisms may offer therapeutic potential for OSA.