Abstract
Purpose
Prior studies evaluating Eustachian tube physiology, baseline middle ear pressure (MEP), and the effects of continuous positive airway pressure (CPAP) have been performed on awake patients. No study to date has specifically investigated MEP during sleep despite the fact that the average individual spends a third of their lifetime sleeping. The primary objectives of the current study are to quantify normal physiologic MEP during sleep and to evaluate the effects of escalating CPAP levels.
Materials and methods
Prospective observational study at a tertiary academic referral center evaluating serial tympanometry on sleeping adult patients during polysomnography. MEP was recorded awake, at 1-hour intervals during diagnostic polysomnography, and at all CPAP levels during titration. Changes in MEP with duration of sleep and escalating CPAP levels were analyzed.
Results
Ten adults were included (4 females; 6 males; mean age 58 years). The mean MEP while awake was 3 decapascals (daPa). The mean MEP during sleep without CPAP rose steadily from 14 daPa at 1 hour to 41 daPa at 4 hours ( r = 0.52; p < 0.001). The mean MEP during sleep at a CPAP level of 5 cm of water was 54 daPa. The mean MEP rose steadily with increasing CPAP levels, and was 104 daPa at 10 cm of water, ( r = 0.82; p < 0.001). The mean MEP during sleep without CPAP was 26 daPa, which was significantly lower than the mean MEP during sleep with CPAP between 5–10 cm H 2 O ( p < 0.01).
Conclusions
MEP naturally increases with duration of sleep. CPAP therapy causes a supraphysiologic elevation in MEP that rises with increasing pressure levels. These findings may help guide future studies examining the safety of CPAP following otologic surgery and the potential therapeutic benefit in patients with chronic middle ear disease.
1
Introduction
Maintenance of normal middle ear pressure (MEP) by an appropriately functioning eustachian tube (ET) is vital to the health of the middle ear. ET dysfunction resulting in chronic negative MEP has been implicated in many significant otologic conditions including hearing loss, tympanic membrane (TM) retraction, and chronic otitis media. Prior studies evaluating middle ear and ET physiology have been performed on awake patients with normal or negative MEP . To the authors’ knowledge, no study to date has specifically investigated MEPs during sleep despite the fact that the average individual sleeps nearly a third of their lifetime. Many organ systems have normal physiologic changes during sleep. In patients without middle ear disease, studies have shown that MEP is most commonly positive upon waking, but quickly normalizes toward zero after swallowing and chewing maneuvers . These findings suggest that middle ear and ET physiology also change during sleep.
Continuous positive airway pressure (CPAP) therapy, a highly effective treatment for obstructive sleep apnea (OSA), provides a pneumatic stent for the upper airway and prevents apnea during sleep. It is highly plausible that positive pressure may be transmitted to the middle ear through the ET during CPAP use. This can occur during periodic ET opening or when nasopharyngeal airway pressures exceed the resting pressure keeping the ET closed. A recent study demonstrated a linear increase in MEP with increasing CPAP levels in awake patients . We hypothesized that MEP would rise slowly with duration of sleep and that escalating CPAP levels would cause proportional elevations in MEP during sleep.
2
Materials and methods
Following Institutional Review Board approval (IRB No. 12-005787), adult patients undergoing polysomnography at a tertiary academic referral center were prospectively enrolled. All research subjects were provided informed consent. Study participation was limited to patients without prior middle ear disease or a history of otologic surgery. Each eligible participant was further screened using otomicroscopy and tympanometry (Madsen OTOflex 100; GN Otometrics North America, Schaumburg, IL), and all patients with evidence of active ET dysfunction, middle ear disease, TM perforation, or a non-Type A tympanogram were excluded. One subject was excluded because of ongoing ET dysfunction with TM retraction and a Type C tympanogram. Each patient was then fitted with a tympanometry probe in one ear that was sealed in place with polyvinylsiloxane ear impression molding (Oaktree Products Inc., Chesterfield, MO) using a manual impression gun ( Fig. 1 ). Tympanometry was performed and MEP was recorded in decapascals (daPa) in supine subjects. Two additional patients were excluded; one could not tolerate sleeping with the tympanometry probe in place, and in the other, a seal could not be kept with the probe in the ear to obtain accurate pressure readings. MEP readings were taken just before sleep initiation and during the diagnostic portion of the polysomnogram at 1-hour intervals following sleep onset. Confirmation of sleep was performed using electroencephalography (EEG). Following diagnostic polysomnography, if the patient met criteria for OSA with an apnea-hyponea index (AHI) ≥ 5 events/hour, they were fitted with a CPAP device. The CPAP level, in centimeters of water (cm H 2 O), was titrated during sleep until the patient’s OSA was adequately treated. Tympanometry was performed and MEP readings were taken prior to the initiation of CPAP, and at each level of CPAP during the titration. MEP mean values, standard deviations, and ranges were calculated for each category. Paired t-tests were used for comparison of MEP with and without CPAP use while asleep. Spearman’s rank correlation coefficient ( r ) was utilized to compare MEP with time asleep and CPAP level.
2
Materials and methods
Following Institutional Review Board approval (IRB No. 12-005787), adult patients undergoing polysomnography at a tertiary academic referral center were prospectively enrolled. All research subjects were provided informed consent. Study participation was limited to patients without prior middle ear disease or a history of otologic surgery. Each eligible participant was further screened using otomicroscopy and tympanometry (Madsen OTOflex 100; GN Otometrics North America, Schaumburg, IL), and all patients with evidence of active ET dysfunction, middle ear disease, TM perforation, or a non-Type A tympanogram were excluded. One subject was excluded because of ongoing ET dysfunction with TM retraction and a Type C tympanogram. Each patient was then fitted with a tympanometry probe in one ear that was sealed in place with polyvinylsiloxane ear impression molding (Oaktree Products Inc., Chesterfield, MO) using a manual impression gun ( Fig. 1 ). Tympanometry was performed and MEP was recorded in decapascals (daPa) in supine subjects. Two additional patients were excluded; one could not tolerate sleeping with the tympanometry probe in place, and in the other, a seal could not be kept with the probe in the ear to obtain accurate pressure readings. MEP readings were taken just before sleep initiation and during the diagnostic portion of the polysomnogram at 1-hour intervals following sleep onset. Confirmation of sleep was performed using electroencephalography (EEG). Following diagnostic polysomnography, if the patient met criteria for OSA with an apnea-hyponea index (AHI) ≥ 5 events/hour, they were fitted with a CPAP device. The CPAP level, in centimeters of water (cm H 2 O), was titrated during sleep until the patient’s OSA was adequately treated. Tympanometry was performed and MEP readings were taken prior to the initiation of CPAP, and at each level of CPAP during the titration. MEP mean values, standard deviations, and ranges were calculated for each category. Paired t-tests were used for comparison of MEP with and without CPAP use while asleep. Spearman’s rank correlation coefficient ( r ) was utilized to compare MEP with time asleep and CPAP level.
