Abbreviated Method for Assessing Upper Airway Function in Obstructive Sleep Apnea

Boudewyns, An; Punjabi, Naresh M.; Heyning, Paul Van de; Backer, Wilfried A. De; O’Donnell, Christopher P.; Schneider, Hartmut; Smith, Philip L.; Schwartz, Alan R.

doi:10.1378/chest.118.4.1031

Cited by 119 publications

(142 citation statements)

References 18 publications

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“…OSA tends to be worse in the supine position when the upper airway is intrinsically more collapsible, probably because of the effects of gravity. 28,29 In the supine position, neck fluid accumulation may increase the collapsibility of an already compromised upper airway sufficiently to increase the number of apneas and hypopneas. In contrast, in the non-supine position, when the upper airway is less collapsible, neck fluid accumulation may have a lesser effect on the AHI.…”

Section: Fluid Shift and Sleep Apnea Variabilitymentioning

confidence: 99%

Night-to-night Variability in Obstructive Sleep Apnea Severity: Relationship to Overnight Rostral Fluid Shift

White

Lyons

Yadollahi

et al. 2015

Journal of Clinical Sleep Medicine

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Study Objectives: Overnight rostral fl uid shift from the legs to the neck may narrow the pharynx and contribute to obstructive sleep apnea (OSA) pathogenesis. We hypothesized that night-to-night changes in the apneahypopnea index (AHI) would be associated with changes in overnight rostral fl uid shift. Methods: Twenty-six patients with OSA (AHI ≥ 10) underwent two polysomnograms 14 days apart with measurement of neck and leg fl uid volumes (LFV), neck circumference and upper-airway cross-sectional area before and after sleep. Results: Although mean AHI did not differ between polysomnograms, 35% of patients had a difference in AHI > 10, indicating signifi cant intra-individual variability. There were direct correlations between change in non-rapid-eye movement (NREM), but not REM AHI and change in evening LFV between polysomnograms (r = 0.440, p = 0.036 and r = 0.005, p = 0.982, respectively) and between change in supine, but not non-supine AHI and change in evening LFV (r = 0.483, p = 0.020 and r = 0.269, p = 0.280, respectively). An increase in evening LFV between polysomnograms was associated with a greater overnight decrease in LFV (r = 0.560, p = 0.005) and a greater overnight increase in neck fl uid volume (r = 0.498, p = 0.016). Additionally, a greater overnight increase in neck circumference was associated with a greater overnight increase in neck fl uid volume between polysomnograms (r = 0.453, p = 0.020) and a greater overnight decrease in upperairway cross-sectional area (r = −0.587, p = 0.005). Conclusion: Intra-individual variability in OSA severity may be partly explained by day-to-day changes in evening leg fl uid volume and overnight rostral fl uid shift, which may be most important in the pathogenesis of OSA during NREM and supine sleep. S C I E N T I F I C I N V E S T I G AT I O N S BRIEF SUMMARYCurrent Knowledge/Study Rationale: Overnight rostral fl uid shift from the legs to the neck may narrow the upper airway and contribute to obstructive sleep apnea (OSA) pathogenesis. Intra-individual night-tonight variability in OSA severity may relate to night-to-night variations in overnight rostral fl uid shift. Study Impact: This study found that intra-individual variability in OSA severity may be partly explained by day-to-day changes in evening leg fl uid volume and overnight rostral fl uid shift, which may be most important in the pathogenesis of OSA during NREM and supine sleep. S everity of obstructive sleep apnea (OSA) can vary considerably from night to night, but the reasons for this are unclear. Previous studies found a change in the frequency of apneas and hypopneas per hour of sleep (apnea-hypopnea index, AHI) greater than 10 in 18% to 65% of patients undergoing polysomnograms (PSGs) on consecutive nights or one month apart. [1][2][3][4] Furthermore, in one study, 50% of patients undergoing consecutive night PSGs met criteria for OSA diagnosis (AHI ≥ 10) on one PSG but not on the other. Few studies have examined the reasons for this AHI variability. While one study found increased variabi...

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Section: Fluid Shift and Sleep Apnea Variabilitymentioning

confidence: 99%

Night-to-night Variability in Obstructive Sleep Apnea Severity: Relationship to Overnight Rostral Fluid Shift

White

Lyons

Yadollahi

et al. 2015

Journal of Clinical Sleep Medicine

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“…PFR were obtained during a second, overnight study, using modifications of previously published techniques (6,9,18). Upper airway function was measured under the following conditions, in random order:…”

Section: Measurement Of Pfr and Upper Airway Responsesmentioning

confidence: 99%

Upper Airway Dynamic Responses in Children with the Obstructive Sleep Apnea Syndrome

et al. 2005

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Normal children have a smaller upper airway than adults, but, nevertheless, snore less and have less apnea. We have previously shown that normal children have an upper airway that is resistant to collapse during sleep. We hypothesized that this resistance to collapse is due to preservation of upper airway neuromotor responses during sleep. Furthermore, we hypothesized that upper airway responses would be diminished in children with the obstructive sleep apnea syndrome (OSAS). We therefore compared the upper airway pressure-flow relationship during sleep between children with OSAS and controls. Measurements were made by correlating maximal inspiratory airflow with the level of nasal pressure applied via a mask. Neuromotor upper airway activation was assessed by evaluating the upper airway response to 1) hypercapnia and 2) intermittent, acute negative pressure. We found that children with OSAS had no significant response to either hypercapnia or negative pressure during sleep, compared with the normal children. After treatment of OSAS by tonsillectomy and adenoidectomy, there was a trend for normalization of upper airway responses. We conclude that upper airway dynamic responses are decreased in children with OSAS but recover after treatment. We speculate that the pharyngeal airway neuromotor responses present in normal children are a compensatory response for a relatively narrow upper airway. Further, we speculate that this compensatory response is lacking in children with OSAS, most likely due to either habituation to chronic respiratory abnormalities during sleep or to mechanical damage to the upper airway. In children, OSAS is related to adenotonsillar hypertrophy. Most children with OSAS have large tonsils and adenoids, and improve after T&A (1). Nevertheless, studies suggest that childhood OSAS is not due to anatomic abnormalities alone. Most obvious is the fact that patients with OSAS do not obstruct during wakefulness, when upper airway muscle tone is high. Although the upper airway may be narrower in children with OSAS than in those without, there is overlap between the groups (2). A small percentage of children with adenotonsillar hypertrophy but no other known risk factors for OSAS are not cured by T&A (1). Furthermore, a small percentage of children who were cured of their OSAS by T&A have been reported to develop a recurrence during adolescence (3,4). Thus, it appears that childhood OSAS is a dynamic process resulting from a combination of structural and neuromotor abnormalities, rather than from structural abnormalities alone. The upper airway above the level of the cartilaginous airway is a collapsible muscular tube that usually remains patent but has the potential to collapse to facilitate such functions as speech and swallowing. It comprises more than 30 pairs of muscles (5). Thus, neuromotor control of this area is important to maintain airway patency. Upper airway collapsibility during sleep is modulated by the central ventilatory drive (6). The upper airway dilatory muscles are respiratory musc...

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“…After an adequate level of sedation was attained, the subjects were initially allowed to breathe under atmospheric pressure while nasal pressure was gradually increased to a holding pressure until inspiratory airflow limitation was eliminated, as previously described (Schwartz et al, 1998b;Boudewyns et al, 2000). Thereafter, nasal pressure was maintained at a holding level and was subsequently lowered progressively by 1 to 2 cm H 2 O every 5 or 6 breaths until zero flow occurred (Fig.…”

Section: Measurement Of Upper-airway Collapsibilitymentioning

confidence: 99%

“…At each level of nasal pressure, breaths were evaluated for the presence of inspiratory airflow limitation, as previously described (Schwartz et al, 1988(Schwartz et al, , 1989Boudewyns et al, 2000). Maximal inspiratory airflow (VImax) was measured in the last 3 flowlimited inspirations at each level of nasal pressure, as previously described (Schwartz et al, 1998a).…”

Section: Upper-airway Pressure Relationshipmentioning

confidence: 99%

Mouth-opening Increases Upper-airway Collapsibility without Changing Resistance during Midazolam Sedation

et al. 2004

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Sedative doses of anesthetic agents affect upper-airway function. Oral-maxillofacial surgery is frequently performed on sedated patients whose mouths must be as open as possible if the procedures are to be accomplished successfully. We examined upper-airway pressure-flow relationships in closed mouths, mouths opened moderately, and mouths opened maximally to test the hypothesis that mouth-opening compromises upper-airway patency during midazolam sedation. From these relationships, upper-airway critical pressure (Pcrit) and upstream resistance (Rua) were derived. Maximal mouth-opening increased Pcrit to −3.6 ± 2.9 cm H2O compared with −8.7 ± 2.8 (p = 0.002) for closed mouths and −7.2 ± 4.1 (p = 0.038) for mouths opened moderately. In contrast, Rua was similar in all three conditions (18.4 ± 6.6 vs. 17.7 ± 7.6 vs. 21.5 ± 11.6 cm H2O/L/sec). Moreover, maximum mouth-opening produced an inspiratory airflow limitation at atmosphere that was eliminated when nasal pressure was adjusted to 4.3 ± 2.7 cm H2O. We conclude that maximal mouth-opening increases upper-airway collapsibility, which contributes to upper-airway obstruction at atmosphere during midazolam sedation.

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Abbreviated Method for Assessing Upper Airway Function in Obstructive Sleep Apnea

Cited by 119 publications

References 18 publications

Night-to-night Variability in Obstructive Sleep Apnea Severity: Relationship to Overnight Rostral Fluid Shift

Night-to-night Variability in Obstructive Sleep Apnea Severity: Relationship to Overnight Rostral Fluid Shift

Upper Airway Dynamic Responses in Children with the Obstructive Sleep Apnea Syndrome

Mouth-opening Increases Upper-airway Collapsibility without Changing Resistance during Midazolam Sedation

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