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LETTER TO THE EDITOR
Rembold, Christopher M., and Paul M. Suratt. An upper airway resonator model of high-frequency inspiratory sounds in children with sleep-disordered breathing. J Appl Physiol 99: 1855–1861, 2005. First published December 23, 2004; doi:10.1152/japplphysiol.01231.2004.— The goal of this study was to determine how high-frequency inspiratory sounds (HFIS) are generated by sleeping children with obstructive sleep-disordered breathing (OSDB). We hypothesized that HFIS are generated when a high-velocity jet of air, generated by a narrowed upper airway, induces the upper airway to act as a resonating chamber. We tested two predictions of this hypothesis: 1) the upper airway is narrowed in children who make HFIS and 2) the length of the upper airway, calculated from HFIS harmonic intervals, is similar to that calculated from magnetic resonance imaging (MRI) scans. The study was conducted in the setting of a sleep laboratory. Participants included 29 children between 6 and 12 yr of age with adenotonsillar hypertrophy suspected of having OSDB. Minimum cross-sectional airway area and airway long dimensions (lips to larynx or soft palate) were measured in awake children with MRIs. Later that night, sound was recorded with a microphone suspended above their bed while the children underwent polysomnography. Sounds were later analyzed with fast Fourier transforms. We found that sleeping children who generated HFIS had significantly narrower upper airways compared with children who did not make HFIS [minimum airway area 20.5 ± 4.4 vs. 70.9 ± 22.5 mm2 (mean ± SE), respectively; P = 0.02]. There was a significant inverse correlation between the log10 of the narrowest airway area and the number of HFIS recorded per hour (r2 = 0.55, P < 0.00001). The harmonics characteristics of HFIS predicted that they were generated by sound resonating in chamber whose length was 12.0 ± 0.9 cm, which is similar to the MRI measured distance from the lips to the larynx of 12.8 ± 0.4 cm. In conclusion, these data suggest that children generate HFIS when 1) they have a narrowed upper airway and 2) their upper airway acts as a resonating chamber.
To the Editor: We wish to congratulate Drs. Rembold and Suratt for their interesting paper on high-frequency inspiratory sounds in children with obstructive sleep-disordered breathing (2). One of their conclusions was that the airway of the children that they studied is narrowest at the level of the adenoids. They then went on to say that: "Our findings differed from those of Fregosi et al. [see Ref. 1], who found that the narrowest area was at the level of the tonsils" (page 1860 in Ref. 2). This statement is not a completely accurate description of our findings. The major finding in our study (using magnetic resonance imaging techniques) was that, compared with normal control subjects, the airway of children with sleep-disordered breathing was significantly narrower in the region where the tonsils, adenoids, and soft palate overlap. This was stated very clearly in the abstract and in the first paragraph of the discussion, and it is depicted graphically in Fig. 5 (1). In our paper, we also defined the retropalatal airspace [ratio of the cross-sectional area (CSA) of the retropalatal airway to the CSA of the soft palate; see Fig. 6 in Ref. 1], and we demonstrated that this index correlated inversely and significantly with the obstructive apnea hypopnea index (i.e., children with higher obstructive apnea hypopnea indexes had a smaller retropalatal air space). Although we showed a significant correlation between the obstructive apnea hypopnea index and tonsil CSA, there were additional significant correlations between the obstructive apnea hypopnea index and the CSA of the soft palate, the volume of the pharyngeal airway, and the smallest oropharyngeal airway diameter (Fig. 3 in Ref. 1). Nevertheless, these correlations provide no information on what part of the airway is "narrowest," only that there is a correlation. This is why we analyzed airway narrowing as a function of airway length, and we found that the region where tonsils, adenoids, and soft palate overlap is significantly narrower in children with sleep-disordered breathing compared with age-matched controls. Although the distinction between "at the level of the tonsils" (2) and "where tonsils, adenoids, and soft palate overlap" (1) may be subtle, it may be important in the pathophysiology of sleep-disordered breathing in children. Moreover, these misinterpretations of our findings lead Drs. Rembold and Surratt to the conclusion that our findings were the result of methodological issues (2). Thus it was incumbent on us to clarify their statement in the form of this letter. We wish to thank the editor, and Drs. Rembold and Suratt, for their kind consideration of this important clarification.
REFERENCES
Stuart F. Quan2
2Department of Medicine and Respiratory Sciences Center
University of Arizona
Tucson, Arizona
REFERENCES
Paul Suratt
2Sleep Disorders Center
Pulmonary and Critical Care Division
Department of Internal Medicine
University of Virginia Health System
Charlottesville, Virginia
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