Glottal Aperture and Buccal Airflow Leaks Critically Affect Forced Oscillometry Measurements.
BACKGROUND
The forced oscillation technique (FOT) measures respiratory resistance and reactance; however, the upper airways may affect the results. We quantified the impact of glottal aperture and buccal air leaks.


METHODS
In the glottal aperture study (1) 10 healthy subjects (aged 34 ± 2 years) performed a total lung capacity maneuver followed by 10-s breath-hold with and without total glottal closure and (2) the effects of humming (incomplete glottal narrowing) on FOT measurements were studied in six healthy subjects. Glottal narrowing was confirmed by direct rhinolaryngoscopy. In the air leak study, holes of increasing diameter (3.5, 6.0, and 8.5 mm) were made to the breathing filters. Eleven healthy subjects (aged 33 ± 2 years) and five patients with COPD (aged 69 ± 3 years) performed baseline FOT measurements with the three modified filters.


RESULTS
Narrow glottal apertures and humming generated whole-breath resistance at 5 Hz (R5) peaks, increased R5 (1.49 ± 0.37 kPa/L/s vs 0.34 ± 0.01 kPa/L/s, P < .001), and decreased whole-breath reactance at 5 Hz (X5) values (-2.10 ± 0.51 kPa/L/s vs -0.09 ± 0.01 kPa/L/s, P < .001). The frequency dependency of resistance was increased. Holes in the breathing filters produced indentations on the breathing trace. Even the smaller holes reduced R5 in healthy subjects (0.33 ± 0.02 to 0.24 ± 0.02 kPa/L/s, P < .01) and patients with COPD (0.50 ± 0.04 to 0.41 ± 0.04 kPa/L/s, P < .05), whereas X5 became less negative (from -0.09 ± 0.01 to -0.05 ± 0.01 in healthy subjects, P < .01; from -0.22 ± 0.06 to -0.11 ± 0.03 kPa/L/s in patients with COPD, P < .05).


CONCLUSIONS
Visual inspection of the data is required to exclude glottal narrowing and buccal air leaks identified as R5 peaks and volume indentations, respectively, because these significantly affect FOT measurements.
Airway Disease Section, National Heart and Lung Institute, Imperial College London and Royal Brompton Hospital, London, England; Department of Pulmonology, Semmelweis University, Budapest, Hungary.
Andres
A
Bikov
Airway Disease Section, National Heart and Lung Institute, Imperial College London and Royal Brompton Hospital, London, England.
Neil B
NB
Pride
Airway Disease Section, National Heart and Lung Institute, Imperial College London and Royal Brompton Hospital, London, England.
Michael D
MD
Goldman
Airway Disease Section, National Heart and Lung Institute, Imperial College London and Royal Brompton Hospital, London, England.
James H
JH
Hull
Department of Pulmonology, Semmelweis University, Budapest, Hungary.
Ildiko
I
Horvath
Airway Disease Section, National Heart and Lung Institute, Imperial College London and Royal Brompton Hospital, London, England.
Peter J
PJ
Barnes
Airway Disease Section, National Heart and Lung Institute, Imperial College London and Royal Brompton Hospital, London, England.
Omar S
OS
Usmani
Airway Disease Section, National Heart and Lung Institute, Imperial College London and Royal Brompton Hospital, London, England. Electronic address: p.paredi@imperial.ac.uk.
Paolo
P
Paredi
D000328:Adult; D000368:Aged; D000403:Airway Resistance / Q000502:physiology*; D005260:Female; D005931:Glottis / Q000502:physiology*; D064368:Healthy Volunteers; D006801:Humans; D007828:Laryngoscopy; D008297:Male; D009991:Oscillometry / Q000379:methods*; D029424:Pulmonary Disease, Chronic Obstructive / Q000503:physiopathology*