**3. Conclusion**

Percent AUC tended to be greater in OSA patients while seated indicating the presence of mechanisms maintaining upper airway patency while supine. By contrast, in COPD patients AUC% was greatest in supine posture, almost twice the value when seated. Thus, mecha‐ nisms preserving patency in supine COPD patients seem not to be as effective as in supine obese or OSA individuals. Reductions in lung volume (as occur in supine posture) result in decreases in caudal traction on the upper airway and concomitant increases in upper airway collapsibility (Owens et al., 2010; Squire et al., Thut et al., 1993; Van de Graaf, 1991). In addi‐ tion, supine positioning promotes laryngeal edema and upper airway narrowing (Jafari & Mohsenin, 2011; Shepard et al., 1996). In COPD, mobilization of secretions when supine may have contributed to this finding. Yet, the finding of an overall increase in EFL% in supine position without concomitant increases in AUC% (or AUC/% EFL%) in most other cohorts indicated a greater degree of intrathoracic tidal EFL [as defined by Koulouris et al (1995)]

132 Oncogenesis, Inflammatory and Parasitic Tropical Diseases of the Lung

than extrathoracic FL. This is likely related to decrease in lung volume when supine.)

ity of EFL within cohorts.

and genioglossus activity in that posture.

still greater than the preceding control flow) during NEP.

The differing findings amongst cohorts can be explained thus: During early expiration, there is post-inspiratory inspiratory activity (PIIA) which may negate the effect of NEP. At the be‐ ginning of expiration, PIIA may oppose NEP (resistance posed by pliometric contraction [= lengthening] of the inspiratory muscles) (Shee et al., 1985). This implies that NEP should not be applied too early in expiration (when PIIA is high). In our subjects, NEP was applied im‐ mediately after the onset of expiratory flow so that PIIA is likely to have influenced variabil‐

Our method for computing AUC% was similar to that of Tamisier et al. (2005) who de‐ vised a quantitative index corresponding to the ratio of the area under the expiratory flow-volume curves between NEP and control tidal volume. They did not, however, study subjects with mild OSA (BMI 5-15), and their control subjects were younger than ours. They also applied NEP near end-expiratory volume which stimulates activation of the genioglossus (Tantucci et al., 1998). This can change the area under the terminal por‐ tion of the NEP curve, affecting the quantitative index used to assess the upper airway collapsibility. Our results suggest that obese and OSA patients are more likely to experi‐ ence upper airway narrowing while seated than COPD patients, indicating reduced PIIA

There were some methodological limitations in this investigation. This study and those of others (Baydur et al., 2004, 2012; Insalaco et al., 2005; Liistro et al., 1999; Rouatbi et al., 2009; Van Meerhaeghe et al., 2004; Verin et al., 2002) assumed that upper airway collapsibility can be identified solely when expiratory flow during NEP decreases below the control curve. As such, detecting upper airway collapsibility only by computing the span of the preceding control tidal volume over which the NEP curve drops below the control breath may be mis‐ leading. It is possible that in this study some patients with upper airway narrowing may not have been identified if they exhibited only a reduction in the increase of expiratory flow (but

Another limitation in this study was that sleep studies were not obtained in COPD patients and controls. Sleep-related disordered breathing (SDB) and nocturnal desaturations have been reported in COPD patients, giving rise to an "overlap syndrome" although not all SDB In conclusion, the EFL% and AUC% methods are useful in determining the magnitude of intrathoracic or extrathoracic FL in patients with COPD and OSA, but fail to distinguish co‐ horts on the basis of EFL quantification using the area under the curve method because of interindividual variabilities. In this respect, our findings were similar to those of Ferretti, et al. (2006). Pattern recognition of NEP tracings remains the best way to differentiate intra‐ thoracic from extrathoracic EFL.

While the NEP method may be regarded as the new standard for the detection of tidal flow limitation (Koulouris, & Hardavella, 2011), further research should include its validation in conditions other than COPD that exhibit intrathoracic EFL. Comparison with other techni‐ ques such as the esophageal balloon, forced oscillation and abdominal compression (proba‐ bly the easiest and least uncomfortable) methods should provide additional information in this regard. In the assessment of extrathoracic airway FL, the NEP technique offers a means to evaluate upper airway dynamics in patents with OSA, but is not able to differentiate snor‐ ers from those with OSA.
