Flow-limitation and upper airways.

We read with interest in the February 1995 issue of The European Respiratory Journal the article by KOULOURIS et al. [1] "A simple method to detect expiratory flowlimitation during spontaneous breathing". The authors applied negative pressure at the mouth (-5 cmH2O) during a tidal expiration (NEP) to 22 patients with chronic obstructive lung disease. They conclude that this provides a simple, noninvasive method for the detection of expiratory, intrathoracic, flow-limitation. Their reasoning is as follows. Application of NEP during expiration increases the pressure gradient between the alveoli and the airway opening. In non-flow-limited subjects, the expiratory flow should increase with NEP. By contrast, in flow-limited patients, application of NEP should not change the expiratory flow. The readers would like to check the hypothesis of the authors, by comparing the flow rate before and after negative pressure is applied at the mouth. However, no mention of the flow rate, before and after NEP, can be found in the results section or elsewhere. To demonstrate the correctness of their approach, the authors present instead two figures, as "representative" examples. The reasoning of the authors would be correct in the absence of extrathoracic upper airways. It would also be correct if upper extrathoracic airways are rigid structures, uninfluenced by transmural pressure changes; or, if these airways are bypassed (see below). Upper airways are in fact compliant structures. A negative pressure applied at the mouth induces a negative intraluminal pressure in these airways. Since outside pressure is atmospheric pressure, transmural pressure would become negative. A negative transmural pressure will narrow the upper airways, thus creating a flow-limiting segment. In other words, flow-limitation would be located at the extrathoracic, and not intrathoracic level. KOULOURIS et al. [1] are probably aware of the interference of the upper airways upon their results, since they emphasize that none of their patients had a history of obstructive sleep apnoea or any evidence of upper airway obstruction. Furthermore, they state that the negative pressure that they applied, i.e. -5 cmH2O, is considerably less than the negative pressure applied by SURATT et al. [2], who have shown that in supine subjects, "collapse" of the pharyngeal airway did not occur at negative pressures between -11 and -40 cmH2O. This is true except that SURATT et al. [2] were speaking about "closure" of upper airways, and therefore zero flow and not flowlimitation. A much lower negative transmural pressure is needed to narrow than to close these airways. In a previous study, published recently by the same authors [3], the same method was used to demonstrate flow-limitation in patients during mechanical ventilation. However, in that study, a cuffed endotracheal tube was used to intubate the patients, thus bypassing the upper airways. This was not the case in their study [1] published recently in The Journal. We have recently shown [4] in supine, relaxed, healthy volunteers, that negative pressure at the mouth, during expiration, induces flow-limitation of the upper airways. Since these airways are unstable structures, a negative pressure of only -2 cmH2O was enough to induce flow-limitation. When subjects contracted their upper airway muscles, "to resist" the applied pressure, there was no flow-limitation. By measuring supraglottic pressure and visualizing the oropharynx, we have demonstrated that flow-limitation was produced by narrowing of the upper airways.