Rebuttal from James P. Butler, Robert L. Owens, Atul Malhotra and Andrew Wellman

Authors


Email: jbutler@hsph.harvard.edu

We challenge the arguments presented in the ‘PRO’ side of this debate by our friends and colleagues, Schwartz & Smith (2013), in two important areas.

(1) They claim that the effective peripharyngeal pressure is Pcrit. We dispute this on several grounds. Pcrit itself is a construct, most often measured by extrapolation to the intraluminal pressure that would be required to effect near or complete obstruction (Gleadhill et al. 1991). The appropriate peripharyngeal pressure for a Starling resistor would be analogous to peribronchial pressure in intrathoracic airways, which is a relatively well defined concept (Mead et al. 1970). But absent a significant stress jump across the air/tissue interface in the pharynx, there is a continuous pressure variation in the tissues from intraluminal pressure to atmospheric pressure at the body surface (Strohl et al. 2012). Thus, the very concept of an extraluminal (or tissue) pressure is vague and Fig. 1 in Schwartz & Smith (2013) is potentially misleading.

(2) For infinitely compliant conduits, their claim is that, as downstream pressure decreases, flow increases up to a point of flow limitation; beyond this, flow remains constant at a plateau (Elliott & Dawson, 1977). This is true in some individuals. In others, increasingly negative downstream pressures do cause the flows to decrease, often substantially, and even, in some, to complete or near occlusion (Schwartz et al. 1988; Owens et al. 2012). This behaviour is inconsistent with the properties of a Starling resistor. When negative effort dependence (NED) is marked, their interpretation is that somehow nasal or upstream pressure (Pus) must have decreased below Pcrit. While Pus < Pcrit can clearly cause closure, individuals with a negative Pcrit can also exhibit profound NED all the way to pharyngeal closure. This finding disproves the assertion made in their figure (‘Occluded’ panel), which implies that occlusion only happens when Pus < Pcrit. Similarly, the finding of significant NED disproves the assertion in the ‘Flow-Limited’ panel, implying a flow-limited plateau with increasingly negative downstream pressure when Pus > Pcrit.

These ideas may suffice for a simple floppy tube, but are unable to explain the profound reductions in inspiratory airflow observed frequently in sleep apnoea patients.

Finally, we remark that clinical Pcrit features (pressure gradients determining severity of obstruction, efficacy of CPAP, decreases in neuromuscular tone leading to obstruction, phenotypic factors of age, weight, sex, etc.) do not constitute evidence for Starling resistor behaviour, insofar as other models (e.g. the distributed tippy tongue model) also fits these variations as well. For us, the important features are these: (a) the simple Starling resistor does not explain the flow/pressure relationship of the upper airways in individuals with marked NED, and (b) NED is important clinically and woefully underappreciated.

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