where y is a measure of parenchymal distortion. Thus increased alveolar pressure leads to increased tethering stress. An increase in tethering stress is then connected with an increase in transmural pressure and thus airway radius; this leads to increased airway calibre and hence decreased resistance Raw ; and thus to increased alveolar pressure via Eq. (1). This completes the feedback loop. As such, an increase in flow drives an increase in alveolar pressure, which in turn increases tethering stress and hence increases airway calibre and further increases flow. The equivalent feedback loop in the opposite direction is that a decrease in flow reduces alveolar pressure, and hence reduces parenchymal tethering stress leading to further airway constriction and reduction in flow. Thus very small initial differences between airways can be magnified by this feedback mechanism into significant heterogeneity. It is important to note that this mechanism requires flow driven at the entrance, generally by volume (but also more recently by pressure [37]), as in mechanical ventilation. The feedback mechanism does not function under flow driven by negative pressure at the periphery, such as spontaneous breathing.