We revisit the airway wall model of Lambert et. al. (JAP 1993:2771). We examine in detail the notion of a general airway bi-stability such that the airway lumen can suddenly decrease from a relative open to a relatively closed condition without needing additional increase in active airway smooth muscle (ASM) tension during the stimulation. The onset of this bi-stability is an emergent consequence of the balance of forces associated with airway wall properties, parenchymal tissue properties, maximum lung elastic recoil, and the maximum stress that the ASM can generate. In healthy lungs we find that all these properties reside in conditions that largely prevent the emergence of the bi-stability even during maximum ASM stimulation. In asthmatic airways, however the airway wall and ASM remodeling conditions can tip the balance so as to promote the onset of the bi-stability at a lower dose of ASM stimulation (enhanced sensitivity) and then work to amplify the maximum constriction reached by each airway (enhanced reactivity). Hence, a larger fraction of asthmatic airways can display overall airway hyperreactivity (AHR). Simulations studies also examine the role of increasing ASM maximum tension, airway wall stiffening, reduced lung volume, and decreased parenchymal tethering. Results predict that the single most important factor causing this AHR is amplified maximum ASM tension, and not a thickening of the airway wall per se.