Abstract
Clustered ventilation defects are a hallmark of asthma, typically seen via imaging studies during asthma attacks. The mechanisms underlying the formation of these clusters is of great interest in understanding asthma. Because the clusters vary from event to event, many researchers believe they occur due to dynamic, rather than structural, causes. To study the formation of these clusters, we formulate and analyze a lattice-based model of the lung, considering both the role of airway bistability and a mechanism for organizing the spatial structure. Within this model we show how and why the homogeneous ventilation solution becomes unstable, and under what circumstances the resulting heterogeneous solution is a clustered solution. The size of the resulting clusters is shown to arise from structure of the eigenvalues and eigenvectors of the system, admitting not only clustered solutions but also (aphysical) checkerboard solutions. We also consider the breathing efficiency of clustered solutions in severely constricted lungs, showing that stabilizing the homogeneous solution may be advantageous in some circumstances. Extensions to hexagonal and cubic lattices are also studied.