The Estimation of Lung Mechanics Parameters in the Presence of Pathology: A Theoretical Analysis

Mechanical lung function is frequently assessed in terms of lung resistance (RL), lung elastance (EL), and airway resistance (Raw). These quantities are determined by measuring input impedance at various oscillation frequencies, and allow lung tissue resistance (Rt) to be estimated as the difference between RL and Raw. These various parameters change in characteristic ways in the presence of lung pathology. In particular, the ratio Rt/EL (known as hysteresivity, (η) has been shown both experimentally and in numerical simulations to increase when regional heterogeneities in mechanical function develop throughout the lung. In this study, we performed an analytical investigation of a two-compartment lung model and showed that while heterogeneity always leads to an increase in EL, η will increase only initially. When heterogeneity becomes extreme, η stops increasing and starts to decrease. However, there are no experimental reports of η decreasing under conditions in which heterogeneity would be expected to exist. We speculate that this is because liquid bridges invariably form across airway lumen that narrow to a certain point, thereby preventing them from achieving arbitrarily small non-zero radii. We also show that recruitment of closed lung units during lung inflation may lead to variables responses in both η and EL.

[1]  J. Bates,et al.  Respiratory mechanics in the normal dog determined by expiratory flow interruption. , 1989, Journal of applied physiology.

[2]  J. Bates,et al.  Two-compartment modelling of respiratory system mechanics at low frequencies: gas redistribution or tissue rheology? , 1991, The European respiratory journal.

[3]  Z. Hantos,et al.  Mechanical impedances of lungs and chest wall in the cat. , 1992, Journal of applied physiology.

[4]  J. Bates,et al.  A nonstatistical approach to estimating confidence intervals about model parameters: application to respiratory mechanics , 1992, IEEE Transactions on Biomedical Engineering.

[5]  David W. Kaczka,et al.  Partitioning airway and lung tissue resistances in humans: effects of bronchoconstriction. , 1997, Journal of applied physiology.

[6]  Béla Suki,et al.  Variable tidal volume ventilation improves lung mechanics and gas exchange in a rodent model of acute lung injury. , 2002, American journal of respiratory and critical care medicine.

[7]  K. Lutchen,et al.  Partitioning of lung tissue response and inhomogeneous airway constriction at the airway opening. , 1997, Journal of applied physiology.

[8]  J. Bates,et al.  Effect of stochastic heterogeneity on lung impedance during acute bronchoconstriction: a model analysis. , 1997, Journal of applied physiology.

[9]  J. Bates,et al.  Transient mechanical benefits of a deep inflation in the injured mouse lung. , 2002, Journal of applied physiology.

[10]  J. Bates,et al.  Dynamic mechanical consequences of deep inflation in mice depend on type and degree of lung injury. , 2004, Journal of applied physiology.

[11]  J. Bates,et al.  Acute pulmonary response to intravenous histamine at fixed lung volume in dogs. , 1993, Journal of applied physiology.

[12]  N. Krug,et al.  Dysfunction of pulmonary surfactant in asthmatics after segmental allergen challenge. , 1999, American Journal of Respiratory and Critical Care Medicine.

[13]  J. Bates,et al.  Comparative respiratory system mechanics in rodents. , 2000, Journal of applied physiology.

[14]  Kenneth R. Lutchen,et al.  How Heterogeneous Bronchoconstriction Affects Ventilation Distribution in Human Lungs: A Morphometric Model , 2004, Annals of Biomedical Engineering.

[15]  D. Stamenović,et al.  On the imperfect elasticity of lung tissue. , 1989, Journal of applied physiology.

[16]  Toyohiro Hirai,et al.  Effects of deep inspiration on bronchoconstriction in the rat. , 2001, Respiration physiology.

[17]  J. Bates,et al.  Acute pulmonary response to intravenous histamine using forced oscillations through alveolar capsules in dogs. , 1994, Journal of applied physiology.

[18]  J. Bates,et al.  Effects of lung volume on lung and chest wall mechanics in rats. , 1999, Journal of applied physiology.

[19]  Jason H T Bates,et al.  The allergic mouse model of asthma: normal smooth muscle in an abnormal lung? , 2004, Journal of applied physiology.

[20]  G. N. Franz,et al.  Asymmetric and Axisymmetric Constant Curvature Liquid-Gas Interfaces in Pulmonary Airways , 2005, Annals of Biomedical Engineering.

[21]  J. Fredberg,et al.  Input impedance and peripheral inhomogeneity of dog lungs. , 1992, Journal of applied physiology.

[22]  Louis A Gatto,et al.  Positive end-expiratory pressure after a recruitment maneuver prevents both alveolar collapse and recruitment/derecruitment. , 2003, American journal of respiratory and critical care medicine.

[23]  J. Bates,et al.  Airway and tissue mechanics in a murine model of asthma: alveolar capsule vs. forced oscillations. , 2002, Journal of applied physiology.

[24]  K. Lutchen,et al.  Tissue heterogeneity in the mouse lung: effects of elastase treatment. , 2004, Journal of applied physiology.

[25]  M. Cosio,et al.  Alpha1-antitrypsin determines the pattern of emphysema and function in tobacco smoke-exposed mice: parallels with human disease. , 2002, American journal of respiratory and critical care medicine.

[26]  H. Stanley,et al.  Size distribution of recruited alveolar volumes in airway reopening. , 2000, Journal of applied physiology.

[27]  J. Bates,et al.  injurious ventilation in rats Pulmonary impedance and alveolar instability during , 2005 .

[28]  Robert B. Darling,et al.  Effects of low work function metals on the barrier height of sulfide‐treated n‐type GaAs(100) , 1992 .

[29]  B Suki,et al.  How inhomogeneities and airway walls affect frequency dependence and separation of airway and tissue properties. , 1996, Journal of applied physiology.

[30]  G. Hedenstierna,et al.  Effect of different pressure levels on the dynamics of lung collapse and recruitment in oleic-acid-induced lung injury. , 1998, American journal of respiratory and critical care medicine.