Biomedical subjects

Adam G Polak

Publications and source records attributed to Adam G Polak.

3 recordsLinked to original sources

PubMed2005

Simulation of lung function evolution after heart-lung transplantation using a numerical model.

A morphometry-based computational model for expiratory flow in humans was used to study the unusual configuration of the maximum expiratory flow-volume (MEFV) curve associated with alterations in lung function after heart-lung transplantation (HLT). The postoperative MEFV curve showed a peak, followed by a gently sloping plateau over the midvolume range, ending in a knee where the flow suddenly fell, instead of the usual observed uniform decrease in expiratory flow. We have tested several hypotheses about the relationship between the pattern of changes in the configuration of the MEFV curve and pathological changes in the airway mechanics through computer simulations. Principally, effects of lung denervation and airway obstruction, associated with the development of bronchiolitis obliterans in the lung periphery, have been investigated. The calculated curves are similar in appearance to the measured postoperative flow-volume curves and confirm reliability of the earlier hypotheses. We conclude that the plateau-knee configuration of the MEFV curve can result from flow limitation in one of the first airway generations, that this flow limitation coupled with an increase in peripheral airway resistance results in plateau shortening, and that flows exceeding predicted values during the second part of expiration may be produced by lung denervation. Additionally our results demonstrate that airways larger than the transitional and respiratory bronchioles can be involved in pulmonary function deterioration observed in patients affected with obliterative bronchiolitis. Our findings indicate that the computational model, based on a symmetrical dichotomous branching structure of the bronchial tree, along with pathological data, can be employed to evaluate the effects of heterogeneous changes in the lung periphery. Index Terms-Airway mechanics, forced expiration, lung transplantation, mathematical modeling, maximal expiratory flow-volume curve.

Computer Simulation↗

PubMed2004

Nonlinear model for mechanical ventilation of human lungs.

A complex nonlinear model for mechanical ventilation, its computer implementation and validation are presented. The model includes the morphometry-based symmetrical structure of the 23 airway generations, dynamic properties of the respiratory system, as well as the description of a ventilator. Distributed character of airway mechanical properties is taken into account when determining airway inertance, resistance and compliance, including turbulence of flow, airway collapsing and the wave speed theory. In effect, the airway parameters vary within the ventilatory cycle and their values are nonlinear functions of control signals. Results of simulations corresponding to normal conditions and airway narrowing are consistent with the published experimental data. The model enables investigations on how specific pathological changes influence the signals and physiological variables during mechanical ventilation, as well as testing known and developing new algorithms tracking time-variability of the respiratory parameters.

Airway Resistance↗

PubMed2003

Computational model for forced expiration from asymmetric normal lungs.

We present a computational model to predict maximal expiration through a morphometry-based asymmetrical bronchial tree. A computational model with the Horsfield-like geometry of the airway structure, including wave-speed flow limitation and taking into consideration separate airflows from several independent alveolar compartments has been derived. The airflow values are calculated for quasistatic conditions by solving a system of nonlinear differential equations describing static pressure losses along the airway branches. Calculations done for succeeding lung volumes result in the semidynamic maximal expiratory flow-volume (MEFV) curve. Simulations performed show that the model captures the main phenomena observed in vivo during forced expiration: effort independence of the flow-volume curve for the most of vital capacity, independence of limited flow on the properties of airways downstream to the choke points, characteristic differences of lung regional pressures and volumes, and a shape of their variability during exhalation. Some new insights into the flow limitation mechanism were achieved. First, flow limitation begins at slightly different time instants in individual branches of the bronchial tree, however after a short period of time, all regional flows are limited in a parallel fashion. Hence, total flow at the mouth is limited for most of the expired lung volume. Second, each of the airway branches contribute their own flow-volume shape and just these individual flows constitute the measured MEFV curve. Third, central airway heterogeneity can play a crucial role in modification of the entire flow. Fourth, the bronchial tree asymmetry is responsible for a nongravitational component of regional volume variability. Finally, increased inhomogeneity yields results that cannot be explained nor re-created with the use of a symmetrical structure of the bronchial tree.

Air Pressure↗