TY - THES
AU - Heijmans, Franciscus R. C.
PY - 1985
TI - A computer simulation of the pulmonary microvascular exchange system - alveolar flooding
KW - Thesis/Dissertation
LA - eng
M3 - Text
AB - Previous models of the pulmonary microvascular exchange system (28,29) have been restricted to the study of fluid and solute exchange between the pulmonary microcirculation, interstitial tissue space, and lymphatics. In severe pulmonary edema the capacities of the lymphatics and tissue space are exceeded. The fluid and solutes entering the interstitium from the circulation will, then, be transported Into the air space. The accumulation of fluid in the air space impairs the diffusion of gas (oxygen and carbon dioxide) between the air space and blood circulation; if this fluid accumulation is excessive a patient's health may be compromised.
In this thesis severe pulmonary edema is studied by including the air space as a fourth compartment into the interstitial model developed by Bert and Pinder (29).
A computer simulation of the four compartment (alveolar) model was developed on a digital computer. Tests of the model were made to study the effect of the parameters which were introduced into the alveolar model. These parameters include: a filtration coefficient that describes the alveolar membrane fluid conductivity, an extravascular fluid volume that represents the point at which fluid enters the air space, the alveolar fluid pressure at the onset of fluid flow into the air space, and the rate of alveolar fluid pressure change relative to an alveolar fluid volume change. For each case the dynamic response of the exchange system was recorded. In addition, two types of pulmonary edema were simulated: 1) hydrostatically induced edema, and 2) edema induced by changes to the fluid and solute permeability of the porous membrane separating the circulatory and interstitial compartments.
Due to the limited data available on the interaction of the air space with the other three compartments of the pulmonary microvascular exchange system, only partial verification of the appropriate range of values of the alveolar model parameters and the predictions of the simulations was possible. The alveolar model developed in this thesis is an initial approximation but appears to provide a satisfactory approach for the inclusion of the air space in the pulmonary microvascular exchange system.
N2 - Previous models of the pulmonary microvascular exchange system (28,29) have been restricted to the study of fluid and solute exchange between the pulmonary microcirculation, interstitial tissue space, and lymphatics. In severe pulmonary edema the capacities of the lymphatics and tissue space are exceeded. The fluid and solutes entering the interstitium from the circulation will, then, be transported Into the air space. The accumulation of fluid in the air space impairs the diffusion of gas (oxygen and carbon dioxide) between the air space and blood circulation; if this fluid accumulation is excessive a patient's health may be compromised.
In this thesis severe pulmonary edema is studied by including the air space as a fourth compartment into the interstitial model developed by Bert and Pinder (29).
A computer simulation of the four compartment (alveolar) model was developed on a digital computer. Tests of the model were made to study the effect of the parameters which were introduced into the alveolar model. These parameters include: a filtration coefficient that describes the alveolar membrane fluid conductivity, an extravascular fluid volume that represents the point at which fluid enters the air space, the alveolar fluid pressure at the onset of fluid flow into the air space, and the rate of alveolar fluid pressure change relative to an alveolar fluid volume change. For each case the dynamic response of the exchange system was recorded. In addition, two types of pulmonary edema were simulated: 1) hydrostatically induced edema, and 2) edema induced by changes to the fluid and solute permeability of the porous membrane separating the circulatory and interstitial compartments.
Due to the limited data available on the interaction of the air space with the other three compartments of the pulmonary microvascular exchange system, only partial verification of the appropriate range of values of the alveolar model parameters and the predictions of the simulations was possible. The alveolar model developed in this thesis is an initial approximation but appears to provide a satisfactory approach for the inclusion of the air space in the pulmonary microvascular exchange system.
UR - https://open.library.ubc.ca/collections/831/items/1.0058699
ER - End of Reference