Experimental Studies of Respiration and Apnea
The use of physiologically-based computational models of chemoreflex control of ventilation has provided general insights into the roles of specific mechanisms in the genesis of periodic breathing and apneas. Our early studies utilized formal mathematical
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Experimental Studies of Respiration and Apnea Eugene N. Bruce
Abstract The use of physiologically-based computational models of chemoreflex control of ventilation has provided general insights into the roles of specific mechanisms in the genesis of periodic breathing and apneas. Our early studies utilized formal mathematical approaches to simplify complex models of this type so that their behaviors could more easily be predicted from various combinations of physiological and environmental parameters. Because it is difficult to apply such models to individual patients, we subsequently pursued a “black-box” approach in which the objective was to characterize the dynamic properties of the system for individual subjects, then relate these properties to physiological and environmental parameters. By stimulating ventilation through pseudorandom variations in inspired CO2 (or O2 ) level, we estimated input–output models, both open-loop (i.e., from end-tidal PCO2 to ventilation) and closed-loop (i.e., from inspired CO2 to ventilation). We found that the dynamic properties of the resulting models differ between normal subjects and both sleep apnea patients and heart failure patients. We also demonstrated in normal subjects that the closed-loop model does not change between wakefulness and quiet sleep, even though the gain of the openloop (or controller) model decreases. To explore the mechanistic basis for these findings using a detailed, physiologically-based, chemoreflex model, we enhanced the typical model of this type by improving the representation of O2 transport and distribution beyond the usual, single lumped-compartment, approach. In our new model, brain and muscle tissue each comprise two subcompartments with intercompartmental diffusion and arterio-venous shunting, as well as O2 binding to myoglobin in muscle. We use this model to predict changes in brain tissue PO2 during sleep apnea. Chapter 8 provides another approach to respiratory control system modeling while Chap. 6 discusses the role of transport delay in respiratory control.
E.N. Bruce () Center for Biomedical Engineering, University of Kentucky, Lexington, KY, USA e-mail: [email protected] J.J. Batzel et al. (eds.), Mathematical Modeling and Validation in Physiology, Lecture Notes in Mathematics 2064, DOI 10.1007/978-3-642-32882-4 7, © Springer-Verlag Berlin Heidelberg 2013
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E.N. Bruce
7.1 Introduction The use of physiologically-based computational models of chemoreflex control of breathing has provided general insights into the roles of specific mechanisms involved in the feedback control of ventilation in sleep apnea and periodic breathing (see also Chap. 8). These models are based on the principle of conservation of mass, usually applied to oxygen and carbon dioxide. Typically the models include lumped, uniform compartments representing the lungs, arterial blood, various large tissues (e.g., skeletal muscles, brain), and venous blood. In addition, these models usually incorporate equations to predict the chemoreflex control of venti
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