Abstract
Heart-lung interaction mechanisms are generally not well understood. Mechanical ventilation, for example, accentuates such interactions and could compromise cardiac activity. Thereby, assessment of ventilation-induced changes in cardiac function is considered an unmet clinical need. We believe that mathematical models of the human cardiopulmonary system can provide invaluable insights into such cardiorespiratory interactions. In this article, we aim to use a mathematical model to explain heart-lung interaction phenomena and provide physiologic hypotheses to certain contradictory experimental observations during mechanical ventilation. To accomplish this task, we highlight three model components that play a crucial role in heart-lung interactions: 1) pericardial membrane, 2) interventricular septum, and 3) pulmonary circulation that enables pulmonary capillary compression due to lung inflation. Evaluation of the model’s response under simulated ventilation scenarios shows good agreement with experimental data from the literature. A sensitivity analysis is also presented to evaluate the relative impact of the model’s highlighted components on the cyclic ventilation-induced changes in cardiac function.
Highlights
T HE human body is a complex dynamic system with sophisticated neurohumoral control mechanisms
The cardiopulmonary model (CP Model) presented in this paper captures the main mechanisms of cardiorespiratory interactions and it includes a pericardial membrane, an interventricular septum, and a pulmonary circulation model that accounts for the effects of pulmonary capillary compression during inhalation
We have hereby presented a mathematical cardiopulmonary model with a pericardial membrane, an interventricular septum, and a pulmonary circulation model that accounts for the compression of the pulmonary peripheral vessels due to lung inflation
Summary
T HE human body is a complex dynamic system with sophisticated neurohumoral control mechanisms. Besides autonomic and humoral regulatory processes, direct mechanical heart-lung interactions exist. Respiratory activity causes cyclic variations in lung volume and in intrathoracic (pleural) pressure Such variations are, in turn, transferred to all cardiovascular structures within the thoracic cavity, such as thoracic veins, heart, pulmonary circulation, and aorta, leading to cyclic changes in cardiac function. In turn, transferred to all cardiovascular structures within the thoracic cavity, such as thoracic veins, heart, pulmonary circulation, and aorta, leading to cyclic changes in cardiac function These respiratory-induced cardiac variations appear in normal breathing (pulsus paradoxus) [1], but they become accentuated in mechanically ventilated subjects under positive pressure ventilation (reversed pulsus paradoxus) [2]
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