Acute cardiovascular response to isocapnic hypoxia. I. A mathematical model.

Abstract

A mathematical model of the acute cardiovascular response to isocapnic hypoxia is presented. It includes a pulsating heart, the systemic and pulmonary circulation, a separate description of the vascular bed in organs with the higher metabolic need, and the local effect of O(2) on these organs. Moreover, the model also includes the action of several reflex regulatory mechanisms: the peripheral chemoreceptors, the lung stretch receptors, the arterial baroreceptors, and the hypoxic response of the central nervous system. All parameters in the model are given in accordance with the physiological literature. The simulated overall response to a deep hypoxia (28 mmHg) agrees with the experimental data quite well, showing a biphasic pattern. The early phase (8-10 s), caused by activation of peripheral chemoreceptors, exhibits a moderate increase in mean systemic arterial pressure, a decrease in heart rate, a quite constant cardiac output, and a redistribution of blood flow to the organs with higher metabolic need at the expense of other organs. The later phase (20 s) is characterized by the activation of lung stretch receptors and by the central nervous system hypoxic response. During this phase, cardiac output and heart rate increase together, and blood flow is restored to normal levels also in organs with lower metabolic need. The model may be used to gain a deeper understanding of the role of each mechanism in the overall cardiovascular response to hypoxia.