A mathematical model of the acute cardiovascular response to isocapnic hypo
xia 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. Moreov
er, the model also includes the action of several reflex regulatory mechani
sms: the peripheral chemoreceptors, the lung stretch receptors, the arteria
l baroreceptors, and the hypoxic response of the central nervous system. Al
l parameters in the model are given in accordance with the physiological li
terature. The simulated overall response to a deep hypoxia (28 mmHg) agrees
with the experimental data quite well, showing a biphasic pattern. The ear
ly phase (8-10 s), caused by activation of peripheral chemoreceptors, exhib
its a moderate increase in mean systemic arterial pressure, a decrease in h
eart rate, a quite constant cardiac output, and a redistribution of blood f
low 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 r
estored to normal levels also in organs with lower metabolic need. The mode
l may be used to gain a deeper understanding of the role of each mechanism
in the overall cardiovascular response to hypoxia.