Changes in heart beat timing: reactivity, resetting, or perturbation?

A widely held hypothesis within behavioral medicine is that cardiovascular reactivity is a risk factor for cardiovascular disease. The measurement model for this cardiovascular reactivity is rather simple. A basal level of function is seen to increase while the organism is stressed and then return to basal function. We argue that this model is incomplete and that other forms of 'reactivity' may be relevant to pathophysiology. A pathophysiological hypothesis is discussed which assumes a cyclic heart beat generation mechanism that is sensitive to stimulation only at certain phases of its cycle. Implications of this hypothesis for measurement are developed to illustrate the point that models of normal function can determine the measures most relevant to pathophysiology.