A quantitative, theory-driven model of hemodynamics was developed,
relating reactivity in blood pressure to orthogonal dimensions
of “hemodynamic profile” and “compensation
deficit,” which were derived from the (multiplicative)
interaction of cardiac output and total peripheral resistance.
A Finapres 2300e was used to estimate blood pressure, cardiac
output, and total peripheral resistance in 100 healthy men and
women during mental arithmetic and cold pressor tasks on two
occasions. Results were consistent with model predictions. As
predicted, cardiac output and peripheral resistance reactions
were curvilinearly related, and blood pressure reactivity was
strongly related to compensation deficit (r =
.76–.89). Conversely, the orthogonally defined hemodynamic
profile remained independent of blood pressure reactivity
(r = .11 or less). The data show that the present model
overcomes several difficulties and inconsistencies in previous
attempts to obtain an independent measure of hemodynamic profile.
The new model could help to elucidate sources of cardiovascular
pathogenesis not suggested from the study of blood pressure
reactivity alone.