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.