TY - JOUR
T1 - A new model of individual differences in hemodynamic profile and blood pressure reactivity
AU - Gregg, M. Elizabeth
AU - Matyas, Thomas A.
AU - James, Jack E.
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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.
KW - Blood pressure reactivity
KW - Blood pressure regulation
KW - Cardiac output
KW - Hemodynamic profile
KW - Individual differences
KW - Total peripheral resistance
UR - http://www.scopus.com/inward/record.url?scp=0036198907&partnerID=8YFLogxK
U2 - 10.1111/1469-8986.3910064
DO - 10.1111/1469-8986.3910064
M3 - Article
C2 - 12206296
AN - SCOPUS:0036198907
SN - 0048-5772
VL - 39
SP - 64
EP - 72
JO - Psychophysiology
JF - Psychophysiology
IS - 1
ER -