The role of arterial elastance in ventricular-arterial coupling in normal gravity and altered acceleration environments.
The role of physiological elastance (Ep) in maximizing external work (EW) transfer is not well understood and has not been investigated during microgravity and increased acceleration conditions. By better understanding this relationship, cardiovascular control mechanisms for meeting metabolic demands during normal gravity and altered acceleration stresses may be elucidated. Therefore, the objectives of this study were to determine the effect of Ep in maximizing EW of the left ventricle and to investigate this relationship during altered acceleration states. Ventricular and arterial parameters were estimated using established lumped parameter models from isolated beats of experimental data. These data were obtained during parabolic flight (0 and approximately 2 Gz) and centrifuge runs (approximately 1 to approximately 4 Gz) where acceleration was used to drive the cardiovascular system into a wide range of physiologic operating and coupling conditions. Parameter estimates at each Gz level were used in a series of computer simulations in which Ep was varied over a wide range to find the point of maximum EW for that coupling condition. Cardiac output and mean arterial pressure were maintained throughout the simulation process by adjusting heart rate. Results of the simulation showed that as arterial elastance decreased from its initially estimated (physiologic) value, external work increased slightly and as elastance increased, external work decreased. In particular, we found that the arterial elastance was set at a point near that which would produce maximal external work. In addition, it was found that altered Gz states may affect the Ep-EW relationship.
Schroeder
M J
MJ
Department of Electrical Engineering, North Dakota State University, Fargo, USA. mjs@yahoo.com
Phaniraj
V
V
Koenig
S C
SC
Latham
R D
RD
Ewert
D L
DL
D000818:Animals; D001158:Arteries / Q000502:physiology; D002302:Cardiac Output; D003198:Computer Simulation; D006112:Gravitation; D006339:Heart Rate; D006439:Hemodynamics; D008297:Male; D010215:Papio / Q000502:physiology; D014655:Vascular Resistance; D016277:Ventricular Function, Left