THE IMPORTANCE OF ONLINE RECORDING OF VENTRICULAR VOLUME

Authors
Citation
P. Schiereck, THE IMPORTANCE OF ONLINE RECORDING OF VENTRICULAR VOLUME, Journal of cardiovascular diagnosis and procedures, 13(2), 1996, pp. 171-176
Citations number
8
Categorie Soggetti
Radiology,Nuclear Medicine & Medical Imaging","Cardiac & Cardiovascular System
ISSN journal
10737774
Volume
13
Issue
2
Year of publication
1996
Pages
171 - 176
Database
ISI
SICI code
1073-7774(1996)13:2<171:TIOORO>2.0.ZU;2-1
Abstract
Since Frank (1898)((1)) and Starling (1918)((2)) showed that the quant ified pressure-volume relationship of the heart offers a good view of the transfer of energy by the heart, many attempts have been made to u se this relationship in diagnostics. The basis of the description is f ound in the microscopic structure of the striated muscle cell in which a simple relation can be found between force, developed after full ac tivation of the muscle cell, and the length of the contractile unit, t he sarcomere. The advantage was that factors affecting the geometry of the cell could be separated from those affecting the biochemical proc esses from excitation to contraction. The relationship gives insight i nto the mechanisms of oxygen consumption and work performed by the hea rt.((4)) In this study we used isolated rat hearts, perfused in a modi fied Langendorff system. Filling of the heart is controlled by the FDP . This filling of the left ventricle runs along the EDP-EDV relationsh ip. The slope of this relation represents the stiffness of the diastol ic myocardium. We show that the diastolic stiffness is the sum of two separated elastic elements: a calcium-independent, passive, and a calc ium-dependent, active, element. Both elements can be affected. Pharmac ological interventions (Ca channel blocking, beta-receptor stimulation /blocking, etc.) can change the contribution of the active element. Pa thological changes (hypertrophy, diabetes mellitus) affect the passive part. If in medical treatment the intracellular calcium is decreased, the EDV is found to be increased based on the changed diastolic stiff ness. To maintain a comparable cardiac output, EDP has to increase. Th is mechanism shifts the cardiac reserve toward the region in which dec ompensation occurs. It is evident that reliable, and possibly noninvas ive recording of the diastolic pressure-volume relationship prevents u nexpected mechanisms.