Independent determinants of systolic effectiveness: growth ability, contractility and mobility.
The left ventricle of the heart is a thick-walled chamber. In such a chamber, cavity dimensions do not express overall wall stretch, so fractional cavity-surface displacements are not ideal performance expressions, and the intercepts and slopes of relations between intensive variables (pressure, stress, resistance, viscosity) and cavity dimensions do not express wall properties. By contrast, there is a midwall isobar whose enclosed volume (Vm) does express distension and stretch, so fractional midwall-volume displacement is an ideal expression of systolic performance, and characteristics of P-Vm and sigma-Vm relations do relate consistently to wall properties. The midwall volume at average basal end-diastolic distension is calculated: Vmu = Vcu Vou (ln Vou - ln Vcu)/(Vou - Vcu), where Vcu is cavity volume and Vou is chamber volume (cavity + wall) at average basal end-diastolic distension. At other distensions, midwall volume departs from Vmu as cavity volume departs from Vcu: Vm = Vmu + Vc - Vcu. Midwall ejection fraction (Jmv) is the difference between end-diastolic midwall volume (Vmd) and end-systolic midwall volume (Vms) divided by Vmd:Jmv = (Vmd - Vms)/Vmd. It depends on preload, afterload and two tensile characteristics. The cleanest separation of tensile characteristics is not in the intercept and slope but in the amplitude and spread of the sigma-Vm relation. Amplitude (sigma su) is the height of the relation at the average basal end-diastolic distension to which the chamber is accustomed. Spread (M sigma v) is the normalized difference between x intercept (Vmx) and Vmu: M sigma v = (Vmu - Vmx)/Vmu. It is the Jmv which would occur if preload were normal and afterload were zero. These considerations give rise to a new system for expressing and evaluating systolic performance and its determinants. The system is valid for the ranges of wall/cavity ratios, P-V-curve shapes and chamber shapes seen in left ventricles.
Regen
D M
DM
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232.
D000818:Animals; D001024:Aortic Valve Stenosis / Q000503:physiopathology; D001794:Blood Pressure; D006321:Heart / Q000502:physiology*; D006352:Heart Ventricles; D006801:Humans; D009200:Myocardial Contraction; D013318:Stroke Volume; D013599:Systole