Left ventricular function: time-varying elastance and left ventricular aortic coupling

Abstract

Many aspects of left ventricular function are explained by considering ventricular pressure-volume characteristics. Contractility is best measured by the slope, Emax, of the end-systolic pressure-volume relationship. Ventricular systole is usefully characterized by a time-varying elastance (ΔP/ΔV). An extended area, the pressure-volume area, subtended by the ventricular pressure-volume loop (useful mechanical work) and the ESPVR (energy expended without mechanical work), is linearly related to myocardial oxygen consumption per beat. For energetically efficient systolic ejection ventricular elastance should be, and is, matched to aortic elastance. Without matching, the fraction of energy expended without mechanical work increases and energy is lost during ejection across the aortic valve. Ventricular function curves, derived from ventricular pressure-volume characteristics, interact with venous return curves to regulate cardiac output. Thus, consideration of ventricular pressure-volume relationships highlight features that allow the heart to efficiently respond to any demand for cardiac output and oxygen delivery.

Figures

Fig. 1

This classic ventricular function curve relates input of the heart (end-diastolic pressure in mmHg) to output of the heart (cardiac output in liters per minute). The ventricular function curve shifts up and to the left when ventricular systolic contractility increases. However, increased diastolic compliance and decreased afterload can also shift the ventricular function curve up and to the left

Fig. 2

For an isolated rabbit trabecular muscle strip, force, expressed as force per area = tension, is plotted against starting length. Passive tension during diastole is plotted as open circles. Normal active tension after electrical stimulation is plotted as closed circles. Contractions following a second rapid electrical stimulation, which increases the calcium concentration at actin/myosin sliding filaments and therefore increases contractility (Potentiated), is plotted as open triangles

Fig. 3

Left ventricular pressure volume relationships. A cardiac cycle is illustrated by the loop labeled as “a”, “b”, “c”, and “d”. ESPVR end-systolic pressure–volume relationship, LV left ventricular

Fig. 4

Three differently loaded cardiac cycles. The end-systolic pressure–volume points all lie on a line termed the end-systolic pressure–volume relationship (ESPVR). The slope of the ESPVR is Emax, maximum elastance. At any time during systolic contraction (e.g., 50-ms time points are shown as filled circles) a line can be drawn connecting pressure–volume points from each of the differently loaded contractions defining elastance (ΔP/ΔV) at that time point. Ventricular systolic contraction can therefore be regarded as a time-varying elastance

Fig. 5

Pressure–volume area (PVA) is the area within the cardiac cycle pressure–volume (P-V) loop plus the area under the ESPVR. PVA linearly correlates with myocardial oxygen consumption. LV left ventricular

Fig. 6

Stroke volume, derived from the left-hand panel, multiplied by heart rate yields cardiac output on the right-hand panel. Thus, for a given ESPVR, diastolic pressure–volume relationship, and afterload, a range of end-diastolic pressures on the left-hand panel yield the ventricular function curve on the right-hand panel. LV left ventricular

Fig. 7

An arterial elastance line can be added to a PVA diagram (Fig. 5) by considering the rise in pressure within the arterial system with an increase in arterial volume (equals the decrease in ventricular volume). Compared with the healthy state (top panel), a decrease in ventricular elastance and an increase in arterial elastance mean that more energy is wasted on the PVA diagram. LV left ventricular, P-V pressure–volume

Fig. 8

Lowering right atrial pressure increases blood flow back to the heart—venous return. This venous return curve can be shifted, primarily by an increase in the x-axis intercept—mean systemic pressure. RVR resistance to venous return

Fig. 9

Ventricular function curves can be plotted on the same set of axes and venous return curves. In steady state cardiac output must equal venous return so the intersection (filled circle) identifies the cardiac output and end-diastolic pressure of the cardiovascular system. A decrease in cardiac function results in a decrease in cardiac output and an increase in end-diastolic pressure (open circle)

Fig. 10

Top: in a normal heart increased contractility does not change the normally steep ventricular function curve so this does not change cardiac output much. In contrast, changes in venous return cause large changes in cardiac output so, in health, cardiac output is primarily controlled by the peripheral circulation. Bottom: in a failing heart changes in venous return curves no longer result in substantial changes in cardiac output but raise venous pressure (solid circle to open circle on bottom ventricular function curve). Now an increase in contractility results in a substantial increase in cardiac output and decrease in end-diastolic pressure (filled circle on lower ventricular function curve to filled circle on upper ventricular function curve)