The left ventricular pressure–volume loop provides a useful representation of left ventricular performance through the cardiac cycle (Figure 31.1; see also Chapter 28, Figure 28.1).
Figure 31.1 Pressure–volume loop of the normal left ventricle (BP = blood pressure).
In a normal left ventricle (LV), the pressure–volume loop is approximately rectangular and can be divided into four phases:
Isovolumetric contraction, a vertical line representing the increase in intraventricular pressure without a change in ventricular volume.
Ventricular ejection, in which the stroke volume (SV) is ejected into the aorta.
Isovolumetric relaxation, a vertical line representing the fall in intraventricular pressure without a change in ventricular volume.
Diastolic ventricular filling, in which the ventricle fills with blood ready for the next contraction.
Preload can be thought of as the volume of blood within the ventricle prior to contraction (see Chapter 29). For the LV, it is the left ventricular end-diastolic volume (LVEDV). According to Starling’s law, an increase in preload results in a greater diastolic stretch of the contractile myocardial fibres (see Chapter 30). The stretched sarcomeres contract more forcefully, thus increasing SV (Figure 31.2).
Figure 31.2 illustrates a number of important features:
The width of the pressure–volume loop, which represents SV, is increased due to the increase in LVEDV. The left ventricular end-systolic volume (LVESV) increases slightly due to an increase in afterload (aortic pressure) caused by the greater cardiac output.
The end-diastolic pressure–volume relationship (EDPVR) line reflects the passive diastolic compliance of the LV. Beyond a certain preload, left ventricular end-diastolic pressure (LVEDP) increases sharply, reflecting the nonlinear compliance of the left ventricular wall. This is due to the elastic proteins and connective tissue within the myocardium reaching their elastic limit.
Afterload is the stress developed in the left ventricular wall during ejection, and it reflects the force opposing the shortening of cardiac myocytes. As afterload increases (e.g. due to an increase in diastolic aortic pressure), both the rate and extent of sarcomere shortening decrease, resulting in a reduction in SV:
As a reduced volume of blood is ejected from the LV, the LVESV is increased.
In turn, the addition of the venous return leads to an increase in LVEDV.
According to Starling’s law, an increase in LVEDV causes an increase in myocardial contractility. Thus, SV increases, returning LVEDV to near normal.
Overall, the increase in LVESV is greater than that of LVEDV. SV is slightly decreased, and the left ventricular pressure–volume loop looks taller and thinner (Figure 31.3a).