Ventricular Pressure-Volume Relationship

To illustrate the pressure-volume relationship for a single cardiac cycle, the cycle can be divided into four basic phases: ventricular filling (phase a, diastole), isovolumetric contraction (phase b, systole), ejection (phase c, systole), and isovolumetric relaxation (phase d, diastole). Point 1 on the PV loop is the pressure and volume at the end of ventricular filling (diastole) and therefore represents the end-diastolic pressure and end-diastolic volume (EDV) for the ventricle. As the ventricle begins to contract isovolumetrically (phase b), the mitral valve closes and the LVP increases, but the LV volume remains the same, therefore resulting in a vertical line (all valves are closed). Once LVP exceeds aortic diastolic pressure, the aortic valve opens (point 2) and ejection (phase c) begins. During this phase, the LV volume decreases as LVP increases to a peak value (peak systolic pressure) and then decreases as the ventricle begins to relax. When the aortic valve closes (point 3), ejection ceases and the ventricle relaxes isovolumetrically, the LVP falls but the LV volume remains unchanged; therefore, the line is vertical (all valves are closed). The LV volume point on the loop is the end-systolic (i.e., residual) volume (ESV). When the LVP falls below the left atrial pressure, the mitral valve opens (point 4) and the ventricle begins to fill. Initially, the LVP continues to fall as the ventricle fills because the ventricle is still relaxing. However, once the ventricle is fully relaxed, the LVP gradually increases as the LV volume increases. The width of the loop represents the difference between EDV and ESV, which is by definition the stroke volume (SV). The area within the loop is the ventricular stroke work. 

Ventricular filling occurs along the end-diastolic pressure-volume relationship (EDPVR), or passive filling curve for the ventricle. The slope of the EDPVR is the reciprocal of ventricular compliance. Therefore, changes in ventricular compliance alter the slope of the passive filling curve. For example, in ventricular hypertrophy the ventricle is less compliant (i.e., it is stiffer) and therefore the slope of the filling curve is increased. This results in higher pressures during filling at a given ventricular volume. Another example of how the EDPVR can be altered is when a ventricle chronically dilates (remodels) as occurs in dilated cardiomyopathy or in valve disease. A dilated ventricle has a higher passive compliance and therefore the slope of the filling curve is reduced. This results in lower ventricular pressures during filling at any given ventricular volume.

The maximal pressure that can be developed by the ventricle at any left ventricular volume is defined by the end-systolic pressure-volume relationship (ESPVR), which represents the inotropic state of the ventricle. The slope and x-intercept of the ESPVR is generated experimentally by occluding the inferior vena cava (IVC), which reduces venous return to the heart (see figure). This decreases ventricular preload (EDV) and causes the PV loop to shift to the left and get smaller over several heart beats; decreased preload reduces SV (loop width). Peak systolic pressure (loop height) also decreases because arterial pressure falls as the cardiac output declines during IVC occlusion. Therefore, afterload is decreased along with the preload. The ESPVR is determined by the line intersecting the upper left corners of the loops. A linear relationship occurs within a narrow range of pressures and volumes (several consecutive beats). After several seconds, the ESPVR becomes non-linear with a steeper slope as baroreflexes increase ventricular inotropy. It is important to note that the pressure-volume loop cannot cross over the ESPVR because that relationship defines the maximal pressure that can be generated at a specific inotropic state.

The end-diastolic and end-systolic pressure-volume relationships are analogous to the passive and total tension curves used to analyze isolated muscle function.

The PV loop will change as the preload, afterload and inotropic state of the heart change. To see how these affect PV loops, CLICK HERE.

Click below to see how the following conditions affect PV loops:

• Systolic dysfunction
• Diastolic dysfunction
• Valve disease

Mini-Lecture: Generation of Ventricular Pressure-Volume Loops (Time = 8.7 minutes)

 

Revised 11/04/2023