end-diastolic volume

By definition, the volume of blood within a ventricle immediately before a contraction is known as the end-diastolic volume.

The term end-diastolic volume is better suited to the clinic, although not exactly equivalent to the strict definition of preload.

This results in a heart with normal rhythm and contractility, but reduced preload and end-diastolic volume.

In diastolic dysfunction, a greater portion of end-diastolic volume results from late filling rather than early filling.

The stroke volume is the difference between the end-diastolic volume and the end-systolic volume.

Ejection fraction can then be obtained by dividing stroke volume by end-diastolic volume as described above.

Reduced heart rate prolongs ventricular diastole (filling), increasing end-diastolic volume, and ultimately allowing more blood to be ejected.

Increasing venous compliance elevates the capacitance of the veins, reducing venous return and therefore end-diastolic volume.

The stroke volume may also increase as a result of greater contractility of the cardiac muscle during exercise, independent of the end-diastolic volume.

Similarly with tamponade, the degree of diastolic dysfunction is inversely proportional to the LV end-diastolic volume.

Mitral stenosis impairs LV filling so that there is a decrease in end-diastolic volume (preload).

However, stroke volume depends on several factors such as heart size, contractility, duration of contraction, preload (end-diastolic volume), and afterload.

Therefore, because end-diastolic volume decreases more than end-systolic volume decreases, the stroke volume decreases.

Because nearly two-thirds of the blood in the systemic circulation is stored in the venous system, end-diastolic volume is closely related to venous compliance.

Along with end-diastolic volume, ESV determines the stroke volume, or output of blood by the heart during a single phase of the cardiac cycle.

This reduction in afterload (particularly aortic diastolic pressure) enables the end-systolic volume to decrease slightly, but not enough to overcome the decline in end-diastolic volume.

Since the next ventricular contraction will come at its regular time, the filling time for the LV increases, causing an increased LV end-diastolic volume.

In terms of the Frank-Starling curve, the end-diastolic volume will be very high, such that further increases in volume result in less and less efficient contraction.

Hence the relationship between ventricular end-diastolic volume and dP/dt is a more accurate index of contractility than dP/dt alone.

This results in higher ventricular end-diastolic pressures (EDP) at any given end-diastolic volume (EDV).

In left ventricular dysfunction, the ejection fraction will decrease significantly, causing reduction in stroke volume, hence causing an increase in end-diastolic volume.

Its value is obtained by subtracting end-systolic volume (ESV) from end-diastolic volume (EDV) for a given ventricle.

The increased end-diastolic volume (increased preload) activates the Frank-Starling mechanism to increase the force of contraction, LV systolic pressure, and stroke volume.

Preload is related to the ventricular end-diastolic volume; a higher end-diastolic volume implies a higher preload.

In cardiovascular physiology, end-diastolic volume (EDV) is the volume of blood in the right and/or left ventricle at end load or filling in (diastole).