afterload

This response enables the heart to maintain a normal stroke volume despite the increase in afterload.

Left ventricular afterload is affected by various disease conditions.

Increased afterload or decreased inotropy shifts the curve down and to the right.

The pulmonary hypertension will cause the right ventricle to face increased afterload.

An increase in afterload will increase contractility (through the Anrep effect).

Conversely, a hypertrophied left ventricle has a lower afterload.

Increased afterload may be found in aortic stenosis and arterial hypertension.

Decreased afterload and increased inotropy shifts the curve up and to the left.

These improve both preload and afterload, and aid in improving cardiac function.

This pressure gradient, resisting the contraction of the left ventricle, causes an increase in afterload.

Since the afterload imposed on the ventricle is reduced, end-systolic volume can be smaller than normal.

The stroke volume is affected by changes in preload, afterload and inotropy (contractility).

That is, it actively deflates in systole, increasing forward blood flow by reducing afterload through a vacuum effect.

This increased pressure fills the ventricle to a greater extent, but stroke volume decreases due to an increase in afterload.

This eventually leads to elevation of pulmonary vascular resistance and increased right ventricular afterload.

The Anrep effect is an autoregulation method in which myocardial contractility increases with afterload.

Many positive inotropes affect preload and afterload.

The narrower the vessels are (especially the smaller ones), the higher the resistance is, and the higher the afterload of the heart is.

These morphological adjustments can be seen as a positive adaptation to simultaneously reduce afterload on the heart and improve blood flow to peripheral tissues.

Elevated afterload (commonly measured as the aortic pressure during systole) reduces stroke volume.

As afterload increases, cardiac output decreases.

This decrease is caused by a reduction in heart rate, afterload and wall stress, leading to less contraction force needed by the myocardium.

It was experimentally determined that increasing afterload caused a proportional linear increase in ventricular inotropy.

The goal in using these pharmacologic agents is to decrease the afterload so that the left ventricle is somewhat spared.

Cardiac imaging is a somewhat limited modality in defining afterload because it depends on the interpretation of volumetric data.