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Heart during ventricular diastole.

In cardiac physiology, preload is the pressure stretching the ventricle of the heart,[1] after passive filling of the ventricle and subsequent atrial contraction. If the chamber is not mentioned, it is usually assumed to be the left ventricle.

Preload is theoretically most accurately described as the initial stretching of a single cardiac myocyte prior to contraction. This cannot be measured in vivo and therefore other measurements are used as estimates. Estimation is inaccurate, for example in a chronically dilated ventricle new sarcomeres may have formed in the heart muscle allowing the relaxed ventricle to appear enlarged. The term end-diastolic volume is better suited to the clinic, although not exactly equivalent to the laboratory term preload.



Quantitatively, preload can be calculated as

\frac{LVEDP \cdot LVEDR}{2h}

where LVEDP=Left ventricular end diastolic pressure, LVEDR= Left ventricular end diastolic radius (at the ventricle's midpoint), and h=thickness of the ventricle. This calculation is based on the Law of Laplace.

Factors affecting preload

Preload is affected by venous blood pressure and the rate of venous return. These are affected by venous tone and volume of circulating blood.

Preload relates to the ventricular end-diastolic volume: a higher end-diastolic volume implies a higher preload, but the relationship is not simple, because of the restriction of the term preload to single myocytes. Single myocytes are not connected simply, but in an interdigitated manner.

Mathematical expression of a titrated Preload is then (narrowly) volumetrically suggested by the inexpensive echocardiographic measurement end diastolic volume or EDV. Extrapolation to performance of a single cardiomyocyte is a worthy endeavor but subject to shading study of the overall performance of the myocardium to the trees rather than the forest.

Preload increases with exercise (slightly), increasing blood volume (overtransfusion, polycythemia) and neuroendocrine excitement (sympathetic tone).

An arteriovenous fistula can increase preload.[2 ]

See also


External links

simply, the load or volume exerted on the ventricleat end diastole;determines the force of contraction;Frank-Starling Law(as with valvular regurtation and/or septal defects



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