What is preload???

Another facts about physiology of heart.

In cardiac physiology, preload is the pressure stretching the ventricle of the heart, 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 cardiomyocyte 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 strict definition of preload.

Calculation
Quantitatively, preload can be calculated as
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 is related to the ventricular end-diastolic volume; a higher end-diastolic volume implies a higher preload. However, the relationship is not simple because of the restriction of the term preload to single myocytes.
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.

What Is Stroke Volume?

In cardiovascular physiology, stroke volume (SV) is the volume of blood pumped from one ventricle of the heart with each beat. It is calculated by subtracting the volume of the blood in the ventricle at the end of a beat (called end-systolic volume) from the volume of blood just prior to the beat (called end-diastolic volume). The term stroke volume applies equally to both left and right ventricles of the heart. These two stroke volumes are generally equal, both approximately 70 ml in a healthy 70-kg man.
Stroke volume is an important determinant of cardiac output, which is the product of stroke volume and heart rate. Because stroke volume decreases in certain conditions and disease states, stroke volume itself correlates with cardiac function.

Calculation
Its value is obtained by subtracting end-systolic volume (ESV) from end-diastolic volume (EDV) for a given ventricle.
SV = EDV − ESV
In a healthy 70-kg man, EDV is approximately 120 mL and ESV is approximately 50 mL, giving a difference of 70 mL for the stroke volume.
"Stroke work" refers to the work, or pressure of the blood ("P") multiplied by the stroke volume.

Determinants
Men, on average, have higher stroke volumes than women due to the larger size of their hearts. However, stroke volume depends on several factors such as heart size, contractility, duration of contraction, preload (end-diastolic volume), and afterload.

Exercise
Prolonged aerobic exercise training may also increase stroke volume, which frequently results in a lower (resting) heart rate. Reduced heart rate prolongs ventricular diastole (filling), increasing end-diastolic volume, and ultimately allowing more blood to be ejected.

Preload
Stroke volume is intrinsically controlled by preload (the degree to which the ventricles are stretched prior to contracting). An increase in the volume or speed of venous return will increase preload and, through the Frank-Starling law of the heart, will increase stroke volume. Decreased venous return has the opposite effect, causing a reduction in stroke volume.

Afterload
Elevated afterload (commonly measured as the aortic pressure during systole) reduces stroke volume. Though not usually affecting stroke volume in healthy individuals, increased afterload will hinder the ventricles in ejecting blood, causing reduced stroke volume. Increased afterload may be found in aortic stenosis and arterial hypertension.