Preload is defined as the degree of myocardial distension prior to contraction, and is therefore related to sarcomere length. The force of myocyte contraction depends on the length to which they are stretched; however, since this length cannot be determined in the intact heart, other indices of preload are used in clinical practice, such as ventricular end-diastolic volume or pressure. Factors that can increase preload include: Increased venous return, for example: Increased blood volume through renal sodium and water retention, whether due to decreased
renal perfusion or increased sympathetic tone Increased muscle activity, as in exercise or stress Decreased venous compliance, as during haemorrhage Increased volume to be pumped out of either ventricle, as with pulmonary or aortic valve regurgitation Factors that can decrease preload include: Decreased venous return Increased pulmonary vascular resistance Decreased volume to be pumped out of either ventricle, as with mitral valve stenosis. When preload increases, there is an increase in end-diastolic volume and an increase in stroke volume.