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, its force of contraction, duration of contraction, preload (end-diastolic volume), and afterload. Corresponding to the oxygen uptake, women's need for blood flow does not decrease and a higher cardiac frequency makes up for their smaller stroke volume.

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 and afterload

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.

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

Stroke volume index

Similar to cardiac index, stroke volume index is a method of relating the stroke volume (SV) to the person's body surface area (BSA).

${\displaystyle SVI=\frac{SV}{BSA}=\frac{(CO/HR)}{BSA}=\frac{CO}{HR\times BSA}}$