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In cardiovascular physiology, stroke volume (SV) is the volume of blood pumped from one ventricle of the heart with each beat. SV is calculated using measurements of ventricle volumes from an echocardiogram and 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 can apply to each of the two ventricles of the heart, although it usually refers to the left ventricle. The stroke volumes for each ventricle are generally equal, both being 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, and is also used to calculate ejection fraction, which is stroke volume divided by end-diastolic volume. Because stroke volume decreases in certain conditions and disease states, stroke volume itself correlates with cardiac function.
|Measure||Typical value||Normal range|
|end-diastolic volume (EDV)||120 mL[non-primary source needed]||65–240 mL[non-primary source needed]|
|end-systolic volume (ESV)||50 mL[non-primary source needed]||16–143 mL[non-primary source needed]|
|stroke volume (SV)||70 mL||55–100 mL|
|ejection fraction (Ef)||58%||55–70%|
|heart rate (HR)||75 bpm||60–100 bpm|
|cardiac output (CO)||5.25 L/minute||4.0–8.0 L/min|
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.
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.
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.
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. 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.
Similar to cardiac index, is a method of relating the stroke volume to the size of the person.