Stroke volume

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Overview

Stroke volume is the amount of blood pumped by the left ventricle of the heart in one contraction.

The stroke volume is not all of the blood contained in the left ventricle. The heart does not pump all the blood out of the ventricle. Normally, only about two-thirds of the blood in the ventricle is put out with each beat. What blood is actually pumped from the left ventricle is the stroke volume and it, together with the heart rate, determines the cardiac output.

Calculation

Its value is obtained by subtracting end-systolic volume (ESV) from end-diastolic volume (EDV) for a given ventricle:

In a healthy 70-kg man, the left ventricular EDV is 120 ml and the corresponding ESV is 50 ml, giving a stroke volume of 70 ml.

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 may also increase stroke volume, which frequently results in a slower 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.

See also

References

  • Berne, Robert M., Levy, Matthew N. (2001). Cardiovascular Physiology. Philadelphia, PA: Mosby. ISBN 0-323-01127-6.
  • Boron, Walter F., Boulpaep, Emile L. (2005). Medical Physiology: A Cellular and Molecular Approach. Philadelphia, PA: Elsevier/Saunders. ISBN 1-4160-2328-3.

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