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 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.^[1]

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.

References

1. ^ Katz, Arnold M. (2006). Physiology of the heart. Hagerstwon, MD: Lippincott Williams & Wilkins. pp. 337. ISBN 0-7817-5501-8. 

• 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. 

External links

• The Gross Physiology of the Cardiovascular System