Stroke volume

Last updated October 10, 2024

In cardiovascular physiology, stroke volume (SV) is the volume of blood pumped from the ventricle per beat. Stroke volume 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 ^{[note 1]}) 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 when not explicitly stated it refers to the left ventricle and should therefore be referred to as left stroke volume (LSV). The stroke volumes for each ventricle are generally equal, both being approximately 90 mL in a healthy 70-kg man. Any persistent difference between the two stroke volumes, no matter how small, would inevitably lead to venous congestion of either the systemic or the pulmonary circulation, with a corresponding state of hypotension in the other circulatory system. A shunt (see patent foramen ovale and atrial septal defect) between the two systems will ensue if possible to reestablish the equilibrium.

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.^{[ citation needed ]}

Calculation

Example values in healthy 70-kg man
Ventricular volumes view talk edit
Measure	Right ventricle	Left ventricle
End-diastolic volume	144 mL (± 23 mL)^[1]	142 mL (± 21 mL)^[2]
End-diastolic volume / body surface area (mL/m²)	78 mL/m² (± 11 mL/m²)^[1]	78 mL/m² (± 8.8 mL/m²)^[2]
End-systolic volume	50 mL (± 14 mL)^[1]	47 mL (± 10 mL)^[2]
End-systolic volume / body surface area (mL/m²)	27 mL/m² (± 7 mL/m²)^[1]	26 mL/m² (± 5.1 mL/m²)^[2]
Stroke volume	94 mL (± 15 mL)^[1]	95 mL (± 14 mL)^[2]
Stroke volume / body surface area (mL/m²)	51 mL/m² (± 7 mL/m²)^[1]	52 mL/m² (± 6.2 mL/m²)^[2]
Ejection fraction	66% (± 6%)^[1]	67% (± 4.6%)^[2]
Heart rate	60–100 bpm ^[3]	60–100 bpm ^[3]
Cardiac output	4.0–8.0 L/minute ^[4]	4.0–8.0 L/minute ^[4]

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, ESV is approximately 50 mL and EDV is approximately 140mL, giving a difference of 90 mL for the stroke volume.

Stroke work refers to the work, or pressure of the blood ("P") multiplied by the stroke volume.^[5]

Determinants

Men, on average, have higher stroke volumes than women due to the larger size of their hearts.^[7] 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.^[7]

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.^[8]

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.^[9]

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.^[10]

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).

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

Note

↑ In short, the remaining blood volume left in the left ventricle not pumped out after a systole.

Related Research Articles

Heart murmurs are unique heart sounds produced when blood flows across a heart valve or blood vessel. This occurs when turbulent blood flow creates a sound loud enough to hear with a stethoscope. The sound differs from normal heart sounds by their characteristics. For example, heart murmurs may have a distinct pitch, duration and timing. The major way health care providers examine the heart on physical exam is heart auscultation; another clinical technique is palpation, which can detect by touch when such turbulence causes the vibrations called cardiac thrill. A murmur is a sign found during the cardiac exam. Murmurs are of various types and are important in the detection of cardiac and valvular pathologies.

In cardiac physiology, cardiac output (CO), also known as heart output and often denoted by the symbols $,, or, is the volumetric flow rate of the heart's pumping output: that is, the volume of blood being pumped by a single ventricle of the heart, per unit time. Cardiac output (CO) is the product of the heart rate (HR), i.e. the number of heartbeats per minute (bpm), and the stroke volume (SV), which is the volume of blood pumped from the left ventricle per beat; thus giving the formula:$

A ventricle is one of two large chambers located toward the bottom of the heart that collect and expel blood towards the peripheral beds within the body and lungs. The blood pumped by a ventricle is supplied by an atrium, an adjacent chamber in the upper heart that is smaller than a ventricle. Interventricular means between the ventricles, while intraventricular means within one ventricle.

An ejection fraction (EF) is the volumetric fraction of fluid ejected from a chamber with each contraction. It can refer to the cardiac atrium, ventricle, gall bladder, or leg veins, although if unspecified it usually refers to the left ventricle of the heart. EF is widely used as a measure of the pumping efficiency of the heart and is used to classify heart failure types. It is also used as an indicator of the severity of heart failure, although it has recognized limitations.

In cardiovascular physiology, end-diastolic volume (EDV) is the volume of blood in the right or left ventricle at end of filling in diastole which is amount of blood present in ventricle at the end of diastole. Because greater EDVs cause greater distention of the ventricle, EDV is often used synonymously with preload, which refers to the length of the sarcomeres in cardiac muscle prior to contraction (systole). An increase in EDV increases the preload on the heart and, through the Frank-Starling mechanism of the heart, increases the amount of blood ejected from the ventricle during systole.

End-systolic volume (ESV) is the volume of blood in a ventricle at the end of contraction, or systole, and the beginning of filling, or diastole.

Afterload is the pressure that the heart must work against to eject blood during systole. Afterload is proportional to the average arterial pressure. As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles respectively. Afterload changes to adapt to the continually changing demands on an animal's cardiovascular system. Afterload is proportional to mean systolic blood pressure and is measured in millimeters of mercury.

Diastole is the relaxed phase of the cardiac cycle when the chambers of the heart are refilling with blood. The contrasting phase is systole when the heart chambers are contracting. Atrial diastole is the relaxing of the atria, and ventricular diastole the relaxing of the ventricles.

Aortic regurgitation (AR), also known as aortic insufficiency (AI), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. As a consequence, the cardiac muscle is forced to work harder than normal.

Mitral regurgitation (MR), also known as mitral insufficiency or mitral incompetence, is a form of valvular heart disease in which the mitral valve is insufficient and does not close properly when the heart pumps out blood. It is the abnormal leaking of blood backwards – regurgitation from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts. Mitral regurgitation is the most common form of valvular heart disease.

In cardiac physiology, preload is the amount of sarcomere stretch experienced by cardiac muscle cells, called cardiomyocytes, at the end of ventricular filling during diastole. Preload is directly related to ventricular filling. As the relaxed ventricle fills during diastole, the walls are stretched and the length of sarcomeres increases. Sarcomere length can be approximated by the volume of the ventricle because each shape has a conserved surface-area-to-volume ratio. This is useful clinically because measuring the sarcomere length is destructive to heart tissue. It requires cutting out a piece of cardiac muscle to look at the sarcomeres under a microscope. It is currently not possible to directly measure preload in the beating heart of a living animal. Preload is estimated from end-diastolic ventricular pressure and is measured in millimeters of mercury (mmHg).

The cardiac cycle is the performance of the human heart from the beginning of one heartbeat to the beginning of the next. It consists of two periods: one during which the heart muscle relaxes and refills with blood, called diastole, following a period of robust contraction and pumping of blood, called systole. After emptying, the heart relaxes and expands to receive another influx of blood returning from the lungs and other systems of the body, before again contracting to pump blood to the lungs and those systems.

Pulsus paradoxus, also paradoxic pulse or paradoxical pulse, is an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. Pulsus paradoxus is not related to pulse rate or heart rate, and it is not a paradoxical rise in systolic pressure. Normally, blood pressure drops less precipitously than 10 mmHg during inhalation. Pulsus paradoxus is a sign that is indicative of several conditions, most commonly pericardial effusion.

Cardiovascular physiology is the study of the cardiovascular system, specifically addressing the physiology of the heart ("cardio") and blood vessels ("vascular").

Impedance cardiography (ICG) is a non-invasive technology measuring total electrical conductivity of the thorax and its changes in time to process continuously a number of cardiodynamic parameters, such as stroke volume (SV), heart rate (HR), cardiac output (CO), ventricular ejection time (VET), pre-ejection period and used to detect the impedance changes caused by a high-frequency, low magnitude current flowing through the thorax between additional two pairs of electrodes located outside of the measured segment. The sensing electrodes also detect the ECG signal, which is used as a timing clock of the system.

Venous return is the rate of blood flow back to the heart. It normally limits cardiac output.

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart. A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot. A number of methods have been determined for measuring PV-loop values experimentally.

$<span class="mw-page-title-main">Heart failure with preserved ejection fraction</span> Medical condition$

Heart failure with preserved ejection fraction (HFpEF) is a form of heart failure in which the ejection fraction – the percentage of the volume of blood ejected from the left ventricle with each heartbeat divided by the volume of blood when the left ventricle is maximally filled – is normal, defined as greater than 50%; this may be measured by echocardiography or cardiac catheterization. Approximately half of people with heart failure have preserved ejection fraction, while the other half have a reduction in ejection fraction, called heart failure with reduced ejection fraction (HFrEF).

The main pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction, hypertension and cardiac amyloidosis. Over time these increases in workload will produce changes to the heart itself:

References

1 2 3 4 5 6 7 Maceira AM, Prasad SK, Khan M, Pennell DJ (December 2006). "Reference right ventricular systolic and diastolic function normalized to age, gender and body surface area from steady-state free precession cardiovascular magnetic resonance" (PDF). European Heart Journal. 27 (23): 2879–88. doi:10.1093/eurheartj/ehl336. PMID 17088316.
1 2 3 4 5 6 7 Maceira A (2006). "Normalized Left Ventricular Systolic and Diastolic Function by Steady State Free Precession Cardiovascular Magnetic Resonance". Journal of Cardiovascular Magnetic Resonance. 8: 417–426. doi:10.1080/10976640600572889.(subscription required)
1 2 Normal ranges for heart rate are among the narrowest limits between bradycardia and tachycardia. See the Bradycardia and Tachycardia articles for more detailed limits.
1 2 "Normal Hemodynamic Parameters – Adult" (PDF). Edwards Lifesciences LLC. 2009.
↑ Katz AM (2006). Physiology of the heart. Hagerstwon, MD: Lippincott Williams & Wilkins. p. 337. ISBN 0-7817-5501-8.
↑ Betts JG (2013). Anatomy & physiology. OpenStax College, Rice University. pp. 787–846. ISBN 978-1938168130 . Retrieved 11 August 2014.
1 2 Cotes, John E.; Maynard, Robert L.; Pearce, Sarah J.; Nemery, Benoit B.; Wagner, Peter D.; Cooper, Brendan G. (2020). Lung Function. John Wiley & Sons. p. 450. ISBN 9781118597354.
↑ Clancy, John; McVicar, Andrew (2017). Physiology and Anatomy for Nurses and Healthcare Practitioners: A Homeostatic Approach, Third Edition. CRC Press. p. 336. ISBN 978-1444165289.
↑ Chang, David W. (2013). Clinical Application of Mechanical Ventilation. Cengage Learning. p. 31. ISBN 978-1285667348.
↑ Pocock, Gillian; Richards, Christopher D.; Richards, David A. (2018). Human Physiology. Oxford University Press. p. 437. ISBN 978-0198737223.

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[1] In short, the remaining blood volume left in the left ventricle not pumped out after a systole.

[RV_Volumes-2] 1 2 3 4 5 6 7 Maceira AM, Prasad SK, Khan M, Pennell DJ (December 2006). "Reference right ventricular systolic and diastolic function normalized to age, gender and body surface area from steady-state free precession cardiovascular magnetic resonance" (PDF). European Heart Journal. 27 (23): 2879–88. doi:10.1093/eurheartj/ehl336. PMID 17088316.

[LV_Volumes-3] 1 2 3 4 5 6 7 Maceira A (2006). "Normalized Left Ventricular Systolic and Diastolic Function by Steady State Free Precession Cardiovascular Magnetic Resonance". Journal of Cardiovascular Magnetic Resonance. 8: 417–426. doi:10.1080/10976640600572889.(subscription required)

[bpm_note-4] 1 2 Normal ranges for heart rate are among the narrowest limits between bradycardia and tachycardia. See the Bradycardia and Tachycardia articles for more detailed limits.

[edwards-5] 1 2 "Normal Hemodynamic Parameters – Adult" (PDF). Edwards Lifesciences LLC. 2009.

[isbn0-7817-5501-8-6] Katz AM (2006). Physiology of the heart. Hagerstwon, MD: Lippincott Williams & Wilkins. p. 337. ISBN 0-7817-5501-8.

[CNX2014-7] Betts JG (2013). Anatomy & physiology. OpenStax College, Rice University. pp. 787–846. ISBN 978-1938168130 . Retrieved 11 August 2014.

[Cotes-8] 1 2 Cotes, John E.; Maynard, Robert L.; Pearce, Sarah J.; Nemery, Benoit B.; Wagner, Peter D.; Cooper, Brendan G. (2020). Lung Function. John Wiley & Sons. p. 450. ISBN 9781118597354.

[Clancy-9] Clancy, John; McVicar, Andrew (2017). Physiology and Anatomy for Nurses and Healthcare Practitioners: A Homeostatic Approach, Third Edition. CRC Press. p. 336. ISBN 978-1444165289.

[Chang-10] Chang, David W. (2013). Clinical Application of Mechanical Ventilation. Cengage Learning. p. 31. ISBN 978-1285667348.

[Pocock-11] Pocock, Gillian; Richards, Christopher D.; Richards, David A. (2018). Human Physiology. Oxford University Press. p. 437. ISBN 978-0198737223.

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