SECTION 6.5
Stroke volume and cardiac output
Relate stroke volume, heart rate and cardiac output, and explain how each factor is adjusted to meet the body’s demand.
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How much blood does the heart move? Two values answer the question. Stroke volume is the amount ejected by one ventricle in one beat, roughly 70 millilitres at rest. Heart rate is the number of beats per minute, roughly 75 at rest. Multiplying them gives cardiac output, the volume pumped each minute, which is about five litres at rest — approximately the entire blood volume. Cardiac output must change constantly: it rises several-fold during exercise and falls during rest or sleep. The body adjusts it by changing the rate, the stroke volume, or both. Stroke volume itself depends on three factors, named preload, contractility and afterload, and understanding these three explains how the heart matches its output to demand and what goes wrong in heart failure.
Key Concepts & Topics
Two numbers and one equation
Stroke volume (SV) is the volume ejected by one ventricle in one beat. It is calculated from two volumes: the end-diastolic volume (EDV), the amount in the ventricle just before contraction, and the end-systolic volume (ESV), the amount left just after ejection. So SV = EDV − ESV. At rest, EDV is about 130 mL and ESV about 60 mL, giving an SV of roughly 70 mL. The ejection fraction is the proportion of EDV that is ejected, normally about 55–70%, and it is a useful measure of pumping efficiency. Cardiac output (CO) is the volume pumped each minute: CO = heart rate × stroke volume. With a rate of 75 beats per minute and an SV of 70 mL, CO is about 5,250 mL, or roughly 5 litres per minute.
For example: If stroke volume falls but heart rate rises proportionally, cardiac output can stay the same; the equation shows why both factors matter.
Preload and the Frank–Starling relationship
Preload is the degree to which the ventricular wall is stretched just before it contracts, and it is determined mainly by how much blood has returned to the heart. Within limits, more filling stretches the muscle fibres, and stretched fibres contract more forcefully, so a larger EDV produces a larger SV. This is the Frank–Starling law of the heart: the heart pumps what it receives. It matters because it matches the output of the two ventricles automatically; if the right ventricle sends more blood to the lungs, more returns to the left ventricle, which then ejects more. Preload is influenced by blood volume, by the tone of the veins, by the skeletal muscle pump and by breathing. When preload becomes too low, as in severe bleeding, stroke volume falls; when it becomes too high, the heart may be unable to cope, and fluid backs up.
For example: When you exercise, the muscle pump and faster breathing increase venous return, which raises preload and helps increase stroke volume.
Contractility
Contractility is the force of contraction at a given fibre length, independent of preload. Two hearts can be filled to the same volume yet eject different amounts if one contracts more forcefully. Sympathetic stimulation and circulating epinephrine increase contractility by raising calcium availability inside the muscle cells, so the same preload produces a larger stroke volume. This is a positive inotropic effect. Factors that reduce contractility include severe oxygen lack, acidosis, some drugs and damage to the myocardium, and are called negative inotropic effects. Contractility is what allows the heart to increase its output during exercise beyond what preload alone would produce, and its loss is a central feature of heart failure, in which the ventricle is often dilated yet ejects too little.
For example: During exercise, sympathetic signals raise both rate and contractility, so stroke volume increases even before preload changes much.
Afterload
Afterload is the resistance the ventricle must overcome to eject blood. In practice it is related mainly to arterial pressure and to the resistance of the vessels, and it is also increased by narrowing of the outlet valve. A higher afterload means the ventricle must generate more pressure for the same flow, so less blood is ejected and ESV rises. This is why untreated high blood pressure reduces stroke volume and increases the work of the heart, and why aortic stenosis impairs ejection. The heart can compensate for a raised afterload by thickening its wall, but this eventually reduces the ability of the ventricle to relax and fill. Afterload is therefore a key target in treating hypertension and heart failure: lowering it makes it easier for the ventricle to eject.
For example: A patient with severe aortic stenosis has a pressure overload, so the left ventricle thickens and may eventually fail to fill and eject adequately.
Cardiac reserve and failure
Cardiac reserve is the difference between the output at rest and the maximum the heart can achieve. In a healthy young adult, cardiac output can rise from about 5 litres per minute at rest to 20 litres or more during intense exercise, an increase achieved by raising both heart rate and stroke volume. Stroke volume rises because preload increases, contractility increases and, in some tissues, afterload falls as vessels dilate. As people age or develop heart disease, reserve shrinks. When the heart cannot deliver enough blood to meet demand, the result is heart failure, in which output is inadequate at rest or during ordinary activity. Because stroke volume depends on preload, contractility and afterload, treatment aims at the same three factors: optimise filling, improve contractility where possible, and reduce afterload.
For example: In heart failure with reduced ejection fraction, the ventricle is dilated and ejects a low fraction of its volume, so cardiac output is maintained only by a faster rate.
Key facts to remember
- Stroke volume = end-diastolic volume − end-systolic volume, about 70 mL at rest.
- Cardiac output = heart rate × stroke volume, about 5 L/min at rest.
- Preload is the stretch before contraction; by the Frank–Starling law, more filling normally produces a larger stroke volume.
- Contractility is the force at a given fibre length; sympathetic activity and epinephrine increase it, while oxygen lack and acidosis reduce it.
- Afterload is the resistance to ejection, related mainly to arterial pressure; higher afterload reduces stroke volume.
Example · During exercise, cardiac output rises from about 5 to 20 litres per minute. Heart rate increases because sympathetic activity dominates. Stroke volume rises because venous return increases preload, sympathetic stimulation increases contractility, and dilated vessels in working muscle lower afterload. The three determinants of stroke volume therefore all move in the direction that increases output. In heart failure, reserve is reduced, so the same exercise produces a much smaller rise and the patient becomes breathless because output cannot meet demand.
Read full notes
Read one topic at a time. These notes explain the mechanisms and relationships behind the key facts.
Two numbers and one equation
The equation is useful because it separates the two ways the heart can change its output. Heart rate can change quickly through the autonomic nervous system, but it cannot rise indefinitely: at very high rates, diastole shortens so much that filling and coronary supply fail, and output actually falls. Stroke volume changes more gradually and depends on three factors. Because output is the product, a fall in one factor can sometimes be offset by a rise in the other, which is why a patient may maintain a normal output with a low stroke volume and a high rate, or the reverse. Clinically, this means that measuring only the pulse or only the blood pressure gives an incomplete picture of how well the heart is working.
Preload and the Frank–Starling relationship
The Frank–Starling relationship is a self-regulating mechanism. Because a stretched fibre contracts more forcefully, the heart automatically ejects what it receives, within limits. This keeps the outputs of the two ventricles equal over time without central coordination: if more blood enters the right side, more is pumped to the lungs, more returns to the left side, and more is pumped to the body. Preload also explains why factors that increase venous return, such as exercise, pregnancy or a slower heart rate, tend to increase stroke volume, and why factors that reduce it, such as bleeding, dehydration or prolonged standing, tend to reduce it. Beyond a certain point, however, further stretching becomes inefficient, and the relationship flattens or reverses.
Contractility
Contractility is what separates a heart that is merely full from a heart that is strong. Two ventricles may have identical preload, yet the one with greater contractility ejects more and leaves less behind. Sympathetic stimulation and epinephrine increase contractility by increasing calcium entry and release inside the muscle cells, and this is the main way the heart increases stroke volume during exercise. Conversely, hypoxia, acidosis, electrolyte disturbance and myocardial damage reduce it. In heart failure, contractility is often reduced, so the ventricle dilates and retains more blood after each beat; the ejection fraction falls, and the heart relies increasingly on a faster rate to maintain output. Treatments that improve contractility therefore increase stroke volume and reduce the work of compensation.
Afterload
Afterload is the pressure the ventricle must overcome to open its outlet valve and eject. It is determined mainly by arterial pressure and vascular resistance, and by any narrowing of the valve itself. The relationship is simple: a higher afterload means a higher pressure must be generated before ejection can begin, so less blood is ejected, more remains in the ventricle and the wall must work harder. Chronic high afterload causes the myocardium to thicken, which helps for a time but reduces the ventricle’s ability to relax and fill. This is why treating high blood pressure and narrowing of the aortic valve protects the heart, and why drugs that reduce afterload improve stroke volume in heart failure.
Cardiac reserve and failure
Cardiac reserve is the measure of how much the heart can increase its output above rest. In a healthy person, output can rise fourfold or more because rate, preload, contractility and afterload all change in the right direction at once. Reserve declines with age and with disease, and it is the first thing lost in many cardiac conditions: a patient may be comfortable at rest and yet breathless on stairs. Heart failure is the clinical state in which output is inadequate for demand, and it can involve reduced contractility, impaired filling, excessive afterload or a combination. Because stroke volume depends on three clear determinants, treatment is organised around them: improve filling where possible, support contractility, and reduce the resistance against which the heart must work.
Explore the diagram
Start with the whole view, then select a numbered structure. Compare the additional illustrations to connect what a structure looks like with what it does.
From one beat to one minute
Reduced motion · use the slider to explore each state.
Blood ejected by one ventricle per beat.
Educational schematic · selected major pathways, not to scale. Motion shows a slowed trace or comparison, not real-time physiology or disease progression.
Connect the illustrations to the key ideas
PRELOAD · venous return stretches the ventricle
By the Frank–Starling law, more filling normally means a larger stroke volume.
CONTRACTILITY · force at a given fibre length
Sympathetic activity and epinephrine raise it; hypoxia and acidosis lower it.
AFTERLOAD · resistance to ejection
Higher arterial pressure or a narrowed valve reduces stroke volume and increases work.
Core Concepts Defined
- Stroke volume (SV)
- The volume ejected by one ventricle in one beat.
- End-diastolic volume (EDV)
- The volume in a ventricle at the end of filling.
- End-systolic volume (ESV)
- The volume remaining in a ventricle after ejection.
- Ejection fraction
- The proportion of end-diastolic volume that is ejected, normally about 55–70%.
- Cardiac output (CO)
- The volume pumped by the heart each minute; heart rate × stroke volume.
- Heart rate
- The number of heartbeats per minute.
- Preload
- The stretch of the ventricular wall before contraction, set mainly by venous return.
- Frank–Starling law
- Within limits, a greater preload stretches the fibres and produces a stronger contraction and larger stroke volume.
- Contractility
- The force of contraction at a given fibre length, independent of preload.
- Inotropic effect
- A change in the force of contraction.
- Afterload
- The resistance the ventricle must overcome to eject blood, related mainly to arterial pressure.
- Venous return
- The volume of blood returning to the heart, the main determinant of preload.
- Cardiac reserve
- The difference between resting cardiac output and the maximum achievable.
- Heart failure
- The inability of the heart to deliver enough blood to meet the body’s needs.
Go deeper · worked example
Raising cardiac output during exercise
- Start from the equation. Cardiac output equals heart rate multiplied by stroke volume, so output can rise by increasing either factor or both.
- Raise the rate. Sympathetic activity increases and vagal activity falls, so the SA node fires faster and heart rate climbs.
- Raise preload. The skeletal muscle pump and faster breathing increase venous return, so the ventricle fills more and, by the Frank–Starling law, contracts more forcefully.
- Raise contractility. Sympathetic stimulation and circulating epinephrine increase calcium availability in the muscle cells, adding further force at the same filling volume.
- Lower afterload in working tissue. Vessels in active muscle dilate, reducing the resistance the left ventricle must overcome, so ejection is easier and stroke volume rises further.
Explain it yourself · Explain why a person with heart failure becomes breathless during exercise that a healthy person finds easy.
Reveal a model explanation
Exercise requires cardiac output to rise several-fold, achieved by increasing both heart rate and stroke volume. In heart failure, contractility is reduced, so stroke volume cannot increase as much; the ventricle may also be stiff or overloaded, limiting filling and raising afterload. The heart tries to compensate by beating faster, but a faster rate shortens diastole and reduces filling and coronary supply further. Because output cannot match demand, blood backs up, pressure rises in the lungs and the patient becomes breathless. The problem is not effort itself but a reduced cardiac reserve.
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OpenStax, Anatomy and Physiology 2e, 19.4 Cardiac Physiology; Tortora & Derrickson, Principles of Anatomy and Physiology, 12e, ch. 20. Author review only; medical and French-language expert review pending.
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