Cardiac Physiology: Preload, Afterload, Contractility and Cardiac Output
Originally published 23 July 2025 · Content reviewed 21 October 2026
Every time the heart beats, it has one job: move enough blood forwards to supply the body.
But the amount of blood leaving the ventricle with each beat is not fixed. It changes depending on how much blood enters the ventricle, how well the myocardium can contract and how difficult it is to push that blood out.
Those three parts of the pump are what we mean by preload, contractility and afterload.
Once those three make sense, stroke volume and cardiac output stop looking like separate pieces of cardiovascular terminology. They become the result of what happened while the ventricle filled, contracted and ejected.
First, the ventricle has to fill
Start during diastole. The ventricular myocardium is relaxed and blood is entering the ventricle. As the ventricle fills, its muscle fibres are stretched.
The degree of myocardial stretch at the end of diastole is called preload.
You will often see preload discussed alongside end-diastolic volume (EDV), which is the volume of blood in the ventricle immediately before it contracts. They are closely related, because increasing ventricular filling generally increases myocardial stretch. They are not exactly the same thing, though. Preload describes the stretch placed on the myocardial fibres, rather than simply the volume of blood inside the chamber.
Where did that filling come from? From blood returning to the heart. This is why venous return has such an important influence on preload.
Imagine a patient who has had severe diarrhoea and vomiting. They have lost fluid from the circulation. With less circulating volume, venous return can fall. Less blood reaches the ventricle during diastole, ventricular filling falls and preload may fall with it.
Now think about what happens when that ventricle contracts. It is beginning the beat with less filling than before, so the amount it can eject may also fall.
Why filling affects the strength of the next beat
The relationship between ventricular filling and contraction is described by the Frank–Starling mechanism.
How to read this graph: the horizontal axis represents increasing ventricular filling, often shown as end-diastolic volume or a measure of filling pressure; the vertical axis shows stroke volume or cardiac output, depending on the graph. The curve for a healthy ventricle rises as filling increases and gradually flattens as further filling adds less forward flow. The curve for a ventricle with impaired systolic function lies lower and is often flatter, so an increase in filling may produce little extra stroke volume. These curves illustrate physiology, not a target for giving intravenous fluids. End-diastolic volume and filling pressure are not interchangeable, particularly when the ventricle has become stiff (Delicce and Makaryus, 2023).
Within physiological limits, when more blood enters the ventricle during diastole, the myocardial fibres are stretched further. That stretch improves the interaction of the contractile proteins within the cardiac muscle, allowing the next contraction to generate more force. The ventricle can therefore eject a larger stroke volume.
This allows the heart to match its output to the blood returning to it. If venous return increases, a healthy heart can usually eject more blood on the next beat rather than allowing that additional volume simply to accumulate.
There is a limit to this relationship. A ventricle with impaired systolic function does not respond to additional filling in the same way as a healthy ventricle. As filling pressure rises, there may be relatively little improvement in stroke volume. Instead, pressure begins to build behind the failing ventricle.
On the left side of the heart, raised filling pressures can be transmitted backwards towards the pulmonary circulation. Fluid can accumulate in the lungs and the patient may become increasingly breathless. This is one reason a patient with heart failure can be fluid overloaded while still having an inadequate cardiac output.
So preload should never be translated into “more fluid means better cardiac output”. It tells you about the filling and stretch experienced by the ventricle. Whether increasing that filling is useful depends on the ventricle and the patient.
Next, the myocardium has to squeeze
Once the ventricle has filled, the myocardial cells have to generate enough force to eject blood. Their intrinsic ability to generate that force is called contractility.
Contractility is influenced by what is happening inside cardiac muscle cells, particularly calcium availability and the interaction of the contractile proteins. Sympathetic stimulation and circulating catecholamines can increase calcium availability and increase the force of contraction. This is a positive inotropic effect.
A stronger contraction can leave less blood behind in the ventricle after systole and increase the amount ejected with that beat.
The opposite can happen when the myocardium is damaged or dysfunctional. Imagine an area of left ventricular muscle affected by a myocardial infarction. If part of the myocardium cannot contract normally, the ventricle may eject less effectively even if it has filled adequately.
This is why contractility and preload are different. A ventricle can be well filled and still pump poorly.
It is also why contractility is not the same as heart rate. Chronotropy describes changes in heart rate, whereas inotropy describes changes in contractile force. Sympathetic stimulation can increase both, but a heart beating faster is not necessarily ejecting more blood with each beat.
Then the ventricle has to push the blood out
The ventricle does not eject blood into an empty tube. It has to generate enough pressure to open the outflow valve and push blood into the circulation.
The load the ventricle has to overcome during ejection is called afterload.
For the left ventricle, arterial pressure and systemic vascular resistance contribute to that load. Ventricular geometry and wall stress are also part of the physiology, so afterload is more than simply another name for blood pressure or vascular resistance.
At a practical level, imagine the difference between ejecting blood into a circulation with relatively low resistance and trying to eject against a markedly raised arterial pressure. The second situation requires the left ventricle to generate greater pressure before and during ejection.
If afterload rises and the ventricle cannot compensate, less blood may be ejected and more remains in the chamber at the end of systole. Over time, persistent pressure loading such as longstanding hypertension can also change the structure of the left ventricle, including the development of left ventricular hypertrophy.
The right ventricle has afterload too, but it pumps into the pulmonary circulation rather than the systemic circulation. A large pulmonary embolism can suddenly obstruct pulmonary blood flow and increase pulmonary vascular resistance. The right ventricle is then faced with a rapid increase in afterload. If it cannot maintain forward flow, right ventricular output falls, less blood reaches the left side of the heart and systemic cardiac output can fall as well.
So afterload is easiest to remember as the load the ventricle faces when it tries to eject.
These three influences determine stroke volume
We can now put the beat together.
The ventricle fills, creating preload. The myocardium contracts with a particular degree of contractility. During that contraction it has to overcome afterload to eject blood.
The amount of blood ejected by one ventricle during one contraction is the stroke volume (SV).
Another way of calculating it is to look at what was in the ventricle before and after contraction:
SV = end-diastolic volume − end-systolic volume
If the ventricle contains 120 mL at the end of diastole and 50 mL remains after systole:
SV = 120 − 50 = 70 mL
For orientation, resting stroke volume in healthy adults is often around 60–100 mL per beat. It varies with body size, fitness, heart rate and clinical circumstances. These are approximate reference figures, not a bedside diagnosis or treatment threshold (Khalil, Foster and Launico, 2026).
That 70 mL is the result of the whole beat. Change the filling, the ability of the myocardium to contract or the load against ejection and the stroke volume may change too.
This also explains why a low stroke volume does not tell you what has gone wrong. One patient may be underfilled after haemorrhage. Another may have impaired contractility following myocardial injury. Another may have a sudden rise in right ventricular afterload from a pulmonary embolism. The result can be reduced forward flow, but the physiology producing it is different.
From one beat to one minute: cardiac output
Stroke volume tells us how much blood leaves with each beat. To know how much the heart pumps each minute, we also need the heart rate.
Cardiac output (CO) = heart rate (HR) × stroke volume (SV)
If the heart rate is 70 beats per minute and stroke volume is 70 mL:
CO = 70 × 70 = 4,900 mL/min, or approximately 4.9 L/min
A typical resting adult cardiac output is around 4–8 L/min, averaging close to 5 L/min. Because a larger person may require a greater output, clinicians sometimes use the cardiac index (CI), which adjusts cardiac output for body size: CI = CO ÷ body surface area (BSA). With a CO of 4.9 L/min and a BSA of 1.8 m², the CI is approximately 2.7 L/min/m². A usual adult resting CI is around 2.5–4.0 L/min/m². These reference ranges help interpret measurements in the appropriate clinical setting; they cannot tell you by themselves whether an individual's organs are adequately perfused (King and Lowery, 2023; Patel et al., 2024).
Now imagine that stroke volume falls. The sympathetic nervous system can increase heart rate in an attempt to preserve cardiac output. This is one reason tachycardia can appear when circulating volume falls.
Initially, that compensation may help. But a faster heart rate does not guarantee a good cardiac output. As the rate becomes very fast, diastole shortens. The ventricles have less time to fill between beats, and reduced filling can reduce stroke volume further. Myocardial oxygen demand also increases.
So a patient with a heart rate of 120 beats per minute may have a high cardiac output, a normal cardiac output or an inadequate cardiac output depending on what is happening to stroke volume. The heart rate alone cannot tell you.
Ejection fraction: a proportion, not a cardiac output
Another term you may see on an echocardiogram report is left ventricular ejection fraction (LVEF). It is the percentage of the ventricle's end-diastolic volume ejected during one beat. It is not the volume pumped in a minute and it is not a direct measurement of intrinsic contractility.
EF = (stroke volume ÷ end-diastolic volume) × 100. Using our earlier example, (70 ÷ 120) × 100 = approximately 58%. The British Society of Echocardiography describes a left ventricular EF of 55% or more as normal with its specified two-dimensional echocardiographic technique. The measurement method influences the appropriate reference range, and a normal EF does not guarantee that stroke volume or cardiac output is adequate (Harkness et al., 2020).
It is also possible to have heart failure with preserved ejection fraction (HFpEF). In this condition, the ventricle may be stiff or relax poorly during diastole. It can eject a normal-looking proportion of what it contains while filling at abnormally high pressure. Breathlessness and pulmonary congestion can follow even when EF is 50% or higher. HFpEF requires clinical assessment and evidence of relevant structural or functional abnormalities; an EF figure on its own does not establish the diagnosis. This is one reason NICE distinguishes reduced, mildly reduced and preserved EF when discussing heart-failure management (NICE, 2025).
Cardiac output only has a purpose if the blood reaches the tissues
This is where the physiology meets the patient.
The reason the heart maintains cardiac output is to provide blood flow to the organs. If effective forward flow falls, the body tries to protect perfusion through compensatory responses. Sympathetic activation can increase heart rate, increase contractility and constrict peripheral blood vessels.
Peripheral vasoconstriction can help maintain arterial pressure and prioritise blood flow towards vital organs, but it also means the skin and extremities may receive less blood. That is one reason an unwell patient with circulatory compromise may develop cool peripheries and prolonged capillary refill.
The kidneys are also sensitive to changes in circulation. Falling renal perfusion can contribute to reduced urine output and, if the problem persists, acute kidney injury. Significant cerebral hypoperfusion may contribute to altered mental state or reduced consciousness.
Blood pressure belongs in this assessment, but blood pressure and cardiac output are not the same thing. A simplified physiological relationship is:
mean arterial pressure ≈ cardiac output × systemic vascular resistance
If cardiac output begins to fall, vasoconstriction can increase systemic vascular resistance and help defend the blood pressure for a time. The patient may therefore already show signs of poor peripheral perfusion before severe hypotension develops.
This is why circulation is assessed as a pattern. Heart rate and rhythm, blood-pressure trend, capillary refill, peripheral temperature, urine output, mental state, fluid balance, respiratory findings and the patient's symptoms all add information. None of them gives you a bedside measurement of preload or cardiac output by itself.
Put it back into one patient
A patient has had repeated vomiting and diarrhoea. Their heart rate is now 116 beats per minute. Their blood pressure has fallen from their usual level, their hands feel cool and they have passed very little urine during the last few hours.
Start with what has happened to the circulation. Fluid loss may have reduced circulating volume. That can reduce venous return, so the ventricles fill less during diastole. Reduced filling means reduced preload and may reduce stroke volume.
The body detects the circulatory change and activates compensatory responses. Heart rate and contractility increase, while peripheral vasoconstriction helps support arterial pressure. Those same responses can help explain the tachycardia and cool hands. If renal perfusion is falling, urine output may decrease.
Now change just one part of the story. Imagine the patient instead has significant left ventricular systolic dysfunction and pulmonary congestion. Their problem may not be insufficient filling at all. Their ventricle may be unable to convert the filling it already has into effective forward flow. Increasing intravascular volume could then increase filling pressures and worsen congestion rather than substantially improve stroke volume.
That comparison is the reason these terms are worth learning. Preload, contractility and afterload give you a way of thinking about why cardiac output has changed rather than treating every abnormal heart rate or blood pressure as the same circulatory problem.
What this means during a ward shift
Return to the patient with vomiting, diarrhoea, a pulse of 116 and reduced urine output. You cannot measure their preload from a blood-pressure cuff, but you can recognise possible deterioration and gather a fuller picture. Work with your supervising registered nurse to begin an ABCDE assessment, obtain a complete set of observations and calculate NEWS2 where used locally. Review the trend in respiratory rate, oxygen saturation, pulse and rhythm, blood pressure relative to baseline, temperature and consciousness, alongside symptoms, capillary refill and peripheral perfusion. If the patient is becoming unwell, escalate promptly. A blood pressure that looks acceptable, or even a low NEWS2 score, must not override clinical concern (Royal College of Physicians, 2017).
Review the fluid balance chart and check that oral and intravenous intake, vomiting, diarrhoea and urine output have been recorded accurately. Consider weight trends where available. Look for possible congestion as well as losses: worsening breathlessness, crackles, raised jugular venous pressure and peripheral oedema may change the interpretation. No single sign reliably separates low circulating volume from heart failure. An assessment of the patient's condition, rather than an assumption about preload, should guide the team's decisions about fluids (NICE, 2013).
Medicines also connect to the pump. A diuretic such as furosemide promotes salt and water excretion, relieving fluid retention and congestion. The team monitors urine output, renal function, electrolytes and blood pressure. Vasodilators can reduce vascular resistance; some also affect venous tone and filling. Inotropes increase the force of contraction, while vasopressors primarily increase vascular tone to support blood pressure and may increase afterload. They are used according to the clinical problem, not as interchangeable fixes for a low blood pressure. NICE does not recommend giving inotropes or vasopressors routinely for acute heart failure, although they may be considered in selected patients with potentially reversible cardiogenic shock, in an appropriately monitored setting (NICE, 2014; NICE, 2025).
When you hand over, use SBAR: explain what has changed, give the observations and trend, describe losses or signs of congestion, and state your concern about possible impaired circulation and the need for review. That is more useful than saying the patient “has low preload”, which you have not directly measured.
Follow the pump
When the terminology starts to blur together, return to what the ventricle is actually doing.
Preload: how much stretch is present at the end of filling.
Contractility: how effectively the myocardium can generate force.
Afterload: the load the ventricle must overcome to eject.
Together, these influence stroke volume, the amount ejected with each beat. Stroke volume combined with heart rate gives cardiac output, the amount pumped each minute.
And cardiac output has one final purpose: maintaining enough blood flow to support the tissues.
That is the whole story this terminology is describing: fill the ventricle, squeeze, push the blood out, and keep it moving around the body.
References
Delicce, A.V. and Makaryus, A.N. (2023) 'Physiology, Frank Starling Law', StatPearls, updated 30 January. Available at: NCBI Bookshelf.
Hall, J.E. and Hall, M.E. (2021) Guyton and Hall Textbook of Medical Physiology. 14th edn. Philadelphia: Elsevier.
Harkness, A., Ring, L., Augustine, D.X., Oxborough, D., Robinson, S. and Sharma, V. (2020) 'Normal reference intervals for cardiac dimensions and function for use in echocardiographic practice', Echo Research & Practice, 7(1), pp. G1–G18. Available at: https://doi.org/10.1530/ERP-19-0050.
Khalil, B., Foster, C. and Launico, M.V. (2026) 'Physiology, Stroke Volume', StatPearls, updated 19 June. Available at: NCBI Bookshelf.
King, J. and Lowery, D.R. (2023) 'Physiology, Cardiac Output', StatPearls, updated 17 July. Available at: NCBI Bookshelf.
National Institute for Health and Care Excellence (NICE) (2013, updated 2017) Intravenous fluid therapy in adults in hospital (CG174). Available at: NICE CG174 recommendations.
National Institute for Health and Care Excellence (NICE) (2014) Acute heart failure: diagnosis and management (CG187). Available at: NICE CG187 recommendations.
National Institute for Health and Care Excellence (NICE) (2018, updated 2025) Chronic heart failure in adults: diagnosis and management (NG106). Available at: NICE NG106 recommendations.
Patel, N. et al. (2024) 'Physiology, Cardiac Index', StatPearls. Available at: NCBI Bookshelf.
Royal College of Physicians (2017) National Early Warning Score (NEWS) 2: Standardising the assessment of acute-illness severity in the NHS. London: RCP. Available at: RCP NEWS2 resources.