Cardiac Output

Cardiac output is the volume of blood pumped by one ventricle of the heart per unit time, usually expressed in liters per minute. It represents one of the most important measures of cardiovascular function because it describes how much blood the heart delivers to the circulation each minute.

Cardiac output is determined primarily by two variables: heart rate, the number of cardiac cycles per minute, and stroke volume, the amount of blood ejected by a ventricle during each beat.

Cardiac output changes continuously according to physiological requirements. Exercise, posture, autonomic activity, blood volume, venous return, myocardial contractility, vascular resistance, and numerous other factors can alter the amount of blood pumped by the heart.

Cardiac Output Equation

Cardiac output is calculated from heart rate and stroke volume:

Cardiac Output = Heart Rate × Stroke Volume

For example, a heart rate of 70 beats per minute and a stroke volume of 70 mL per beat produce a cardiac output of approximately 4.9 L/min.

Components of Cardiac Output

Variable	Definition
Heart rate	Number of heartbeats per minute
Stroke volume	Volume ejected by one ventricle during each beat
Cardiac output	Volume pumped by one ventricle per minute

Heart Rate

Heart rate is the number of cardiac cycles occurring each minute.

Under normal conditions, the sinoatrial node establishes the basic cardiac rhythm, while autonomic nervous system activity continuously modifies the rate.

Effect of Heart Rate on Cardiac Output

If stroke volume remains constant, an increase in heart rate increases cardiac output.

However, very high heart rates shorten diastole and may reduce ventricular filling sufficiently to decrease stroke volume. Therefore, the relationship between heart rate and cardiac output is not unlimited.

Stroke Volume

Stroke volume is the amount of blood ejected from one ventricle during a single contraction.

It is determined by the difference between ventricular end-diastolic volume and end-systolic volume.

Stroke Volume Equation

Stroke Volume = End-Diastolic Volume − End-Systolic Volume

End-diastolic volume represents ventricular filling before systole, while end-systolic volume represents the blood remaining after ventricular ejection.

Determinants of Stroke Volume

The three major physiological determinants of stroke volume are preload, contractility, and afterload.

Determinant	General Effect
Preload	Greater physiological filling tends to increase stroke volume
Contractility	Greater contractility tends to increase stroke volume
Afterload	Greater afterload tends to oppose ventricular ejection

Preload

Preload refers to the degree of myocardial fiber stretch before ventricular contraction and is related to ventricular filling.

End-diastolic volume and end-diastolic pressure are commonly used as indicators of ventricular preload, although preload itself refers more specifically to myocardial wall stress or fiber stretch before contraction.

Venous Return

Venous return is the flow of blood returning to the heart through the venous circulation.

In a stable circulation, venous return and cardiac output must be equal when averaged over time because the pulmonary and systemic circulations form a closed circuit.

Venous Return and Preload

Increased venous return generally increases ventricular filling and end-diastolic volume.

This increases myocardial fiber stretch and can increase stroke volume through the Frank-Starling mechanism.

Frank-Starling Mechanism

The Frank-Starling mechanism describes the intrinsic ability of the heart to adjust its force of contraction in response to changes in ventricular filling.

Within physiological limits, increased end-diastolic filling stretches ventricular muscle fibers and increases the force of the subsequent contraction.

Functional Importance of Frank-Starling Regulation

The Frank-Starling mechanism helps the heart match its output to the amount of blood returning through the venous circulation.

It also helps maintain balance between right and left ventricular output over time.

Contractility

Contractility, or inotropy, describes the intrinsic ability of cardiac muscle to generate force at a given loading condition.

Increased contractility allows the ventricle to eject more blood at a given preload and afterload, generally decreasing end-systolic volume and increasing stroke volume.

Positive Inotropy

A positive inotropic effect increases myocardial contractile force.

Sympathetic stimulation and circulating catecholamines are important physiological causes of increased ventricular contractility.

Sympathetic Stimulation

Sympathetic activation stimulates beta-adrenergic receptors in ventricular myocardium.

This increases intracellular calcium availability and enhances force development during systole.

Afterload

Afterload is the load against which a ventricle must contract and eject blood.

For the left ventricle, arterial pressure and systemic vascular properties are important contributors. For the right ventricle, pulmonary arterial pressure and pulmonary vascular resistance are important contributors.

Effect of Increased Afterload

An acute increase in afterload makes ventricular ejection more difficult.

If other factors remain unchanged, stroke volume may decrease and end-systolic volume may increase.

End-Diastolic Volume

End-diastolic volume (EDV) is the volume of blood within a ventricle immediately before ventricular systole.

It reflects ventricular filling during diastole and contributes importantly to preload.

End-Systolic Volume

End-systolic volume (ESV) is the amount of blood remaining in a ventricle after systolic ejection.

It is influenced strongly by myocardial contractility and afterload.

Relationship Between Ventricular Volumes and Output

Variable	Relationship
EDV increases	Can increase stroke volume through Frank-Starling effects
ESV decreases	Stroke volume increases if EDV is unchanged
Stroke volume increases	Cardiac output increases if heart rate is unchanged

Ejection Fraction

Ejection fraction is the proportion of end-diastolic volume ejected during ventricular systole.

It is calculated by dividing stroke volume by end-diastolic volume and is commonly expressed as a percentage.

Ejection Fraction Equation

Ejection Fraction = Stroke Volume ÷ End-Diastolic Volume × 100

Ejection fraction is an important measure of ventricular systolic performance, although it is not equivalent to cardiac output and does not describe every aspect of cardiac function.

Cardiac Index

Cardiac index adjusts cardiac output for body size by dividing cardiac output by body surface area.

This permits more meaningful comparison of cardiac pumping performance among individuals of different sizes.

Cardiac Index Equation

Cardiac Index = Cardiac Output ÷ Body Surface Area

Resting Cardiac Output

In a typical resting adult, cardiac output is commonly around 5 L/min, although normal values vary with body size, age, physiological state, and measurement method.

Cardiac output may change substantially even in healthy individuals according to metabolic demand.

Cardiac Output During Exercise

Exercise increases cardiac output to deliver additional oxygen and nutrients to active skeletal muscle and other tissues.

The increase is produced by a combination of increased heart rate and increased stroke volume.

Exercise and Heart Rate

During exercise, parasympathetic withdrawal and increased sympathetic activity accelerate sinoatrial nodal firing.

The resulting rise in heart rate is a major contributor to increased cardiac output.

Exercise and Stroke Volume

Stroke volume can increase during exercise because of increased venous return, enhanced myocardial contractility, and changes in ventricular loading conditions.

The relative contribution of stroke volume varies with exercise intensity, posture, training status, and individual cardiovascular characteristics.

Muscle Pump

Contraction of skeletal muscles compresses veins and helps propel blood toward the heart.

Venous valves limit backward flow, allowing the skeletal muscle pump to increase venous return during movement and exercise.

Respiratory Pump

Changes in thoracic and abdominal pressures during respiration influence venous return.

During inspiration, reduced intrathoracic pressure generally favors systemic venous flow toward the right atrium.

Blood Volume

Blood volume influences venous return and ventricular filling.

A reduction in circulating volume can reduce preload and cardiac output, while expansion of effective circulating volume can increase filling under appropriate conditions.

Venous Tone

Veins contain a large proportion of the circulating blood volume and function as capacitance vessels.

Sympathetic venoconstriction can reduce venous capacitance and shift blood toward the central circulation, increasing venous return.

Autonomic Regulation

The autonomic nervous system can rapidly modify cardiac output by altering heart rate, contractility, and vascular tone.

Sympathetic Effects

Target	Effect
SA node	Increases heart rate
Ventricular myocardium	Increases contractility
Veins	Increases venous tone and can augment venous return
Arterioles	Changes resistance according to vascular bed and receptor distribution

Parasympathetic Effects

Parasympathetic activity acts prominently on the sinoatrial and atrioventricular nodes.

Its principal direct effect on cardiac output is usually mediated through a reduction in heart rate, while direct parasympathetic effects on ventricular contractility are comparatively limited.

Cardiac Output and Arterial Pressure

Cardiac output is one of the major determinants of arterial pressure.

Mean arterial pressure depends on the interaction between cardiac output, systemic vascular resistance, arterial compliance, and other hemodynamic factors.

Systemic Vascular Resistance

Systemic vascular resistance represents the resistance to blood flow offered by the systemic circulation.

Arterioles are major sites of adjustable vascular resistance and therefore play an important role in determining arterial pressure and ventricular afterload.

Cardiac Output and Tissue Perfusion

Cardiac output supplies the blood that is distributed among the organs of the systemic circulation.

Individual organ blood flow is then regulated by local metabolic mechanisms, neural control, hormones, vascular resistance, and perfusion pressure.

Distribution of Cardiac Output

Cardiac output is not distributed equally among tissues.

The proportion received by different organs changes according to physiological conditions such as rest, exercise, digestion, temperature regulation, and stress.

Right and Left Ventricular Output

The right ventricle pumps blood through the pulmonary circulation, while the left ventricle pumps blood through the systemic circulation.

Over time, the outputs of the two ventricles must remain essentially equal because the circulations are connected in series.

Temporary Differences Between Ventricular Outputs

Small transient differences between right and left ventricular output can occur.

The Frank-Starling mechanism and redistribution of blood within the pulmonary circulation help restore balance between the two sides.

Cardiac Output and Oxygen Delivery

Cardiac output is an important determinant of systemic oxygen delivery.

Oxygen delivery depends on both blood flow and the oxygen content of arterial blood.

Fick Principle

The Fick principle can be used to calculate cardiac output from whole-body oxygen consumption and the difference in oxygen content between arterial and mixed venous blood.

The principle relates the amount of oxygen consumed by tissues to the amount delivered and removed from the circulating blood.

Fick Cardiac Output

Using oxygen as the measured substance, cardiac output can be calculated as:

Cardiac Output = Oxygen Consumption ÷ Arteriovenous Oxygen Content Difference

Thermodilution

Thermodilution is an invasive method of estimating cardiac output using changes in blood temperature after injection of a known quantity of indicator through a pulmonary artery catheter.

The resulting temperature-time curve is used to calculate flow.

Echocardiographic Estimation

Echocardiography can estimate stroke volume using measurements of blood-flow velocity and the cross-sectional area of an outflow tract.

Stroke volume multiplied by heart rate can then provide an estimate of cardiac output.

Other Measurement Methods

Method	General Principle
Fick method	Uses substance consumption and arterial-venous concentration difference
Thermodilution	Uses indicator temperature dilution
Echocardiography	Estimates stroke volume from flow velocity and anatomical measurements
Indicator dilution	Uses dilution of an injected indicator to estimate flow

Factors That Increase Cardiac Output

Cardiac output commonly increases when metabolic demand rises or cardiovascular reflexes increase heart rate, venous return, or contractility.

• Exercise
• Increased sympathetic activity
• Increased venous return
• Increased myocardial contractility
• Appropriate increases in heart rate

Factors That Decrease Cardiac Output

Cardiac output may decrease when ventricular filling, contractility, heart rate, or effective ejection becomes inadequate.

• Severe blood loss
• Marked reduction in venous return
• Severe myocardial dysfunction
• Extreme bradycardia
• Very rapid tachycardia that compromises filling
• Markedly increased afterload

Effect of Posture

Moving from a supine to an upright position causes blood to shift toward dependent veins because of gravity.

This initially reduces central venous return and ventricular filling, triggering cardiovascular reflexes that help maintain arterial pressure and cardiac output.

Baroreceptor Reflex

Arterial baroreceptors detect changes in stretch associated with arterial pressure.

When arterial pressure falls, reflex increases in sympathetic activity and reductions in parasympathetic activity can increase heart rate, contractility, and vascular tone.

Cardiac Reserve

Cardiac reserve refers to the ability of the heart to increase cardiac output above its resting level.

Cardiac reserve is particularly important during exercise and other conditions that substantially increase tissue metabolic requirements.

Clinical Significance

Low Cardiac Output

Inadequate cardiac output can reduce tissue perfusion and oxygen delivery.

The consequences depend on the severity, duration, underlying cause, and ability of compensatory mechanisms to maintain perfusion of vital organs.

Heart Failure

Heart failure can impair the ability of the heart to provide adequate output at normal filling pressures.

Compensatory increases in sympathetic activity, fluid retention, and changes in vascular tone may initially support circulation but can also contribute to disease progression.

Cardiogenic Shock

Cardiogenic shock is a state of severe circulatory failure caused primarily by inadequate cardiac pump function.

Markedly reduced cardiac output can lead to hypotension and insufficient perfusion of vital organs.

Hypovolemic Shock

Loss of circulating blood or fluid reduces venous return and ventricular preload.

If severe, the resulting reduction in stroke volume can substantially lower cardiac output.

Distributive Shock

In distributive forms of shock, abnormal vascular tone and distribution of blood volume alter venous return and tissue perfusion.

Cardiac output may be low, normal, or elevated depending on the cause and stage of the condition.

Arrhythmias

Abnormal heart rhythms can alter cardiac output by changing heart rate, ventricular filling, atrioventricular coordination, or ventricular contraction.

Both severe bradyarrhythmias and rapid tachyarrhythmias can reduce effective cardiac output.

Atrial Fibrillation

Atrial fibrillation eliminates coordinated atrial systole and produces an irregular ventricular rhythm.

Cardiac output may decline when loss of atrial contribution to ventricular filling or an excessively rapid ventricular response significantly reduces stroke volume.

Valve Disease

Stenotic or regurgitant cardiac valves can alter ventricular loading and reduce effective forward output.

The hemodynamic consequences depend on the valve involved, severity of disease, and compensatory ventricular changes.

Hypertension

Systemic hypertension increases left ventricular afterload.

Chronic pressure loading can produce ventricular hypertrophy and eventually alter both systolic and diastolic function.

Key Relationships

Relationship	Meaning
CO = HR × SV	Cardiac output depends on heart rate and stroke volume
SV = EDV − ESV	Stroke volume depends on ventricular filling and residual volume after ejection
Increased preload	Can increase stroke volume through Frank-Starling regulation
Increased contractility	Generally increases ventricular emptying and stroke volume
Increased afterload	Generally opposes ventricular ejection
Venous return	Must equal cardiac output over time in a stable closed circulation

Key Features of Cardiac Output

Feature	Key Point
Definition	Volume pumped by one ventricle per minute
Primary determinants	Heart rate and stroke volume
Stroke volume determinants	Preload, contractility and afterload
Typical unit	Liters per minute
Resting magnitude	Approximately 5 L/min in a typical adult, with physiological variation
Body-size adjustment	Cardiac index
Major physiological regulator	Autonomic nervous system and venous return
Clinical importance	Determines systemic blood flow and contributes to tissue oxygen delivery

Anatomical and Physiological Importance

Cardiac output integrates the mechanical performance of the heart with the requirements of the entire circulation. Heart rate determines how often the ventricles eject blood, while stroke volume determines how much blood is delivered with each contraction.

Stroke volume itself reflects the interaction of ventricular filling, myocardial contractility, and the load against which the ventricles eject. Venous return and the Frank-Starling mechanism allow the heart to adjust output to incoming blood flow, while autonomic regulation provides rapid changes in heart rate, contractility, and vascular tone.

Cardiac output is therefore not a fixed property of the heart. It is a continuously regulated variable that links cardiac anatomy, electrophysiology, ventricular mechanics, vascular function, and tissue metabolism. Maintaining an appropriate cardiac output is essential for adequate organ perfusion and systemic oxygen delivery.