Katana VentraIP

Cardiac output

In cardiac physiology, cardiac output (CO), also known as heart output and often denoted by the symbols , , or ,[2] 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 (usually measured per minute). 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:

Values for cardiac output are usually denoted as L/min. For a healthy individual weighing 70 kg, the cardiac output at rest averages about 5 L/min; assuming a heart rate of 70 beats/min, the stroke volume would be approximately 70 mL.


Because cardiac output is related to the quantity of blood delivered to various parts of the body, it is an important component of how efficiently the heart can meet the body's demands for the maintenance of adequate tissue perfusion. Body tissues require continuous oxygen delivery which requires the sustained transport of oxygen to the tissues by systemic circulation of oxygenated blood at an adequate pressure from the left ventricle of the heart via the aorta and arteries. Oxygen delivery (DO2 mL/min) is the resultant of blood flow (cardiac output CO) times the blood oxygen content (CaO2). Mathematically this is calculated as follows: oxygen delivery = cardiac output × arterial oxygen content, giving the formula:


With a resting cardiac output of 5 L/min, a 'normal' oxygen delivery is around 1 L/min. The amount/percentage of the circulated oxygen consumed (VO2) per minute through metabolism varies depending on the activity level but at rest is circa 25% of the DO2. Physical exercise requires a higher than resting-level of oxygen consumption to support increased muscle activity. In the case of heart failure, actual CO may be insufficient to support even simple activities of daily living; nor can it increase sufficiently to meet the higher metabolic demands stemming from even moderate exercise.


Cardiac output is a global blood flow parameter of interest in hemodynamics, the study of the flow of blood. The factors affecting stroke volume and heart rate also affect cardiac output. The figure at the right margin illustrates this dependency and lists some of these factors. A detailed hierarchical illustration is provided in a subsequent figure.


There are many methods of measuring CO, both invasively and non-invasively; each has advantages and drawbacks as described below.

Clinical significance[edit]

When Q increases in a healthy but untrained individual, most of the increase can be attributed to an increase in heart rate (HR). Change of posture, increased sympathetic nervous system activity, and decreased parasympathetic nervous system activity can also increase cardiac output. HR can vary by a factor of approximately 3—between 60 and 180 beats per minute—while stroke volume (SV) can vary between 70 and 120 mL (2.5 and 4.2 imp fl oz; 2.4 and 4.1 US fl oz), a factor of only 1.7.[71][72][73]


Diseases of the cardiovascular system are often associated with changes in Q, particularly the pandemic diseases hypertension and heart failure. Increased Q can be associated with cardiovascular disease that can occur during infection and sepsis. Decreased Q can be associated with cardiomyopathy and heart failure.[69] Sometimes, in the presence of ventricular disease associated with dilatation, EDV may vary. An increase in EDV could counterbalance LV dilatation and impaired contraction. From equation (3), the resulting cardiac output Q may remain constant. The ability to accurately measure Q is important in clinical medicine because it provides for improved diagnosis of abnormalities and can be used to guide appropriate management.[74]

Related measurements[edit]

Ejection fraction[edit]

Ejection fraction (EF) is a parameter related to SV. EF is the fraction of blood ejected by the left ventricle (LV) during the contraction or ejection phase of the cardiac cycle or systole. Prior to the start of systole, during the filling phase (diastole), the LV is filled with blood to the capacity known as end diastolic volume (EDV). During systole, the LV contracts and ejects blood until it reaches its minimum capacity known as end systolic volume (ESV). It does not completely empty. The following equations help translate the effect of EF and EDV on cardiac output Q, via SV.

VO2 consumption per minute using a (with the subject re-breathing air) and a CO2 absorber

spirometer

the oxygen content of blood taken from the pulmonary artery (representing mixed venous blood)

the oxygen content of blood from a cannula in a peripheral artery (representing arterial blood)

Arthur Guyton

Venous return

Right atrial pressure

Central venous pressure

Archived 11 December 2022 at the Wayback Machine

Hemodynamics training for Junior Medical Staff

The Gross Physiology of the Cardiovascular System

The Determinants of Cardiac Output (online video)

Archived 4 June 2023 at the Wayback Machine

Basic Principles in Cardiac Physiology