Cardiac output is the quantity of blood pumped into the aorta each minute by
Unit – liter (ml) / min.
CO = SV multiplied by Heart Rate (HR) or Pulse Rate (PR)
Cardiac Output = Arterial Pressure / Total Peripheral Resistance
Cardiac output varies widely with the level of activity of the body.
The following factors directly affect cardiac output:
(1) The basic level of body metabolism,
(2) Whether the person is exercising or not,
(3) The person's age, and
(4) Size of the body.
Stroke volume ( SV ) is the volume of blood pumped from one ventricle of
the heart with each beat.
Unit of SV measurement is ml / beat.
SV 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 ) from the volume of blood just prior to
the beat ( called end - diastolic volume ).
SV = EDV – ESV
The term stroke volume can apply to each of the two ventricles of the
heart, although it usually refers to the left ventricle.
The stroke volumes for each ventricle are generally equal, both being approximately
70 ml in a healthy 70 kg man. Stroke volume is an important determinant of cardiac
output, which is the product of stroke volume and heart rate
When the heart contracts strongly, the end - systolic volume can be decreased
to as little as 10 to 20 millilitres.
Conversely, when large amounts of blood flow into the ventricles during
diastole, the ventricular end - diastolic volumes can become as great as 150 to
180 millilitres in the healthy heart.
By both increasing the end - diastolic volume and decreasing the end - systolic
volume, the stroke volume output can be increased to more than double
Men, on average, have higher stroke volumes than women due to the larger size
of their hearts.
However, stroke volume depends on several factors such as contractility,
duration of contraction, preload (end - diastolic volume) and after load.
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 enddiastolic volume, and ultimately allowing more blood to be ejected
(cardiovascular conditioning in athletes).
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.
Elevated after load (commonly measured as the aortic pressure during systole)
reduces stroke volume. Though not usually affecting stroke volume in healthy
individuals, increased after load will hinder the ventricles in ejecting blood,
causing reduced stroke volume.
The resistance to the ejection of blood by the ventricle is called afterload.
The left ventricle, for example, must create sufficient pressures during systole to
overcome diastolic arterial pressure and systemic vascular resistance before any
blood is ejected.
While preload enhances contractility and stroke volume, high pressures in the
arterial vessels during ventricular end diastole is inversely related to stroke
While systemic vascular resistance is not easily determined without a
pulmonary artery catheter, diastolic blood pressure is easily measured.
So while an accurate estimate of afterload is often not clinically practical, a
patient’s diastolic pressure provides a good indication of the resistance the left
ventricle must overcome.
In general, the higher the diastolic pressure, the higher the afterload.
Afterload is also tied to cardiac hypertrophy.
As the resistance to chamber contraction increases, the chamber
adapts to this increased workload with the accumulation of
increased fiber within the myocardial cells.
This makes the cells stronger but also bulks up the cells, ultimately
resulting in chamber hypertrophy.
Unfortunately, these thicker chamber walls can be associated with
additional complications such as decreased contractility, reduced
stroke volume, and cardiac dysrhythmias.
For young, healthy men, resting cardiac output averages about 5.6 L / min.
For women, this value is about 4.9 L / min.
With increasing age, body activity diminishes; the average cardiac output for the
resting adult is often stated to be almost exactly 5 L / min.
Experiments have shown that the cardiac output increases approximately in
proportion to the surface area of the body.
Therefore, cardiac output is frequently stated in terms of the cardiac index,
which is the cardiac output per square meter of body surface area.
The normal human being weighing 70 kilograms has a body surface area of
about 1.7 square meters, which means that the normal average cardiac index
for adults is about 3 L/min/m2 of body surface area.
Cardiac output is regulated throughout life almost directly in proportion to the
overall bodily metabolic activity. Therefore, the declining cardiac index is
indicative of declining activity with age.
Frank - Starling law of the heart states that when there is increased
quantities of blood flow (venous return – pre load) into the
heart, the cardiac muscle contracts with increased force, and this
empties the extra blood that has entered from the systemic
circulation. And so there is increased cardiac output.
The venous return to the heart is the sum of all the local blood
flows through all the individual tissue segments of the peripheral
circulation. Therefore, it follows that cardiac output regulation is
the sum of all the local blood flow regulations.
When the total peripheral resistance (after load) increases above
normal, the cardiac output falls; conversely, when the total
peripheral resistance decreases, the cardiac output increases.
Two types of factors usually can make the heart a better pump
(1) Nervous stimulation: Increased sympathetic & inhibited
parasympathetic activity leads to both increased heart rate &
strength of heart contraction leading to increased cardiac
(2) Hypertrophy of the heart muscle: A long-term increased
workload, but not so much excess load that it damages the
heart, causes the heart muscle to increase in mass and
contractile strength in the same way that heavy exercise causes
skeletal muscles to hypertrophy leading to increased cardiac
Low cardiac output, whether it be a peripheral factor or a cardiac
factor, if ever the cardiac output falls below that level required for
adequate nutrition of the tissues, the person is said to suffer
Cardiac index is calculated mainly in this type of patient for early
detection of shock.
In the human, except in rare instances, cardiac output is measured
by indirect methods that do not require surgery.
Two of the methods commonly used are the oxygen Fick’s method
and the indicator dilution method.
Why cardiac output is vital to our well-being ?
Simply, cardiac output is intimately connected to energy
Sufficient perfusion to the tissues yields an abundant energy
Poor tissue perfusion results in critical shortages of energy and
often diminished function.
Sufficient cardiac output is necessary to deliver adequate supplies
of oxygen and nutrients (glucose) to the tissues.
Table No. 1 : Example values in healthy 70 kg man
Typical value Normal range
End - diastolic volume ( EDV ) 120 ml
65 - 240 ml
End - systolic volume ( ESV )
16 - 143 ml
Stroke volume ( SV )
55 - 100 ml
Ejection fraction ( Ef )
55 to 70 %
Heart rate ( HR )
60 to 100 bpm
Cardiac output ( CO )
5.25 L / minute 4.0 - 8.0 L / min
Of the total CO, 75 % is distributed to the vital organs –
Liver, kidney, brain, lung, heart
Table No. 2 : Effect of various Physiologic
conditions on Cardiac Output
Condition or Factor
Moderate changes in environmental
Anxiety and excitement ( 50 – 100 % )
Eating ( 30 % )
Exercise ( up to 700 % )
High environmental temperature
Pregnancy ( Later months )
High Altitude due to hypoxia
Day time according to metabolic activity
Decrease Sitting or standing from lying position
( 20 – 30 % )
Factors regulating HR
Body temp. – Marey’s law
Drugs – E, NE, Bainbridge reflex
↑ in ICP – bradycardia – Cushing reflex
Pain – superficial & deep, respiration – sinus arrhythmia
Factors controlling HR
Cardiac innervation by ANS
Medullary Cardiovascular centers: VMC, CVC
HR & Respiration – Role of inspiratory neurons
Role of baroreceptors – NTS – CVC, Resting vagal
Role of chemoreceptors - hypoxia
Pathway relating interaction of cardiac
and respiratory reflexes