 By
the end of this lecture the students are
expected to:
 Define cardiac output, stroke volume, enddiastolic and end-systolic volumes.
 Define physiological conditions affecting CO
 List causes of high and low output
pathological states.
 Define venous return and describe factors
controlling venous return

Cardiac output is the amount of blood pumped by each
ventricle per minute (5L/min). It varies physiologically
with age, body mass index, physical activity, sleep, meals,
pregnancy, etc.. But there are pathological conditions that
lead to a significant increase in CO including
hyperthyroidism, anemia and conditions decreasing CO as
myocardial infarction. CO is well controlled and regulated
by Many Factors: venous return, ABP , blood volume and
nervous regulation. This lecture will focus on Venous
return as an important factor determining CO. Venous
return represents the amount of blood returning to the
heart per minute. Venous return is controlled by many
factors:1) Frank-Starling’s mechanism, 2) mean systemic
filling pressure, 3) tissue metabolism, 4) thoracic pump, 5)
Gravity, 6) Muscle pump, 7) blood volume.
Cardiac output (CO):
Amount of blood pumped by each
ventricle per minute. It equals 5L/min.
 Stroke volume (SV):
Volume of blood is ejected by each
ventricle/beat.(70 ml/beat).
S V times the number of beats per minute
(heart rate, HR), equals the cardiac output (CO).

CO = SV · HR
 Stroke volume is expressed in ml/beat and heart
rate in beats/minute. Therefore, cardiac output
is in ml/minute. Cardiac output may also be
expressed in liters/minute.

End-diastolic volume (EDV):
Amount of blood remaining in the heart by the end
of diastole.(140 mL)
End-systolic volume (ESV):
Amount of blood remaining in the heart by the end
of systole.
=70 mL
SV = EDV-ESV
Cardiac index:
=Cardiac output/BSA:
This allows direct comparison of the cardiac index
of large and small patients.
The percentage of blood that is pumped out of
a filled ventricle as a result of a heartbeat.
The heart does not eject all the blood in the
ventricle. Only about 2/3 of the blood is
normally pumped out with each beat, and that
fraction is referred to as the ejection fraction.
It decreases when the cardiac muscle becomes
diseased.
SV = EDV - ESV.
 This measurement can be affected by changes in
the heart's ability to contract, the force of
contraction, the volume of blood available to be
pumped or other variables such as resistance
within the circulatory system that can affect or
alter these factors. Severe hemorrhage or shock,
heart damage or extreme infections can change
the heart's ability to pump effectively.
 It is affected by cardiac contractility, preload,
and afterload.

 An
increase in heart rate due to stimulation
or excitation by activity, drugs, medications
or other sources, will result in an increase in
cardiac output. A decrease in the heart rate
due to an electrical abnormality and some
medications can result in a decreased
cardiac output.
 When
heart rates become excessively fast,
the heart may not have enough time to
adequately fill with blood between beats;
this can result in a decreased cardiac output.
 When heart rates are too slow the cardiac
output can also decrease significantly, and
interventions may be required to increase
the heart rate. Implanted pacemakers may
be surgically placed to ensure a consistent
adequate heart rate.
Exercise (up to 700%)
Eating ( 30%)
High environmental temperature ( )
Pregnancy ( )
Anxiety ( 50-100%)
Sympathomimitics, epinephrine ( )
Sitting or standing from lying position ( 2030%)
Increasing CO:
 Fever
 Hyperthyroidism
 Anemia
Decreasing CO:
 Hypothermia.
 Hypothyroidism
 Myocardial diseases e.g. infarction, failure…
 Rapid arrhythmias
VR
ABP
Preload (Venous return):
It represents the amount of blood returning to the
heart per minute.
Venous return is controlled by many factors:
1) Frank-Starling’s mechanism,
2) mean systemic filling pressure,
3) tissue metabolism,
4) thoracic pump,
5) Gravity,
6) Muscle pump,
7) blood volume.
8) Valsalva maneuvour

Venous return (VR) is the
flow of blood back to the
heart. Under steady-state
conditions, venous return
must equal cardiac output
(CO) when averaged over
time because the
cardiovascular system is
essentially a closed loop.
Otherwise, blood would
accumulate in either the
systemic or pulmonary
circulations. Although
cardiac output and venous
return are
interdependent, each can
be independently
regulated .
Mean systemic filling pressure:
 Sympathetic fibers supply veins (sympathetic
venoconstrictor tone).
 This is important to maintain venous pressure
and hence creates gradient to push blood to
the right atrium.
 Acute venous dilation can lead to significant
drop in VR and so Cardiac output.
Ability
of the heart to change its
force of contraction and therefore
stroke volume in response to
changes in venous return .
Also
defined as the ability of the
heart to pump all blood coming to it
without allowing systemic stasis,
within limits.
Echocardiography
 Record real-time changes in
ventricular dimensions, thus
computing stroke volume,
which when multiplied by
heart rate, gives cardiac
output.
Fick Principle :


An old technique.
Equation used:

CO = VO2/(O2art – O2ven)



Compute cardiac output (CO) indirectly from:
body oxygen consumption (VO2),
the mixed venous (O2ven), and
arterial oxygen contents (O2arterial blood)

To calculate CO, the oxygen contents of arterial and venous blood
samples are measured, and at the same time, whole body
oxygen consumption is measured by analyzing expired air.

The blood contents of oxygen are expressed as ml O2/ml blood,
and the VO2 is expressed in units of ml O2/min.
If O2art and O2ven contents are 0.2 ml and 0.15
ml O2/ml blood, respectively, and VO2 is 250 ml
O2/minute, then , how much will be the CO?
Then , CO= 250 mlO2/min /(0.2-0.15) mlO2/ml
blood= 5000 ml/min, or 5 L/min.
Ventricular stroke volume = CO/HR.