STROKE VOLUME
Prof. Sultan Ayoub Meo
MBBS, M.Phil, Ph.D (Pak), PG Dip Med Ed, M Med Ed (Scotland)
FRCP (London), FRCP (Dublin), FRCP (Glasgow), FRCP (Edinburgh)
Professor and Consultant, Department of Physiology,
College of Medicine, King Saud University, Riyadh, Saudi Arabia
LECTURE OUTLI NES / OBJECTIVES
STUDENTS ABLE TO UNDERSTAND:
•
Understand the concept of preload and after-load
•
Determine factors effecting the end-diastolic
Volume
• Explain how cardiac contractility affect stroke
volume
•
Describe the pressure volume loop
STROKE VOLUME
The amount of blood pumped out of each ventricle per beat is
called stroke volume (SV). 70 ml.
The output of the heart per unit time (minute) is called cardiac
output. Cardiac Out put= Stroke Volume x Hear Rate
[70 mL x 72 beats / min= 5040 ml. Approx]
 Cardiac Index: There is a correlation between resting cardiac
output and body surface area. The output per minute per square
meter of body surface is called cardiac index. Averages 3.2 L.
STROKE VOLUME
SV = EDV - ESV
Stroke volume is also defined as the difference between the ventricular
End Diastolic Volume [EDV] and the End Systolic Volume [ ESV].
EDV is the filled volume of ventricle prior to contraction
ESV is the residual volume of blood remaining in the ventricle after
ejection.
The EDV is about 120 ml of blood and the ESV about 50 ml of blood.
The difference in these two volumes 70 ml represents the SV. Factor
that alters either the EDV or the ESV will change SV.
Example: Increase in EDV increases SV, whereas an increase in
ESV decreases SV.
STROKE VOLUME
When the heart contracts strongly, the end-systolic volume can
be decreased to as little as 10 to 20 milliliters.
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 milliliters in healthy heart.
By both increasing the end-diastolic volume and decreasing the
end-systolic volume, the stroke volume output can be increased
STROKE VOLUME
Preload affect the SV through the increase in venous return to the
heart, increases the filled volume (EDV) of the ventricle, which
stretches the muscle fibers thereby increasing their preload. This
leads to an increase in the force of ventricular contraction
Afterload is related to the pressure that the ventricle generate to
eject blood into the aorta. Changes in afterload affect the ability
of the ventricle to eject blood and thereby alter ESV and SV.
increase in afterload, increase aortic pressure, decreases SV, and
causes ESV to increase.
STROKE VOLUME
STROKE VOLUME
STROKE VOLUME / CARDIAC OUT PUT
Factor
No change
Sleep
Moderate changes in environmental temperature
Increase
Anxiety and excitement (50–100%)
Eating (30%)
Exercise (up to 700%)
High environmental temperature
Pregnancy
Epinephrine
Decrease
Sitting or standing from lying position (20–30%)
Rapid arrhythmias, Heart disease
PRESSURE VOLUME LOOP
10
There are only three ways that the body
regulates stroke volume from minute-tominute:
• Filling pressure (preload)
• Aortic pressure (afterload)
• Contractility
11
PRESSURE VOLUME LOOP
The ejection loop
12
PRESSURE VOLUME LOOP
Changing filling
pressure changes stroke
volume only by
changing LVEDV
This could be an
example of
transfusion
Lowering LVEDP
has the opposite
effect (hemorrhage)
13
Lowering the aortic
pressure causes the
ventricle to empty
more completely.
The stroke volume
increases by an
amount equal to the
fall in LVESV.
LVEDV is not
affected.
Raising aortic
pressure has the
opposite effect
14
PRESSURE VOLUME LOOP
Increasing
contractility
decreases LVESV
and thus increases
stroke volume.
LVEDV is not
affected.
Heart failure has
the opposite
effect
15
PRESSURE VOLUME LOOP
Decreasing the
diastolic compliance
decreases LVEDV
and stroke volume
but has no effect on
LVESV
16
The real ejection loop has a
rounded top since the blood
pressure increases during
ejection (auxotonic beat)
17
Decreased compliance occurs only in
disease and is not a physiological
regulator
18
Hypertrophy
Normal
Dilation
19
Hypertrophy
Normal
Dilation
Hypertrophy results from
increased afterload over
several months.
Dilation results from
persistently elevated
preload over several days.
20
Hypertrophy
Normal
Dilation
Hypertrophy results from
increased afterload over
several months.
Dilation results from
persistently elevated
preload over several days.
Fiber slippage at the
desmosomes will occur
before the fibers will extend
beyond Lo
21
Hypertrophy
Normal
Dilation
Hypertrophy results from
increased work load over
several months.
Increased mass
Dilation results from
persistently elevated
preload over several days.
Same mass
The large chamber diameter
and thin wall puts the
dilated heart at a
mechanical disadvantage.
22
Notice that stroke
volume change in a
reciprocal manner.
Stroke Work = P x Vol
As P goes up V
naturally goes down so
their product remains
constant.
Stroke work should be
independent of any
change in blood
pressure.
23
If aortic pressure is held
constant stroke volume
increases with contractility.
Stroke volume goes down as
aortic pressure goes up.
Since stroke volume changes
reciprocally with aortic pressure
their product (stroke work) is
relatively independent of aortic
pressure
24
How can we measure contractility in the patient?
Ejection fraction = (LVEDV-LVESV) / LVEDV
The fraction of
the ventricular
contents at end
diastole that is
ejected.
25
How can we measure contractility in the patient?
Ejection fraction = (LVEDV-LVESV) / LVEDV
A normal
ejection fraction
should be above
0.50.
Ejection fractions
of 0.30-0.50 are
of concern.
Values below
0.30 carry a poor
prognosis.
26
How can we measure contractility in the patient?
Ejection fraction = (LVEDV-LVESV) / LVEDV
Can be easily
measured by
•X-ray
• Nuclear
techniques
• Echo
50-60 normal
35-49 concern
<35 serious
27
Often contractility is lost in just a region of the
heart as occurs in a myocardial infarction.
Regional dysfunction can be seen with
ultrasound or with a X-ray of the ventricle.
Normal
Regional akinesis
28