Cardiac Output and Venous Return
Learning objectives
• Define venous return. Understand the concept
of “resistance to venous return” and know what
factors determine its value.
• Understand the principles underlying cardiac
output measurements using the Fick principle,
dye dilution, and thermodilution methods.
• Know how cardiac function (output) curves are
generated and how factors which cause changes
in contractility in the heart can alter the shape
of cardiac function curves.
Learning objectives
• Construct a vascular function curve. Predict how
changes in total peripheral resistance, blood
volume, and venous compliance influence this
curve.
• Use the intersection point of the cardiac function
curve and vascular function curve to predict how
interventions such as hemorrhage, heart failure,
autonomic stimulation, and exercise will affect
cardiac output and right atrial pressure.
Cardiac output
• Amount of blood ejected by each ventricle per
minute is called cardiac output (CO). Its value is
almost same for both the ventricles & is about
5L/min. in a normal adult male
• Cardiac output = heart beat rate X stroke volume
(stroke volume is amount of blood ejected/ventricle/beat or
stroke = EDV-ESV)
• CO = 72/min X 70ml = 5 L/min (approx.)
Cardiac index: CI is the cardiac output per
square meter of body surface area. Normal
value is about 3 L/min/m2
(2.6 to 4.2 L/min/m2 )
Measurement of Cardiac Output
• Calculation of flow through the pulmonary
circuit provides a measure of the CO.
Required data are:
• oxygen consumption of the organ
• A – V oxygen content (concentration)
difference across the organ (not PO2)
• In a test subject, oxygen consumption was
measured at 700 mL/min.Pulmonary artery
oxygen content was 140 mL per liter of blood
and brachial artery oxygen content was 210
mL per liter of blood. Cardiac out-put was
which of the following?
a. 4.2 L/min
b. 7.0 L/min
c. 10.0 L/min
d. 12.6 L/min
e. 30.0 L/min
Regulation of cardiac output
• Factors effecting
Regulation of Heart rate
• Sympathetic &
parasympathetic
(vagus) nerves
control the heart
beat rate.
• A normal heart beat
is maintained by
slow continuous
discharge from
sympathetic nerves
• The vagal fibers are
distributed mainly
to atria than
ventricles
Regulation of Heart rate
• Strong sympathetic stimulation can increase the heart rate from
normal 70 beats / min. upto 180-200 beats / min.
• Strong vagal stimulation bring down the rate to 20 40beats/min & also can decrease strength of heart muscle
contraction by 20-30%
14-8
The output per minute per square meter of body
surface is called
A. Cardiac output
B. Stroke volume
C. Afterload
D. Cardiac index
E. Preload
Baroreceptor Reflex
Bainbridge Reflex, Atrial Receptors,
and Atrial Natriuretic Peptide
Respiratory Sinus Arrhythmia
Determinants of Cardiac Output
• Venous parameters, not arterial parameters,
normally determine cardiac output.
• Heart rate does not normally affect cardiac output
but very low and very high heart rates impede
venous return and cardiac output.
• Increased resistance of arteries raises blood pressure
but does not affect venous return and cardiac
output.
• For instance, aortic stenosis, coarc-tion of the aorta,
and hypertension do not decrease cardiac output if
the heart if able to pump against the increased
afterload.
Stroke Volume
• Is determined by 3 variables:
– Preload/End diastolic volume (EDV) = volume of blood in
ventricles at end of diastole
– Afterload/Total peripheral resistance (TPR) = impedance
to blood flow in arteries
– Contractility/Inotropy = strength of ventricular
contraction
14-9
Regulation of Stroke Volume
• EDV is workload (preload) on heart prior to
contraction
– SV is directly proportional to preload &
contractility
• Total peripheral resistance = afterload which
impedes ejection from ventricle
– SV is inversely proportional to TPR
• SV is directly proportional to Contractility.
Regulation of stroke volume
1. Preload :Passive tension in the muscle
when it is being filled during diastole.
• End diastolic volume
• Venous return
• Frank-Starling’s law (Energy of
contraction is proportional to the initial length
of cardiac muscle fibres)
Preload
General features
• Preload is the load on the muscle in the
relaxed state.
• More specifically, it is the load or prestretch
on ventricular muscle at the end of diastole.
• Preload on ventricular muscle is not measured
directly; rather, indices are utilized.
• Indices of left ventricular preload:
– Left ventricular end-diastolic volume (LVEDV)
– Left ventricular end-diastolic pressure (LVEDP)
• somewhat less reliable indices of left
ventricular preload are those measured in the
venous system.
– Left atrial pressure
– Pulmonary venous pressure
– Pulmonary wedge pressure
• Measurement of systemic central venous
pressure is an index of preload on the right
ventricle
Question time again-
In skeletal muscle the resting muscle length is
approximately the optimal length at which maximal tension
can be developed during a subsequent contractionA)True
B)False.
Frank-Starling Law of the Heart
(a) is state of myocardial
sarcomeres just
before filling
Actins overlap, actinmyosin interactions
are reduced &
contraction would be
weak
In (b, c & d) there is
increasing
interaction of actin
& myosin allowing
more force to be
developed
• The Frank–Starling law of the heart states
that the stroke volume of the heart increases
in response to an increase in the volume of
blood filling the heart (the end diastolic
volume) when all other factors remain
constant.
• Important in Balancing left and right
ventricular Cardiac output.
Fig. -. Frank-Starling Law of the heart. The graph illustrates the
relationship between SV and changes in ventricular end-diastolic
volume. The insets showing diagrammatic sarcomeres, illustrate the
relationship between end-diastolic volume and myofilament overlap.
Length-force relationships in intact heart:
a Frank-Starling curve
Optimal Length
Figure 14-28
Factors affecting end-diastolic volume, e.g. the degree to which
cardiac muscle is stretched
Increase
• Stronger atrial contraction
• Increased total blood volume
• Increased venous tone
• Increased pumping action of skeletal muscle
• Increased negative intrathoracic pressure
Decrease
• Standing
• Increased intrapericardial pressure(Cardiac tamponade)
• Decreased ventricular compliance
•Pathological conditions
such as ventricular
systolic failure and valve
defects such as aortic
stenosis, aortic
regurgitation (pulmonary
valve stenosis and
regurgitation have similar
effects on right ventricular
preload).
B. Extrinsic Regulation of Stroke Volume
• Any changes in the strength of cardiac contraction that occur
independently of changes in EDV are referred to as changes in
myocardial contractility
• A change in myocardial contractility (Inotropism) is
mechanistically different from the altered vigor of contraction seen
with changes in muscle length
• Changes in contractility are direct result of changes in the rate
and extent of Ca2+ movement into the cytoplasm
• Increased firing of cardiac sympathetic nerve results in  in both
the rate (chronotropic action) and extent (inotropic action) of
myocardial contractions
Relationship between contractility and intracellular Ca2+ : contractility is a
result of cytoplasmic Ca2+ concentration. This is the result of both release of
Ca2+ from the sarcoplasmic reticulum and influx of Ca2+ from the
extracellular space. Increased Ca2+ results in activation of additional
crossbridges (indicated in red)
sympathetic
Fig. 14. Effect of changes in myocardial contractility on the FrankStarling curve. The curve shifts downward and to the right as
contractility is decreased. The major factors influencing contractility are
summarized on the right (dashed lines indicate portions of the curve where
maximum contractility has been exceeded). W.Ganong. Review of Medical
Physiology
Ejection Fraction – is the fraction of the enddiastolic volume that is ejected with each beat,
that is, it is stroke volume (SV) divided by enddiastolic volume (EDV).
stroke volume / end diastole volume X 100%,
normal range, 55-65%.
Commonly used as a clinical index for evaluating
the inotropic state of the heart.
Fig. . Changes in SV due to changes in contractility are mechanistically
different from those occurring as a result of EDV. The two mechanisms can
operate simultaneously to  SV (lower panel). EDV = end- diastolic volume;
ESV = end-systolic volume; SV = stroke volume (Human Physiology)
Afterload and Cardiac Performance
• Afterload: all the factors that impede fiber
shortening, in this case it would be all the
factors that impede the ejection of blood from
the ventricle. What the heart has to pump
against
•
•
•
•
Volume of blood in the arterial circulation
Pressure in aorta at onset of ejection (DAP)
Compliance of aorta
Size of outflow orifice
Factors that affect stroke volume.
Myocardial Hypertrophy
Concentric
• Cross sectional area of a
muscle increases when
repeatedly exposed to an
elevated work load over a
sustained period of time
• In cardiac muscle this can be
the result of increased wall
tension caused by increased
preload or increased after load
.
51
eccentric
Changes in the radius of the ventricles (curvature of the
ventricle) can affect ventricular pressure (Laplace’s Law) and
efficiency of the heart as a pump
• The pressure generated in a sphere is directly proportional to the
wall tension (T) developed, and inversely related to the radius of
the sphere (r) (Law of Laplace)
P = 2T/r
• In normal conditions, during ejection phase of cardiac cycle the
volume of blood in the V falls, and the r of the V decreases. As the
radius falls, the tension in the V walls is more effective in
ventricular pressure
• In chronic cardiac failure the contractility is reduced and the heart
becomes less effective as a pump and dilates radius of the
ventricles and reduces its curvature, and ejection gets more
difficult as it proceeds
Normal P-V loop
Increased Afterload
Increased Preload
Increased Contractility
1. The figure below shows pressure volume loops for two
situations. When compared with loop A, loop B
demonstrates
(A) Increased preload
(B) Decreased preload
(C) Increased contractility
(D) Increased afterload
(E) Decreased afterload
Which of the following would cause a
decrease in stroke volume, compared with
the normal resting value?
(A) Reduction in afterload
(B) An increase in end-diastolic pressure
(C) Stimulation of the vagus nerves
(D) Electrical pacing to a heart rate of 200
beats/min
(E) Stimulation of sympathetic nerves to the
heart
Point Y in the figure below is the control point. Which point
corresponds to a combination of increased contractility and
increased ventricular filling?
(A) Point A
(B) Point B
(C) Point C
(D) Point D
(E) Point E
Summary of the regulation of Cardiac Output
The Cardiac output is the volume of blood pumped by
each ventricle and equals the product of heart rate and
stroke volume
• Heart rate is  by stimulation of the sympathetic nerves
to the heart (NE) and by epinephrine (E); it is  by
stimulation of the parasympathetic nerves to the heart
• Stroke volume is increased mainly by an  in enddiastolic volume (the Frank-Starling mechanism) and by
an  in contractility due to sympathetic-nerve stimulation
or to epinephrine. Afterload can also play a significant role
in certain situations
Swollen legs
A 47 year old woman was brought to the hospital because of severe
shortness of breath and swelling of her lower body. Over the last year *she
had noticed periods of shortness of breath while doing her housework
(exertional dyspnea). She also had shortness of breath while lying down
(orthopnea). The patient often awoke at night with a sensation of not getting
enough air and she had to sit or stand to obtain relief (paroxysmal nocturnal
dyspnea). #More recently she noticed swelling first of her lower extremities
and then of her lower abdomen. The swelling was
worse through the day and decreased overnight. She reported awakening
three to four times a night to urinate. The patient did not remember any ill
health before these problems began.
Physical examination revealed a woman sitting up in bed in mild to moderate
respiratory distress. Her blood pressure was 100/70, pulse was 120 and weak.
Respirations were 26 per minute and labored. There was jugular venous
distension, even while she was sitting. Palpation of the sternum revealed a
restrosternal lift. Auscultation of the heart revealed an opening snap and a
long diastolic rumble at the apex. Auscultation of the lungs revealed crackles
halfway up the lungs. There was also severe lower extremity edema. During
her hospitalization, as part the work-up, the following studies were done.
O2 consumption(VO2)
Arterial-venous O2 content
difference
Heart rate
Mean Pulmonary Capillary
Wedge Pressure
Right Ventricular Systolic
pressure
End-Diastolic pressure
Right Ventricular End
Diastolic volume
Patient
Normal
188 ml/min
5.3 ml/dl blood
200-250mL/min
3.0-5.0 ml/dl blood
122
25 mm Hg
60-100 beats/min
<15 mmHg
80 mm Hg
16 mm Hg
<28mmHg
<8mmHg
140 ml/m2
60-88mL/m2
•Use the data in the table above to calculate cardiac output and ejection fraction
· Evaluate the mean electrical axis of the heart using the ECG shown overleaf