Cardiac Output and Venous Return
Learning objectives
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Define Cardiac Output and Venous Return.
Define the factors that affect cardiac output.
Explain how alteration in (preload,contractility,afterload) change the cardiac
output.
Describe the effects of changing total peripheral resistance on cardiac output.
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.
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
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
14-14
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:
– End diastolic volume (EDV) = volume of blood in
ventricles at end of diastole
– Total peripheral resistance (TPR) = impedance to blood
flow in arteries
– Contractility = strength of ventricular contraction
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Regulation of Stroke Volume
• EDV is workload (preload) on heart prior to
contraction
– SV is directly proportional to preload &
contractility
• Strength of contraction varies directly with
EDV
• Total peripheral resistance = afterload which
impedes ejection from ventricle
– SV is inversely proportional to TPR
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)
Venous Return
• Is return of blood to
heart via veins
• Controls EDV & thus SV
& CO
• Dependent on:
– Blood volume & venous
pressure
– Vasoconstriction caused
by Symp
– Skeletal muscle pumps
– Pressure drop during
inhalation
Fig 14.7
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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
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 preload effect can be explained on the
basis of a change in sarcomere length
Frank-Starling Law of the Heart
• States that strength
of ventricular
contraction varies
directly with EDV
– Is an intrinsic
property of
myocardium
– As EDV increases,
myocardium is
stretched more,
causing greater
contraction & SV
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• 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.
The contractility factor in systolic
performance (inotropic state)
• Contractility is the change in systolic
performance at a given preload.
• Contractility is a change in the force of
contraction at any given sarcomere length.
• Acute changes in contractility are due to
changes in the intracellular dynamics of
calcium.
Indices of contractility
–dp/dt (change in pressure vs.
change in time) = rate of pressure
development during isovolumetric
contraction.
–ejection fraction (stroke
volume/end-diastolic volume)
Effects of increased contractility
• Both an increased preload and an increased
contractility will be accompanied by an
increased peak left ventricular pressure, but
only with an increase in contractility will there
be a decrease in the systolic interval.
Regulation of stroke volume
3 Contractility (Inotropic state)
Independence of preload and contractility
Preload and Contraction in acute situation
• In summary,
A → B increased performance due entirely to
preload
A → C increased performance due entirely to
contractility
A → D increased performance due to an
increase in both preload and contractility
Regulation of stroke volume
• 3 Afterload –
• It is the load on the muscle during contraction
• It represents the force that the muscle must
generate to eject the blood into the aorta
Indices of afterload
• An approximation for the left ventricle is
aortic diastolic pressure, which is primarily
determined by the resistance of the arterioles
(TPR).
• Other acceptable indices of afterload on the
left ventricle are the following:
a. Mean aortic pressure
b. Peak left ventricular pressure
Regulation of stroke volume
2 Afterload
• Usually measured as arterial pressure
• ↑PR → ↑BP → ↑Afterload → ↓CO
• ↓PR → ↓BP → ↓Afterload → ↑CO
CHRONIC INCREASE IN AFTERLOAD
Systolic dysfunction
Diastolic dysfunction
• An abnormal reduction
in ventricular emptying
due to impaired
contractility or
excessive afterload.
• Decrease in ventricular
compliance during the
filling phase of the
cardiac cycle due to
either changes in tissue
stiffness or impaired
ventricular relaxation.
• The consequence is a
diminished FrankStarling mechanism
An increase in afterload can be due to a pressure
or a volume overload.
Pressure Overload
1. Hypertension and aortic stenosis
2. Initially, increased performance due to
(increased contractility); no decrease in CO
3. Chronically, in an attempt to normalize wall
tension (actually internal wall stress), the
ventricle develops a concentric hypertrophy.
There is a dramatic increase in wall thickness
and a decrease in chamber diameter.
• The consequence of concentric hypertrophy
(new sarcomes laid down in parallel, i.e., the
myofibril thickens)
• is a decrease in ventricular compliance and
diastolic dysfunction,
• followed eventually by a systolic dysfunction
and ventricular failure.
Volume Overload
• mitral and aortic insufficiency, patent ductus
arteriosus.
• Chronically, in an attempt to normalize wall
tension (actually internal wall stress), the
ventricle develops an eccentric hypertrophy
(new sarcomeres laid down end-to-end, i.e.,
the myofibril lengthens. All cardiac volumes
increase.)
• There is a modest increase in wall thickness
that does not reduce chamber size.
• Compliance of the ventricle is not
compromised and diastolic function is
maintained.
• Eventual failure is usually a consequence of
systolic dysfunction
Effect of Various Conditions on
Cardiac Output.
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
The cardiac function (cardiac output) curve
• A cardiac function curve is generated by
keeping contractility constant and following
ventricular performance as preload increases.
• depicts the Frank-Starling relationship for the
ventricle.
• shows that cardiac output is a function of enddiastolic volume.
The preload dependence of Cardiac output is defined by cardiac function curve
• Starting at N, which represents a normal,
resting individual:
• A = decreased performance due to a
reduction in preload
• B = increased performance due to an
increased preload
• C represents an increased performance due
almost entirely to increased contractility (close
to the situation during exercise)
• Points C, D, and E represent different levels of
performance due to changes in preload only;
all three points have the same contractility.
Q
• Haemorrhage and volume overload: how
does it affects preload , performance and
contractility?
• Vector I: consequences of a loss in preload,
e.g., hemorrhage, venodilators (nitro-glycerin)
• Vector II: consequences of a loss in
contractility, e.g., congestive heart failure
• Vector III: consequences of an acute increase
in contractility
• Vector IV: consequences of an acute increase
in preload, e.g., volume loading the individual
going from the upright to the supine position
Vascular function curves
• Defines the changes in central venous
pressure that are caused by changes in cardiac
output.
• The vascular function (venous return) curve
depicts the relationship between blood flow
through the vascular system (or venous
return) and right atrial pressure.
cardiac failure
• What parameter is reduced in cardiac failure?
cardiac contractility
• How the kidneys are involved in the
compensatory mechanism to cardiac failure.
Sympathetic NS acts on Beta-1 cells in the
kidney to release renin secretion. This
increases blood volume and induces
venoconstriction.
• Q. How does cardiac failure affect CO and
RAP?
slight fall in CO
Increase RAP
Use the diagram below to answer the following three questions. The point marked control
represents the state of the cardiovascular system in the resting state.
An increase in total peripheral resistance and contractility is repre-sented by a shift from the resting
state to point