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In some case, the order of the topics and the objectives have been modify
01. Understand the principles underlying cardiac output measurements made using a) The
Fick’s method and b) indicator dilution methods using a Swan-Ganz catheter
Calculate CO by using Fick’s method
02. Understand the concept of “mean systemic pressure”, its normal value, and how various
factors can alter its value.
Construct a vascular function curve. Identify on the curve the normal central venous
pressure and mean circulatory pressure. Predict how the curve is altered by a) changes
in resistance to venous return and b) changes in blood volume or vascular compartment
size.
Define venous return. Understand the concept of “resistance to venous return” and know
that factors determine its value theoretically, what factors are most important in practice,
and how various interventions would change the resistance to venous return.
03. Know how cardiac function (output) curves are generated and how actors which cause
hyper effective or hypo effective changes (contractility) in the heart can alter the shape of
cardiac function curve.
04. Use a combined cardiac output / venous return graph to predict how interventions such as
hemorrhage, increase in preload, acute and chronic heart failure, autonomic stimulation or
ihibition, and exercise will affect cardiac output and right atrial pressure. Predict how
physiological compensatory changes would alter acute changes.
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I. Cardiac output (CO)
Is the volume of blood pumped into the aorta each minute by the left ventricle.
For a 70kg man normal values are HR=70/min and SV=70ml, giving a cardiac output of about
5litre/min. . CO can be increased to 20 l/min depending on the body’s demand for O2.
A. The cardiac index is the cardiac output per square meter of body surface area, normal
2
values range from 2.5-4.0 litre/min/m .
Body surface area normalizes for different shapes, heights and weights. Tables are available
that estimate body surface area from weight and height. An average surface area is 1.73 square
2
meters (m ). Therefore a person with an average cardiac output of 5 l/min would have a Cardiac
2 2
Index of: 5 l/min ÷ 1.73 m = 2.89 l/min/m .
1. Fick’s principle
2. Dye dilution
3. Thermodilution
4. Doppler techniques
Flow can be measured by adding (or removing) a substance to the liquid as it passes through
the tube.
Blood is pumped from the venous system through the lungs to the arterial system. In the lungs,
O2 is taken up into the blood stream. The total uptake of O2 by the lung per minute has to be
equal to the product of the pulmonary blood flow per min. and the difference in O2 concentration
in pulmonary venous and pulmonary arterial blood.
The O2 uptake can be measured by spirometry. Arterial and venous O2 concentrations can be
measured by withdrawing and analyzing blood from both vessels.
Therefore:
Cardiac Output = O2 consumption/min ÷ (aO2 - vO2)
2. Indicator-dilution method
A known quantity of a dye is injected into the right atrium via catheter. A measured quantity of
an indicator (dye) is injected into a large central vein or into the right side of the heart through a
catheter. Arterial blood is continuously drown and passes through a photosensitive device that
measures the dye concentration. The resulting curve measures dye concentration as a function
of time.
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The area under the dye-dilution curve can be calculated and approximates the average
concentration of dye over time. Knowing the quantity of dye injected, the cardiac output can be
determined by:
Cardiac output = Quantity of dye injected ÷ area under the curve
3. Thermo-dilution technique
The procedure is the same, but blood temperature is measured instead of dye color. A cold
dextrose solution (2.5-10 ml) is injected through one part (proximal opening) of a double
lumen catheter which is positioned near right atrium and a small thermistor attached to catheter
tip lies in pulmonary artery and measures the profile of temperature change with time.
The degree of change in the temperature is inversely proportional to the cardiac output. Then:
Plotting this temperature change against the time it took for the cooler fluid to reach the
thermistor gives us a thermo dilution curve, a computer built into the monitor calculates and
integrates the area under the thermo dilution curve, and gives a digital readout of the cardiac
output in L/min
4. Doppler techniques
Is a non-invasive technique. The machines transmit an ultrasonic vibration into the body and
record the change in the frequency of the signal that is reflected off the red blood cells, so
Doppler techniques measure velocity, not flow. The flow could be obtained by integrating the
signal over the cross-sectional area of the vessel.
The velocity of blood in the ascending aorta may be measured using the Doppler effect. The
length of a column of blood passing through the aorta in unit time is estimated and then
multiplied by the cross-sectional area of the aorta to give stroke volume.
The central venous pressure (CVP) measures the filling pressure of the right ventricular (RV); it
gives an estimate of the intravascular volume status and is an interplay of the (1) circulating
blood volume (2) venous tone and (3) right ventricular function.
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A. Waveforms in CVP
The normal CVP waveform consists of three upwards deflections (a, c, & v waves) and two
downward defections (x and y descents). These waves are produced as follows:
1. The ‘a’ wave is produced by right atrial contraction and occurs just after the P wave on the
ECG.
2. The ‘c’ wave occurs due to isovolumic ventricular contraction forcing the tricuspid valve to
bulge upward into the right atrium. (RA)
3. The pressure within the RA then decreases as the tricuspid valve is pulled away from the
atrium during right ventricular ejection, forming the X descent.
4. The RA continues to fill during late ventricular systole, forming the V wave.
5. The Y descent occurs when the tricuspid valve opens and blood from the RA empties rapidly
into the RV during early diastole.(1
The pulmonary artery catheter (PAC) help to monitoring the pulmonary artery (PA) pressure,
pulmonary capillary wedge pressure (PCWP) as well as central venous pressure (CVP).
The PCWP under most circumstances provides an accurate estimate of the diastolic filling
(preload) of the left heart.
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C. Factors that influence RAP:
Atrial contraction
Intrapleural pressure
Posture
Blood volume
Intrinsic venous tone
Sympathetic neural tone to veins
Venous pump (exercise
Over time cardiac output and venous return must be equal for each ventricle, although transient
differences can occur. Changes in posture, such as lying down, can briefly increase venous
return. The resulting change in the preload should increase cardiac output. But the vascular
system is a closed circuit, blood pumped from the heart returns to the heart, therefore, venous
return must equal cardiac output over time.
CO = HR x SV
A. Heart rate: is determined by the rate of spontaneous depolarization at the sinoatrial node
and is modified by the autonomic nervous system. The vagus nerve acts on muscarinic
receptors to slow the heart, whereas the cardiac sympathetic fibers stimulate beta-adrenergic
receptors and increase heart rate.
As the EDV (end-diastolic volume) increases and stretches the muscle fiber, the energy of
contraction and stroke volume increase, until a point of over-stretching when stroke volume may
actually decrease, as in the failing heart. Cardiac output will also increase or decrease in
parallel with stroke volume if there is no change in heart rate.
2. Afterload: is the resistance to ventricular ejection. This is caused by the resistance to flow
in the systemic circulation and is the systemic vascular resistance. The resistance is determined
by the diameter of the arterioles and pre-capillary sphincters; the narrower or more constricted,
the higher the resistance. The level of systemic vascular resistance (total peripheral resistance
TPR) is controlled by the sympathetic system which controls the tone of the muscle in the wall
of the arteriole, and hence the diameter.
3. Contractility describes the ability of the myocardium to contract in the absence of any
changes in preload or afterload. In other words, it is the "power" of the cardiac muscle. The
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most important influence on contractility is the sympathetic nervous system. Norepinephrine
stimulate Beta-1 adrenergic receptors, and contractility increases.
State the relationship of right atrial pressure (RAP) and venous return (VR). When graphed the
independent variable is the CO, and the dependent variable is the CVP.
1. Is the systemic filling pressure . This is the difference between peripheral venous
pressure and right atrial pressure (Right atrial pressure is typically ~ 2 mmHg with a mean
systemic filling pressure of 7 mmHg. At this pressure difference (7 - 2) and the low resistance of
the venous system, venous return is approximately 5 l/min.
2. Blood transfusion or retention of salt and water results in an increase of Pcm, then would
increase the pressure difference and increase venous return
Hemorrhage would reduce peripheral venous pressure and reduce venous return for a given
right atrial pressure.
The vascular function curves by effect of changing circulatory volume are parallel to each other.
This principle illustrates the relationship between cardiac output (CO) and left ventricular end
diastolic volume (LVEDV), or the relationship between
stroke volume and right atrial pressure.
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An increase in preload (going from point A to B or from
C to D in the graph at the right) will increase the
cardiac output until very high end diastolic volumes are
reached. At this point cardiac output will not increase
with any further increase in preload, and may even
decrease after a certain preload is reached.
B. Change in contractility
Any increase or decrease in the contractility of the
cardiac muscle for a given end diastolic volume will act
to shift the curve up or down, respectively. (see graph
at the left)The curves show how the heart performs at
different states of contractility, ranging from the normal
heart to one in cardiogenic shock. This is a condition
where the heart is so damaged by disease that cardiac
output is unable to maintain tissue perfusion. Also
shown are increasing levels of physical activity which
require a corresponding increase
D. Afterload
Relationship
between stroke volume and afterload. A series of curves
illustrates the effects of increasing afterload on systemic
vascular resistance.
Simultaneous plots of cardiac output and venous return as a function of end diastolic volume (or
right atrial pressure.
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D. Equilibrium point:
This is the steady-state where the two curves intersect; it reflects the point where cardiac output
is equal to venous return.
1. Inotropic Changes:
b. Negative inotropic agents have the opposite effect, decreasing contractility and CO, and
increasing RAP.
Changes: TPR is determined by the resistance of the arterioles. Changes in TPR will change
the slope of both the cardiac function curve and the venous return curve.
a. An increase in TPR (left side
graph) will cause blood to be
retained on the arterial side of
circulation and will increase the
aortic pressure against which the
heart must pump.
This will act to shift both slopes
downward. As a result of this
simultaneous change, both the
cardiac output and the venous return
are decreased, however the right
atrial pressure remains the same .
3. Exercise.
Cardiac output will change to match changing metabolic demands of the body. The outputs of
both ventricles must be identical, and also equal the venous return of blood from the body.
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During exercise the cardiac output and venous return are balanced. Blood vessels dilate in
exercising muscle groups because of increased metabolism, and blood flow increases. This
increases venous return and right ventricular preload.
More blood is delivered to the left ventricle and cardiac output increases.
Associated with exercise there is an increase in sympathetic activity that will lead to an
increased contractility and heart rate, further increasing cardiac output to meet tissue
requirements.
A. Changes in HR alters:
B. Graph analysis
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X. CONGESTIVE HEART FAILURE
A. Definition:
Fatigue
Low exercise tolerance
Venous congestion and edema
Dyspnea
Reduced ejection fraction
E. Compensations
F. Causes of hypertrophy/failure
1. Pressure overload causes concentric hypertrophy where the ventricle remodels inwardly
causing low lumen volume and thick wall. Caused by hypertension or outflow track
obstruction.
2. Volume overload leads to eccentric hypertrophy. The heart remodels outwardly to give a
large lumen volume and a thin wall. Caused by regurgitant aortic valve or AV fistulas.
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