This document discusses methods of measuring cardiac output. It begins with a brief history noting Adolf Fick first developed a technique for measuring cardiac output in 1870 using what is now called the Fick principle. It then describes several methods including invasive techniques using a pulmonary artery catheter and non-invasive options like echocardiography, esophageal Doppler, and impedance cardiography. The document emphasizes the importance of cardiac output for oxygen delivery and assessing cardiovascular function in critically ill patients.

1. Cardiac Output MeasurementsCardiac Output Measurements
By Yerukneh Solomon
1Prepared by Yerukneh Solomon07/18/17

2. Outlines
General consideration of cardiac output measurement
• Historical perspective cardiac output measurement
• Importance of cardiac output measurement
• Features of an ideal Cardiac Output monitor
• Factors affecting selection of cardiac output monitoring devices
Methods of measuring cardiac output
• Types of cardiac output measurement
cardiac reserve
• Mechanisms of cardiac reserve:Mechanisms of cardiac reserve:
Cardiac index
2Prepared by Yerukneh Solomon07/18/17

3. Adolf Eugen Fick ( 1829 – 1901)
•1855- Introduced a law
of diffusion called Fick’s
law of diffusion
•1870- Was the first one
to develop a technique
for measuring cardiac
output
3Prepared by Yerukneh Solomon07/18/17

4. Cardiac output
•Is volume of blood pumped into the aorta each minute
by the left vetricle .
•It is the determinant of global oxygen transport to the
body
•It reflects the efficiency of cardiovascular system
•There no absolute value for cardiac output
measurement
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5. Cardiac Output Measurement
•AIM : hemodynamic monitoring and support in the
critically ill so as to optimize oxygen delivery to the
tissues
•Oxygen delivery is determined by Cardiac Output
and amount of oxygen carried in the blood
•Allows us to assess the blood flow to the tissues,
and provides information on how to best support
a failing circulation
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6. Why should we measure?
1.The recognition that in many critically ill patients, low
cardiac output leads to significant morbidity and mortality
2.The clinical assessment of cardiac output is unreliable/
inaccurate
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7. When should we monitor?
•High risk critically ill surgical patients in whom
large fluid shifts are expected along with bleeding
and hemodynamic instability
•An important component of goal directed therapy
(GDT), i.e., when a monitor is used in conjunction
with administration of fluids and vasopressors to
achieve set therapeutic endpoints thereby
improving patient care and outcome
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8. Features of an ideal Cardiac Output monitor
•Safe and accurate
•Quick and easy to use both in terms of set-up and
interpretation of information
•Operator independent i.e. the skill of the operator doesn’t
affect the information collected
•Provide continuous measurement
•Reliable during various physiological states07/18/17 Prepared by Yerukneh Solomon 8

9. Methods of measuring cardiac output
Invasive
• Pulmonary Artery Catheter
(Dye, Thermodilution)
Fick Principle
Non-Invasive
I. TEE / Esophageal Doppler
II. Endotracheal Cardiac
Output Monitor (ECOM)
III. Trans Thoracic
Echocardiography (TTE)
IV. impedance Cardiography
(ICG)
Prepared by Yerukneh Solomon 907/18/17

10. Factors affecting selection of cardiac
output monitoring devices
07/18/17 Prepared by Yerukneh Solomon 10

11. Methods of measuring cardiac output
Simple method:
• CO(L/min) = HR(beats /min) x SV(L/beat.)
• SV: volume ejected during each beat , depends on venous
return, can be equal to venous return.
• CO (at rest) = 5-6 L/min.
• HR=72 beats/min , SV=0.07L/min (70ml) .
• CO increases when metabolic need (eg. Exercise), Therefore,
HR or SV or both can increase. 11Prepared by Yerukneh Solomon07/18/17

12. Methods of measuring cardiac output
Fick Principle: “Gold standard”
•Fick Principle relies on the total uptake of a substances
by peripheral tissue is equal to the product of blood
flow to the peripheral tissue and arterial – venous
concentration difference of the substances 12Prepared by Yerukneh Solomon07/18/17

13. 13Prepared by Yerukneh Solomon07/18/17

14. Mixed venous blood is usually obtained
•Through a catheter inserted into:
The brachial vein of the forearm,
Through the subclavian vein,
Down to the right atrium,
The right ventricle or pulmonary artery
Systemic arterial blood can then be obtained from
any systemic artery in the body. 14Prepared by Yerukneh Solomon07/18/17

15. •Fick cardiac outputs are infrequently used because
difficulties in collecting and analyzing exhaled gas
concentration in critically ill patients because may
not have normal VO2 value.
15Prepared by Yerukneh Solomon07/18/17

16. Indicator dilution method
•Based on how fast the flowing blood can dilute the
substances introduced into the circulation
•A known amount of a substance, such as a dye, is injected
into a large systemic vein or, preferably, into the right
atrium.
•The concentration of the dye is recorded as the dye passes
through one of the peripheral arteries, giving a curve
16Prepared by Yerukneh Solomon07/18/17

17. Stewart-Hamilton Equation
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18. Area under the curve is inversely proportion to the
rate of blood flow.
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19. is Thermodilution Method, in which the indicator
used is cold saline.
•Affected by the phase of respiration and should be
measured at the same point of respiratory cycle
•Variations in the speed of cold water injection can
result in altered measurement
19Prepared by Yerukneh Solomon07/18/17

20. Thermodilution: A popular indicator
dilution technique
•A cold solution of D/W 5% or normal saline
(temperature 0°C) is injected into the right atrium from
a proximal catheter port
•This solution causes a decrease in blood temperature
in right heart and flows to the pulmonary artery where
the temperature is measured by a thermistor placed in
the pulmonary artery catheter
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21. 07/18/17 Prepared by Yerukneh Solomon 21

22. •The thermistor records the change in blood
temperature with time and sends this information
to an electronic instrument that records and
displays a temperature-time curve /
Thermodilution curve
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23. 07/18/17 Prepared by Yerukneh Solomon 23

24. • The Cardiac Output can be derived from the Modified
Stewart-Hamilton conservation of heat equation
• CO= V1( Tb- T1) K1
K2
ξ ΔTb (t) dt
Where,
V1= injectate volume in ml
Tb= temperature of pulmonary artery blood
T1= injectate temperature °C
K1
= density factor
K2
= computation constant taking in account the catheter
dead-space and heat exchange in transit ; both
computation constant
Denominator: change in temp and change in time:
corresponds to the area under thermodilution curve
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25. •The degree of change is inversely
proportional to cardiac output
•Temperature change is minimal if there is a
high blood flow but Temperature change high
if blood flow is low
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26. Prepared by Yerukneh Solomon 26
Non Invasive Methods
07/18/17

27. Endotracheal Cardiac Output Monitor
(ECOM)
• ECOM (Con-Med, Irvine, Calif, United States) measures CO
using impedance plethysmography
• Is based on the principle of bio-impedance
• Current is passed through electrodes attached to endotracheal
tube shaft and cuff
• Current is passed from electrode on the shaft of endotracheal
tube and change in impedance secondary to aortic blood flow is
detected by electrode on the cuff07/18/17 Prepared by Yerukneh Solomon 27

28. •An algorithm calculates SV based on impedance
changes and CO can be calculated
•Impedance is affected by aortic blood flow
•Limitations:
•Electro cautery affects its accuracy
•Coronary blood flow is not calculated
•Is still adequately not validated in humans
•Is costly and has not become very popular
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29. Trans Esophageal Echocardiography (TEE) /
Doppler
•A widely used monitor in perioperative setting
•Is an important tool for the assessment of
cardiac structures, filling status and cardiac
contractility
•Aortic pathology can also be detected by TEE
•Doppler technique is used to measure CO by
Simpson’s rule measuring SV multiplied by HR
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30. •Measurement can be done at the level of pulmonary
artery, mitral or aortic valve
•TEE can quantify Cardiac Output more precisely by
measuring both the velocity and the cross-sectional
area of blood flow at appropriate locations in the heart
or great vessels
i.e. Flow = CSA X Velocity
SV= flow X ET ( Systolic Ejection time)
CO=SV X HR
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31. 07/18/17 Prepared by Yerukneh Solomon 31

32. 07/18/17 Prepared by Yerukneh Solomon 32

33. Advantages
• Minimally invasive
• Minimal interference
form bone, lungs and
soft tissue (as seen with
transthoracic route)
• Quickly inserted and
analyzed
• Little training required
• Very few complications
Disadvantages
• May require sedation
• User dependent
• Probe may detect other
vessels e.g. intracardiac,
intrapulmonary
• Contraindicated in
Esophageal Surgeries
• Depends on accurate
probe positioning
Prepared by Yerukneh Solomon 3307/18/17

34. Trans Thoracic Echocardiography (TTE)
•Echocardiography is cardiac ultrasound
•Can be used to estimate Cardiac Output by direct
visualization of the contracting heart in real time
•Gaining acceptance as one of the safest and
most widely used cardiac output monitors in the
critically ill
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35. •Be used to assess cardiac output (intermittently)
•The USCOMTM
device targets the pulmonary and
aortic valves accessed via the parasternal and
suprasternal windows in order to assess cardiac
output completely non-invasively
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36. Advantages
•Non-invasive
•Quick
•Allows for
measurement of the
ventricles,
visualization of the
valves, estimation of
ejection fraction
Disadvantages
 User dependent
 Possible
interference from
bone, lung and
soft tissues
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37. Cardiac reserve
•Cardiac reserve refers to the heart's ability to adjust to
the demands placed upon it.
Cardiac reserve =
[cardiac output during stress - cardiac output at rest.]
•In the normal young adult the resting cardiac output is
about 5-6 L/min and the cardiac reserve is nearly 30
L/min.
37Prepared by Yerukneh Solomon07/18/17

38. Prepared by Yerukneh Solomon
Short term mechanisms Long term mechanisms
Mechanisms of cardiac reserve:Mechanisms of cardiac reserve:
-Rapid onset.
- Increase CO according
to moment to moment
increase in body needs.
-Slow and gradual.
-Occur in cases of prolonged
excess work done by heart
eg: Increased ABP
(hypertension).
3807/18/17

39. Prepared by Yerukneh Solomon
Short term mechanisms:
1. Heart rate (HR) reserve:
The possibility of the increase of heart rate up to 2 – 3 times.
•Heart rate reserve is limited because the increase in heart rate above
180 beats/min causes decrease in the CO.
As this marked increase in the heart rate will be associated with
marked decrease in diastolic period causing:
Decrease in ventricular filling Decrease in coronary blood flow
Decrease in SV and CO Decrease in myocardial contraction
Decrease in CO
3907/18/17

40. 2. Stroke volume reserve:
•Increase in SV causes increase of CO.
•This mechanism is mediated by either:
Increase of the EDV Decrease of the ESV
(EDV reserve) (ESV reserve)
40Prepared by Yerukneh Solomon07/18/17

41. 2.1. EDV reserve:
• Increase of the venous return (as in Ms exercise) increases
EDV  stretch of ventricular muscle fibers
Increases force of contraction of cardiac muscle and
increases SV and CO.(Starling law.)
This mechanism is limited as the marked increase in EDV
causes overstretch of ventricular muscle fibers decreases
force of contraction of cardiac muscle. This will decrease 41Prepared by Yerukneh Solomon07/18/17

42. Prepared by Yerukneh Solomon
 2.2 ESV reserve:
• Increased sympathetic stimulation to the heart increases
the force of cardiac muscle contraction and decreases the
ESV. This will increase SV and CO.
• This mechanism is also limited as the marked decrease in
ESV causes myocardial injury (athletic injury).
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43. Long term mechanisms:
1. Cardiac muscle hypertrophy:
•It is the increase in the size of the individual cardiac muscle
fiber (increase its protein content). This increases the force
of contraction of cardiac muscle increase SV and CO.
•Marked hypertrophy of the myocardium is not
associated with parallel increase in coronary blood flow.
•This cause myocardial ischemia with subsequent
decrease in the force of contraction of cardiac muscle.
This will decrease the SV and CO.
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44. 2. Dilatation of cardiac chambers:
• This mechanism occurs when the blood accumulated
inside the cardiac chambers as in case of heart failure.
• This dilatation of the cardiac chambers causes stretch of
the cardiac muscle fibers Increases its force of
contraction according to Starling law.
• Marked increase in EDV causes overstretch of ventricular
muscle fibers and decreases force of contraction of cardiac
muscle.
• This will decrease the SV and the CO.Prepared by Yerukneh Solomon 4407/18/17

45. •In severe heart failure the cardiac reserve can be
markedly diminished or totally abolished
•The cardiac reserve is affected by a number of
different factors like:
The percentage of fibrosis,
The degree of apoptosis or necrosis and
Presence of auto-antibodies against the β1-
adrenoceptor in the heart.
45Prepared by Yerukneh Solomon07/18/17

46. Cardiac IndexCardiac Index
•Both of these people’s
hearts pump 3 liters of
blood per minute.
•Who feels better?
•The smaller one!
•Why ?
•Less body surface area.
Prepared by Yerukneh Solomon 4607/18/17

47. Cardiac Index
• Is the cardiac output per square meter of body surface area
• Cardiac output is frequently stated in terms of the cardiac
index
• Average human being who weighs 70 kilograms has a body
surface area of about 1.7 square meters, which means that the
normal average cardiac index for adults is about 3 L/min/m2
of
body surface area
07/18/17 Prepared by Yerukneh Solomon 47

48. Variation of Cardiac Index with age07/18/17 Prepared by Yerukneh Solomon 48

49. THANK YOU!!!
Prepared by Yerukneh Solomon 4907/18/17

50. • Ganong’s Review of Medical Physiology - 23rd
Ed
• Medical physiology : a cellular and molecular approach /
[edited by] Walter F. Boron, Emile L. Boulpaep. 2nd
ed.
• Guyton and hall textbook of medical physiology, 13th
edition
• http://heart.bmj.com/content/79/3/289#BIBL
• Chew MS, Aneman A. Haemodynamic monitoring using
arterial waveform analysis. Curr Opin Crit Care.
2013;19:234-41
Prepared by Yerukneh Solomon 5007/18/17