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Cardiac output

Cardiac output (Q) is the volume of blood being pumped by the heart, in particul
ar by a Left or Right ventricle in the Time interval of one minute. CO may be me
asured in many ways, for example dm3/min (1 dm3 equals 1000 cm3 or 1 litre). Q i
s furthermore the combined sum of output from the right ventricle and the output
from the left ventricle during the phase of Systole of the heart. An average ca
rdiac output would be 5 L/min for a human male and 4.5 L/min for a female.[citat
ion needed]
Q=Stroke Volume × Heart rate
Contents
1 Clinical uses
2 Measuring cardiac output
2.1 The Fick Principle
2.2 Finapres Methodology - BMEYE Nexfin Monitor
2.3 Dilution methods
2.4 Ultrasound Dilution method
2.5 Pulmonary Artery Thermodilution (Trans-right-heart Thermodilution)
2.6 Doppler ultrasound method
2.6.1 Echocardiography
2.6.2 Transcutaneous Doppler: USCOM
2.6.3 Transoesophageal Doppler: TOD
2.7 Pulse Pressure Methods
2.7.1 Non-invasive PP – Sphygmomanometry and Tonometry
2.7.2 Invasive PP
2.7.2.1 Calibrated PP – PiCCO, LiDCO
2.7.2.2 Uncalibrated PP — FloTrac
2.7.2.3 Uncalibrated, pre-estimed demographic data-free — PRAM
2.8 Impedance cardiography – BioZ-NICCOMO
2.9 Electrical Cardiometry
2.10 Magnetic Resonance Imaging
3 Cardiac Output and Vascular Resistance
4 Cardiac Output and Respiration
5 Combined cardiac output
6 Example values
7 External links
8 References
Clinical uses
The function of the heart is to transport the blood to deliver oxygen, nutrients
and chemicals to the cells of the body to ensure their survival and proper func
tion and to remove the cellular wastes. Q indicates how well the heart is perfor
ming this function. Q is regulated principally by the demand for oxygen by the c
ells of the body. If the cells are working hard, with a high metabolic oxygen de
mand then the Q is raised to increase the supply of oxygen to the cells, while a
t rest when the cellular demand is low, the Q is said to be baseline. Q is regul
ated not only by the heart as it pumps, but also by the function of the vessels
of the body as they actively relax and contract thereby increasing and decreasin
g the resistance to flow.
When Q increases in a healthy but untrained individual, most of the increase can
be attributed to an increase in heart rate (HR). Change of posture, increased s
ympathetic nervous system activity, and decreased parasympathetic nervous system
activity can also increase cardiac output. HR can vary by a factor of approxima
tely 3, between 60 and 180 beats per minute, while stroke volume (SV) can vary b
etween 70 and 120 ml, a factor of only 1.7.[1][2][3]
A parameter related to SV is Ejection Fraction (EF). EF is the fraction of blood
ejected by the Left Ventricle (LV) during the contraction or ejection phase of
the cardiac cycle or Systole. Prior to the start of Systole, the LV is filled wi
th blood to the capacity known as End Diastolic Volume (EDV) during the filling
phase or diastole. During Systole, the LV contracts and ejects blood until it re
aches its minimum capacity known as End Systolic Volume (ESV), it does not empty
completely. Clearly the EF is dependent on the ventricular EDV which may vary w
ith ventricular disease associated with ventricular dilatation. Even with LV dil
atation and impaired contraction the Q may remain constant due to an increase in
EDV.
Stroke Volume (SV) = EDV – ESV
Ejection Fraction (EF) = (SV / EDV) × 100%
Cardiac Output (Q) = SV × HR
Cardiac Index (CI) = Q / Body Surface Area (BSA) = SV × HR/BSA
HR is Heart Rate, expressed as BPM (Beats Per Minute)
BSA is Body Surface Area in square metres.
Diseases of the cardiovascular system are often associated with changes in Q, pa
rticularly the pandemic diseases of hypertension and heart failure. Cardiovascul
ar disease can be associated with increased Q as occurs during infection and sep
sis, or decreased Q, as in cardiomyopathy and heart failure. The ability to accu
rately measure Q is important in clinical medicine as it provides for improved d
iagnosis of abnormalities, and can be used to guide appropriate management. Q me
asurement, if it were accurate and non-invasive, would be adopted as part of eve
ry clinical examination from general observations to the intensive care ward, an
d would be as common as simple blood pressure measurements are now. Such practic
e, if it were adopted, may revolutionise the treatment of many cardiovascular di
seases including hypertension and heart failure. This is the reason why Q measur
ement is now an important research and clinical focus in cardiovascular medicine
.
Measuring cardiac output
Circulation is a critical and variable function of human physiology and disease.
An accurate and non-invasive measurement of Q is the holy grail of cardiovascul
ar assessment. This would allow continuous monitoring of central circulation and
provide improved insights into normal physiology, pathophysiology and treatment
s for disease. Invasive methods are well accepted, but there is increasing evide
nce that these methods are neither accurate nor effective in guiding therapy, so
there is an increasing focus on development of non-invasive methods.[4][5][6]
There are a number of clinical methods for measurement of Q ranging from direct
intracardiac catheterisation to non-invasive measurement of the arterial pulse.
Each method has unique strengths and weaknesses and relative comparison is limit
ed by the absence of a widely accepted “gold standard” measurement. Q can also be af
fected significantly by the phase of respiration; intra-thoracic pressure change
s influence diastolic filling and therefore Q. This is especially important duri
ng mechanical ventilation where Q can vary by up to 50% across a single respirat
ory cycle. Q should therefore be measured at evenly spaced points over a single
cycle or averaged over several cycles.
The Fick Principle
The Fick principle was first described by Adolf Eugen Fick in 1870 and assumes t
hat the rate at which oxygen is consumed is a function of the rate of blood flow
s and the rate of oxygen picked up by the red blood cells. The Fick principle in
volves calculating the oxygen consumed over a given period of time from measurem
ent of the oxygen concentration of the venous blood and the arterial blood. Q ca
n be calculated from these measurements:
VO2 consumption per minute using a spirometer (with the subject re-breathing air
) and a CO2 absorber
the oxygen content of blood taken from the pulmonary artery (representing mixed
venous blood)
the oxygen content of blood from a cannula in a peripheral artery (representing
arterial blood)
From these values, we know that:
VO2 = (Q×CA) - (Q×CV)
where
CA = Oxygen content of arterial blood
CV = Oxygen content of venous blood.
This allows us to say
Q = (VO2/[CA - CV])*100
and therefore calculate Q. While considered to be the most accurate method for Q
measurement, Fick is invasive, requires time for the sample analysis, and accur
ate oxygen consumption samples are difficult to acquire. There have also been mo
difications to the Fick method where respiratory oxygen content is measured as p
art of a closed system and the consumed Oxygen calculated using an assumed oxyge
n consumption index which is then used to calculate Q. Other modifications use i
nert gas as tracers and measure the change in inspired and expired gas concentra
tions to calculate Q (Innacor, Innovision A/S, Denmark).
Additionally, the calculation of the arterial and venous oxygen content of the b
lood is a straightforward process. Almost all oxygen in the blood is bound to he
moglobin molecules in the red blood cells. Measuring the content of hemoglobin i
n the blood and the percentage of saturation of hemoglobin (the oxygen saturatio
n of the blood) is a simple process and is readily available to physicians. Usin
g the fact that each gram of hemoglobin can carry 1.34 ml of O2, the oxygen cont
ent of the blood (either arterial or venous) can be estimated by the following f
ormula:
Finapres Methodology - BMEYE Nexfin Monitor
In 1967 the Czech physiologist Jan Peñáz invented and patented the volume clamp meth
od to measure continuous blood pressure. The principle of the volume clamp metho
d is to provide equal pressures dynamically on either side of the wall of an art
ery: inside pressure (= intra-arterial pressure) equals outside pressure (= fing
er cuff pressure) by clamping the artery to a certain volume. He decided that th
e finger was the optimal site to apply this volume clamp method.
In 1978 scientists at BMI-TNO, the research unit of Netherlands Organization for
Applied Scientific Research at The University of Amsterdam, invented and patent
ed a series of additional key elements to make the volume clamp work in clinical
practice, among them: the use of modulated infra-red light in the optical syste
m inside the sensor, the light-weight, easy to wrap finger cuff with Velcro fixa
tion, a new pneumatic proportional control valve principle and last but not leas
t the invention of a setpoint strategy for the determination and tracking of the
correct volume at which to clamp the finger arteries – the Physiocal system. An a
cronym for PHYSIOlogical CALibration of the finger arteries, this Physiocal trac
ker turned out to be surprisingly accurate, robust and reliable and was never ch
anged since its invention.
The Finapres methodology was developed to use this information to accurately cal
culate arterial pressure from the finger cuff pressure data. A generalized algor
ithm to correct for the pressure level difference between the finger and brachia
l sites within an individual patient was developed and this correction worked un
der all circumstances that it was tested, even when it was not designed for it,
since it applied general physiological principles. The first implementation of t
his innovative brachial pressure waveform reconstruction was in the Finometer, t
he successor of Finapres that BMI-TNO introduced in the market in 2000.
The availability of a continuous, high-fidelity, calibrated blood pressure wavef
orm opened up the perspective of beat-to-beat computation of integrated hemodyna
mics, based on two notions: 1. That pressure and flow are inter-related at each
site in the arterial system by their so-called characteristic impedance and 2. T
hat at the proximal aortic site, the 3-element Windkessel model of this impedanc
e can be modeled with sufficient accuracy in an individual patient when age, gen
der, height and weight are known.
For the next generation Finapres, Nexfin, researchers developed a pulse contour
method, CO-TREK, that uses the measured systolic pressure-time integral and the
heart’s afterload determined from the Windkessel model to calculate CO. As a resul
t, the Nexfin CO-TREK confidence interval in estimating the initial mean level o
f CO is +/- 15-18% (SD) which gives it about the same (in-) accuracy as a standa
rd single thermodilution (TD) with a pulmonary artery catheter. This third gener
ation CO method is only available in BMEYE’s Nexfin monitor. The Nexfin developmen
t was started in April 2005, and the Nexfin monitor obtained CE mark in June 200
7 and was approved by the FDA in December 2007 for the US market.
Dilution methods
This method was initially described using an indicator dye and assumes that the
rate at which the indicator is diluted reflects the Q. The method measures the c
oncentration of a dye at different points in the circulation, usually from an in
travenous injection and then at a downstream sampling site, usually in a systemi
c artery. More specifically, the Q is equal to the quantity of indicator dye inj
ected divided by the area under the dilution curve measured downstream (the Stew
art (1897)-Hamilton (1932) equation):
The trapezoid rule is often used as an approximation of this integral.
Ultrasound Dilution method
Ultrasound Dilution method was firstly introduced in 1995.[7], and it was used e
xtensively to measure flow and volumes with extracorporeal circuits condition su
ch as ECMO[8][9] and Hemodialysis[10][11], leading more than 150 peer reviewed p
ublications, and now it has adapted to Intensive Care Units (ICU) settings as CO
status (Transonic System Inc. Ithaca, NY).
COstatus uses body temperature normal saline (NS) as an indicator to measure car
diac output, plus a group of important hemodynamic Blood Volumes (BV) variables,
such as total end-diastole volume (TEDV), central blood volume (CBV) and active
circulation volume (ACVI).
COstatus technology is based on ultrasound indicator dilution[12]. Blood ultraso
und velocity (1560–1585 m/s) is a function of total blood protein concentration (s
ums of proteins in plasma and in red blood red cells), temperature etc. Injectio
n of body temperature normal saline (ultrasound velocity of saline is 1533m/sec)
into a unique AV loop decreases blood ultrasound velocity, and produce dilution
curves.
COstatus establishes an extracorporeal circulation through its unique AV loop wi
th two preexisting arterial and central venous lines in ICU patients. When the s
aline indicator is injected into the A-V loop, it is detected by the venous clam
p-on sensor on the AV loop before it enters the patient’s right heart atrium. Afte
r the indicator traverses the heart and lung, the concentration curve in the art
erial line is recorded and displayed on the COstatus HCM101 Monitor. Cardiac out
put is calculated from the area of the concentration curve by the classic Stewar
t-Hamilton equation. It is a non-invasive procedure only by connection the AV lo
op and two lines of a patient. There lacks general methods to measure cardiac ou
tput in pediatric ICU patients, COstatus has been demonstrated to be a safe and
reproducible tool.
Pulmonary Artery Thermodilution (Trans-right-heart Thermodilution)
The indicator method was further developed with replacement of the indicator dye
by heated or cooled fluid and temperature change measured at different sites in
the circulation rather than dye concentration; this method is known as thermodi
lution. The pulmonary artery catheter (PAC), also known as the Swan-Ganz cathete
r, was introduced to clinical practice in 1970 and provides direct access to the
right heart for thermodilution measurements.
The PAC is balloon tipped and is inflated, which helps "sail" the catheter ballo
on through the right ventricle to occlude a smaller branch of the pulmonary arte
ry system. The balloon is deflated. The PAC thermodilution method involves injec
tion of a small amount (10ml) of cold glucose at a known temperature into the pu
lmonary artery and measuring the temperature a known distance away (6–10 cm) using
the same catheter.
The Q can be calculated from the measured temperature curve (The “thermodilution c
urve”). High Q will change the temperature rapidly, and low Q will change the temp
erature slowly. Usually three or four repeated measures are averaged to improve
accuracy. However it is complex to perform and there are many sources of inaccur
acy in the method.[13][14] Modern catheters are fitted with a heating filament w
hich intermittently heats and measures the thermodilution curve providing serial
Q measurement. However, these take an average of measurements made over 2–9 minut
es, depending on the stability of the circulation, and thus do not provide conti
nuous monitoring.
PAC use is complicated by arrhythmias, infection, pulmonary artery rupture, and
right heart valve damage. Recent studies in patients with critical illness, seps
is, acute respiratory failure and heart failure suggest use of the PAC does not
improve patient outcomes.[4][5][6] PAC use is in decline as clinicians move to l
ess invasive technologies for monitoring hemodynamics.
Doppler ultrasound method
This method uses ultrasound and the Doppler effect to measure Q. The blood veloc
ity through the heart causes a Doppler shift in the frequency of the returning
ultrasound waves. This Doppler shift can then be used to calculate flow velocit
y and volume and effectively Q using the following equations:
Q = SV × HR
SV = vti × CSA
where:
CSA = valve orifice cross sectional area; use pr²
r = valve radius
vti = the velocity time integral of the trace of the Doppler flow profile
Doppler ultrasound is non-invasive, accurate and inexpensive and is a routine pa
rt of clinical ultrasound with high levels of reliability and reproducibility ha
ving been in clinical use since the 1960s.
Echocardiography
Echocardiography uses a conventional ultrasound machine and a combined two dimen
sional (2D) and Doppler approach to measure Q. 2D measurement of the diameter (d
) of the aortic annulus allows calculation of the flow CSA (cross-sectional area
) which is then multiplied by the vti of the Doppler flow profile across the aor
tic valve to determine the flow volume or SV. Multiplying SV by HR produces Q. E
chocardiographic measurement of flow volume is clinically well established and o
f proven accuracy but requires training and skill, and may be time consuming to
perform effectively. The 2D measurement of the aortic valve diameter is challeng
ing and associated with significant error, while measurement of the pulmonary va
lve to calculate right sided Q is even more difficult.
Transcutaneous Doppler: USCOM
An Ultrasonic Cardiac Output Monitor (USCOM) (Uscom Ltd, Sydney, Australia) uses
Continuous Wave Doppler (CW) to measure the Doppler flow profile vti, as in ech
ocardiography, but uses anthropometry to calculate aortic and pulmonary valve di
ameters so both the right and left sided Q can be measured. Real time Automatic
tracing of the Doppler flow profile allows for beat to beat right and left sided
Q measurement. This single method has been used in neonates, children and adult
s for low and high Q measurement.
Transoesophageal Doppler: TOD
Transoesophageal Doppler (TOD), also known as esophageal Doppler monitor (EDM),
supports a CW sensor on the end of a probe which can be introduced via the mouth
or nose and positioned in the oesophagus so the Doppler beam aligns with the de
scending thoracic aorta (DTA) at a known angle. Because the transducer is close
to the blood flow the signal is clear, however correct alignment may be difficul
t to maintain, especially during patient movement. This method has good validati
on, particularly for measuring changes in blood flow. As it only measures DTA fl
ow and not true Q, it may be potentially influenced by disproportionate changes
in blood flow between upper and lower body though this does not appear to be pro
blematic in most clinical situations. This method generally requires patient sed
ation and is accepted for use in both adults and children.
Pulse Pressure Methods
Pulse Pressure (PP) methods measure the pressure in an artery over time to deriv
e a waveform and use this information to calculate cardiac performance. The prob
lem is that any measure from the artery includes the changes in pressure associa
ted with changes in arterial function (compliance, impedance, etc..).
Physiologic or therapeutic changes in vessel diameter are assumed to reflect cha
nges in Q. Put simply, PP methods measure the combined performance of the heart
and the vessels thus limiting the application of PP methods for measurement of Q
. This can be partially compensated for by intermittent calibration of the wavef
orm to another Q measurement method and then monitoring the PP waveform. Ideally
, the PP waveform should be calibrated on a beat to beat basis.
There are invasive and non-invasive methods of measuring PP:
Non-invasive PP – Sphygmomanometry and Tonometry
The sphygmomanometer or cuff blood pressure device was introduced to clinical pr
actice in 1903 allowing non-invasive measurements of blood pressure and providin
g the common PP waveform values of peak systolic and diastolic pressure which ca
n be used to calculate mean arterial pressure (MAP). The pressure in the arterie
s, measured by sphygmomanometry, is often used as a guide to the function of the
heart. Put simply, the pressure in the heart is conducted to the arteries, so t
he arterial pressure approximately reflects the function of the heart or the Q.
The pressure in the heart rises as blood is forced into the aorta
The more stretched the aorta, the greater the pulse pressure (PP)
In healthy young subjects, each additional 2 ml of blood results in a 1 mmHg ris
e in pressure
Therefore:
SV = 2 ml × Pulse Pressure
Q = 2 ml × Pulse Pressure × HR
By resting a more sophisticated pressure sensing device, a tonometer, against th
e skin surface and sensing the pulsatile artery, continuous PP wave forms can be
acquired non-invasively and analysis made of these pressure signals. Unfortunat
ely the heart and vessels can function independently and sometimes paradoxically
so that changes in the PP may both reflect and mask changes in Q. So these meas
ures represent combined cardiac and vascular function only. Another similar syst
em that uses the arterial pulse is the pressure recording analytical method (PRA
M).
Invasive PP
Invasive PP involves inserting a manometer (pressure sensor) into an artery, usu
ally the radial or femoral artery and continuously measuring the PP waveform. Th
is is usually done by connecting the catheter to a signal processing and display
device. The PP waveform can then be analysed to provide measurements of cardiov
ascular performance. Changes in vascular function, the position of the catheter
tip, or damping of the pressure waveform signal will all affect the accuracy of
the readings. Invasive PP measurements can be calibrated or uncalibrated.
Calibrated PP – PiCCO, LiDCO
PiCCO (PULSION Medical Systems AG, Munich, Germany) and PulseCO (LiDCO Ltd, Lond
on, England) generate continuous Q by analysis of the arterial PP waveform. In b
oth cases, an independent technique is required to provide calibration of the co
ntinuous Q analysis, as arterial PP analysis cannot account for unmeasured varia
bles such as the changing compliance of the vascular bed. Recalibration is recom
mended after changes in patient position, therapy or condition.
In the case of PiCCO, transpulmonary thermodilution is used as the calibrating t
echnique. Transpulmonary thermodilution uses the Stewart-Hamilton principle, but
measures temperatures changes from central venous line to a central arterial li
ne (i.e. femoral or axillary) arterial line. The Q derived from this cold-saline
thermodilution is used to calibrate the arterial PP contour, which can then pro
vide continuous Q monitoring. The PiCCO algorithm is dependent on blood pressure
waveform morphology (i.e. mathematical analysis of the PP waveform) and calcula
tes continuous Q as described by Wesseling and co-workers.[15] Transpulmonary th
ermodilution spans right heart, pulmonary circulation and left heart; this allow
s further mathematical analysis of the thermodilution curve, giving measurements
of cardiac filling volumes (GEDV), intrathoracic blood volume, and extravascula
r lung water. While transpulmonary thermodilution allows for less invasive Q cal
ibration, the method is also less accurate than PA thermodilution and still requ
ires a central venous and arterial line with the attendant infection risks.
In the case of LiDCO, the independent calibration technique is lithium dilution,
again using the Stewart-Hamilton principle. Lithium dilution uses a peripheral
vein to a peripheral arterial line; however, it does not provide information on
cardiac filling volumes and extravascular lung water. Calibration measurements c
annot be performed too frequently, and can be subject to error in the presence o
f certain muscle relaxants. The PulseCO algorithm used by LiDCO is based on puls
e power derivation and is not dependent on waveform morphology.
Uncalibrated PP — FloTrac
This technology involves inserting a manometer tipped arterial catheter into the
mid flow portion of an artery, usually radial or femoral, and then by time doma
in sampling converts the arterial PP to Q. While this method involves one less l
ine than the calibrated PP Q systems, it remains uncalibrated and so is only mea
suring arterial PP invasively. While it estimates upstream Q, any independent ch
anges in Q and SVR cannot be detected by this method. However, SVR can be comput
ed if there is a central line in place and those values are slaved into the moni
tor. Its accuracy and ability to follow trends is however open to question as ma
ny studies show poor agreement against comparator techniques.
Uncalibrated, pre-estimed demographic data-free — PRAM
Pressure Recording Analytical Method (PRAM), exclusively available in MostCare d
evice (Vytech, Padova, Italy) estimates Q just from the analysis of the pressure
wave profile, mininvasively obtained from an arterial catheter (choice of radia
l or femoral access); thanks to Physic Perturbation theory application to the ph
ysiology issue, all the elements determining Q can be simultaneously and beat-to
-beat taken in consideration. Uniquely sampled at 1000Hz, the detected pressure
curve is so precise to be effectively submitted to an equally sophisticated anal
ysis; the result is the calculation of the real (relative to the patient under e
xamination) and actual (beat-to-beat) Stroke Volume; no constant value of impeda
nce, deriving from an external calibration neither form pre-estimated in vivo/in
vitro data are needed.
PRAM has been validated against the considered gold standard methods in stable c
ondition[16] and in various hemodynamic states[17]; it can be used to monitor pe
diatric[18] and mechanically supported[19] patients.
A part to generally monitored hemodynamic values and to fluid responsiveness par
ameters, an exclusive reference is also provided by PRAM: Cardiac Cycle Efficien
cy (CCE). Expressed by a pure number ranging from 1 (the best) and -1 (the worse
) it indicates the overall heart-vascular response coupling; the ratio between t
he heart performed and consumed energy, represented as CCE “stress index”, can be of
paramount importance in understanding patient present and next future course[20
].
Impedance cardiography – BioZ-NICCOMO
Impedance cardiography (often related as ICG or TEB) BioZ-NICCOMO (BioZ - Cardio
dynamics San Diego USA, Niccomo Medis GmbH - Ilmenau - GERMANY) is a method whic
h calculates Q from the measurement of changes in impedance across the chest ove
r the cardiac cycle. Lower impedance indicates greater the intrathoracic fluid v
olume, and as the only fluid volume which changes beat to beat within the thorax
is the blood, the change in impedance can be used to calculate the SV and, comb
ined with HR, the Q. This technique has progressed clinically (often called BioZ
-Niccomo, i.e. biologic impedance, as promoted by the leading manufacturer in th
e US) and allows non-invasive estimations of Q and total peripheral resistance u
sing only 4 paired skin electrodes.
While the method is desirably non-invasive and inexpensive, it has achieved an a
cceptable reliability and reproducibility required of a useful clinical tool (se
e www.impedancecardiography.com), and the evolution of algorithms to convert imp
edance signals to Q across a variety of outputs and in a variety of diseases con
tinues.
Electrical Cardiometry
Electrical Cardiometry is a non-invasive method similar to Impedance cardiograph
y, in the fact that both methods measure thoracic electrical bioimpedance (TEB).
The underlying model is what differs, being that Electrical Cardiometry attribu
tes the steep increase of TEB beat to beat to the change in orientation of red b
lood cells. Four standard ECG electrodes are required for measurement of cardiac
output. Electrical Cardiometry is a method trademarked by Cardiotronic, Inc., a
nd shows promising results in a wide range or patients (is currently US market a
pproved for use in adults, pediatrics, and neonates). Electrical Cardiometry mon
itors have shown promise in postoperative cardiac surgical patients (both hemody
namicially stable and unstable).[21]
Magnetic Resonance Imaging
Velocity encoded phase contrast Magnetic Resonance Imaging (MRI)[22] is the most
accurate technique for measuring flow in large vessels in mammals. MRI flow mea
surements have been shown to be highly accurate compared to measurements with a
beaker and timer[23] and less variable than both the Fick principle[24] and ther
modilution.[25]
Velocity encoded MRI is based on detection of changes in the phase of proton pre
cession. These changes are proportional to the velocity of the movement of those
protons through a magnetic field with a known gradient. When using velocity enc
oded MRI, the result of the MRI scan is two sets of images for each time point i
n the cardiac cycle. One is an anatomical image and the other is an image where
the signal intensity in each pixel is directly proportional to the through-plane
velocity. The average velocity in a vessel, i.e. the aorta or the pulmonary art
ery, is hence quantified by measuring the average signal intensity of the pixels
in the cross section of the vessel, and then multiplying by a known constant. T
he flow is calculated by multiplying the mean velocity by the cross-sectional ar
ea of the vessel. This flow data can be used to graph flow versus time. The area
under the flow versus time curve for one cardiac cycle is the stroke volume. Th
e length of the cardiac cycle is known and determines heart rate, and thereby Q
can be calculated as the product of stroke volume and heart rate. MRI is typical
ly used to quantify the flow over one cardiac cycle as the average of several he
art beats, but it is also possible quantify the stroke volume in real time on a
beat-for-beat basis.[26]
While MRI is an important research tool for accurately measuring Q, it is curren
tly not clinically used for hemodynamic monitoring in the emergency or intensive
care setting. Cardiac output measurement by MRI is currently routinely used as
a part of clinical cardiac MRI examinations.[27]
Cardiac Output and Vascular Resistance
The vascular beds are a dynamic and connected part of the circulatory system aga
inst which the heart must pump to transport the blood. Q is influenced by the re
sistance of the vascular bed against which the heart is pumping. For the right h
eart this is the pulmonary vascular bed, creating Pulmonary Vascular Resistance
(PVR), while for the systemic circulation this is the systemic vascular bed, cre
ating Systemic Vascular Resistance (SVR). The vessels actively change diameter u
nder the influence of physiology or therapy, vasoconstrictors decrease vessel di
ameter and increase resistance, while vasodilators increase vessel diameter and
decrease resistance. Put simply, increasing resistance decreases Q; conversely,
decreased resistance increases Q.
This can be explained mathematically:
By simplifying Darcy s Law, we get the equation that
Flow = Pressure/Resistance
When applied to the circulatory system, we get:
Q = (MAP – RAP)/TPR
Where MAP = Mean Aortic (or Arterial) Blood Pressure in mmHg,
RAP = Mean Right Atrial Pressure in mmHg and
TPR = Total Peripheral Resistance in dynes-sec-cm-5.
However, as MAP>>RAP, and RAP is approximately 0, this can be simplified to:
Q ˜ MAP/TPR
For the right heart Q ˜ MAP/PVR, while for the left heart Q ˜ MAP/SVR.
Physiologists will often re-arrange this equation, making MAP the subject, to st
udy the body s responses.
As has already been stated, Q is also the product of the heart rate (HR) and the
stroke volume (SV), which allows us to say:
Q ˜ (HR × SV) ˜ MAP / TPR
Cardiac Output and Respiration
Q is affected by the phase of respiration with intra-thoracic pressure changes in
ng diastolic heart filling and therefore Q. Breathing in reduces intra-thoracic
pressure, filling the heart and increasing Q, while breathing out increases intr
a-thoracic pressure, reduces heart filing and Q. This respiratory response is ca
lled stroke volume variation and can be used as an indicator of cardiovascular h
ealth and disease. These respiratory changes are important, particularly during
mechanical ventilation, and Q should therefore be measured at a defined phase of
the respiratory cycle, usually end-expiration.
Combined cardiac output
Combined cardiac output (CCO) is the sum of the outputs of the right and left si
de of the heart. It is a useful in fetal circulation, where the cardiac output f
rom both sides of the heart partly work in parallel by the foramen ovale and duc
tus arteriosus, both directly supplying the systemic circulation.[28]
Example values
Measure
view • talk • edit
Typical value Normal range
end-diastolic volume (EDV) 120 ml[29] 65 - 240 ml[29]
end-systolic volume (ESV) 50 ml[29] 16 - 143 ml[29]
stroke volume (SV) 70 ml 55 - 100 ml
ejection fraction (Ef) 58% 55 to 70%[30]
heart rate (HR) 72 bpm
cardiac output (CO) 4.9 L/minute 4.0 - 8.0 L/min[31]
External links
Hemodynamics training for Junior Medical Staff
The Gross Physiology of the Cardiovascular System
The Determinants of Cardiac Output (online video)
Basic Principles in Cardiac Physiology
Cardiovascular system, physiology: cardiovascular physiology
Heart
Volumes
Stroke volume = End-diastolic volume – End-systolic volume
Cardiac output = Heart rate  Stroke volume
Afterload  Preload
Frank–Starling law of the heart  Cardiac function curve  Venous return curve
Aortic valve area calculation  Ejection fraction  Cardiac index
Dimensions
Fractional shortening = (End-diastolic dimension – End-systolic dimension) / End-d
iastolic dimension
Interaction diagrams
Cardiac cycle  Wiggers diagram  Pressure volume diagram
Tropism
Chronotropic (Heart rate)  Dromotropic (Conduction velocity)  Inotropic (Contrac
tility)  Batmotropic (Excitability)  Lusitropic (Relaxation)
Conduction system /
Cardiac electrophysiology
Cardiac action potential (Atrial action potential, Ventricular action potential)
 Effective refractory period  Pacemaker potential  EKG (P wave, PR interval, QRS
complex, QT interval, ST segment, T wave, U wave)  Hexaxial reference system
Chamber pressure
Central venous pressure/right atrial pressure → Right ventricular pressure → Pulmona
ry artery pressure → Pulmonary wedge pressure/left atrial pressure → Left ventricula
r pressure → Aortic pressure
Other
Ventricular remodeling
Vascular system/
Hemodynamics
Blood flow
Compliance  Vascular resistance (Total peripheral resistance)  Pulse  Perfusion
Blood pressure
Pulse pressure (Systolic - Diastolic)  Mean arterial pressure
Jugular venous pressure
Portal venous pressure
Regulation of BP
Baroreflex  Kinin-kallikrein system  Renin-angiotensin system  Vasoconstrictors/V
asodilators  Autoregulation (Myogenic mechanism, Tubuloglomerular feedback)  Par
aganglia (Aortic body, Carotid body, Glomus cell)
M: HRT
anat/phys/devp
noco/cong/tumr, sysi/epon
proc, drug (C1A/1B/1C/1D)
M: VAS
anat(a:h,u,t,a,l,v:h,u,t,a,l)/phys/devp/cell
noco/syva/cong/tumr, sysi/epon
proc, drug(C2s/n,C3,C4,C5,C7,C8,C9)