The PiCCO Monitor

The PiCCO Monitor
Achikam Oren-Grinberg, MD, MS

Harvard Medical School
Boston, Massachusetts
’ Introduction
Hemodynamic optimization is a complex task requiring, among

other things, monitoring of arterial and venous pressures, urine output,
acid-base balance, and oxygen content/delivery. These parameters,
however, reflect the overall circulatory state and not the basic physiologic
determinants of cardiac output (CO), which include preload, afterload,
and contractility. To help determining these basic physiologic determi-
nants, the pulmonary artery catheter (PAC) has been used by clinicians for
almost 4 decades where it became the mainstay of patient monitoring in
the operating room and in the intensive care unit (ICU) setting. It
provides direct information on pressure variables such as pulmonary
artery pressure, pulmonary artery occlusion pressure, and central venous
pressure. It can also provide flow-related data such as CO and mixed
venous oxygen saturation. Despite its extensive use, the clinical value of
data obtained from pulmonary artery catheters remains unproven.1
Therefore, an alternative approach to the PAC monitoring has been
proposed—the functional hemodynamic monitoring. This approach
focuses on the effects of positive pressure ventilation on left ventricular
(LV) output; positive pressure ventilation induces phasic changes in LV
stroke volume through similar cyclic changes in venous return. This is a
‘‘normal’’ phenomenon for all patients ventilated with positive pressure
ventilation, and can be advantageous in situations of hypovolemia.
REPRINTS: ACHIKAM OREN-GRINBERG, MD, MS, HARVARD MEDICAL SCHOOL, BETH ISRAEL DEACONESS MEDICAL
CENTER, BOSTON, MA 02215. E-MAIL: [email protected]
INTERNATIONAL ANESTHESIOLOGY CLINICS

Volume 48, Number 1, 57–85
r 2010, Lippincott Williams & Wilkins
www.anesthesiaclinics.com | 57
58 ’ Oren-Grinberg
These cyclic changes can be used to predict fluid responsiveness as

it has been shown that hypovolemic patients—those who are on the
ascending limb of the Frank-Starling curve—are very sensitive to these
changes. To date, several functional parameters have been described
and used clinically to assess fluid responsiveness. These parameters
include the systolic pressure variation, the pulse pressure variation
(PPV), and the stroke volume variation (SVV) and are utilized clinically
by currently available invasive monitors. They are considered the
standard of care in the assessment of fluid responsiveness.
The PiCCO monitor (Fig. 1) uses the dynamic parameters to predict
fluid responsiveness. In addition, it has other hemodynamic indices that
are very useful in understanding the individual patient physiological
state:
1. Fluid responsiveness: PPV and SVV
2. CO measurement
a. Transpulmonary thermodilution
b. Pulse contour analysis
3. Extravascular lung water index (EVLWI): a good surrogate assess-
ment of pulmonary edema
4. Global end-diastolic volume index (GEDI): a volumetric preload
assessment
5. Cardiac function index: a calculated index of cardiac function
Figure 1. The newly designed PiCCO2 monitor is a user-friendly touch screen monitor.
www.anesthesiaclinics.com
The PiCCO Monitor ’ 59
Thus, the PiCCO monitor is an ‘‘all inclusive’’ alternative to current

hemodynamic monitors and is very important in the management of
hemodynamically unstable patients in the operating room or ICU.
’ Fluid Responsiveness
In the assessment and management of critically ill patients, the actual

hemodynamic monitoring questions are physiological in their language
but need to be practical and concrete in their application. Perhaps the
most frequent hemodynamic question when managing patients in the
operating room or ICU is: Will CO increase with volume loading?
Data from numerous studies have documented repeatedly that
neither right atrial pressure or pulmonary artery occlusion pressure
predict well the subsequent response of the subject to an intravascular
fluid challenge.2–10 Furthermore, measures of absolute LV volumes are
only slightly better at predicting preload responsiveness.7,10–13 In
contrast, the dynamic parameters have been shown to be very useful
in discriminating between patients who respond to fluid therapy from
those who do not.5,14–16
Physiological Rationale of the Dynamic Parameters

Positive pressure ventilation is associated with simultaneous but
different effects on the left and right sides of the heart. A positive pressure
breath results in increased intrathoracic pressure, which in turn leads to
increased LV filling of blood due to compression of the pulmonary venous
system. The end result is an acute increase in LV stroke volume.
Simultaneously, however, the increased intrathoracic pressure causes a
decrease in venous return to the right side of the heart due to compression
of the inferior vena cava. During exhalation there is a decrease in stroke
volume; the heart is relatively ‘‘empty’’—the pulmonary veins have been
‘‘squeezed’’ during the positive pressure breath and the right ventricle is
relatively ‘‘empty’’ due to decreased venous return as above. This is a
‘‘normal’’ physiology during positive pressure ventilation (Figs. 2, 3).
As the left ventricle is more sensitive to preload changes when it is on
the ascending limb, or steep portion of the Frank-Starling curve, these
variations have been used clinically to assess preload status and predict
fluid responsiveness in deeply sedated patients under positive pressure
ventilation. Among the dynamic parameters described above, the
PiCCO monitor calculates and displays only the PPV and SVV.
PPV
The PPV extends the concept of cyclic variations in LV stroke
volume during positive pressure ventilation (Fig. 4). The arterial
pulse pressure—the difference between the systolic and the diastolic
Figure 2. Schematic diagram showing the increase in stroke volume and pulse pressure during a
positive pressure breath.
pressure—is directly proportional to stroke volume and inversely

related to arterial compliance.17 It is calculated as:
PPV ¼ ðPPmax rmPPmin Þ=mean 100
An index of 13% discriminates between fluid responders (increase

in CO >15% from baseline) from nonresponders (increase in CO
<15% from baseline). In addition to patients following coronary artery
bypass surgery,18 PPV was found to predict the effect of volume
Figure 3. A photo of an arterial waveform tracing depicting normal variation in stroke volume
and blood pressure during positive pressure ventilation.
Figure 4. Schematic diagram showing the variation in pulse pressure during one mechanical breath.
expansion on CO also in septic shock hypotensive patient5 and acute

lung injury.19
SVV
SVV is determined by analysis of the continuous arterial pulse
contour. This method uses the area under the systolic portion of the
arterial pressure curve for beat-to-beat determination of stroke volume (in
relative values) and their variation over the respiratory cycle. Its feasibility
and appropriateness in estimating cardiac preload and volume responsive-
ness has been reported in several clinical trials (Fig. 5).14,20–22
Similarly to the PPV, it is calculated as:
SSV ¼ ðSVmax SVmin Þ=mean times100
Figure 5. Schematic diagram showing the variation in stroke volume during one mechanical breath.
An SVV of 10% is considered as a cutoff discriminating between

fluid responders and nonresponders; if SVV is less than 10% CO
will not increase in response to volume loading and thus may be avoi-
ded as a therapeutic challenge. SVV is now accepted as an index
of fluid responsiveness and was validated in ventilated postcardiac
patients,21,23,24 in the operating room during neurosurgery20 and in
septic shock patients.14
Limitations of the Dynamic Parameters
1. Need for positive pressure ventilation: The respiratory variation in

stroke volume and arterial pressure has been validated as a predictor
of fluid responsiveness only in mechanically ventilated patients. This
limits the use of these parameters only to ventilated patients in the
operating room and ICU.
2. Need for paralysis or heavy sedation: The dynamic parameters have
been validated only in patients who are paralyzed or heavily sedated,
provided there is no patient initiation of the ventilator. As such, they
can be used to analyze fluid responsiveness only in these circum-
stances. In case where the patient is either initiating the ventilator or
breathing spontaneously thorough an endotracheal tube, one cannot
use the dynamic parameters to assess fluid responsiveness. This may
limit the clinical usefulness of arterial pressure variation in the ICU
where current practice guidelines recommend to lower the level of
sedation.25,26 As a result of these guidelines, many patients today are
ventilated with minimal respiratory support and breathe sponta-
neously.
3. Cardiac rhythm: The beat-to-beat variation in stroke volume may
no longer reflect the effects of mechanically ventilation in patients
with arrhythmias. This is mostly true in patients with atrial
fibrillation. Although significant cardiac ectopy will interfere with
the continuous and automatic monitoring of dynamic parameters, it
is still appropriate to analyze the arterial pressure curve in patients
with few extrasystoles, provided that the rhythm is regular during at
least one respiratory cycle.
4. Atherosclerosis: Systolic and pulse pressures depend not only on

stroke volume, but also on arterial compliance.17 Thus, PPV could
vary from one patient to another according to the arterial
compliance. Therefore, if arterial compliance is low (eg, patients
with significant peripheral vascular disease), this can be translated to
large changes in arterial pressure despite small changes in stroke
volume. Conversely, if arterial compliance is high (eg, young patients
without vascular disease), small changes in arterial pressure could
be seen despite large changes in stroke volume.
5. Variation in pleural pressure: Changes in pleural pressure can affect
the dynamic parameters by either falsely decreasing or increasing the
variations.
A. Small variations: During positive pressure ventilation, small
variations in pleural pressure can be seen when small tidal
volumes are used27 (eg, 6 mL/kg) or when chest compliance is
increased. Theoretically, if the pleural pressure generated during
positive pressure ventilation is not high enough to affect venous
return, this may affect the dynamic parameters and ability to
discriminate between fluid responders and nonresponders.
Indeed, SVV has been found to be a reliable predictor of fluid
responsiveness only in patients with a tidal volume ranging
between 8 and 15 mL/kg.5,23,28,29 In this regard, caution should be
exercised before concluding that a patient will not respond to a
fluid challenge because no variation in blood pressure is observed
if the tidal volume is low or increased chest compliance.
B. Large variations: Conversely, large variations in pleural pressure
can be seen when large tidal volumes are used or when chest
compliance is low. It has been shown that increasing tidal
volume29,30 or reducing chest compliance31,32 leads to increases
in stroke volume and blood pressure variations. Similarly,
decreasing chest compliance also affect stroke volume and blood
pressure variation as recently shown that opening the chest by
sternotomy decreased stroke volume and increased cardiac
preload.33 Thus, by inducing a rightward shift on the Frank-
Starling curve, the decrease in chest compliance decreased the
sensitivity of the heart to fluid challenge.
6. Technical
A. Similar to any invasive pressure monitoring, the arterial pressure
curve obtained from the fluid-filled catheter is subjected to
technical problems (eg, kinks, air bubbles, clots, excessive tubing
length, tube compliance), which could affect the dynamic response
of the monitoring system.34
B. The site of arterial pressure monitoring can also affect the
observed pressures. The recognized fact of pulse amplification
from aortic root to the peripheral circulation characterized by
increase in systolic pressure and slight decrease in diastolic

pressure in healthy individual35 is untrue in patients with sepsis36
or postcardiopulmonary bypass.37 In these patients, lower systolic
pressures have been documented in peripheral arteries. To
overcome this problem, the PiCCO catheter is placed in central
artery; brachial, axillary, or femoral arteries.
In theory, any state which increase venocapacitance and decrease
return of blood to the heart (eg, anesthetics and venodilators) may
affect the dynamic parameters; decrease return of blood to the heart
will lead to increase in the dynamic parameters which will lead to a state
of fluid responsiveness. This is not an artifact, but rather a ‘‘true’’ state
whereby a fluid bolus will result in increased CO. However, this does
not mean that fluid bolus is needed. In general, after answering the
question ‘‘will cardiac output increase with volume loading?’’ one has to
decide if fluid therapy is needed. The fact that a patient is fluid
responsive should not translate automatically to administration of
fluids. Fluid therapy should be given only if the patient is fluid
responsive and there is evidence of hypoperfusion (eg, low urine
output, tachycardia, hypotension, increased lactate, etc.). As an
example, all healthy individuals operate on the ascending limb of the
Frank-Starling curve and are fluid responsive, yet do not require fluid
bolus or therapy to maintain adequate perfusion.
’ CO
The PiCCO monitor measures CO by 2 ways: the transpulmonary

themodilution method and the pulse contour analysis.
Transpulmonary Thermodilution
The indicator-dilution techniques for measurement of CO was
introduced at the end of the 19th century by Stewart38 who first used
these techniques to measure the volume of blood in the heart and
lungs. Stewart’s model was developed and extended by Hamilton and
his colleagues39 who emphasized the use of mean circulation time to
determine the volume of a vascular bed. The consequence of Stewart
and Hamilton work was the establishment of the fundamental
relationship of volume, flow, and circulation time.40
Volume ¼ flow mean circulation time
The validity of this method of measurement of flow depends on
the assumption that the dye is distributed throughout a ‘‘central’’
pool of blood as it passes from the vein into the right heart chambers,
the lungs, and the left heart and out into the arterial system of vessels.
The validity and accuracy of the method for determining rates of flow
in mechanical systems and the CO in animals and human participants

have been later determined.39,41
A simple explanation of this elaborate work goes as follows: when
an exogenous substance (an ‘‘indicator’’) is injected into the vascular
space it is quickly diluted by flowing blood. Just how quickly or slowly
this dilution takes place is a function of the magnitude of flow. If flow
between these 2 points is high, then the concentration of the injected
substance (eg, ‘‘cold’’) will be diluted quickly. At the downstream
detection point, then, the concentration-time curve will change
relatively little. Conversely, if flow is low, the concentration of the
substance at the detection site will not be diluted as much and
temperature change will build and fall less quickly.
With the PiCCO technology the indicator (15 to 20 mL of cold
saline) is injected into the circulation at a central vein. The
concentration of the thermodilution indicator is measured at some
other point downstream from the injection site using a 4 or 5 Fr
thermistor-tipped catheter. The catheter should be placed in a central
artery—either the femoral, brachial, or axillary arteries (the PiCCO
monitor cannot use a radial arterial line due to the inaccuracy of a
peripheral arterial waveform as described later under complications).
Any in situ central venous catheter can be used, including a femoral
one. If the arterial catheter is in a femoral position and a femoral
central catheter is planned—it should be placed in the contralateral
side to prevent the ‘‘cross talk’’ phenomenon.42 Thus, when
measuring CO using the PiCCO monitor, a thermodilution bolus
passes through the right side of the heart (right atrium and ventricle),
the lungs, the left side of the heart (left atrium and ventricle), and the
aorta and smaller artery, depend where the catheter is placed (eg,
axillary, brachial, or femoral).
Comparison with the PAC thermodilution technique:
1. The temperature-time curves obtained during transpulmonary
thermodilution measurements are broader and lower in magni-
tude than when obtained via a PAC (Fig. 6), which makes them
more vulnerable to errors caused by baseline drift and miscorrec-
tions for indicator recirculation. In contrast, and for the same
reason, the transpulmonary method is less vulnerable to errors
caused by respiratory variation in blood temperature. The greater
sensitivity to baseline drift can be minimized in part by using
a larger injectate volume of ice-cold saline (the recommen-
ded volume is 15 to 20 mL rather than the 10 mL of room
temperature saline often used for thermodilution measurements
via a PAC.43
2. As with any thermodilution technique, intracardiac shunts and
valvular insufficiencies may affect absolute CO values. In left
to right shunts, recirculation of the indicator splays out the
Figure 6. Comparison between the transpulmonary thermodilution curve and the pulmonary
artery catheter (PAC) thermodilution curve. The transpulmonary thermodilution curve is broader
and lower in magnitude than when obtained via a PAC, but the area under the curve is similar.
Dashed arrow indicates central venous injection point of cold injectate. Full arrow indicates detection
point downstream in a large artery.
thermodilution curve and CO is underestimated. Conversely, right

to left shunts result in overestimation due to premature delivery
of the indicator. The direction and magnitude of the error
introduced by valvular regurgitation is more difficult to predict,
and will depend on several factors including the site and severity
of the regurgitation and the actual CO. These conditions may less
likely to affect the temperature time curve as detected by the
transpulmonary measurements of CO.43 However, caution should
be taken in interpreting the transpulmonary CO measurement
of patients with significant tricuspid regurgitation (moderate to
severe), as it may still lead to inaccurate measurement. In such
circumstances, a reasonable alternative approach would be to
measure the actual CO ‘‘going forward’’ by the pulse contour
analysis (see below), or by echocardiography.
3. The assumption (in the Stewart-Hamilton model) that there is no
unaccounted loss of thermal indicator is more likely to be an error
during transpulmonary measurements of CO in the presence of
extrapulmonary ‘‘sinks’’ for the thermal indicator (such as peri-
cardial or pleural effusions).44
These differences between PAC and transpulmonary thermodilution
CO measurements do not seem to have clinical significance; a high
degree of correlation between the 2 thermodilution CO technique has
been established in multiple experimental and clinical settings including
cardiac surgery patients, intensive care patients, septic patients, and
burn victims.45–48
Pulse Contour Analysis

The theory behind using the arterial pulse waveform to measure CO
dates back to 1899 where Otto Frank developed a model describing
the loads faced by the heart when pumping against the pulmonary or
systemic circulation and the relationship between the arterial blood
pressure and flow in the systemic and pulmonary arteries (Windkessel
model). It was Frank’s goal to be able to calculate CO from arterial pulse
pressure.49
In 1904, Erlanger and Hooker hypothesized that CO was propor-
tional to arterial pulse pressure. It was only in the last several years,
however, that the technology to accurately measure CO with the arterial
waveform has become available. The limiting factor in this process was
the realization that some other method was needed to calibrate the
system to accurately measure CO using the pulse waveform. In addition,
the compliance of the arterial tree was a major obstacle to the accurate
measurement of CO because it was determined that the compliance
of the arterial tree is nonlinear; when a volume of blood is introduced
into the vasculature at higher pressures, the compliance decreases more
rapidly than when the same volume of blood is introduced at a lower
pressure.49
The principle of pulse contour analysis is based on the physiological
relationship between stroke volume and the area under the systolic
portion of the aortic pressure waveform on a beat-to-beat basis.50
Pulse Contour Algorithm

The basic algorithm for the determination of CO from pulse-
contour was developed by Wesseling and co-workers in 1974.51–53
According to this algorithm, LV stroke volume is computed by dividing
the measured area under the systolic portion of the arterial pressure
waveform by the aortic impedance. A subsequent multiplication by the
heart rate yields pulse-contour CO. To adjust for aortic impedance,
which differs from patient to patient, the PiCCO monitor uses the
thermodilution measurement of CO for the calibration of the system.54
The calculation is as follows: CO ¼ heartrate Asys=Zao
where Zao = SVpc/SVtd
Asys, area under systolic pressure waveform; Zao, aortic impedance;
SVpc, uncalibrated stroke volume based on pulse-contour; and SVtd,
stroke volume by thermodilution.
PiCCO’s new pulse-contour algorithm is a more sophisticated
formula that analyzes the actual shape of the pressure waveform in
addition to the area under the systolic portion of the pressure wave.54 In
addition, the software takes into account the individual aortic compli-
ance and systemic vascular resistance. An explanation to these conside-
rations is that during the systole phase of a heartbeat, blood is ejected
into the aorta. Simultaneously, blood flows out of the aorta into the
peripheral vascular system. However, during the ejection phase the sum
of all blood flowing into the aorta is larger than the blood volume
entering the peripheral vascular system. Thus, the volume of the aorta
increases. In the subsequent diastole, most of the remaining blood will
empty into the peripheral vasculature and coronaries. This behavior is
dependent on the ability of the aorta to expand and contract in response
to ejected volumes (Fig. 7). The volume change and subsequent
pressure change is described as the compliance function of the aorta.
The relationship between blood flow out of the aorta and pressure
measured at the end of the aorta (femoral artery or other large artery) is
determined by the compliance function. The compliance function can
therefore be characterized by measuring blood pressure and blood flow
(CO) simultaneously. Transpulmonary thermodilution CO determined
simultaneously with continuous arterial pressure measurement is utilized
to calibrate the pulse contour analysis to each individual patient’s aortic
compliance function (Fig. 8). For the continuous calculation of pulse
contour CO the a calibration factor (cal) determined by thermodilution
CO measurement and the heart rate, as well as the integrated values for
the area under the systolic part of the pressure curve [P(t)/SVR], the
aortic compliance [C(p)] and the shape of the pressure curve represented
by change of pressure over change of time (dP/dt) (Fig. 8).
This method of CO measurement has been studied extensively and
validated in a variety of patient populations.45,46,54–57 Although there is
a bias between the measurements of the pulmonary thermodilution
technique and pulse contour analysis of – 0.71 L/min58 to 0.22 L/m/m2,59
bias and precision are clinically acceptable. Concerns that the use of
pulse-contour analysis for continuous CO monitoring during profound
changes in hemodynamic status might become unreliable were raised by
some investigators.60,61 Interestingly, several other authors have been
unable to confirm this problem.45,59,62,63 In addition, it has been shown
recently that the PiCCO pulse-contour new algorithm is reliable and
accurate during hemodynamic instability54 and is currently accepted as
a continuous CO measurement.64,65
’ EVLW
Pulmonary edema is a common finding in many critically ill patients.

The pathophysiological mechanism leading to pulmonary edema is
accumulation of fluid in the interstitial and alveolar space in the lungs,
a phenomenon termed extravascular lung water. EVLW is a marker
for the severity of lung injury, the knowledge of which may improve
the outcome in some critically ill patients by guiding volume of fluid
therapy.66,67 The ability to measure EVLW at the bedside to allow for
direction in fluid management is of immense significance. The
Figure 7. Characteristic compliance during heart phases. Upper part—heart in systolic phase.
Lower part—heart in diastolic phase.
measurement of EVLW using intravascular indicator-dilution techniques

was proposed by Chinard in 1954.68 Radioactively labeled indicators were
used—iodinated albumin for the intravascular space, and tritiated water
for the total intravascular and extravascular water space. Several
descriptions of EVLW measurement using these indicators were reported
during the subsequent 15 years, but results were disappointing.69
Figure 8. Top, A diagram showing the themodilution cardiac output measurement as a reference
for the continuous pulse contour cardiac output measurement. Bottom, The PiCCO monitor pulse
contour cardiac output analysis algorithm, which incorporates the aortic compliance, the area under
the systolic portion of the arterial waveform, a patient-specific calibration factor based on the
thermodilution measurement of cardiac output, and the shape of the pressure curve.
The Double Dye Technique

Gee and Stage70 were the first to report use of a thermal indicator
with indocyanine green dye as an intravascular volume indicator. In
anesthetized dogs, they injected the indicators into the pulmonary
artery, sampled in the aorta, and utilized transform functions to correct
mean transit times for the response times of the measuring systems. In
an unspecified number of dogs, they found that mean EVLW was
6.2 mL/kg body weight, which represented 87% of the gravimetrically
measured EVLW.69 These initial studies were followed by numerous
others, validated against the reference gravimetric method, even in
humans71–73 and yields EVLW measurements with a good reproduci-
bility.74 EVLW estimated by transpulmonary thermodilution has been
shown to correlate quite closely with EVLW assessed by the double-
indicator dilution technique.75,76 In animals, this method works also
quite well compared with the reference gravimetric method but with a
systematic bias due to different and species-dependent relationships
between GEDV and intrathoracic blood volume (ITBV).77–81
Transpulmonary Thermal Technique

The first use of a thermal indicator to detect water content of the
lungs, and the first indication that it would fully detect the actual water
content was reported by Pearce and Beazell.82 They injected a thermal
Figure 9. A diagram showing the volume in the chest and the derivation of the extravascular lung
water. CO indicates cardiac output; DStcold, down-slope time of cold injectate; EVLW, extravascular
lung water; GEDV, global end-diastolic volume; ITBV, intrathoracic blood volume; ITTV,
intrathoracic thermal volume; MTtcold, mean transit time of cold injectate; PTV, pulmonary thermal
volume.
bolus into the right atrium in 7 dogs, and detected it with a thermistor
advanced into the distal airways. Extravascular thermal volume
measured by this thermal technique averaged 8.3 mL/kg body weight.
The dilution methods are based on mathematical concepts and models
described in the 1950s,83,84 allowing the calculation of the volume of
distribution of an indicator injected into the circulation. On the basis of
these mathematical and experimental models, if an indicator is injected
into a system composed of several mixing chambers organized in series
and detected at the exit of the system (dilution curve), the product of the
flow passing through the system by the mean transit time of the indicator
gives the total volume of distribution between the site of injection and the
site of detection.38,84,85 This can also be seen mathematically from the
Stewart-Hamilton principle described above, whereas the relationship
between volume, flow and mean transit time is described as:
Volume ¼ Flow mean circulation time
As water is a very good thermal conductor, with the thermal indicator

technique the volume of distribution will include not only the intravascular
but also the EVLW space (without any distinction between interstitial and
alveolar water). From the measurement of volume of distribution of the
thermal indicator, the EVLW—a surrogate marker for pulmonary edema
can be calculated using the formula as follows (Fig. 9):
Intrathoracic Thermal Volume

The intrathoracic thermal volume (ITTV) is the volume of
distribution of the thermal indicator, which includes the volume of the
heart (4 chambers) and lungs (intravascular volume, as well as interstitial
and alveolar volumes). It is calculated as:
ITTV = CO MTtcold
whereas CO, cardiac output and MTtcold, mean transit time of cold
indicator.
Pulmonary Thermal Volume

Pulmonary thermal volume (PTV) is based on the work done by
Newman et al in the 1950s.84 In a mathematical experimental model
using bottles with different volumes arranged in series, Newman
showed that the down-slope shape of the dilutional thermal curve is
very important; the exponential down-slope time relates to the largest
chamber in a system. If using the thermodilution curve—the down-
slope time relates to the lungs, as the lungs represent the largest
chamber in the heart-lung volume system. The PTV includes the
intravascular, as well as the interstitium and alveoli volumes of the lungs.
It is calculated as:
PTV ¼ CO DStcold
whereas CO, cardiac output and DStcold, down-slope time of cold

indicator.
GEDV
This is a volumetric preload index which includes the volume in the
4 chambers of the heart. It is calculated by subtracting the PTV from the
ITTV. Although not as good as the dynamic indices for predicting fluid
responsiveness, it may help in specific situations such as when a patient
with normal sinus rhythm converts to atrial fibrillation and with this
loosing the ability to follow the dynamic parameters.
ITBV
The ITBV is the volume within the thoracic vasculature. It includes
blood in the 4 chambers of the heart and within the pulmonary
vasculature. This volume is closely related to GEDV as showed by Sakka
et al,75 and is calculated as:
ITBV ¼ 1:25 GEDV
EVLW
The EVLW is the volume within the interstitium and the alveoli and is
a very good clinical surrogate marker of pulmonary edema. It is calculated
by subtracting the ITBV from the ITTV:
EVLW = ITTV– ITBV.
Limitation of the Dilution Method

Like any other modality, this technique has limitations and familiari-
zation with these limitations is important if one is to minimize misinter-
pretation and maximize patient benefit from data measured.
Vascular Obstruction The thermal indicator cannot equilibrate

within the extravascular water space if it is not delivered sufficiently
close to reach that space by conduction. Therefore, vascular obstruction
may cause errors in EVLW measurement.86,87 This explains the
observation during experimental obstruction of large pulmonary
arteries of a significant underestimation of EVLW.88 Despite this concern
of major pulmonary vessel obstruction (mostly due to pulmonary emboli),
in clinical practice clinicians are more concerned about pulmonary
vasculature micro-obstruction that may occur in patients with acute
respiratory distress syndrome (ARDS) [either due to microthrombi or
application of high levels of positive end expiratory pressure (PEEP)].
Underestimation of EVLW has been observed in experimental models
when vessels Z500 mm in size are obstructed.87 This is not necessarily the
case when smaller vessels are embolized,89 which may be explained by the
high conduction speed of water for temperature, which is much greater
than the diffusion speed of small molecules,71 allowing thermal equilibra-
tion within embolized or underperfused regions from adjacent well-
perfused vessels.90
Effect of PEEP The effect of PEEP on EVLW measurement is still

controversial since the use of high levels of PEEP could potentially lead
to pulmonary vascular defect. This may explain the observation by some
experimental studies a decrease in EVLW measured by dilution techniques
during PEEP application.91 In contrast, PEEP may induce a redistribution
of pulmonary blood flow toward previously excluded areas and hence

artificially ‘‘increase’’ EVLW by recruiting the lungs.87,92 It is important to
appreciate that in addition to potentially affecting measurement of EVLW
by dilution method, PEEP may also have an effect on the real amount of
EVLW; in case of elevated pulmonary capillary pressure due to LV dys-
function, the application of PEEP may decrease EVLW by decreasing
pulmonary capillary pressure.93,94 In contrast, PEEP may increase EVLW
by increasing central venous pressure leading to reduced lymph flow from
the lungs (and thus lymphatic congestion), and by increasing lung volume
leading to vascular congestion and edema.95 In summary, one must keep in
mind that PEEP may affect both the amount and the measurement of
EVLW by dilution methods. Finally, a recent study showed that despite
these concerns, compared with quantitative computed tomography scan (a
technique not affected by perfusion defects), dilution methods are very
accurate in assessment of EVLW in patients with ARDS ventilated with high
levels of PEEP (10 to 20 cm H2O).96
Focal Lung Injury In case of focal or regional pulmonary injury,

there is a theoretical concern that the redistribution of blood flow away
from injured areas may lead to an underestimation of EVLW, as been
described in models of unilateral smoke inhalation97 or during HCl
instillation.98–100 These experimental models are known to induce
heterogeneous lung injuries. In human beings, new data may suggest
that the redistribution of regional blood flow may not be as of a problem
as in animal models. The redistribution of pulmonary blood flow during
cardiogenic pulmonary edema or acute lung injury has been recently
studied. Using positron emission tomography scan to assess both
pulmonary perfusion and EVLW, it was well demonstrated101 that
hypoxic pulmonary vasoconstriction is severely blunted in this clinical
context, such that there is no appreciable perfusion redistribution away
from regions with edema. Therefore, in human beings with pulmonary
edema, it is unlikely that the accuracy of dilution techniques may be
affected by a redistribution phenomenon of pulmonary blood flow, as
corroborated by these recent findings.96
Lung Resection Lung resection affects the accuracy of transpul-

monary thermodilution. The estimation of EVLW by thermodilution
is based on the equation ITBV = 1.25 GEDV. This indicates a ratio
between GEDV and ITBV is consistently equals to 4:5. The difference
between ITBV and GEDV is the pulmonary blood volume and thus, any
decrease in pulmonary blood volume (eg, due to lung resection) may
affect the GEDV/ITBV ratio and hence the estimation of EVLW. As an
example, after pneumonectomy, the 50% reduction in pulmonary blood
volume is not taken into account by the equation above. This leads to
overestimation of the ITBV by approximately 10%. As EVLW is
calculated as the difference between ITTV and ITBV (which is overesti-

mated), transpulmonary thermodilution underestimates EVLW after
lung resection.
Clinical Utilization of EVLW Measurements

Prognostic Value Eisenberg et al67 were the first to establish a link
between the level of EVLW and mortality. More recently Sakka et al102
retrospectively analyzed 373 critically ill patients in whom EVLW was
assessed by the double-indicator dilution technique. In their study,
nonsurvivors had significantly higher EVLW values than survivors, the
mortality rate being approximately 65% in patients with EVLW
>15 mL/kg and 33% in patients with EVLW<10 mL/kg. On ICU
admission, EVLW as a single variable was found to be as accurate as the
multivariable Acute Physiology and Chronic Health Evaluation II score
for outcome prediction. EVLW may be useful to predict short-term
outcomes in a given patient such as the clinical behavior during
mechanical ventilation. In addition, EVLV may guide invasive ventila-
tion management as shown by Zeravik et al.103,104 In their studies they
showed that high-frequency ventilation is much more efficient in
patients with an elevated EVLW (>15 mL/kg), whereas in contrast, pres-
sure support ventilation is better tolerated in patients with subnormal or
normal EVLW (<11 mL/kg). In theory, estimating EVLW may also be use-
ful to predict weaning failure from mechanical ventilation or to diagnose
LV dysfunction after transfer from mechanical ventilation to spontaneous
breathing, although this is only a theoretical advantage, which has not
been studied yet.
Diagnostic Value
1. Pulmonary edema: The diagnostic accuracy of auscultation and
radiography is poor, particularly in mechanically ventilated patients.
Auscultation—the first bedside step in clinical evaluation—can be
significantly altered by intrathoracic transmission of sounds origi-
nated from the mechanical ventilator. The accuracy of auscultation in
the diagnosis of alveolar-interstitial processes is only 55%.105 Bedside
chest radiograph quality is significantly reduced due to various
technical limitations (chest wall movement, supine position, anterior-
posterior approach, etc.), and its accuracy in diagnosing alveolar-
interstitial processes is slightly higher than auscultation—only
72%.105 In this regard, several studies have underlined the little
value of chest radiograph in detecting a small increase in EVLW and
the overall poor correlation between chest radiograph scores of
pulmonary edema and the real amount of EVLW.67,106 In contrast,
dilution methods can identify small increases in EVLW107 and
therefore are useful in discriminating between pulmonary edema

and atelectasis.108,109
2. ARDS: It has been shown that a significant number (one-fourth to one-
third) of patients with acute lung injury or ARDS criteria have no
significant pulmonary edema.110–112 This is because the chest radio-
graph can be misleading, and the criterion used in the current
American-European criterion definition of ARDS showed high inter-
observer variability.113 In addition, arterial hypoxemia can be due to
other disease processes than pulmonary edema. Therefore, EVLW
measurement could be helpful to better characterize patients with
ARDS and identify those who may benefit from fluid restriction.114,115
3. Differentiating between high and low pressure pulmonary edema:
The ratio between EVLW and ITBV (EVLW/ITBV) may be helpful to
identify the mechanism responsible for pulmonary edema. In an
experimental model of pulmonary edema, the ratio of EVLW to
ITBV was found to be significantly greater in case of permeability
(oleic acid infusion) than in case of hydrostatic (atrial balloon infla-
tion) pulmonary edema.78 A recent study suggests that this ratio may
be useful to discriminate between patients with cardiogenic and
patients with permeability pulmonary edema, the diagnostic being
established on clinical and biological criteria.116
Therapeutic Value
Fluid Therapy Guidance Fluid management of patients with acute
lung injury or ARDS is a topic of ongoing controversy.117,118 Fluid
restriction—or ‘‘drying’’ of the lungs—may improve arterial oxygena-
tion and lung mechanics and accelerate weaning from mechanical
ventilation. However, the concern is that such a fluid-restrictive
approach may worsen or induce hemodynamic instability and may
even lead to organ failure.117 The literature, however, does not support
this concern; Mitchell et al66 showed that a fluid restriction/depletion
therapy based on the measurement of EVLW is able to decrease the
duration of mechanical ventilation and the length of stay in the ICU
compared with a strategy based on occlusion pressure measurement.
A second study by Eisenberg et al67 even found a benefit in terms of
mortality in using such an EVLW-based fluid-restrictive approach in a
small subgroup (n = 15) of patients with acute lung injury (defined by
the association of EVLW >7 mL/kg and occlusion pressure <18 mm
Hg). Despite the positive findings of these studies, one need to recognize
that they were done more than 17 years ago. Improvement in other
aspects of critical care medicine, they may not apply to current practices.
A current ongoing prospective, randomized multicenter fluid restriction
trial based on EVLW is expected to finish in 2010 (personal
communication—Dr Charlie Phillips, Oregon Health Sciences Univer-

sity) and it would be interesting to observe if the positive findings of the
quoted 2 studies could be replicated in current critical care practices.
Finally, a subset of the ARDS-net trail—a large multicenter randomized
trial—showed that the so-called ‘‘conservative’’ strategy (fluid restric-
tion/depletion strategy) in patients with acute lung injury improves lung
function and shortens the duration of mechanical ventilation.119 This
finding emphasizes the potential usefulness of EVLW measurement to
titrate the ‘‘conservative’’ treatment on an individual basis.
Complications
The PiCCO monitor requires a central venous catheter and an
arterial catheter placed in a ‘‘large’’ artery (brachial, axillary, or femoral
arteries). A radial arterial line cannot be used due to site variability
waveform distortion.
Site-variable Waveform Distortion Distinction should be made

between central and peripheral arterial pressure; whereas central
pressure represents blood pressure in proximity of the heart, peripheral
pressure represents blood pressure obtained in smaller, distal arteries.
The relationship between central and peripheral arterial pressure can
be altered by vasoactive agents, anesthetics, core temperature, and
cardiopulmonary bypass.
1. Radial artery: The radial waveform is subject to inaccuracy inherent
to the distal location. Radial catheters may produce an attenuated
waveform with an exaggerated pulse pressure in states of hypovolemia
and vasoconstriction.120 Urzua et al121 prospectively studied the effects
of thermoregulatory vasoconstriction and concluded that the combina-
tion of more forceful cardiac ejection, stiffer arteries, and locally
increased arteriolar resistance produced marked radial waveform
distortion, artificially increasing peak systolic pressure. Finally, Dorman
et al36 studied the adequacy of radial pressure monitoring by using a
prospective observational study during high-dose vasopressor admin-
istration and concluded that radial pressure underestimated central
pressure and resulted in excessive vassopressor administration.
2. Axillary artery: Axillary artery cannulation reflects central pressure and
provides more reliable waveform morphology than of peripheral
catheters; it more accurately reflects systolic blood pressure, and proxi-
mity to the aortic arch affords accurate pressure and waveform, even
during profound vasoconstriction. It may be used during extended
monitoring, owing to a large intraluminal bore. Van Beck et al122
concluded that the axillary artery was the most distal site in upper extre-
mity at which arterial pressure consistently and accurately estimated
central aortic pressure postcardiopulmonary bypass.
3. Femoral artery: Femoral cannulation affords access to central pressure,

a morphologically reliable waveform, and an accurate reflection of sys-
tolic blood pressure. It provides accurate estimation of central pressure
in hypovolemic, vasoconstricted, and central shunting states, with wave-
form changes less than those observed in radial artery during vasoco-
nstriction.121 Femoral systolic pressure exceeding radial systolic pressure
by more than 50 mm Hg has been described.36 Similar to axillary
cannulation, the large intravascular lumen of the femoral artery allows
for extended monitoring.123
This restriction raises concern among many clinicians. Although the
placement of a radial arterial catheter is perceived as safest, this notion is
not supported in the available literature published to date.
Radial Artery The radial artery is the most common site for arterial
cannulation for hemodynamic monitoring.36,124,125 In a clinical review
of complications and risk factors of peripheral arterial cannulation, Scheer
et al124 found that the most common complication from radial arterial
cannulation was temporary occlusion of the artery, the incidence of which
ranged from 1.5%126 to 35%.127 Although temporary occlusion of the
artery has no serious sequela, permanent occlusion can lead to devastating
outcome. Thankfully, this seems to be rare with mean incidence of
0.09%.124 This review included 19,617 arterial cannulations.
Another serious complication described in this review was pseudoa-
neurysm, with a reported mean incidence of 0.09%. Pseudoaneurysm
poses a risk for infection, sepsis, rupture,128–130 and formation of an
extracorporeal pseudoaneurysm.131 Radial catheterization was asso-
ciated with sepsis with mean incidence of 0.13%, whereas local infection
at the cannulation site was reported with mean incidence of 0.72%.
Other complications include abscess, cellulitis, paralysis of the median
nerve, suppurative thromboarteritis, air embolism, compartment syndro-
me, and carpal tunnel syndrome.124
Femoral Artery The review included 3899 femoral cannulations.

Temporary occlusion of the femoral artery was reported with a mean inci-
dence of 1.45%, and serious ischemic complications requiring extremity
amputation was reported with a mean incidence of 0.18%.132 Pseudoaneu-
rysm formation occurred with mean incidence of 0.3%, sepsis was obser-
ved with a mean incidence of 0.44% and local infection was reported with
a mean incidence of 0.78%. Bleeding (generally minor) was observed with
a mean incidence of 1.58%, and hematoma formation was observed with a
mean incidence of 6.1%.124
Axillary Artery In this review, the axillary artery was cannulated in a

total of 1989 reported cases. Serious complications included permanent
ischemic damage with a mean incidence of 0.20%, pseudoaneurysm
formation with a mean incidence of 0.1%, and sepsis with a mean incidence
of 0.51%. Paresthesia of the hand due to pressure on the brachial nerve
plexus was also described.124
This systematic review concluded that ‘‘Incidence rates for major
complications such as permanent ischemic damage, sepsis and pseudo-
aneurysm formation are low and similar for the radial, femoral, and
axillary arteries. They occur in fewer than 1% of cases.’’124
These data suggest that radial artery cannulation is not safer than
axillary or femoral cannulation. Although the most commonly used
cannulation site, the radial artery should probably be used for shorter
period of time and in a state of relative hemodynamic stability. However,
when patients become hemodynamically unstable and for a longer
period (eg, a septic shock patient in the ICU), cannulation of the axillary
or femoral arteries may be beneficial. These arteries better reflect
central blood pressure, may decrease the amount of vasopressors
administered, and the catheter may last longer in comparison with
radial cannulation.
’ Conclusions
The PiCCO monitor is an ‘‘all inclusive’’ hemodynamic monitor. It

allows for assessment of fluid responsiveness using the well-established
dynamic parameters. The PPV and SVV are measured and presented on
the monitor and provides the clinician a continuous assessment of fluid
status.
CO is measured by 2 techniques; the transpulmonary thermodilu-
tion allows for intermittent CO measurement, and the pulse contour
analysis technique allows continuous CO measurement, using the
transpulmonary thermodilution measurement to calibrate the pulse
contour method for better accuracy.
Finally, the transpulmonary thermodilution curve is used to calculate
volumes in the thoracic cavity, the EVLW being one of the most important
ones. Management algorithm based on the EVLW—a surrogate marker for
pulmonary edema—may help clinicians in the management of fluid status
and may help improve outcome.
’ References
1. Sandham JDHR, Brant RF. A randomized, controlled trial of the use of pulmonary-
artery catheters in high-risk surgical patients. N Engl J Med. 2003;348:5–14.
2. Osman DRC, Ray P. Cardiac filling pressures are not appropriate to predict
hemodynamic response to volume challenge. Crit Care Med. 2007;35:64–68.
3. Lichtwarck-Aschoff MZJ, Pfeiffer UJ. Intrathoracic blood volume accurately reflects
circulatory volume status in critically ill patients with mechanical ventilation. Intensive
Care Med. 1992;18:137–138.
4. Reuse CVJ, Pinsky MR. Measurement of right ventricular volumes during fluid
challenge. Chest. 1990;98:1450–1454.
5. Michard FBS, Chemla D. Relation between respiratory changes in arterial pulse
pressure and fluid responsiveness in septic patients with acute circulatory failure. Am
J Respir Crit Care Med. 2000;162:134–138.
6. Calvin JEDA, Sibbald WJ. The hemodynamic effect of rapid fluid infusion in
critically ill patients. Surgery. 1981;90:61–76.
7. Tousignant CPWF, Mazer CD. The use of transesophageal echocardiography for
preload assessment in critically ill patients. Anesth Analg. 2000;90:351–355.
8. Diebel LNWR, Tagett MG. End-diastolic volume. A better indicator of preload in the
critically ill. Arch Surg. 1992;127:817–821.
9. Diebel LWR, Heins J. End-diastolic volume versus pulmonary artery wedge
pressure in evaluating cardiac preload in trauma patients. J Trauma. 1994;37:
950–955.
10. Tavernier BMOLG. Systolic pressure variation as a guide to fluid therapy in patients
with sepsis-induced hypotension. Anesthesiology. 1998;89:1313–1321.
11. van Daele META, van Woerkens LC. Transesophageal echocardiographic monitoring
of preoperative acute hypervolemic hemodilution. Anesthesiology. 1994;81:602–609.
12. Greim CARN, Apfel C. Relation of echocardiographic preload indices to stroke
volume in critically ill patients with normal and low cardiac index. Intensive Care Med.
1997;23:411–416.
13. Feissel MMF, Mangin I. Respiratory changes in aortic blood velocity as an indicator of
fluid responsiveness in ventilated patients with septic shock. Chest. 2001;119:867–873.
14. Mrarx GCT, McCrossan L. Assessing fluid responsiveness by stroke volume variation
in mechanically ventilated patients with severe sepsis. Eur J Anaesthesiol. 2004;21:
132–138.
15. Sander MSC, Berger K. Prediction of volume response under open chest conditions
during coronary artery bypass surgery. Crit Care. 2007;11:1–24.
16. Bendjelid KRJ. Fluid responsiveness in mechanically ventilated patients: a review of
indices used in intensive care. Intensive Care Med. 2003;29:352–360.
17. Chemla DHJ, Coirault C. Total arterial compliance estimated by stroke volume-
to-aortic pulse pressure ratio in humans. Am J Physiol. 1998;274:H500–H505.
18. Kramer AZD, Hawes H. Pulse pressure variation predicts fluid responsiveness
following coronary artery bypass surgery. Chest. 2004;126:1563–1568.
19. Michard FCD, Richard C. Clinical use of respiratory changes in arterial pulse
pressure to monitor the hemodynamic effect of PEEP. J Respir Crit Care Med.
1999;159:935–939.
20. Berkenstadt HMN, Hadani M. Stroke volume variation as a predictor of fluid
responsiveness in patients undergoing brain surgery. Anesth Analg. 2001;92:984–989.
21. Reuter DAKA, Felbinger TW. Usefulness of left ventricular stroke volume variations
to assess fluid responsiveness in patients with reduced left ventricular function. Crit
Care Med. 2003;31:1399–1404.
22. Rex SBS, Metzelder S. Prediction of fluid responsiveness in patients during cardiac
surgery. Br J Anaesth. 2004;93:782–788.
23. Reuter DAFT, Schmidt C. Stroke volume variations for assessment of cardiac
responsiveness to volume loading in mechanically ventilated patients after cardiac
surgery. Intensive Care Med. 2002;28:392–398.
24. Reuter DAKA, Felbinger TW. Optimising fluid therapy in mechanically ventilated
patients after cardiac surgery by on-line monitoring of left ventricular stroke volume
variations: a comparison to aortic systolic pressure variations. Br J Anesth. 2005;88:
124–126.
25. Kress JPPA, O’Connor MF. Daily interruption of sedative infusions in critically ill
patients undergoing mechanical ventilation. N Engl J Med. 2000;342:1471–1477.
26. Girard TDKJ, Fuchs BD. Efficacy and safety of a paired sedation and ventilator
weaning protocol for mechanically ventilated patients in intensive care (Awakening
and Breathing Controlled trial): a randomised controlled trial. Lancet. 2008;371:
126–134.
27. The Acute respiratory Distress Syndrome Network: ventilation with lower tidal
volumes as compared with traditional tidal volumes for acute lung injury and the
acute respiratory distress syndrome. N Engl J Med. 2000;342:1301–1308.
28. Tavernier BMO, Lebuffe G, et al. Systolic pressure variation to guide fluid therapy
in patients with sepsis-induced hypotension. Anesthesiology. 1998;89:1313–1321.
29. Reuter DABJ, Goepfert MS. Influence of tidal volume on left ventricular stroke
volume variation measured by pulse contour analysis in mechanically ventilated
patients. Intensive Care Med. 2003;29:476–481.
30. Szold APR, Segal E. The effect of tidal volume and intravascular volume state
on systolic pressure variation in ventilated dogs. Intensive Care Med. 1989;15:
368–371.
31. Pizov RYaY, Perel A. The arterial pressure waveform during acute ventricular
failure and synchronized external chest compression. Anesth Analg. 1989;68:
150–156.
32. Tournadre JPAB, Cayrel V. Estimation of cardiac preload changes by systolic
pressure variation in pigs undergoing pneumoperitoneum. Acta Anaesthesiol Scand.
2000;44:231–235.
33. Reuter DAGT, Goepfert MS. Effects of mid-line thoracotomy on the interaction
between mechanical ventilation and cardiac filling during cardiac surgery. Br
J Anaesth. 2004;92:808–813.
34. Gardner RM. Direct blood pressure measurement: dynamic response requirements.
Anesthesiology. 1981;54:227–236.
35. Smulyan HSM. Systolic blood pressure revisited. J Am Coll Cardiol. 1997;29:
1407–1413.
36. Dorman TBM, Lipsett PA. Radial artery pressure monitoring underestimates
central arterial pressure during vasopressor therapy in critically ill surgical patients.
Crit Care Med. 1998;26:1646–1649.
37. Stern DHGJ, Allen FB. Can we trust the direct radial artery pressure imme-
diately following cardiopulmonary bypass?. Anesthesiology. 1985;62:557–561.
38. Stewart GN. Researches on the circulation time and on influences which affect it.
J Physiol. 1897;22:159–183.
39. Hamilton WFMJ, Kinsman JI. Studies on the Circulation. IV. Further analysis of the
injection method, and of changes in hemodynamics under physiological and
pathological conditions. Am J Physiol. 1932;99:534–551.
40. Meier PZK. On the theory of the indicator-dilution method for measurement of
blood flow and volume. J Appl Physiol. 1954;6:731–744.
41. Hamilton WFRR, Attyah AM. Comparison of the Fick and dye injection methods of
measuring the cardiac output in man. Am J Physiol. 1948;153:309–321.
42. Michard F. Looking at transpulmonary thermodilution curves: the cross-talk
phenomenon. Chest. 2004;126:656–657.
43. Isakow WSD. Extravascular lung water measurements and hemodynamic monitor-
ing in the critically ill: bedside alternatives to the pulmonary artery catheter.
Am J Physiol Lung Cell Mol Physiol. 2006;291:L1118–L1131.
44. Breukers RBJJ. Pulmonary artery thermodilution cardiac output vs. transpulmon-
ary thermodilution cardiac output in two patients with intrathoracic pathology. Acta
Anaesthesiol Scand. 2004;48:658–661.
45. Goedje OHK, Lichtwarck-Aschoff M. Continuous cardiac output by femoral arterial
thermodilution calibrated pulse contour analysis: comparison with pulmonary
arterial thermodilution. Crit Care Med. 1999;27:2407–2412.
46. Buhre WWA, Kazmaier S. Comparison of cardiac output assessed by pulse-contour

analysis and thermodilution in patients undergoing minimally invasive direct
coronary artery bypass grafting. J Cardiothorac Vasc Anesth. 1999;13:437–440.
47. Marx GST, Siimpelmann R. Comparison of cardiac output measurements by arterial
trans-cardiopulmonary and pulmonary arterial thermodilution with direct Fick in
septic shock. Eur J Anaesthesiol. 2005;22:129–134.
48. Della Rocca GCM, Coccia C. Cardiac output monitoring: aortic transpulmonary
thermodilution and pulse contour analysis agree with standard thermodilution
methods in patients undergoing lung transplantation. Can J Anaesth. 2003;50:
707–711.
49. Funk DJME, Gan TJ. Minimally invasive cardiac output monitoring in the
perioperative setting. Anesth Analg. 2009;108:887–897.
50. Wesseling KHPR, Smith NT. A computer module for the continuous monitoring of
cardiac output in the operating theatre and the ICU. Acta Anaesthesiol Belg.
1976;27(suppl):327–341.
51. Wesseling KHdWB, Weber JAP. A simple device for the continuous measurement of
cardiac output. Adv Cardiovasc Phys. 1983;5:16–52.
52. Wesseling KHSN, Nichols WW. Beat to beat cardiac output from the arterial
pressure pulse contour. In: Course on Measurement in Anaesthesia. Leiden: University
of Leiden Press; 1974.
53. Wesseling KHJJ, Settels JJ. Computation of aortic flow from pressure in humans
using a nonlinear three-element model. J Appl Physiol. 1984;74:2566–2573.
54. Godje OHK, Goetz AE. Reliability of a new algorithm for continuous cardiac output
determination by pulse-contour analysis during hemodynamic instability. Crit Care
Med. 2002;30:52–58.
55. Jansen JRSJ, Mulier JP. A comparison of cardiac output derived from the arterial
pressure wave against thermodilution in cardiac surgery patients. Br J Anaesth.
2001;87.
56. Zollner CBJ, Kilger E. Retrospective analysis of transpulmonary and pulmonary arterial
measurement of cardiac output in ARDS patients. Anaesthesist. 1998;47:912–917.
57. Zollner CHM, Weis M. Beat-to-beat measurement of cardiac output by intravascular
pulse contour analysis: a prospective criterion standard study in patients after
cardiac surgery. J Cardiothorac Vasc Anesth. 2000;14:125–129.
58. Bein BWF, Tonner P. Comparison of esophageal Doppler, pulse contour analysis,
and real-time pulmonary artery thermodilution for the continuous measurement of
cardiac output. J Cardiothorac Vasc Anesth. 2004;18:185–189.
59. Felbinger TWRD, Eltzschig HK. Cardiac index measurements during rapid preload
changes: a comparison of pulmonary artery thermodilution with arterial pulse
contour analysis. J Clin Anesth. 2005;17:241–248.
60. Tannenbaum GAMD, Weissman C. Pulse contour cardiac output in surgical
intensive care unit patients. J Clin Anaesth. 1993;5:471–478.
61. Rodig GPC, Keyl C. Continuous cardiac output measurement: pulse contour
analysis vs. thermodilution technique in cardiac surgical patients. Br J Anaesth.
1999;82:525–530.
62. Gödje OTC, Reichenspurner H. Less invasive, continuous beat-to-beat hemody-
namic monitoring during minimally invasive coronary surgery. Ann Thorac Surg.
1999;68:1532–1536.
63. Jellema WWK, Groenevald ABJ. Continuous cardiac output in septic shock by
simulating a model of the aortic input impedance—a comparison with bolus
injection thermodilution. Anaesthesiology. 1999;90:1317–1328.
64. Sakka SGRK, Wegscheider K. Is the placement of a pulmonary artery catheter still
justified solely for the measurement of cardiac output? J Cardiothorac Vasc Anesth.
2000;14:119–124.
65. Genahr AMA. Transpulmonary thermodilution in the critically ill. Brit J Int Care.
2004;Spring:6–10.
66. Mitchell JPSD, Calandrino FS. Improved outcome based on fluid management in
critically ill patients requiring pulmonary artery catheterization. Am Rev Respir Dis.
1992;145:990–998.
67. Eisenberg PRHJ, Anderson D. A prospective study of lung water measurements
during patient management in an intensive care unit. Am Rev Respir Dis. 1987;
136:662–668.
68. Chinard FPET. Transcapillary pulmonary exchange of water in the dog. Am J Physiol.
1954;178:197–202.
69. Lewis FREV, Hill SL. The Measurement of extravascular lung water by thermal-
green dye indicator dilution. Ann New York Acad Sci. 1982;394–410.
70. Gee MHMP, Stage AF. Estimation of pulmonary extravascular fluid volume by use of
thermodilution. Fed Proc. 1971;30:379.
71. Bock JLF. Clinical relevance of lung water measurement with the thermal-dye
dilution technique. J Surg Res. 1990;48:254–265.
72. Mihm FGFT, Jamieson SW. Thermal dye double indicator dilution measurement of
lung water in man: comparison with gravimetric measurements. Thorax. 1987;42:
72–76.
73. Sturm JA. Development and Significance of Lung Water Measurement in Clinical and
Experimental Practice. Berlin: Springer; 1990:129–139.
74. Gödje OPM, Seebauer T. Reproducibility of double-indicator dilution measure-
ments of intrathoracic blood volume compartments, extravascular lung water, and
liver function. Chest. 1998;113:1070–1077.
75. Sakka SGRC, Pfeiffer UJ. Assessment of cardiac preload and extravascular lung water
by single transpulmonary thermodilution. Intensive Care Med. 2000;26:180–187.
76. Michard FSA, Toens C. Factors influencing the estimation of extravascular lung
water by transpulmonary thermodilution in critically ill patients. Crit Care Med.
2005;33:1243–1247.
77. Kirov MYKV, Kuklin VN. Extravascular lung water assessed by transpulmonary single
thermodilution and postmortem gravimetry in sheep. Crit Care. 2004;8:451–458.
78. Katzenelson RPA, Berkenstadt H. Accuracy of transpulmonary thermodilution
versus gravimetric measurement of extravascular lung water. Crit Care Med.
2004;32:1550–1554.
79. Nirmalan MNM, Willard T. Estimation of errors in determining intrathoracic blood
volume using thermal dilution in pigs with acute lung injury and haemorrhage.
Br J Anaesth. 2004;93:546–551.
80. Nirmalan MWT, Edwards DJ. Estimation of errors in determining intrathoracic
blood volume using the single transpulmonary thermal dilution technique in
hypovolemic shock. Anesthesiology. 2005;103:805–812.
81. Neumann P. Extravascular lung water and intrathoracic blood volume: double
versus single indicator dilution. Intensive Care Med. 1999;25:216–219.
82. Pearce MLBJ. The measurement of pulmonary parenchymal volume by thermal
indicator dilution. Clin Res. 1966;14:182.
83. Meier PZK. On the theory of indicator-dilution method of measurement of blood
flow and volume. J Appl Physiol. 1954;6:731–744.
84. Newman EVMM, Genecin A. The dye dilution method for describing the central
circulation. An analysis of factors shaping the time-concentration curve. Circulation.
1951;4:735–746.
85. Stewart GN. Research on the circulation time in organs and on the influences which
affect it. J Physiol. 1897;15:1–89.
86. Effros RM. Lung water measurements with the mean transit time approach.
J Appl Physiol. 1985;59:673–683.
87. Allison RCCPJ, Gray BA. Thermodilution measurement of lung water. Clin Chest
Med. 1985;6:439–457.
88. Schreiber THL, Schwarzkopf K. Lung perfusion affects preload assessment and
lung water calculation with the transpulmonary double indicator method. Intensive
Care Med. 2001;27:1814–1818.
89. Beckett RCGB. Effects of atelectasis and embolization on extravascular thermal
volume of the lung. J Appl Physiol. 1982;53:1614–1619.
90. Michard F. Bedside assessment of extravascular lung water by dilution methods:
temptations and pitfalls. Crit Care Med. 2007;35:1–7.
91. Myers JCRT, Cloutier CT. Effect of positive end-expiratory pressure on extravascular
lung water in porcine acute respiratory failure. Crit Care Med. 1988;16:52–54.
92. Carlile PVLD, Gray BA. Effect of PEEP and type of injury on thermal-dye estimation
of pulmonary edema. J Appl Physiol. 1986;60:22–31.
93. Colmero-Ruiz MF-ME, Fernandez-Sacristan MA. PEEP and low tidal volume
ventilation reduce lung water in porcine pulmonary edema. Am J Respir Crit Care
Med. 1997;155:964–970.
94. Ruiz-Bailen MF-ME, Hurtado-Ruiz B. Immediate application of positive end
expiratory pressure is more effective than delayed positive end expiratory pressure
to reduce extravascular lung water. Crit Care Med. 1999;27:380–384.
95. Demling RHSN, Edmunds LH Jr. Effect of end-expiratory airway pressure on
accumulation of extravascular lung water. J Appl Physiol. 1975;38:907–912.
96. Patroniti NBG, Maggioni E. Measurement of pulmonary edema in patients with
acute respiratory distress syndrome. Crit Care Med. 2005;33:2547–2554.
97. Prien TTL, Herndon DN. Pulmonary edema with smoke inhalation, undetected by
indicator-dilution technique. J Appl Physiol. 1987;63:907–911.
98. Roch AMP, Lambert D. Accuracy of the double indicator method for measurement
of extravascular lung water depends on the type of acute lung injury. Crit Care Med.
2004;32:811–817.
99. Groeneveld ABJVJ. Is pulmonary edema associated with a high extravascular
thermal volume? Crit Care Med. 2004;32:899–901.
100. Carlile PVGB. Type of lung injury influences the thermal-dye estimation of
extravascular lung water. J Appl Physiol. 1984;57:680–685.
101. Schuster DPAC, Kozlowski J. Regional pulmonary perfusion in patients with acute
pulmonary edema. J Nucl Med. 2002;43:863–870.
102. Sakka SGKM, Reinhart K. Prognostic value of extravascular lung water in critically
ill patients. Chest. 2002;122:2080–2086.
103. Zeravik JPU. Efficacy of high frequency ventilation combined with volume
controlled ventilation in dependency of extravascular lung water. Acta Anaesthesiol
Scand. 1989;33:568–574.
104. Zevarik JBU, Pfeiffer UJ. Efficacy of pressure support ventilation dependent on
extravascular lung water. Chest. 1990;97:1412–1419.
105. Lichtenstein DGI, Mourgeon E. Comparative diagnostic performances of ausculta-
tion, chest radiography, and lung ultrasonography in acute respiratory distress
syndrome. Anesthesiology. 2004;100:9–15.
106. Sivak EDRB, O’Donovan PB. Value of extravascular lung water measurement
versus portable chest x-ray in the management of pulmonary edema. Crit Care Med.
1983;11:498–501.
107. Fernandez-Mondejar ER-FR, Garcia-Delgado M. Small increases in extravascular
lung water are accurately detected by transpulmonary thermodilution. J Trauma.
2005;59:1420–1424.
108. Verheij JvLA, Raijmakers PG. Pulmonary abnormalities after cardiac surgery are
better explained by atelectasis than by increased permeability oedema. Acta
Anaesthesiol Scand. 2005;49:1302–1310.
109. Groeneveld ABVJ, van den Berg FG. Increased pulmonary capillary permeability
and extravascular lung water after major vascular surgery: effect on radiography
and ventilatory variables. Eur J Anaesthesiol. 2006;23:36–41.
110. Michard FZV, Alaya S. Better characterization of acute lung injury/ARDS using lung
water. Chest. 2004;125:1166–1167.
111. Martin GES, Mealer M. Extravascular lung water in patients with severe sepsis:
a prospective cohort study. Crit Care. 2005;9:R74–R82.
112. Groeneveld ABJPK. Acute lung injury, overhydration or both? Crit Care. 2005;9:
136–137.
113. Meade MOCR, Guyatt GH. Interobserver variation in interpreting chest radio-
graphs for the diagnosis of acute respiratory distress syndrome. Am J Respir Crit Care
Med. 2000;161:85–90.
114. Matthay MA. Clinical measurement of pulmonary edema. Chest. 2002;122:
1877–1879.
115. Schuster DP. Identifying patients with ARDS: time for a different approach. Intensive
Care Med. 1997;23:1197–1203.
116. Monnet XAN, Osman D. Assessing pulmonary permeability by transpulmonary
thermodilution allows differentiation of hydrostatic pulmonary edema from ALI/
ARDS. Intensive Care Med. 2007;33:448–453.
117. Rivers EP. Fluid-management strategies in acute lung injury—liberal, conservative,
or both? N Engl J Med. 2006;354:2598–2600.
118. Schuster DP. Fluid management in ARDS: ‘‘keep them dry’’ or does it matter?
Intensive Care Med. 1995;21:101–103.
119. The National Heart, Lung, and Blood Institute. Acute Respiratory Distress
Syndrome (ARDS) Clinical Trials Network: comparison of two fluid-management
strategies in acute lung injury. N Engl J Med. 20006;354:2564–2575.
120. Bryan-Brown CWKK, Lumb PD. The axillary artery catheter. Heart Lung. 1983;12:
492–497.
121. Urzua JSD, Meneses G. Thermoregulatory vasoconstriction increases the difference
between femoral and radial arterial pressures. J Clin Monit. 1994;10:229–236.
122. Van Beck JOWR, Abenstein JP. Thermoregulatory vasoconstriction increases the
difference between femoral and radial arterial pressure. J Clin Monit. 1993;10:
229–236.
123. Cousins TRODJ. Arterial cannulation: a critical review. AANA J. 2004;72:267–271.
124. Scheer BVPA, Pfeiffer UJ. Clinical review: complications and risk factors of
peripheral arterial catheters used for haemodynamic monitoring in anaesthesia
and intensive care medicine. Crit Care. 2002;6:198–204.
125. Durbin CG Jr. Radial arterial lines and sticks: what are the risks? Respir Care.
2001;46:229–230.
126. Soderstrom CAWD, Dunham CM. Superiority of the femoral artery for monitoring.
A prospective study. Am J Surg. 1982;144:309–312.
127. Bedford RF. Wrist circumference predicts the risk of radial-arterial occlusion after
cannulation. Anesthesiology. 1978;48:77–378.
128. Wolf SMD. Pseudoaneurysm: a late complication of radial-artery catheterization.
Anesthesiology. 1980;52:80–81.
129. Fraile JRCJ, Gilsanz F. Postpuncture pseudoaneurysm of the radial artery
[in Spanish]. Rev Esp Anestesiol Reanim. 1989;36:126–127.
130. McEllistrem RFOTD, Keane P. Post-cannulation radial artery aneurysm: a rare
complication. Can J Anaesth. 1990;37:907–909.
131. Arrowsmith JE. Extracorporeal pseudoaneurysm: an unusual complication of radial
artery cannulation. Anesthesia. 1991;46:894–895.
132. Riker AIGR. Vascular complications and femoral artery catheterization in burn
patients. J Trauma. 1996;41:904–905.

The PiCCO Monitor

Uploaded by

Copyright:

Available Formats

The PiCCO Monitor

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

The PiCCO Monitor

Uploaded by

Copyright:

Available Formats

The PiCCO Monitor

Achikam Oren-Grinberg, MD, MS

Hemodynamic optimization is a complex task requiring, among

INTERNATIONAL ANESTHESIOLOGY CLINICS

These cyclic changes can be used to predict fluid responsiveness as

Thus, the PiCCO monitor is an ‘‘all inclusive’’ alternative to current

In the assessment and management of critically ill patients, the actual

Physiological Rationale of the Dynamic Parameters

pressure—is directly proportional to stroke volume and inversely

PPV ¼ ðPPmax rmPPmin Þ=mean 100

An index of 13% discriminates between fluid responders (increase

expansion on CO also in septic shock hypotensive patient5 and acute

An SVV of 10% is considered as a cutoff discriminating between

Limitations of the Dynamic Parameters

1. Need for positive pressure ventilation: The respiratory variation in

4. Atherosclerosis: Systolic and pulse pressures depend not only on

increase in systolic pressure and slight decrease in diastolic

The PiCCO monitor measures CO by 2 ways: the transpulmonary

in mechanical systems and the CO in animals and human participants

thermodilution curve and CO is underestimated. Conversely, right

Pulse Contour Analysis

Pulse Contour Algorithm

Pulmonary edema is a common finding in many critically ill patients.

measurement of EVLW using intravascular indicator-dilution techniques

The Double Dye Technique

Transpulmonary Thermal Technique

Volume ¼ Flow mean circulation time

As water is a very good thermal conductor, with the thermal indicator

Intrathoracic Thermal Volume

Pulmonary Thermal Volume

whereas CO, cardiac output and DStcold, down-slope time of cold

EVLW = ITTV– ITBV.

Limitation of the Dilution Method

Vascular Obstruction The thermal indicator cannot equilibrate

Effect of PEEP The effect of PEEP on EVLW measurement is still

of pulmonary blood flow toward previously excluded areas and hence

Focal Lung Injury In case of focal or regional pulmonary injury,

Lung Resection Lung resection affects the accuracy of transpul-

calculated as the difference between ITTV and ITBV (which is overesti-

Clinical Utilization of EVLW Measurements

therefore are useful in discriminating between pulmonary edema

communication—Dr Charlie Phillips, Oregon Health Sciences Univer-

Site-variable Waveform Distortion Distinction should be made

3. Femoral artery: Femoral cannulation affords access to central pressure,

Femoral Artery The review included 3899 femoral cannulations.

Axillary Artery In this review, the axillary artery was cannulated in a

The PiCCO monitor is an ‘‘all inclusive’’ hemodynamic monitor. It

46. Buhre WWA, Kazmaier S. Comparison of cardiac output assessed by pulse-contour

You might also like