(Chest. 2002;121:559-565.)
© 2002
American College of Chest Physicians
Comparison of Cardiac Output and Circulatory Blood Volumes by Transpulmonary Thermo-Dye Dilution and Transcutaneous Indocyanine Green Measurement in Critically Ill Patients*
Samir G. Sakka, MD;
Konrad Reinhart, MD;
Karl Wegscheider, PhD and
Andreas Meier-Hellmann, MD
*
From the Department of Anesthesiology and Intensive Care Medicine (Drs. Sakka, Reinhart, and Meier-Hellman), Friedrich-Schiller-University of Jena, Jena, Germany; and the Department of Statistics and Econometry (Dr. Wegscheider), University of Hamburg, Hamburg, Germany.
Correspondence to: Samir G. Sakka, MD, DEAA, Department of Anesthesiology and Intensive Care Medicine, Friedrich-Schiller-University of Jena, Bachstrasse 18, D-07740 Jena, Germany; e-mail: Samir. Sakka{at}med.uni-jena.de
 |
Abstract
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|---|
Objective: We prospectively studied the agreement
between transpulmonary aortic fiberoptic-based and pulse dye
densitometry (PDD) measurements of cardiac output and circulatory blood
volumes.
Design: Prospective clinical study.
Setting: Operative ICU of a university hospital.
Patients: Sixteen critically ill, deeply sedated patients
receiving mechanical ventilation with ARDS (n = 8), sepsis/septic
shock (n = 6), subarachnoid hemorrhage (n = 1), and severe head
injury (n = 1).
Measurements and results: Each
patient received a 4F aortic catheter with an integrated fiberoptic and
thermistor that was connected to a computer system for automatic
calculation of the transpulmonary indicator dilution (TPID) technique
for the measurement of cardiac output (COTPID),
intrathoracic blood volume (ITBV), and total blood volume measured by
TPID technique (TBVTPID). In each patient, an indocyanine
green sensor was attached to one nasal wing and connected to an
analyzer for the PDD measurement of cardiac output (COPDD),
central blood volume (CBV), and TBV measured by PDD
(TBVPDD). For all first measurements, linear regression
analysis between COTPID and COPDD revealed that
COPDD = 0.63 x COTPID + 3.69 (L/min)
[r = 0.64, p = 0.008]. Mean bias between both
techniques was - 0.8 L/min (SD, 1.7 L/min). Correlations between
ITBV/CBV (r = 0.52) and
TBVTPID/TBVPDD were only moderate:
TBVPDD = 0.74 x TBVTPID + 2,362 (mL)
[r = 0.60, p = 0.015; mean bias, - 999 mL; SD,
1,353 mL]. Over all 55 measurements, TPID measurements were on average
11.5% (cardiac output) and 17.6% (TBV) higher than PDD measurements.
The differences between both measurements ranged from - 58 to 81%
(cardiac output) and from - 47 to 82% (TBV; 95% reference ranges).
The main source of variation were the intraindividual differences,
resulting in different peaks and trends in the patients’ time courses
depending on which measurement method was used.
Conclusion: PDD measurement of cardiac output and
circulatory blood volumes agrees moderately with transpulmonary
thermo-dye dilution technique in critically ill
patients.
Key Words: cardiac output • circulatory volumes • critically ill patients • indocyanine green • thermodilution
|
Introduction
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|---|
Cardiac
output is an important hemodynamic variable for the assessment of
cardiac function and guiding therapy in the intensive care setting.
Various techniques, each with its own advantages and disadvantages, can
be used for the measurement of cardiac output. Since the introduction
of the pulmonary
artery catheter in 1971 by Ganz et al,1
the pulmonary
artery thermodilution technique has become the "gold standard."
Most commonly, a bolus of cold saline solution is injected into the
right atrium, and a thermistor in the tip of the pulmonary artery
catheter is used to measure the temperature changes. Cardiac output
measured by the transpulmonary indicator dilution (TPID) technique
(COTPID) is also available, which only needs arterial
and central venous catheterization but not pulmonary artery
catheterization. Measurement of cardiac output by transpulmonary
thermodilution is also based on the Stewart-Hamilton
principle2
and has been shown to agree well with pulmonary
artery measurement.3
4
5
6
7
8
9
In general, measurement of cardiac output per se is only of
limited value and becomes much more helpful when cardiac preload is
available at the same time. In contrast to cardiac output and
myocardial afterload, which are readily available or can easily be
calculated, assessment of myocardial preload is more difficult.
Different variables have been suggested for the estimation of cardiac
preload in the clinical setting; however, there is still controversy on
which preload variable to use preferably. For instance, pulmonary
artery catheterization allows the assessment of cardiac preload by
pressure monitoring, ie, measurement of central venous and
pulmonary artery occlusion pressure. More recently, intrathoracic blood
volume (ITBV), which can be obtained from the TPID technique, has been
clinically introduced as an alternative preload variable, and has been
found to be a more appropriate preload indicator in critically ill
patients receiving mechanical ventilation compared to the cardiac
filling pressures.10
11
12
13
Since pulmonary artery catheterization is invasive and the TPID
technique requires placement of an aortic catheter, noninvasive
assessment of hemodynamic parameters would be desirable. A recently
developed and clinically introduced device allows cardiac output
measurement based on transcutaneous dye concentration curves by a
system adapted from the pulse oximetry.14
15
In principle,
comparably to the transpulmonary fiberoptic-based technique,
measurement of indocyanine green (ICG) is based on a spectrophotometric
technology. This system has been suggested to allow measurement of
cardiac output, total blood volume (TBV), and central blood volume
(CBV). In this study, we analyzed the agreement between both
techniques, ie, transpulmonary arterial thermodilution and
transcutaneous dye-dilution based assessment of cardiac output, and
derived variables such as ITBV and TBV in 16 critically ill
patients.
|
Materials and Methods
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|---|
With agreement from our institutional ethics committee, we
studied 16 critically ill patients (10 male and 6 female patients) who
had ARDS (n = 8), sepsis/septic shock (n = 6), subarachnoid
hemorrhage (n = 1), and severe head injury (n = 1). Severity of
illness was characterized by the Simplified Acute Physiology
Score-II16
(52 ± 13; range, 36 to 86) and
Sepsis-Related Organ Failure Assessment score17
(15 ± 1; range, 13 to 18). All patients were deeply sedated with
fentanyl (0.4 to 0.6 mg/h) and droperidol (5 to 7.5 mg/h). If
necessary, midazolam was administered in a dosage up to 15 mg/h.
Patients received mechanical ventilation in a pressure-controlled mode,
and positive end-expiratory pressure was adjusted individually
according to blood gas values. Each patient received a 4F aortic
catheter with an integrated fiberoptic and thermistor (Pulsiocath 4F PV
2024 L; Pulsion Medical Systems; Munich, Germany) that was connected to
a computer system (COLD-Z021; Pulsion Medical Systems) for automatic
calculation of COTPID from thermodilution, ITBV, and TBV
measured by the TPID technique (TBVTPID).18
Based on the principle of the TPID technique, the distribution volume
of a soluble indicator, injected into the central circulation, is
dependent on the flow in the system (ie, cardiac output) and
the mean transit time (MTT) of the indicator. According to the MTT
approach, ITBV can be calculated by the product of cardiac output and
MTT. While cardiac output is obtained from the aortic thermodilution
curve in the transpulmonary technique, MTT is derived from the aortic
dye-concentration curve. The tip of the catheter was placed at the
infradiaphragmatic level as assumed from individual body measures. In
each patient, 30 mg of cooled (0°C to 6°C) ICG (Pulsion Medical
Systems) were injected first through a central venous catheter as a
bolus (15 mL of ICG in a concentration of 2 mg/mL dissolved in 5%
glucose). For verification of COTPID results, two
bolus injections of cooled saline solution followed the ICG injection.
All injections were made manually and were not respirator triggered.
For the simultaneous assessment of the transcutaneous ICG
concentration curve by pulse dye densitometry (PDD) [DDG2001
analyzer; Nihon Kohden; Tokyo, Japan], an ICG sensor was used and an
appropriate baseline signal quality was confirmed according to the
instructions of the manufacturer. Since detection of the first-pass
curve by the finger-clip device was found to be inaccurate, especially
in patients with poor peripheral perfusion, we always attached the ICG
sensor to one nasal wing as recommended.15
Immediately
prior to each measurement, hemoglobin concentration was determined for
calibration of PDD. In this system, cardiac output is derived from the
noninvasive ICG concentration curve and CBV is calculated according to
ITBV as the product of cardiac output and the MTT of the indicator. In
general, CBV will always be somewhat higher than ITBV due to the longer
appearance time explained by the more peripheral indicator detection
site. Mean hemoglobin concentration was 9.5 ± 1.1 g/dL (range, 8.3
to 14.1 g/dL). Body temperature was between 35.5°C and 40.0°C
(mean ± SD, 37.8 ± 1.4°C).
Statistical Methods
Patient characteristics and baseline hemodynamic and respiratory
data are presented as ranges and arithmetic means ± SDs. The
relations between COTPID/cardiac output measured by PDD
(COPDD) and TBVTPID/TBV measured by PPD
(TBVPDD) were analyzed from each first simultaneous
measurement per patient by linear regression and their agreement
according to Bland and Altman.19
Agreement between different methods that try to measure the same
continuous-scale parameter is predominantly judged by using plots by
Bland and Altman.19
These plots allow one to determine a
possible systematic bias and the random variability between both
methods separately. However, the underlying model of the Bland and
Altman plots only holds when either repeated-measurement pairs are
taken in one individual, or when one measurement pair is taken per
patient. In this study, interindividual and intraindividual variability
was present at the same time, requiring a variance component approach
that allows one to distinguish between different sources of variation.
For each of the pairs of methods, COTPID/COPDD
and TBVTPID/TBVPDD, we computed the differences
of the logarithms of the measurements at the same measurement time and
fitted a general linear model including a constant term (measuring
bias), a random patient term (measuring the interindividual variability
of the differences between methods), and an error term (measuring the
intraindividual variability). Logarithms were taken, since it turned
out that relative differences were better suited to describe the
differences between the methods than absolute differences, and model
assumptions were better met after logarithmic transformation. If
differences between logarithms are small, log effects can be
approximately transformed into percentages, and this is what is done
during the following presentation of results. Interindividual and
intraindividual variation are combined to the total random error, and
the total random error again is combined with the bias term to an
estimated root mean square difference (RMSD). The RMSD expresses the
expected total deviation that has to be faced if one of the methods is
used instead of the other in future measurements. Results are
visualized by Bland and Altman19
plots in which the usual
95% reference bands were replaced by two bands. The narrower of these
two bands was calculated using interindividual SD and thus corresponds
to patients’ means, while the outer band was calculated using the
total random error and thus corresponds to single measurements. The
consequences of the use of different measurement methods were studied
by plotting intraindividual courses of cardiac output and TBV
measurements as time series within one diagram.
Statistical analyses were performed using statistical software (SPSS
for Windows, version 9.0; SPSS; Chicago, IL). Bland and
Altman19
plots were produced using graphical software
(HPGL; Hewlett-Packard; Palo Alto, CA). Statistical significance
was considered at p < 0.01.
|
Results
|
|---|
Patient characteristics are listed in Table 1
, and baseline data on hemodynamic and respiratory variables are
shown in Table 2 . For all first measurements (n = 16), range was 4.99 to 11.90 L/min
for COTPID and 3.82 to 10.71 L/min for COPDD.
Linear regression analysis revealed the following:
COPDD = 0.63 x COTPID + 3.69 (L/min)
[r = 0.64, p = 0.008; Fig 1
]. The analysis according to Bland and
Altman19
showed only moderate agreement between both
techniques (mean bias, - 0.8 L/min; SD, 1.7 L/min; Fig 2
).
Correlations between ITBV/CBV (r = 0.52) and
TBVTPID/TBVPDD were
only moderate: TBVPDD =
0.74 x TBVTPID + 2,362 (mL)
[r = 0.60, p = 0.015] with a mean bias of - 999 mL
(SD, 1,353 mL; Fig 3
,
4
). Range was 2,495 to 8,152 mL for TBVTPID
and 1,920 to 8,930 mL for TBVPDD. Measurements
were made during stable global hemodynamics, as can be seen from the
mean ± SD of 0.28 ± 0.21 L/min over all 48 thermodilution
COTPID measurements (ie, one cooled
ICG bolus and two cooled saline solution injections).
Table 3
reports the three different sources of variability and their
combinations for the two method comparisons. RMSDs were as high as 38%
(cardiac output) or 33% (TBV), ie, the expected RMSD
between the two methods in either direction is one third or more of the
lower of the two measurements, in each case. This enormous difference
is mainly due to a large intraindividual variability. It is not obvious
that interindividual differences contribute further to the total
variability (p > 0.05 in both cases). Biases of 12% and 18% toward
higher pulse densitometric values were observed, but may even be chance
effects due to the big variability for cardiac output (p > 0.05). A
more detailed analysis using Bland and Altman19
plots
revealed a tendency toward higher TPID measurements as compared to PDD
measurements when cardiac output increased. While in the range < 5
L/min, cardiac output determinations by TPID were > 20% beneath
the corresponding PDD values; those increased by up to 80% in
the range > 12 L/min (Fig 5
). A similar but less pronounced tendency was observed in TBV
measurements (Fig 6
).
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Figure 5.. Agreement between COTPID and
COPDD according to Bland and Altman19
analysis. Percent differences (y-axis) are plotted against mean cardiac
output determinations (x-axis). The solid line corresponds to bias. The
dotted (dashed) lines define the 95% reference range of individual
means (single measurements).
|
|
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|
Figure 6.. Agreement between TBVTPID and
TBVPDD according to Bland and Altman19
analysis. Percent differences (y-axis) are plotted against mean TBV
determinations (x-axis). The solid line corresponds to bias. The dotted
(dashed) lines define the 95% reference range of individual means
(single measurements).
|
|
In summary, the differences between the methods were considerable in
both cases, with a tendency toward higher values for the transcutaneous
system. The time courses of four patients with at least six measurement
time points demonstrate the consequences for the clinical practice: the
directions of cardiac output/TBV changes as well as the positions of
the minima and maxima depend heavily on the chosen method of
measurement. PDD measurements revealed higher fluctuations than TPID
measurements.
|
Discussion
|
|---|
In this study, we could show that PDD measurement of cardiac
output, CBV, and TBV only moderately correlated with values derived
from a fiberoptic-based transpulmonary thermo-dye dilution
technique.
When analyzing each first measurement per patient, differences between
methods are definitely too big to be ignored. Furthermore, since the
differences between the methods vary considerably within patients, the
interpretation of time courses of cardiac output and TBV in the
individual may seriously depend on the measurement method chosen, as is
obvious from the intraindividual series of measurements. The PDD
technique is more variable, but the fluctuations seem spurious and may
be a result of a more pronounced instability of the method.
In a previous investigation for the validation of cardiac output by
PDD, Iijima et al15
studied eight patients undergoing
coronary bypass grafting. After confirming that transcutaneous ICG
concentrations correlated well with blood values
(r = 0.95), COPDD and cuvette ICG
photometric-derived cardiac output values were reported to correlate by
r = 0.87 in this study. For comparison, pulmonary artery
thermodilution cardiac output (COPA) and cuvette
ICG photometric-derived values correlated by r = 0.88.
Furthermore, the relation between COPDD and
COPA was described by
r = 0.83.15
However, the number of
measurements per patient varied and, thus, may have potentially
influenced the results of this study. Furthermore, these patients, in
contrast to our patients, did not receive vasoactive drugs. It may be
that absolute measurement of ICG concentration, which is required to
allow quantification of the area under the primary curve in order to
calculate cardiac output, becomes inaccurate by the transcutaneous
pulse densitometric device in patients with capillary leakage and
edema. Imai et al20
studied 22 patients with mainly
coronary artery bypass grafting or cardiac valve replacement. In their
analysis, four to six simultaneous COPA and
COPDD measurements per patient were used and
approximately 50% of all patients were only measured prior to surgery.
Overall mean bias between COPA and
COPDD was 0.16 L/min (SD, 0.80 L/min), and
percentage SD was approximately 20%. Clinically relevant differences
of up to 2 L/min with a mean cardiac output of 4 L/min became obvious
in some patients.
Transpulmonary thermodilution has been extensively validated and can be
regarded as accurate enough when compared with pulmonary artery
thermodilution cardiac output.3
4
5
6
7
8
9
Measurement of cardiac
output is crucial for the calculation of ITBV or CBV, since it is one
of two determinants in the product in the MTT approach. ITBV has been
shown to be an appropriate or even better indicator of cardiac preload
in critically ill patients when compared to the cardiac filling
pressures.10
11
12
13
21
However, accurate measurement of both
cardiac output and MTT is required for correct calculation of ITBV,
which is determined by the product of the two variables. Most
importantly, assessment of absolute ICG concentration is required for
the correct determination of cardiac output.
In our study, only a moderate correlation between CBV and ITBV was
found (r = 0.52). Unfortunately, the noninvasive technique
failed in our study to allow accurate measurement of cardiac output.
Accordingly, derived hemodynamic variables that are calculated by
cardiac output cannot be determined accurately. Thus, absolute
concentrations are not detected reliably by the noninvasive device,
although relative changes in the ICG concentration decay curve
have been shown to be reflected well by PDD.22
Moreover, measurement of TBV, which is gaining increasing clinical
interest during anesthesia and in critically ill patients, is based on
the measurement of absolute ICG concentrations.23
Published results by Ishihara et al24
showed that ICG can
accurately measure plasma volume in critically ill patients
independently from its plasma disappearance rate. However,
spectrophotometric ICG quantification and not the pulse densitometry
device was still used in this work. In a study on the accuracy of total
circulating blood volume by PDD, 11 healthy volunteers were studied and
the results were compared to a 131I-human serum
albumin radionuclide technique.25
In the results, total
circulating blood volume estimated by the nostril ICG sensor was found
to correlate well with the blood ICG technique and the radionuclide
approach. In detail, percentage differences between
transcutaneous/131I-human serum albumin and
transcutaneous/blood-derived total circulating blood volumes were
3.99 ± 10.54% and 2.72 ± 9.44%, respectively. Nevertheless, the
fiberoptic catheter-derived TBV may show differences when compared
to a reference technique, ie, the Evans blue
method.18
Correlation between these two techniques was
found to be r2 = 0.83, and
TBVTPID was found to underestimate TBV as
measured by the Evans blue method with a mean bias of 435
mL.18
Furthermore, measurement of ICG plasma disappearance
rate by the fiberoptic system was found to agree well with values from
arterial ICG concentrations (in vitro spectrophotometry) in
critically ill patients.26
Most recently, Imai et
al27
compared TBVPDD with
measurement by 51Cr-labeled RBCs in 11 adult
patients on the first day after cardiac surgery. In their results, a
good accuracy (mean bias < 10%) and repeatability of the pulse
densitometric technique was found.27
As stated by the
authors in their discussion, transcutaneous measurement is limited
during poor peripheral circulation or vasoconstriction, and tissue
factors have been mentioned as cause for the considerable differences
in TBV measurement.27
Noteworthy, only "modest doses of
dopamine and/or dobutamine"27
were infused in this
study. Most likely, vasopressor dosages may be responsible for the
different results in these two studies. In our critically ill patients
who mainly had ARDS or sepsis and required vasoactive drug support, we
could only demonstrate a moderate correlation between
TBVTPID and TBVPDD
(r = 0.60) and, probably due the larger number of
patients, a larger bias of 17.6%.
|
Conclusion
|
|---|
Although the pulse-densitometric system has been found to allow
measurement of ICG-plasma disappearance rate accurately,22
it cannot be recommended for the measurement of cardiac output, CBV,
and TBV in critically ill patients.
|
Footnotes
|
|---|
Abbreviations:
CBV = central blood volume; COPA = pulmonary artery
thermodilution cardiac output; COPDD = cardiac output
measured by pulse dye densitometry; COTPID = cardiac
output measured by the transpulmonary indicator dilution technique;
ICG = indocyanine green; ITBV = intrathoracic blood volume;
MTT = mean transit time; PDD = pulse dye densitometry;
RMSD = root mean square difference; TBV = total blood volume;
TBVPDD\t= total blood volume measured by pulse dye
densitometry; TBVTPID = total blood volume
measured by the transpulmonary indicator dilution technique;
TPID = transpulmonary indicator dilution
Received for publication March 1, 2001.
Accepted for publication August 9, 2001.
|
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Abstract
Introduction
