Skip Navigation LinksHome > July 2013 - Volume 117 - Issue 1 > An Assessment of Global End-Diastolic Volume and Extravascul...
Anesthesia & Analgesia:
doi: 10.1213/ANE.0b013e31828f2c39
Technology, Computing, and Simulation: Research Report

An Assessment of Global End-Diastolic Volume and Extravascular Lung Water Index During One-Lung Ventilation: Is Transpulmonary Thermodilution Usable?

Haas, Sebastian A. MD*; Trepte, Constantin J. C. MD*; Nitzschke, Rainer MD*; Jürgens, Tim P. MD; Goepfert, Matthias S. MD*; Goetz, Alwin E. MD, PhD*; Reuter, Daniel A. MD, PhD*

Free Access
Supplemental Author Material
Article Outline
Collapse Box

Author Information

From the Departments of *Anesthesiology, Center of Anesthesiology and Intensive Care Medicine and Systems Neuroscience, Center for Experimental Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Accepted for publication February 4, 2013

Published ahead of print April 16, 2013

Funding: This study was funded solely from departmental sources.

Conflict of Interest: See Disclosures at the end of the article.

Sebastian A. Haas, MD and Constantin J. C. Trepte, MD contributed equally to the manuscript.

Reprints will not be available from the authors.

Address correspondence to Sebastian Haas, MD, Department of Anesthesiology, Center of Anesthesiology and Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany. Address e-mail to shaas@uke.de.

Collapse Box

Abstract

BACKGROUND: The thermodilution curve assessed by transpulmonary thermodilution is the basis for calculation of global end-diastolic volume index (GEDI) and extravascular lung water index (EVLWI). Until now, it was unclear whether the method is affected by 1-lung ventilation. Therefore, aim of our study was to evaluate the impact of 1-lung ventilation on the thermodilution curve and assessment of GEDI and EVLWI.

METHODS: In 23 pigs, mean transit time, down slope time, and difference in blood temperature (ΔTb) were assessed by transpulmonary thermodilution. “Gold standard” cardiac output was measured by pulmonary artery flowprobe (PAFP) and used for GEDIPAFP and EVLWIPAFP calculations. Measurements were performed during normovolemia during double-lung ventilation (M1), 15 minutes after 1-lung ventilation (M2) and during hypovolemia (blood withdrawal 20 mL/kg) during double-lung ventilation (M3) and again 15 minutes after 1-lung ventilation (M4).

RESULTS: Configuration of the thermodilution curve was significantly affected by 1-lung ventilation demonstrated by an increase in ΔTb and a decrease in mean transit time and down slope time (all P < 0.04) during normovolemia and hypovolemia. GEDIPAFP was lower after 1-lung ventilation during normovolemia (M1: 459.9 ± 67.5 mL/m2; M2: 397.0 ± 54.8 mL/m2; P = 0.001) and hypovolemia (M3: 300.6 ± 40.9 mL/m2; M4: 275.2 ± 37.6 mL/m2; P = 0.03). EVLWIPAFP also decreased after 1-lung ventilation in normovolemia (M1: 9.0 [7.3, 10.1] mL/kg; M2: 7.4 [5.8, 8.3] mL/kg; P = 0.01) and hypovolemia (M3: 7.4 [6.3, 9.7] mL/kg; M4: 5.8 [5.2, 7.4]) mL/kg; P = 0.0009).

CONCLUSION: Configuration of the thermodilution curve and therefore assessment of GEDI and EVLWI are significantly affected by 1-lung ventilation.

Advanced hemodynamic monitoring has become increasingly important as surgical procedures and patients, suffering from various comorbidities, increase the complexity of the perioperative and intensive care setting.1,2 In this context, optimization of cardiac preload guided by global end-diastolic volume index (GEDI) and extravascular lung water index (EVLWI) both derived from transpulmonary thermodilution (TPTD) has been shown to result in improved clinical outcome.3 Methodologically, a central venous bolus injection of an indicator, i.e., cold saline is required. This bolus dilutes within the blood on its passage through the right heart, pulmonary circulation, left heart, and aorta. The change in blood temperature then is detected by a thermosensor located at the tip of an arterial catheter. The resulting thermodilution curve is determined by the difference of blood temperature (ΔTb) and its chronological sequence. Cardiac output (CO) can be assessed based on the modified Stewart-Hamilton equation. Calculation of various volumetric variables derived from the thermodilution curve is also possible. For this purpose, 2 variables are needed: mean transit time (MTT) and down slope time (DST). The MTT is the time required for half of the indicator to pass the thermistor in the femoral artery. MTT divides the area under the thermodilution curve into 2 areas of the same size.2 DST is defined as the exponential elution time. In detail, the time between 85% and 45% of the maximum temperature response is measured.4 This method of thermodilution curve assessment is illustrated in Figure 1. On the basis of CO, MTT, and DST, it is now possible to calculate the intrathoracic thermo volume (ITTV = CO·MTT) and pulmonary thermovolume (PTV = CO·DST). The difference between ITTV and PTV is the global end-diastolic volume (GEDV). Intrathoracic blood volume (ITBV) is calculated by ITBV = 1.25·GEDV.5 The difference in ITTV and ITBV equals the EVLW (Fig. 2).

Figure 1
Figure 1
Image Tools
Figure 2
Figure 2
Image Tools

One-lung ventilation is a routine anesthesia procedure.6 Due to progress in surgical techniques, there is increasing necessity for prolonged intraoperative 1-lung ventilation (lung transplantation, esophagectomy, spinal surgery, minimally invasive cardiac surgery). One-lung ventilation results in the total atelectasis of 1 lung and an increase in the pulmonary vascular resistance provoked by hypoxic pulmonary vasoconstriction. This may influence transit time and contact time of the indicator with the extravascular space resulting in altered indicator loss in the surrounding tissue, especially in the deflated lung.7 Consequently, configuration of the thermodilution curve and thereby all derived volumetric variables for monitoring and guidance of therapy would be questionable if these effects have a significant impact on the accuracy of measurement.

As part of this experimental study, we have already reported that the assessment of CO by TPTD is clinically useful during 1-lung ventilation even if accuracy is reduced.8 Even more clinically important, the validity of GEDI and EVLWI during 1-lung ventilation remains unclear. Therefore, we evaluated the influence of 1-lung ventilation on the configuration of the thermodilution curve and consequently the calculation of GEDI and EVLWI. Measurements were conducted in normovolemic and hypovolemic conditions representing a wide range of preload and CO.

Back to Top | Article Outline

METHODS

The study was approved by the local governmental commission for the care and use of animals. The animals received care in compliance with the “Guide for the Care and Use of Laboratory Animals” (National Institutes of Health publication No. 86-23, revised 1996).

Back to Top | Article Outline
Anesthesia and Instrumentation

Animals were fasted overnight. Premedication was conducted by IM injection of ketamine (10 mg/kg), azaperone (4 mg/kg), midazolam (0.5 mg/kg), and atropine sulfate (1 mg). Thereafter, tracheotomy and placement of an endotracheal tube (8.5 Ch) were performed. Anesthesia was maintained by continuous infusion of fentanyl (0.05 mg·kg−1·h−1) and propofol (10 mg·kg−1·h−1). After securing the airway, a single dose of pancuronium (0.1 mg/kg) was administered to facilitate surgical preparation. Animals were monitored with a 5-lead electrocardiograph and pulse oximetry. Controlled mechanical ventilation was performed using a volume-controlled mode. Tidal volumes were set at 10 mL/kg, inspiration to expiration ratio at 1:1.6, and positive end-expiratory pressure at 5 cm H2O. (Zeus, Drägermedical®, Lübeck, Germany). End-expiratory pCO2 was continuously controlled and maintained at 5.3 to 6.0 kPa by adjusting respiration rate. A saline infusion was given at a rate of 13 mL·kg−1·h−1 to maintain hydration. Body temperature was measured by the arterial catheter and kept constant by using warming blankets and prewarmed infusions. For catheter placement and surgical preparation, animals were placed in the supine position. An 8.5 French central venous catheter was introduced into the right internal jugular vein for drug and fluid administration as well as for central venous pressure measurement, for injection of the cold indicator for thermodilution and detection of injection temperature (Ti) via a thermistor (Pulsion®, Munich, Germany). A 5 French thermistor tipped catheter (PiCCO Catheter, PV 2015L20N, Pulsion) was placed into the femoral artery for estimation of blood temperature (Tb) and ΔTb as well as the thermodilution curve. TPTD was also used for assessment of MTT, DST, ITTVTPTD, GEDITPTD, intrathoracic blood volume index (ITBI)TPTD, and EVLWITPTD for which the DuBois formula was used for indexing variables to body surface area ([m2] = 0.20247·Height [m]0.725·Weight [kg]0.425). Based on the results of CO, Ti, Tb, ΔTb, MTT, and DST, averaged thermodilution curves for double-lung ventilation and 1-lung ventilation in normo- and hypovolemia were reconstructed using MATLAB software (MathWorks® Inc., Natick, MA).

To eliminate any potential falsification of GEDITPTD and EVLWITPTD by less precise measurement of cardiac index (CI) based on TPTD during 1-lung ventilation, an ultrasonic pulmonary artery flowprobe (PAFP) was positioned for “gold standard” CI measurement (CIPAFP).8 For positioning of the PAFP, a median sternotomy was performed. The pericardium was longitudinally incised at midline, the pulmonary artery and ascending aorta were exposed, and the perivascular ultrasonic flowprobe (18 mm, Medistim®, Oslo, Norway) was fit around the pulmonary artery. Acoustic gel was placed between the pulmonary artery and flowprobe to avoid any air hindering for accurate flowprobe measurement.

Back to Top | Article Outline
Measurements and Experimental Protocol

Normovolemia was established with hydroxyethylstarch (Voluven 130/0.46%, Fresenius Kabi®, Bad Homburg, Germany) until the stroke volume variation was below 10%, and then baseline measurement was performed (M1). All TPTD measurements were assessed by 3 sequential central venous injections of 10 mL (Vi = 10 mL) cold saline solution (<8°C), randomly administered throughout the respiratory cycle. All thermodilution curves were examined, and measurements were accepted if none of the 3 consecutive values differed by >10% from the mean. Coefficient of variation of the 3 measurements was calculated. One-lung ventilation was initiated by deflating the left lung. An endobronchial blocker (5 French G44109, CookMedical®, Bloomington, IN) was placed into the left main bronchus using a fiberbronchoscope (BF-P60, Olympus®, Hamburg, Germany). During 1-lung ventilation, tidal volumes were reduced to 6 mL/kg. After an equilibration period of 15 minutes, measurements were repeated (M2), and thereafter, 1-lung ventilation was ceased. The period of 15 minutes was chosen because hypoxic pulmonary vasoconstriction reaches maximum within this period of time.9,10 Hypovolemia was induced by the withdrawal of blood (20 mL/kg) over a period of 30 minutes. After the third set of measurements (M3), 1-lung ventilation was implemented as described before (M4). Simultaneously with every thermodilution measurement, CO from the flowprobe was recorded using EMKA software (EMKA Technologies®, Paris, France) and the mean and coefficient of variation was calculated. After completion of the experimental protocol, the animals were euthanized by rapid injection of 50 mmol potassium chloride during deep anesthesia. Later offline analysis was performed to calculate ITTVPAFP, GEDIPAFP, ITBIPAFP, and EVLWIPAFP based on the PAFPs measurement of CI.

Back to Top | Article Outline
Statistical Analysis

Descriptive statistical analysis was performed using SigmaStat™ (Version 3.5) and SigmaPlot™ (Version 10.0; Systat Software®, Chicago, IL). Because there are insufficient data on the effects of 1-lung ventilation on thermodilution-derived variables GEDI and EVLWI, 15% was defined as the minimal detectable difference for these variables corresponding to a clinically relevant change. The calculated minimally required group size was n = 21 (SD: 17%, α error: 0.05, and power: 0.8). Normal distribution of all absolute data was tested using Kolmogorov-Smirnov test with Lilliefors correction. Normal distribution was assumed if P > 0.2. Results are given as mean ± SD for normally distributed variables and as median (25% percentile, 75% percentile) for non-normally distributed data. Furthermore, absolute and percentaged difference of the mean as well as for estimation of clinical relevance 95% confidence interval of the absolute and percentaged difference of the mean was given.11

The coefficient of variation was calculated for averaged CO measurements as SD divided by the mean.12 Paired Student t test was used for comparison between measurements during double-lung ventilation and 1-lung ventilation for normally distributed data and equal variances. Mann-Whitney-Wilcoxon test was used for non-normally distributed data. Beforehand, testing for normal distribution was performed using Kolmogorov-Smirnov test with Lilliefors correction, and homoscedasticity was ascertained by means of Levene test. Results were regarded statistically significant with P < 0.05 and clinically relevant with a difference of >15%.

Back to Top | Article Outline

RESULTS

Hemodynamics

Twenty-three female German domestic pigs (Landrace) in overt good health were studied. The mean size of the animals was 109.2 ± 6.3 cm, and mean body weight was 36.0 ± 5.6 kg. Hemodynamic variables such as heart rate (/minutes), mean arterial blood pressure (mm Hg), central venous pressure (mm Hg), CI (L·min−1·m−2) measured by TPTD (CITPTD), and CI measured by PAFP (CIPAFP) are given in Table 1. None of the variables was significantly affected by the onset of 1-lung ventilation, in normovolemia or in hypovolemia (P > 0.05).

Table 1
Table 1
Image Tools
Back to Top | Article Outline
Analysis of Transpulmonary Thermodilution

Blood temperature (Tb), injection temperature (Ti), and the difference of both (Tb−Ti) did not change significantly after 1-lung ventilation in normovolemia or in hypovolemia. The delta between maximum and minimum blood temperatures (ΔTb) changed significantly after 1-lung ventilation in normovolemia as well as in hypovolemia. MTT was significantly reduced by 1-lung ventilation by approximately 12% in normovolemia (M1: 189.5 ± 34.4 seconds; M2: 166.9 ± 26.3 seconds; P = 0.02) (difference: −22.6 seconds = −11.9%; 95% confidence interval, −4.4 to −40.8 seconds = −2.3% to −21.5%) and hypovolemia (M3: 229.7 [201.1, 274.6] seconds; M4: 202.0 [168.4, 244.8] seconds; P = 0.04) (difference: −27.7 seconds = −12%; 95% confidence interval, 3.8 to −63.9 seconds = −1.6% to 27.8%). DST decreased significantly after onset of 1-lung ventilation by approximately 15% in normovolemia (M1: 93.8 ± 21.8 seconds; M2: 80.0 ± 16.9 seconds; P = 0.02) (difference: −13.8 seconds = −14.7%; 95% confidence interval, −2.2 to −25.4 seconds = −2.3% to −27.1%) and by approximately 18% in hypovolemia (M3: 123.6 [105.5, 146.3]; M4: 101.0 [87.0, 131.9]; P = 0.02) (difference: −22.6 seconds = −18.3%; 95% confidence interval, 1.1 to −44.2 seconds = 0.9% to −35.8%). Results are presented in Table 2. Reconstructed thermodilution curves based on these results illustrate the alteration of curve configuration after 1-lung ventilation as shown in Figure 3 for normovolemia and in Figure 4 in hypovolemia. One-lung ventilation induced a faster start to the curve, a higher peak, and a faster decline both in normo- and in hypovolemia.

Table 2
Table 2
Image Tools
Figure 3
Figure 3
Image Tools
Figure 4
Figure 4
Image Tools
Back to Top | Article Outline
Volumetric Variables Derived from Transpulmonary Thermodilution

In Table 3, the results of volumetric variables calculated from the CO estimated by TPTD are shown. GEDITPTD remained statistically unchanged in both normovolemia (M1: 554 ± 94.2 mL/m2; M2: 521.8 ± 83 mL/m2; P = 0.23) (difference: −32.2 mL/m2 = −5.8%; 95% confidence interval, 19.9 to −85.5 mL/m2 = 3.6% to −17.9%) and in hypovolemia (M3: 413.5 ± 59.9 mL/m2; M4: 394.8 ± 65.0 mL/m2; P = 0.32) (difference: −18.7 mL/m2 = −4.5%; 95% confidence interval, 18.5 to −55.8 mL/m2 = 4.5% to −13.5%). EVLWITPTD in normovolemia decreased significantly after implementation of 1-lung ventilation (M1: 10.7 [9.5, 12.2] mL/kg; M2: 9.1 [7.5, 11.6] mL/kg; P = 0.035) (difference: −1.6 mL/kg = −15.0%; 95% confidence interval, 0.2 to −2.9 mL/kg = 1.9% to −27.1%). Also, in hypovolemia EVLWITPTD showed a statistically significant reduction (M3: 10.1 [8.6, 13.9] mL/kg; M4: 8.6 [7.4, 10.7] mL/kg; P = 0.037) (difference: −1.5 mL/kg = −14.9%; 95% confidence interval, −0.1 to −3.5 mL/kg = −1% to −34.7%).

Table 3
Table 3
Image Tools

Results of volumetric variables calculated from the CO measured by PAFP are given in Table 4. In normovolemia, GEDIPAFP was M1: 459.9 ± 67.5 mL/m2 and decreased significantly to M2: 397.0 ± 54.8 mL/m2 (P = 0.001) (difference: −62.9 mL/m2 = −13.7%; 95% confidence interval, −26.4 to −99.4 mL/m2 = −5.7% to −21.6%). In hypovolemia, GEDIPAFP also decreased significantly (M3: 300.6 ± 40.9 mL/m2; M4: 275.2 ± 37.6 mL/m2; P = 0.03) (difference: −25.4 mL/m2 = −8.5%; 95% confidence interval, −2.0 to −48.8 mL/m2 = −0.6% to −16.2%). EVLWIPAFP also showed a significant change in normovolemia after 1-lung ventilation (M1: 9.0 [7.3, 10.1] mL/kg; M2: 7.4 [5.8, 8.3] mL/kg; P = 0.01) (difference: −1.6 mL/kg = −17.8%; 95% confidence interval, −0.3 to −3.6 mL/kg = −3.3% to −40%). EVLWIPAFP in hypovolemia was also significantly changed after 1-lung ventilation (M3: 7.4 [6.3, 9.7] mL/kg; M4: 5.8 [5.2, 7.4] mL/kg; P = 0.0009) (difference: −1.6 mL/kg = −21.6%; 95% confidence interval, −0.4 to −2.8 mL/kg = −5.4% to −37.8%).

Table 4
Table 4
Image Tools
Back to Top | Article Outline

DISCUSSION

In this experimental animal study, our data demonstrate that configuration of the thermodilution curve is significantly influenced by 1-lung ventilation consequently introducing errors in the measurement of GEDI and EVLWI calculations especially when the gold standard CO is used. Therefore, in clinical use, GEDI and EVLWI measured by TPTD have to be interpreted with caution when assessed during 1-lung ventilation.

The thermodilution curve is the basis for calculation of all variables that can be derived from TPTD. The 3 variables directly assessed from the thermodilution curve are the area under the thermodilution curve, and thereby CO, as well as MTT and DST. However, various factors affect the validity of the method. These factors include structural malfunction of heart valves such as aortic valve defect, mitral, and tricuspid valve insufficiencies.1,13,14 Intracardiac shunts can also increase the recirculation phenomenon of the thermoindicator falsifying the contour of the thermodilution curve.12

CO is calculated by the modified Stewart-Hamilton method focusing on the area under the thermodilution curve. As we recently published as an independent part of this experimental trial, the CO itself is not significantly changed by 1-lung ventilation. However, we also showed that the methodology of CO assessment by TPTD is influenced by 1-lung ventilation with a significant increase in bias of CITPTD compared with CIPAFP.8 For this reason, we also calculated the volumetric variables based on the CO measured by the PAFP to eliminate any influence from imprecise values.

When considering some aspects of the thermodilution curve, the following holds true. We know that the area under the thermodilution curve, necessary for CI assessment, is not altered by 1-lung ventilation. MTT and DST are derived from the contour of the thermodilution curve. Until now, there was no evidence in the literature as to whether or not physiological changes induced by 1-lung ventilation affected the shape of the thermodilution curve and thereby MTT and DST estimation. In prior studies, microembolization of pulmonary vessels was shown to lead to underestimation of extravascular lung water.15–17 It has to be assumed that hypoxic pulmonary vasoconstriction in the deflated lung, as with embolization, affects the contour of the thermodilution curve, because the thermal indicator cannot pass through and cannot equilibrate within the extravascular water space in the same manner.7,18,19 This probably delays arrival at the detection site to such an extent that a certain portion of the indicator passing through the deflated lung disappears as recirculation phenomena. Due to hypoxic pulmonary vasoconstriction, the passage of the cold indicator shifts from the deflated lung to the ventilated lung and more cold indicator passes through the ventilated lung where this bolus passes more en bloc, resulting in a faster start to the curve, increased peak, and an accelerated decline of the thermodilution curve. This hypothesis is confirmed by our results where the ΔTb was increased, and MTT and DST were both significantly decreased after 1-lung ventilation, as illustrated in Figures 3 and 4.

With this in mind, it may initially be surprising that GEDI was not significantly affected, if based on measurements of CO by TPTD (GEDV = CO·[MTT − DST]). The reason for this is that both MTT and DST decreased, and therefore, the difference between both, paired with a more imprecise CO measurement, resulted in a nonstatistically significant change in GEDI. However, when eliminating the falsification factor of a less accurate CO measurement by TPTD during 1-lung ventilation and calculating GEDI based on the gold standard CO measurement by PAFP, GEDI showed a significant change after onset of 1-lung ventilation. Indeed, the same applied to ITBI, which is also used as a volumetric variable of cardiac preload, because the calculation of ITBV is solely based on multiplying GEDV by 1.25.5 Regarding EVLWI, the other clinically important variable derived from thermodilution, the following applies. EVLWI requires ITTV and ITBV for its calculation (EVLW = ITTV − ITBV). When calculating ITTV, the same phenomenon applies as for the estimation of GEDI and ITBI. ITTV showed a tendency to decrease when calculated with less precise assessment of CO by TPTD; however, a level of statistical significance was not reached. When the calculation was based on CO measured by PAFP, ITTV showed significant changes. When put in the equation to calculate EVLWI, the tendencies to decrease for ITTV in absolute values are much larger than for ITBV adding up to a statistically significant change in EVLWI even if calculation was based on measurement of CO by TPTD.

Some limitations of this study should be considered. The main limitation of our study is that gold standard evaluation for comparison of GEDI and EVLWI was not possible during the special situation of 1-lung ventilation because the experimental reference technique was not available. Other aspects include statistical considerations. In our study after onset of 1-lung ventilation, a statistically significant change was demonstrated for GEDI and EVLWI when calculated on the basis of CO assessed by PAFP. However, one has to differentiate between a statistically significant and a clinically relevant change.11 For the design of our study, we had arbitrarily defined a difference of >15% to be of clinical relevance. However, our results only allow the conclusion that thermodilution-derived variables during 1-lung ventilation do present a statistically significant change and therefore have to be interpreted with caution for clinical use. No final conclusion regarding the magnitude and the clinical relevance of change of thermodilution-derived variables can be drawn from the results, and therefore, our study needs to be considered a pilot study. For an exact determination of the magnitude of change, our study does not provide adequate power to reliably define the magnitude of this change. The question to which extent our findings are clinically relevant lack a definite answer making further studies, probably with a larger sample size and maybe another, possibly lower definition of clinical relevance, necessary to finally conclude this issue. Another aspect is that factors for the calculation of intrathoracic compartments differ from pigs to humans.20–22 Therefore, calculation of absolute values is not correct in our study and is biased by a systematic error. Nonetheless, alterations due to interventions within the same subject, such as 1-lung ventilation in our study, still are reliably detected. Also, midline thoracotomy was performed in our study. In most surgeries requiring 1-lung ventilation, excluding lung transplantation, lateral thoracotomy is usually performed. These different thoracic approaches might have different impacts on TPTD. For practical reasons, we performed 1-lung ventilation of the right lung, excluding the smaller left lung from ventilation as pigs do have an accessory upper lobe branch for the right upper lobe complicating 1-lung ventilation and making it less reliable for experimental purposes. Proportions of left to right lung are 3 to 4. Effects of 1-lung ventilation could therefore have been even more distinct if the right lung was excluded. Nonetheless, we consider the effects achieved by exclusion of the left lung adequate.

In conclusion, during 1-lung ventilation, the thermodilution curve is significantly changed, and consequently, an underestimation of GEDI and EVLWI has to be assumed. As a consequence, both variables have to be evaluated and interpreted with caution for guidance of therapy in this special situation.

Back to Top | Article Outline

DISCLOSURES

Name: Sebastian A. Haas, MD.

Contribution: This author helped design and conduct the study, collect the data, analyze the data, and prepare the manuscript.

Attestation: Sebastian Haas approved the final manuscript. Sebastian Haas attests to the integrity of the original data and the analysis reported in this manuscript. Sebastian Haas is the archival author.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: Constantin J. C. Trepte, MD.

Contribution: This author helped design and conduct the study, collect the data, analyze the data, and prepare the manuscript.

Attestation: Constantin Trepte approved the final manuscript. Constantin Trepte attests to the integrity of the original data and the analysis reported in this manuscript.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: Rainer Nitzschke, MD.

Contribution: This author helped design the study, analyze the data, and prepare the manuscript.

Attestation: Rainer Nitzschke approved the final manuscript. Rainer Nitzschke attests to the integrity of the original data and the analysis reported in this manuscript.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: Tim P. Jürgens, MD.

Contribution: This author helped analyze the data and prepare the manuscript.

Attestation: Tim P. Jürgens approved the final manuscript. Tim P. Jürgens attests to the integrity of the original data and the analysis reported in this manuscript.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: Matthias S. Goepfert, MD.

Contribution: This author helped design the study, analyze the data, and prepare the manuscript.

Attestation: Matthias Goepfert approved the final manuscript. Matthias Goepfert attests to the integrity of the original data and the analysis reported in this manuscript.

Conflicts of Interest: The author has no conflicts of interest to declare.

Name: Alwin E. Goetz, MD, PhD.

Contribution: This author helped design the study, analyze the data, and prepare the manuscript.

Attestation: Alwin Goetz approved the final manuscript. Alwin Goetz attests to the integrity of the original data and the analysis reported in this manuscript.

Conflicts of Interest: Alwin Goetz is member of the editorial board of pulsion medical system.

Name: Daniel A. Reuter, MD, PhD.

Contribution: This author helped design the study, analyze the data, and prepare the manuscript.

Attestation: Daniel Reuter approved the final manuscript. Daniel Reuter attests to the integrity of the original data and the analysis reported in this manuscript.

Conflicts of Interest: Daniel Reuter is member of the editorial board of pulsion medical system.

This manuscript was handled by: Dwayne R. Westenskow, PhD.

Back to Top | Article Outline

REFERENCES

1. Reuter DA, Huang C, Edrich T, Shernan SK, Eltzschig HK. Cardiac output monitoring using indicator-dilution techniques: basics, limits, and perspectives. Anesth Analg. 2010;110:799–811

2. Kiefer N, Hofer CK, Marx G, Geisen M, Giraud R, Siegenthaler N, Hoeft A, Bendjelid K, Rex S. Clinical validation of a new thermodilution system for the assessment of cardiac output and volumetric parameters. Crit Care. 2012;16:R98

3. Goepfert MS, Reuter DA, Akyol D, Lamm P, Kilger E, Goetz AE. Goal-directed fluid management reduces vasopressor and catecholamine use in cardiac surgery patients. Intensive Care Med. 2007;33:96–103

4. Saugel B, Umgelter A, Schuster T, Phillip V, Schmid RM, Huber W. Transpulmonary thermodilution using femoral indicator injection: a prospective trial in patients with a femoral and a jugular central venous catheter. Crit Care. 2010;14:R95

5. Sakka SG, Rühl CC, Pfeiffer UJ, Beale R, McLuckie A, Reinhart K, Meier-Hellmann A. Assessment of cardiac preload and extravascular lung water by single transpulmonary thermodilution. Intensive Care Med. 2000;26:180–7

6. Lohser J. Evidence-based management of one-lung ventilation. Anesthesiol Clin. 2008;26:241–72

7. Michard F. Bedside assessment of extravascular lung water by dilution methods: temptations and pitfalls. Crit Care Med. 2007;35:1186–92

8. Trepte C, Haas S, Meyer N, Gebhardt M, Goepfert MS, Goetz AE, Reuter DA. Effects of one-lung ventilation on thermodilution-derived assessment of cardiac output. Br J Anaesth. 2012;108:922–8

9. Moudgil R, Michelakis ED, Archer SL. Hypoxic pulmonary vasoconstriction. J Appl Physiol. 2005;98:390–403

10. Bindslev L, Jolin A, Hedenstierna G, Baehrendtz S, Santesson J. Hypoxic pulmonary vasoconstriction in the human lung: effect of repeated hypoxic challenges during anesthesia. Anesthesiology. 1985;62:621–5

11. Gibbs NM, Weightman WM. Beyond effect size: consideration of the minimum effect size of interest in anesthesia trials. Anesth Analg. 2012;114:471–5

12. Cecconi M, Rhodes A, Poloniecki J, Della Rocca G, Grounds RM. Bench-to-bedside review: the importance of the precision of the reference technique in method comparison studies–with specific reference to the measurement of cardiac output. Crit Care. 2009;13:201

13. Goldenheim PD, Kazemi H. Cardiopulmonary monitoring of critically ill patients (2). N Engl J Med. 1984;311:776–80

14. Nadeau S, Noble WH. Limitations of cardiac output measurements by thermodilution. Can Anaesth Soc J. 1986;33:780–4

15. Giraud R, Siegenthaler N, Park C, Beutler S, Bendjelid K. Transpulmonary thermodilution curves for detection of shunt. Intensive Care Med. 2010;36:1083–6

16. Beckett RC, Gray BA. Effect of atelectasis and embolization on extravascular thermal volume of the lung. J Appl Physiol. 1982;53:1614–9

17. Oppenheimer L, Elings VB, Lewis FR. Thermal-dye lung water measurements: effects of edema and embolization. J Surg Res. 1979;26:504–12

18. Allison RC, Carlile PV Jr, Gray BA. Thermodilution measurement of lung water. Clin Chest Med. 1985;6:439–57

19. Effros RM. Lung water measurements with the mean transit time approach. J Appl Physiol. 1985;59:673–83

20. Kirov MY, Kuzkov VV, Fernandez-Mondejar E, Bjertnaes LJ. Measuring extravascular lung water: animals and humans are not the same. Crit Care. 2006;10:415

21. Kirov MY, Kuzkov VV, Kuklin VN, Waerhaug K, Bjertnaes LJ. Extravascular lung water assessed by transpulmonary single thermodilution and postmortem gravimetry in sheep. Crit Care. 2004;8:R451–8

22. Rossi P, Wanecek M, Rudehill A, Konrad D, Weitzberg E, Oldner A. Comparison of a single indicator and gravimetric technique for estimation of extravascular lung water in endotoxemic pigs. Crit Care Med. 2006;34:1437–43

© 2013 International Anesthesia Research Society

Login

Become a Society Member