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TECHNOLOGY, COMPUTING, AND SIMULATION

The Reliability of Pulse Contour-Derived Cardiac Output During Hemorrhage and After Vasopressor Administration

From the Department of Anaesthesiology and Intensive Care Medicine, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

Address correspondence and reprint requests to Dr. Berthold Bein, Department of Anaesthesiology and Intensive Care Medicine, University Hospital Schleswig-Holstein, Campus Kiel, Schwanenweg 21, D-24105 Kiel, Germany. Address e-mail to bein{at}anaesthesie.uni-kiel.de.

	Abstract

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BACKGROUND: Reliable measurement of cardiac output (CO) is important in the critically ill. Pulse contour-derived CO (PCCO) has been evaluated during stable hemodynamics, but is sensitive to changes in vascular tone and has not been validated under conditions of changing hemodynamics. Furthermore, PCCO requires calibration for the individual vascular impedance by transpulmonary thermodilution CO (TPCO), and the required frequency of recalibration to maintain accurate measurements, especially during changing conditions, has not been confirmed. We compared PCCO measurements of CO with TPCO and continuous and bolus pulmonary artery CO (CCO and BCO, respectively) during conditions of uncontrolled hemorrhage and resuscitation with norepinephrine.

METHODS: Thirteen pigs were anesthetized and instrumented for determination of CO by BCO and CCO, respectively, as well as bolus TPCO and PCCO. Uncontrolled hemorrhage was accomplished by liver incision. When mean arterial blood pressure was <25 mm Hg, or heart rate declined progressively to <20% of its peak value, vasopressor therapy was started. TPCO and BCO were performed after induction of anesthesia and 15 min after start of therapy, and PCCO and CCO were obtained repeatedly. CO measurements were compared using Bland-Altman analysis.

RESULTS: Mean arterial blood pressure, CO and systemic vascular resistance decreased after hemorrhage (P < 0.001 and <0.01, respectively). Bias and limits of agreement between CCO and PCCO (0.54 L/min; 1.46 L/min) increased after hemorrhage (–3.49; 6.12) and further deteriorated after norepinephrine administration (–8.01; 9.9). After recalibration, bias and limits of agreement returned to –0.51 and 1.28.

CONCLUSIONS: PCCO needs frequent recalibration during hemorrhage and after vasopressor administration.

	Introduction

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Reliable measurement of cardiac output (CO) is useful for evaluating hemodynamic instability in critically ill patients (1). In the past decade, continuous CO (CCO) was commonly obtained by pulmonary artery catheters (PAC) with integrated heating filaments. However, heating filament-based CO measurements show a lack of agreement with intermittent bolus thermodilution (BCO) during rapid hemodynamic changes due to the time constant of the calculation algorithm (2,3). More importantly, the risk–benefit ratio of right heart catheterization simply for CO determination has been questioned due to associated complications and the availability of less invasive alternatives (4).

One of the less invasive methods for measuring CO is pulse contour analysis. Arterial pulse pressure waveform analysis according to the method by Wesseling consists of measuring the area under the systolic portion of the arterial pulse wave from the end of diastole to the end of the ejection phase, thus enabling a beat-to-beat update of the instantaneous CO (5). Pulse contour analysis is not a new technology, but the technique has been implemented in a commercially available device (PiCCO® monitor, Pulsion Medical Systems, Munich, Germany). Since then, the proprietary calculation algorithm has undergone several methodological refinements. Numerous studies have shown good agreement between PiCCO and aortic transpulmonary and pulmonary artery thermodilution during stable hemodynamics, and the technique therefore has gained increasing clinical acceptance (6–8). Pulse contour-derived CO (PCCO) requires calibration for the individual vascular impedance by transpulmonary thermodilution CO (TPCO). Since the contour of the pulse waveform is integral to the CO measurement when using PCCO, changes in that waveform may herald the need for recalibration. It is not clear, however, how frequently recalibration is necessary if the shape of the pulse contour is altered by catecholamines or changing intravascular volume. Some studies found a substantial change of PCCO accuracy after cardiopulmonary bypass (CPB) and vasopressor administration (9–11), while several other authors were unable to confirm this problem (7,12–14). We hypothesized that both hemorrhage and vasopressor administration affect the accuracy of PCCO. Therefore, our study was designed to (1) compare the level of agreement between methods of CO measurement (BCO, CCO, TPCO, and PCCO) often used in daily clinical routine during hemorrhagic shock and during its treatment with fluids and vasopressors and to (2) determine how long PCCO remains calibrated during shock and its treatment in an established animal model of uncontrolled hemorrhage before and after vasopressor administration.

	METHODS

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The project was approved by the local Animal Investigation Committee, and animals were managed in accordance with the American Physiologic Society and guidelines by the National Academy of Science in the Guide for the Care and Use of Laboratory Animals. The study was performed on 13 healthy swine (German domestic pigs), ranging from 12 to 16 wk of age of either gender, weighing 43–48 kg. The pigs were premedicated with azaperone (neuroleptic drug; 8 mg/kg IM) and atropine (0.05 mg/kg IM) 1 h before surgery. Anesthesia was induced with a bolus dose of ketamine (2 mg/kg IV), propofol (1–2 mg/kg IV), and sufentanil (0.3 µg/kg IV) given via a peripheral catheter into the right ear vein. After endotracheal intubation during spontaneous ventilation, the pigs were ventilated with a volume-controlled ventilator (Siemens SV 900C, Germany), with 35% oxygen at 20 breaths per minute, a tidal volume of 8–10 mL/kg adjusted to maintain normocapnia (end-tidal CO₂ from 35 to 40 mm Hg), and a positive end-expiratory pressure of 5 mm Hg. Anesthesia was maintained with a continuous infusion of propofol (8–10 mg · kg^–1 · h^–1) and sufentanil (0.3 µg · kg^–1 · h^–1); paralysis was provided by a continuous infusion of pancuronium (0.1 mg · kg^–1 · h^–1). Ringer's solution (6 mL · kg^–1 · h^–1) was administered in the preparation phase using an infusion pump (Infusomat, Braun, Melsungen, Germany). A standard lead II electrocardiogram was used to monitor cardiac rhythm. Depth of anesthesia was judged according to Bispectral index (BISXP, Aspect Medical Systems, Natick, MA). Throughout the study period, propofol and sufentanil were titrated aiming at BIS values below 50, which, in our experience, is sufficient to indicate lack of pain perception or arousal in pigs. If BIS indicated a reduced depth of anesthesia, additional propofol and sufentanil were administered.

A PAC (Edwards Swan Ganz Combo EDV Thermodilution Catheter, Baxter Laboratories, Irvine, USA) was inserted via an 8.5 F introducer into the right internal jugular vein, advanced under continuous pressure recording into wedge position and then connected to a CO computer system (Vigilance Monitor, Baxter Edwards Critical Care). Bolus pulmonary artery thermodilution was performed using 10 mL ice cold saline injected in the proximal port of the PAC three times randomly assigned to the respiratory cycle. Measurements were averaged independent of their actual value if the decay curve of the PiCCO plus® and PAC monitor was accepted as reliable; otherwise, it was excluded from further analysis and injection was repeated. A 4-F thermodilution catheter (Pulsion Medical Systems, Munich, Germany) was placed in the femoral artery and connected to the pressure transducer for continuous arterial pressure recording. The arterial catheter was connected to a monitor for pulse contour analysis (PiCCO plus, Software Version 6.0, Pulsion Systems, Munich, Germany) and the resulting signal processed to determine hemodynamic variables. To calibrate the PiCCO device for the individual vascular impedance and for determination of global end-diastolic volume (GEDV), 10 mL ice cold saline was injected into the proximal port of the PAC. The mean of three consecutive measurements randomly assigned to the respiratory cycle was used for calibration. BCO and TPCO measurements were performed simultaneously. Body temperature was maintained between 38.0°C and 39.0°C with a heating blanket. Ventilation was monitored using an inspired/ expired gas analyzer that measured oxygen and end-tidal carbon dioxide (M-PRESTN; Datex-Ohmeda; Helsinki, Finland). Oxygen saturation was monitored by a continuous pulse oxymeter placed on the ear (M-CAiOV; Datex-Ohmeda, Helsinki, Finland). Systemic vascular resistance (SVR) was calculated based on CCO readings, since these were obtained more frequently than BCO and TPCO.

Experimental Protocol
The experimental protocol is delineated in Figure 1. At the end of surgical preparation, at least 30 min were allowed for stabilization. After taking baseline values for BCO, TPCO, CCO, and PCCO (baseline), a midline laparotomy was performed, followed by an incision across the right liver lobe (width, 12 cm; depth, 3 cm) to simulate uncontrolled hemorrhage. Blood in the abdominal cavity was continuously removed by suctioning and collected for quantitative measurement. Hemodynamic decompensation was defined as a mean arterial blood pressure of <25 mm Hg, or a heart rate of <20% of its peak value. At that point, Fio₂ was increased to 1.0 and all animals received a hypertonic-isooncotic hydroxyethyl starch solution (Hyperhaes®, Fresenius, Bad Homburg, Germany, 4 mL/kg over 2 min) and norepinephrine (Aventis Pharma GmbH, Frankfurt am Main, Germany); 25 µg/kg followed by a continuous infusion (60 µg · kg^–1 · h^–1). Further blood loss was prevented by liver compression and surgical drapes. TPCO and BCO were performed at baseline and 15 min after start of therapy in triplicate, and BCO additionally 20 min after trauma. To allow for further determination of uncalibrated PCCO values, no TPCO assessment was performed at that point. PCCO and CCO were obtained directly after each calibration and additionally at trauma + 10 min, trauma + 20 min, at initiation of therapy, and at 5, 10, and 30 min after initiation of therapy (Fig. 1). Fluids were warmed with a fluid warming system (Ranger, Arizant Healthcare Inc. Eden Prairie, MN) to 37°C and administered via an introducer in the right femoral vein to prevent interaction with thermodilution measurements. After finishing the experimental protocol, the animals were euthanized with an overdose of propofol, sufentanil, and potassium chloride and subjected to necropsy to check for correct positioning of the intravascular catheters.

View larger version (15K): [in this window] [in a new window]   Figure 1. Experimental protocol. BCO = cardiac output derived from bolus pulmonary artery thermodilution; TPCO = cardiac output derived from bolus transpulmonary thermodilution (= calibration of PCCO); CCO = continuous cardiac output derived from continuous pulmonary artery thermodilution; PCCO = pulse contour-derived cardiac output; HHS = hypertonic-isooncotic hydroxyethyl starch; NE = norepinephrine; BL-Tr = baseline trauma; Tr + 10 = trauma + 10 min; Tr + 20 = trauma + 20 min; BL-Th = baseline therapy; Th + 5 = therapy + 5 min; Th + 15 = therapy + 15 min; Th + 30 = therapy + 30 min.

Statistical Analysis
Statistical comparisons were performed using commercially available statistics software (GraphPad Prism version 4.03 for Windows, GraphPad Software, San Diego, CA). Differences between CCO and PCCO were analyzed using two-way analysis of variance factoring for time and method of CO determination followed by Bonferroni correction for repeated measurements, and BCO and TPCO values were compared with paired Student's t-test. Bland-Altman statistics were used to compare agreement and to determine differences between methods of CO measurements (15). Bias was defined as the mean value of the differences between methods. Precision was defined as 1 sd of the differences, and limits of agreement were defined as bias ±2 sd. Interchangeability of methods was judged according to criteria proposed by Critchley and defined as limits of agreements 30% of the mean CO (16). One-way analysis of variance was used to check for differences between hemodynamic variables at the different experimental stages, and blood loss and GEDV values were analyzed with the Wilcoxon matched pairs test. A P < 0.05 was considered statistically significant.

	RESULTS

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Hemodynamic variables and total amount of blood loss at the different experimental stages are displayed in Table 1. After liver incision, mean arterial blood pressure decreased continuously, while heart rate increased significantly. SVR was significantly reduced at both 10 and 20 min after trauma (P < 0.001 and <0.01, respectively), and increased after norepinephrine administration. Hemodynamic decompensation occurred after 37 ± 6 min. The increasing blood loss was reflected by GEDV that was 1044 ± 151 mL at baseline and significantly (P < 0.001) decreased to 528 ± 123 mL 15 min after initiation of therapy. CO as assessed with CCO and BCO decreased continuously until hemodynamic decompensation, while, in contrast, PCCO values increased in the majority of animals (Fig. 2). Whereas at baseline CCO and PCCO were interchangeable, increasing blood loss and vasopressor administration led to PCCO readings with large bias and unacceptable limits of agreement thereafter (Figs. 2–5). After recalibration, comparing PCCO with TPCO values yielded limits of agreement of 27%, while limits of agreement with CCO and BCO were 41% and 34%. Applying the strict criteria proposed by Critchley, however, BCO, CCO, TPCO, and PCCO were only interchangeable at baseline. Comparison of BCO with CCO and TPCO 15 min after initiation of therapy yielded limits of agreement of 45% and 33% of the mean CO, respectively (Fig. 5).

View larger version (7K): [in this window] [in a new window]   Figure 2. Cardiac output derived from PCCO, CCO, TPCO, and BCO at the different experimental stages. PCCO = pulse contour-derived cardiac output; CCO = continuous cardiac output derived from continuous pulmonary artery thermodilution; TPCO = cardiac output derived from bolus transpulmonal thermodilution; BCO = cardiac output derived from bolus pulmonary artery thermodilution. BL-Tr = baseline trauma; Tr + 10 = trauma + 10 min; Tr + 20 = trauma + 20 min; BL-Th = baseline therapy; Th + 5 = therapy + 5 min; Th + 10 = therapy + 10 min; Th + 15 = therapy + 15 min; Th + 30 = therapy + 30 min. Significant differences are given for between method comparisons. *P < 0.01 versus CCO; **P < 0.001 versus CCO; P < 0.05 versus BCO. Data are mean ± sd.

View larger version (5K): [in this window] [in a new window]   Figure 5. Bias between cardiac output derived from bolus pulmonary artery thermodilution (BCO) and PCCO, CCO and TPCO at the different experimental stages. PCCO = pulse contour-derived cardiac output; CCO = continuous cardiac output derived from continuous pulmonary artery thermodilution; TPCO = cardiac output derived from bolus transpulmonary thermodilution. Th + 15 = therapy + 15 min; Tr + 10 = trauma + 10 min; Th + 30 = therapy + 30 min. Data are mean ± sd. *Methods interchangeable according to Critchley.

View larger version (6K): [in this window] [in a new window]   Figure 3. Bland-Altman Plot comparing CCO and PCCO at trauma + 10 min. CCO = continuous cardiac output derived from continuous pulmonary artery thermodilution; PCCO = pulse contour-derived cardiac output. The thick line represents the bias and the thin lines the limits of agreement (±2 sd); n = 13.

View larger version (6K): [in this window] [in a new window]   Figure 4. Bland-Altman Plot comparing CCO and PCCO at therapy + 30 min. CCO = continuous cardiac output derived from continuous pulmonary artery thermodilution; PCCO = pulse contour-derived cardiac output. The thick line represents the bias and the thin lines the limits of agreement (±2 sd); n = 12.

One pig died directly after hemodynamic decompensation, whereas in the remaining animals, resuscitation was successful.

	DISCUSSION

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Using this pig model, we found that during stable spontaneous circulation, all investigated methods of CO determination were interchangeable. During hemorrhage and treatment of shock, however, PCCO consistently over-estimated CCO values. In contrast, CCO showed acceptable agreement with both TPCO and BCO throughout the study period.

Pulse contour analysis enables a beat-to-beat update of the instantaneous CO. The system is calibrated for the individual vascular impedance by transpulmonary thermodilution, which additionally gives important information concerning the patient's intravascular volume status; for example, a surrogate variable for preload (GEDV). Despite the advantages of PCCO, there is controversy as to the reliability of this technique during rapid hemodynamic changes and after vasopressor administration. Several studies in patients undergoing CPB found a decreased accuracy of PCCO measurements after CPB (9–11). In one of these studies, there was a significant influence of the SVR (10). In our study, increasing hemorrhage resulted in tachycardia and a reduced CO, while SVR initially decreased. Tachycardia, reduced CO (specifically stroke volume), and decreasing SVR clearly influence the shape of the arterial pulse contour (17). After fluid and norepinephrine administration, PCCO accuracy further deteriorated. Since hemodynamics did not change significantly compared with baseline therapy, it remains speculative whether the effect of hyperoncotic fluid on intravascular volume or, alternatively, the effect of norepinephrine on arterial tone were predominantly responsible for this effect. However, in one investigation in patients during the early postoperative period after elective coronary artery bypass graft surgery, intravascular fluid administration did not influence PCCO readings, and therefore the latter reason is highly likely (13).

It has been suggested, that changes in vascular tone 20% have no impact on PCCO accuracy, whereas greater changes (>50%) may affect it (9). In the present investigation, SVR decreased initially about 40% followed by an equal increase up to 5 min after initiation of therapy. This emphasizes that a rapid change of SVR as a global parameter of arterial tone may have an important impact on arterial pulse contour. Our data further suggest that tachycardia and small stroke volumes may be a limitation for pulse contour-based methods of CO determination. Specifically, a major issue is the ability of the underlying algorithm to reliably identify the systolic portion of the pulse contour. A pivotal point in this respect is the correct identification of the dicrotic notch (18). Especially at faster heart rates, this may become increasingly difficult. Interestingly, other alterations in the shape of the pulse contour seem to be less critical, as reported by Pittman et al. (17). Another important issue is the individual vascular impedance. PCCO values are calibrated to account for this unknown factor. This implies, on the other hand, that changes in the vascular impedance after vasopressor administration must affect reliability of PCCO values. Consequently, the most distinct differences between PCCO and the other methods in our study appeared after vasopressor administration. However, we did not store the pulse contour signal from individual animals for further off-line analysis and therefore cannot comment on the way the shape of the pulse contour changed, except for the common clinical observation that the dicrotic notch started to disappear at faster heart rates.

Besides identification of the dicrotic notch, the ability to track changes in CO correctly depends on the algorithm's ability to compensate for changes in arterial characteristics. The three-element Windkessel model underlying the PiCCO® PCCO algorithm uses the characteristic aortic impedance, Windkessel compliance of the arterial system, and both area and shape of the pressure curve for calculation of flow from the arterial curve (14). Anesthesia-induced changes in arterial tone, impaired performance of the arterial catheter-transducer system, altered peripheral vascular reactivity, and varying blood rheology all may influence the shape of the pulse contour (19). If changes in arterial tone occur, then the primary assumptions about the interaction between stroke volume and pressure also change, and the validity of the underlying algorithm becomes questionable. Also, actual vascular conductance among different arterial beds may vary significantly and rapidly during pathological conditions, i.e., hemorrhage (20). Accordingly, if either global arterial tone or blood flow distribution among vascular beds change, then the relation between the arterial pressure profile and stroke volume may vary. From our data, however, we cannot differentiate if failure to identify the dicrotic notch or a change in arterial tone was predominantly responsible for the large measurement error found.

Only two studies address the impact of hemodynamic changes on PCCO performance over a longer period (14,17). In the study by Goedje et al. (14), reliability of PCCO readings was shown in patients up to 44 h after CPB without repeated calibrations, despite considerable changes in CO, SVR, or both. In contrast to the present investigation, however, the time period in which these changes occurred was not reported. It is conceivable that substantial changes occurring over a longer period have less influence on the shape of the pulse contour compared with more rapid ones. Moreover, none of the patients enrolled suffered from severe hemorrhage during the study period. Consequently, the mean CO of patients (5.7–8.6 L/min) was well above values obtained in our study. Interestingly, bias and limits of agreement did not match the criteria of interchangeability with TPCO during the majority of measurements as well. Pittman et al. (17), comparing PCCO with lithium dilution CO in patients after cardiac or major noncardiac surgery found a slight influence of SVR on CO determination by this method, based on another algorithm of pulse contour analysis. Again, in the latter study, no sustained tachycardia or intravascular volume depletion was present, and 97% and 93% of patients had a <15% change in heart rate and a <15% change in mean arterial blood pressure, respectively. Interestingly, the algorithm underlying lithium-calibrated PCCO has only been validated for heart rates between 30 and 120 bpm (18). Therefore, the favorable results reported may be challenged by a clinical scenario comparable to our animal model.

The methods investigated were only interchangeable at baseline, applying the strict criteria proposed by Critchley (16). The higher bias and limits of agreement of CCO readings during hemorrhage and the therapy phase are not surprising, since CCO obtained with a PAC reflects rapid hemodynamic changes with a considerable delay (2). However, throughout the entire study period, CCO was close to the ±30% criterion proposed by Critchley compared with both TPCO and BCO, albeit not inside this range. Importantly, CCO values correctly indicated the way CO trended over time. This may be rooted in the calculation algorithm that is based on a complete new set of data containing several randomly arranged thermodilutions during each measuring cycle (3).

Another major issue is the frequency of PCCO recalibration required to maintain reliable PCCO values. From a clinical standpoint, a pivotal event is the moment the methods studied start to give significantly different results. In our study, this discrepancy started by 20 min after hemorrhage with a significant difference between BCO and PCCO. Most important, there was already a significant difference between CCO and PCCO 5 min after initiation of vasopressor therapy. We would therefore suggest recalibration during continuous and sustained hemorrhage each 20–30 min, and during large dose vasopressor therapy as soon as possible after vasopressor administration.

Some limitations of our study should be noted. The PAC with integrated heating filament is able to perform semicontinuous CO determinations at best, since the time constant of the measurement algorithm leads to a delayed time response in case of rapid hemodynamic changes (2,3). Moreover, none of the methods investigated allow for determination of the "true" CO, and its value remains speculative. Therefore, our conclusions are based on the plausible trends in CO measurement and data on limits of agreement. However, good agreement during hemorrhage (20 min after trauma) between BCO and CCO indicates that values obtained using CCO are more reliable than PCCO values. Intuitively, an increasing CO during sustained hemorrhage is highly unlikely. More important, after recalibration PCCO values again closely approximated CCO. Since time to hemodynamic decompensation varied among animals due to uncontrolled hemorrhage, the total amount of blood loss also differed at the specified experimental stages. Therefore, the shape of the pulse contour was changed over different time intervals, which may explain the large variation between individual animals. Rapid hemorrhage will probably have greater impact on PCCO accuracy compared with more gradual hemorrhage. This is emphasized by the fact that the most rapid change in the vascular tone by vasopressor administration provoked the largest bias of PCCO compared with the other methods of CO determination.

In conclusion, while PCCO, TPCO, BCO, and CCO are interchangeable during stable hemodynamics, PCCO is unreliable for CO determination during continuous hemorrhage and after administration of norepinephrine. These findings suggest that PCCO values should be interpreted with caution if the shape of the pulse contour is altered substantially. During sustained tachycardia, as well as during large dose vasopressor administration, recalibration is recommended whenever changes in PCCO prompt major alteration in patient management.

	ACKNOWLEDGMENTS

 
The authors are indebted to Volkmar Haensel-Bringmann, RN, Department of Anesthesiology and Intensive Care Medicine, for excellent technical assistance and logistic support, and to Juergen Hedderich, PhD, Department of Biostatistics, for statistical advice.

	Footnotes

 
Accepted for publication March 29, 2007.

Funding was restricted to institutional and departmental sources.

No author has a conflict of interest with regard to any device or drug used in this study.

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