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Eur J Cardiothorac Surg 1998;13:533-540
© 1998 Elsevier Science NL

Central venous pressure, pulmonary capillary wedge pressure and intrathoracic blood volumes as preload indicators in cardiac surgery patients¹

Department of Cardiac Surgery, University Hospital Großhadern, Ludwig-Maximilians-Universität München, 81377 Munich, Germany

Received 29 September 1997; received in revised form 16 February 1998; accepted 24 February 1998.

Corresponding author. Tel.: +89 7097 1844; fax: +89 7097 1848; e-mail: doc.olli@www.lrz.uni-muenchen.de

	Abstract

Top Abstract Introduction Patients and methods Results Discussion Appendix A. Conference... References

 
Objective: Monitoring of cardiac preload is mainly performed by measurement of central venous and pulmonary capillary wedge pressure in combination with assessment of cardiac output, applying the pulmonary arterial thermal dilution technique. However, the filling pressures are negatively influenced by mechanical ventilation and the pulmonary artery catheter is criticized because of its inherent risks. Measurement of right atria, right ventricular, global end diastolic and intrathoracic blood volume index by arterial thermal dye dilution utilizing the COLD-system may represent an alternative. Methods: In 30 CABG patients with an uncomplicated postoperative course the mentioned parameters were measured 1, 3, 6, 12 and 24 h postoperatively to prove their qualification as preload indicators: As patients received no inotropic support, changes of cardiac index and stroke volume index must correlate to changes of presumably preload indicating parameters. Results: When arterial and pulmonary arterial thermal dilution were compared, no differences were found; the correlation coefficient being 0.96, the bias 0.16 l/min per m² (2.4%) and coefficients of variation did not exceed 7%. Changes of central venous pressure, capillary wedge pressure, right atrial end diastolic volume index and right ventricular end diastolic volume index did not correlate at all to changes of cardiac and stroke volume index (coefficients ranged from -0.01 to 0.28). In contrast, intrathoracic and global end diastolic blood volume indices with coefficients from 0.76 to 0.87, did show a good correlation to cardiac and stroke volume index. Conclusion: Central venous pressure, capillary wedge pressure, right atrial and right ventricular end diastolic volumes are no suitable preload parameters in cardiac surgery intensive care, compared to intrathoracic and global end diastolic blood volumes. The latter show a higher clinical value and can be obtained by less invasive methods, as no pulmonary artery catheter is required.

Key Words: Thermal dye dilution • Cardiac output measurement • Cardiac preload • Cardiac filling pressures • Intrathoracic blood volume

	Introduction

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Hemodynamic monitoring and treatment of deviation from normovolemia belong to the fundamental and most difficult tasks in intensive care medicine [1] [2]. Usually, monitoring of cardiac output (CO) and preload as the basis to volume therapy is performed with a pulmonary artery catheter (PAC) which allows assessment of CO and measurement of central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP). CVP and PCWP are assumed to reflect central blood volume and hence to be reliable guides to volume therapy. These pressures however, are indirect volume indicators at best, and are influenced by lung compliance and intrathoracic pressures, most pronounced in ventilated patients [2] [3] [4]. Moreover, because of its inherent risks and invasiveness the PAC is met with criticism [5] [6]; a recent study [7] reports a higher patient mortality caused by the mere use of this catheter. As a consequence a re-evaluation of the use of this catheter was recommended [8] [9] [10] [11].

Based on this background, new preload parameters have to be found and investigated. Instead of conventional pulmonary artery thermal dilution (TDpa) with the PAC, the arterial double-indicator thermal dye dilution (TDDart) allows the determination of CO, right atrial (RAEDV) and right ventricular (RVEDV) end diastolic volume, global end diastolic volume (GEDV), which represents the sum of volumes in all chambers of the heart at the time of end-diastole, and intrathoracic blood volume (ITBV), which consists of GEDV plus the pulmonary blood volume. Compared to CVP and PCWP with its indirect access to preload, the latter four parameters may directly reflect cardiac preload by volumetric measurements.

Despite encouraging experimental data and first clinical experiences [12] [13] [14] no publications exist on the use of this method and its parameters concerning volume management in cardiac surgery. The purpose of this study was, to compare conventional preload parameters CVP and PCWP with intrathoracic partial blood volumes as provided by TDDart and to test these parameters on their use as guides to volume therapy.

	Patients and methods

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Patients
The study included thirty patients (26 males/4 females) after uncomplicated coronary artery bypass grafting. Mean age was 66.9±10.2 years (range 44–87 years). The underlying disease was ischemic heart disease in all cases. Patients with extensive peripheral arterial occlusive disease, patients with concomitant heart valve disease, and patients with a known allergy against indocyanine green dye (ICG) were not considered for this investigation. Only patients who did not receive any inotropic support during their stay on the intensive care unit and who had no postoperative complications like bleeding, arrhythmia, prolonged ventilation, stroke, infection or necessity of atrial or ventricular pacing were included in the study. Patients who did not fulfill these conditions were retrospectively excluded. The study was conducted according to the principles of the Helsinki declaration and written informed consent was obtained from all patients prior to the operation.

Methods
As part of our routine monitoring, the PAC (Ohmeda, Erlangen, Germany) was inserted upon induction of anesthesia. For arterial access a 3F thermistor-tipped fibre optic catheter for double indicator dilution (PV 2024, Pulsion Medical Systems, Munich, Germany) was used. It was introduced via a 4F introducing sheath (Arrow, Reading, USA) (with side port for pressure monitoring and blood sampling; no additional arterial access was necessary) in the femoral artery, placed into the descending aorta and connected to a bedside computer (COLD Z-021, Pulsion Medical Systems, Munich, Germany). As the PAC was also attached to this system, a simultaneous measurement of right (COpa) and left (COart) ventricular cardiac output was possible. The double indicator consisted of 1mg/kg body weight indocyanine green dye mixed in 10 ml iced 5% dextrose solution. To maintain a constant indicator temperature and to exclude variations of manual injection, an automatic thermodilution injector (ZI-03, Pulsion Medical Systems, Munich, Germany) was used, which kept the indicator temperature at 4°C and injected it at a constant rate of 10 ml/s.

At 1, 3, 6, 12 and 24 h postoperatively, simultaneous triplicate TDpa and TDDart measurements (measurement interval 3 min) were performed and systemic vascular resistance indices (SVRI) were computed. The indicator bolus was injected into the superior vena cava via the proximal port of the PAC. The dilution curve of the cold was recorded in the pulmonary artery by the thermistor of the PAC, the dilution curves of cold and dye were recorded simultaneously in the descending aorta, using the signals from the thermistor-tipped fibre optic catheter.

Pulmonary arterial and arterial thermal dilution enable determination of COpa, COart and left ventricular stroke volume (SV), using the conventional Stewart–Hamilton formula. Estimation of volumes by thermal-dye-dilution is based on the simultaneous application of two substances that distribute either to the intravascular space of the cardiopulmonary system or to the intra- and extravascular space: The cold indicator distributes within the intra- and extravascular space, thereby marking the intrathoracic thermal volume. The dye ICG, which even with severe lung injuries stays intravascularly [15], immediately after injection binds to plasma proteins, thereby marking the intrathoracic blood volume exclusively. Concerning the extremely rare side effects see Ref. [15].

ITBV is then calculated by multiplying the mean transit time of the dye (between the point of injection and the point of detection) with COart. GEDV is gained by subtracting the pulmonary thermal volume (COart x exponential downslope time of the dye) from the intrathoracic thermal volume (COart x mean transit time of the cold). Multiplying COpa with the downslope time of the cold yields RVEDV. Subtracting RVEDV from right heart end diastolic volume (COpa x mean transit time of the cold) yields RAEDV. For a more detailed description of the method see Pfeiffer et al. [16].

Statistics
For statistical analysis, except for CVP and PCWP all values have been indexed to body surface area as it is frequently done in clinical practice. In order to validate COart, which is the basis of the volumetric measurements of the COLD-system, the `gold standard' COpa was assessed at the same time and linear regression and Bland–Altman [17] analyses were computed. Reproducibility was tested in terms of the coefficient of variation of three successive measurements.

As the patients did not receive inotropic support, it can be assumed, that relevant changes of myocardial inotropic status or afterload did not occur during the study period. As a consequence, changes of cardiac output or stroke volume must depend on changes of cardiac preload, according to the Frank–Starling law. Therefore linear regression analyses were computed between changes of preload dependant left ventricular stroke volume index (SVI) and cardiac index (CI) and the corresponding, presumably preload indicating parameters CVP, PCWP and the indices of RAEDV, RVEDV, ITBV and GEDV (e.g. the change of CVP and the change of CI from the 1 h point of time to the 3 h point of time were computed and used for the regression analysis). Regression analyses have been tested for significance and mean results at different measurement times were compared with the t-test for paired samples. All statistical analyses were computed by SPSS for Windows (Version 7.0, 1995, SPSS Inc. Chicago, IL).

	Results

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All patients studied were extubated between 6 h and 18 h after the operation, left the intensive care unit at the second postoperative day and were discharged from the hospital between day 8 and 11 after the operation.

The comparison of simultaneous CO determination in the pulmonary artery (CIpa) and in the descending aorta (CIart) with the COLD system is given in Fig. 1 . The regression analysis ( Fig. 1a) depicts a correlation coefficient of 0.96. Mean difference between both methods (bias) was 0.16 l/min per m², corresponding to 2.4% as shown in the Bland–Altman plot in Fig. 1b. This means that CIart constantly yielded higher numbers when compared to CIpa. Limits of agreement (2 SD) were +0.79 l/min per m² and -0.44 l/min per m². The mean difference did not depend on the level of CI.

View larger version (21K): [in this window] [in a new window]   Fig. 1. Comparison of cardiac index measurements by arterial and pulmonary arterial thermal dilution with the COLD-system. (a) Regression analysis. (b) Bland–Altman plot. (CIart, cardiac index derived from arterial thermal dilution; CIpa cardiac index derived from pulmonary arterial thermal dilution).

The coefficients of the correlation analyses between changes () of CVP, PCWP, RAEDVI, RVEDI and changes of SVI and CI are depicted in Table 2. None of these parameters showed a clinically sufficient correlation, the highest correlation coefficient was 0.28 (RAEDVI). Higher correlation coefficients than the latter ones were found when the parameters ITBVI and GEDVI were used. ITBVI correlated well with SVI and CI, coefficients were 0.76 and 0.83, respectively ( Fig. 2 ). Correlation coefficients of GEDVI versus SVI/CI were 0.82 and 0.87 ( Fig. 3 ).

View larger version (17K): [in this window] [in a new window]   Fig. 2. Regression analysis between changes of ITBVI and changes of CI (ITBVI, changes of intrathoracic blood volume index; (CI changes of cardiac index).

View larger version (18K): [in this window] [in a new window]   Fig. 3. Regression analysis between changes of GEDVI and changes of CI (GEDVI, changes of global end diastolic volume index; (CI changes of cardiac index).

	Discussion

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All preload parameters measured with the COLD system are based on arterial thermal dilution. Therefore it has to be proved first, whether CIart corresponds to CIpa when both are measured by the thermal dilution technique.

In our study, CIart values were higher when compared with those of CIpa, which supports results from other authors [18] [19] [20] [21] [22]. Two divergent explanations are suggested to account for this discrepancy: The indicator is possibly lost on trans-cardio-pulmonary passage with resulting overestimation of CIart as compared to CIpa [19]. Others could not confirm the assumed loss of indicator [18] [20]. They argue, that a slowing of the heart rate as a reaction of the sinus node to the injected cold influences the estimation of CIpa [21]. Slowing of heart rate however would indeed underestimate the true CI value, as the major impact of the slow heart rate would occur during the short passage of the cold indicator between the vena cava and pulmonary artery. During the longer bolus passage to the descending aorta this influence would tend to level out. Which CI is the true CI can therefore not be decided. In any case, both values were tightly correlated as judged from the correlation coefficient of 0.96 and the Bland–Altman analysis with a mean difference CIart/CIpa of 2.4% only ( Fig. 1a,b). As coefficients of variation show an equal reproducibility for both methods (Table 1), CIpa can be replaced by CIart without restrictions.

The coefficients of variations of the volumes derived from arterial thermal dilution were not higher than 7%. With 8.3% for GEDVI within a single triplicate measurement sequence (Table 1), even the highest coefficient of variation was found to be below 10%. As coefficients of variation lower than 10% are generally accepted in clinical applications, the variabilties of RAEDVI, RHEDVI ITBVI and GEDVI determinations proved to be satisfactory.

Although there exist several publications, which could show a striking discrepancy between CVP and PCWP and the cardiac preload, especially under the condition of mechanical ventilation, the most common used and clinically accepted method for assessing the volume status is still the measurement of CVP and PCWP. Both pressures are wrongly assumed to reflect right or left ventricular end diastolic volumes [2] [3] [4]. Increasing intrathoracic pressure during mechanically ventilation causes a volume shift from intra- to extrathoracic space and thus decreases venous return and right ventricular filling. On the other hand, ventilator pressure dependant CVP and PCWP are elevated, indicating an increase of preload. Although some clinicians try to get an impression of the volume status by short term ventilator removal, this way is misleading, as changes of preload must be related to changes of intrathoracic pressure [14]. During ventilator disconnection, the correct volume status may possibly be indicated by CVP and PCWP, nevertheless, continuing ventilation will cause the volume shift induced preload reduction again [3].

According to the Frank–Starling law, cardiac output depends on end diastolic wall tension; this wall tension however depends on the volume in the heart and not on the pressure. Judging volume by means of measuring intravascular pressure, especially against atmosphere and not against the surrounding intrathoracic pressure, is therefore not correct. Consequently, in our patients there was no correlation between changes of CVP and PCWP and changes of CO, as all correlation coefficients were near zero (Table 2).

One might argue, that our average cardiac surgical patients were not continuously ventilated during the 24 h study period, and in fact, all patients were off the ventilator after 18h. But this still would imply, that at a time when even the easiest routine patients heart is most sensitive (during the first postoperative hours when all patients are ventilated), there is no adequate monitoring tool for preload. One might also argue, that only in the statistic mean, there may be no correlation between the filling pressures and cardiac output, but in each single patient. However the correlation coefficients between changes of CVP and PCWP and changes of CIart in single patients (Table 2) are still far from being acceptable, as the best correlation coefficient we found was 0.33. Of course, volume status of the patients on most intensive care wards today is not guided by static assessment of CVP and PCWP, and it was attempted to assess it by repeated measurements and changes of these parameters and cardiac output following therapeutic manoeuvres. However as the results in Table 2 prove, the assumed relationship between filling pressures and cardiac output does not exist in this way, which was also shown by other authors [3] [4] [13] [14]. Furthermore, concerning volume therapy, such a strategy could result in a fluid overload.

Poor correlation coefficients were found for RAEDVI and RVEDVI in all patients, as well as in single observations (Table 2). These findings may be explained by the fact, that right ventricular myocardial wall tension underlies different regional influences [23], or that cardiac output depends mainly on left ventricular wall tension, vice versa RVEDV has only minor influence on cardiac performance. Although in the literature a positive correlation between RVEDV and left ventricular end diastolic volume was previously shown [24], our data do not support this conclusion. If there exists a correlation between those parameters, RVEDV should be better correlated to overall cardiac output. The fact that RVEDV does not have a major influence on cardiac output may be proved in pediatric cardiac surgery. By a Fontan operation in case of right ventricular absence or hypoplasia, an acceptable cardiac output can be obtained by connecting venous vascular system to the pulmonary arteries. On the other hand, right ventricular dysfunction may be a limiting factor in patient outcome, but this is rather due to reduced left ventricular preload by right heart pump failure. Measurements of right ventricular preload may therefore fail to correlate to cardiac output, even if they truly reflect RVEDV. As RVEDVI shows no satisfying correlation to CI, this is almost impossible for RAEDVI, because it precedes RVEDVI in flow direction.

In this study ITBV and GEDV proved to be most valuable for cardiac preload determination. This may be due to the fact, that these parameters include both, right and left ventricular end diastolic volumes and therefore reflect the overall filling situation of the heart. As discussed above, the main determinant of overall cardiac output is left ventricular preload.

Comparing ITBV with GEDV as preload indicator, GEDV is slightly more indicative. The reason for this may be, that ITBV also includes pulmonary blood volume, whereas GEDV purely sums up right and left heart volumes. Because in GEDV, left ventricular end diastolic volume reflects a relatively greater portion compared to ITBV, its relation to cardiac output is even closer. These results agree quite well with first results in non-cardiac intensive care patients [13] [14].

As a limitation, in patients who conduct their CO by extensive inotropic support, ITBV and GEDV are not the main determinants of CO. However even in those patients, a meticulous preload management is essential [1], because the wrong volume status (whether too high or too low) may be fatal for patients outcome. Measuring ITBV and GEDV in such cases will help the physician to adjust the preload at the optimum.

It might of course have been interesting to test the volumetric parameters under various loading conditions, however, as mentioned above, performing a volume challenge might be dangerous for cardiac patients. Before doing so, it therefore needs to be shown, that the correlation between ITBV/GEDV and cardiac output, which was found in experimental studies and studies in non-cardiac patients [12] [13] [14], exists in cardiac surgical patients also. As these patients often show dilated hearts with a reduced function, results from non-cardiac patients may not automatically be transferred. Furthermore, as we did not compare absolute values, but rather changes of preload and cardiac output from one time-point to the other, we tested all parameters under varying conditions, occurring in a patients postoperative course; extubation, for example, results in a clear change of a patients loading condition.

If, as in the majority of patients, a PAC is not required for monitoring pulmonary artery pressure, another positive aspect of the COLD method is its low invasiveness [25]. ITBV, GEDV, CO and SV are measured without a PAC, requiring only a central venous and an arterial line. The discussion on the use of a PAC for cardiac output and preload determination, as mentioned in the beginning, is therefore truly justified and the use of a PAC should be limited to patients where knowledge of pulmonary arterial pressure is essential. Placing a PAC for the measurement of mixed venous oxygen saturation can also be limited to a very minority of patients, because measurement of lactate levels in blood gives comparable information concerning oxygen-debt, especially since lactate-measurement is possible at the bedside [26].

As with less invasiveness, parameters of a higher clinical value are available, we therefore conclude, that the described method shows considerable potential as a monitoring tool for volume status and hemodynamics in patients after cardiac surgery.

	Footnotes

 
Presented at the 11th Annual Meeting of The European Association for Cardio-thoracic Surgery, Copenhagen, Denmark, September 28 – October 1, 1997. Winner of the Young Investigator's Award.

	Appendix A. Conference discussion

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Dr H. Borst (Munich, Germany): In your abstract you present 180 cases where the central venous pressure and the pulmonary wedge pressure were very low, so I do not think it is so convincing. Did you make these measurements also in patients who are indeed in trouble when they have high pressures?

Dr Gödje: These pressures, which each are the mean of 30 patients, are not really low, as they lie within a range which is generally seen as the normal range for CVP and PCWP. Although it is difficult to compare our patients which are in trouble, I can state that the volume parameters are useful in any patient situation, whereas the pressures do not correlate to preload whether they are 3–4 mmHg or 15–20 mmHg.

Dr G. Szabo (Heidelberg, Germany): I have two comments on your study. First of all, you assumed that the contractile state and afterload do not change during the 24-h period. It would be a very important assumption to apply the Starling law. I think it is very unlikely that over a 24-h period contractility and afterload does not change. You should think about, for example, recovery from ischemia, reperfusion, and so on. The second, this is a mathematical problem. The linear relationship is only described between end diastolic volume and stroke work. Other indexes have no linear relationship, therefore I think to characterize the relation between preload parameters and cardiac output with linear regression is inappropriate.

Dr Gödje: You may be partially right. To come to the first part of your question, of course we can not absolutely exclude that the patients had no changes of contractility or afterload. But, as it is shown in the according manuscript, afterload did not change significantly from one point of time to the next and also not over the 24-h study period. To exclude potential changes of contractility we did perform this study only in patients who required absolutely no vasoactive or catecholamine support. In patients with drug support, this principle would of course not be applicable. And on the other hand, the need for drug support or the reduction of drug support are at least a hint for changing contractility. Concerning the second part of your question, I agree with you that the relation between preload and output is not overall linear, however, it is linear within its physiologic part. No matter of what kind the relation is, we found a positive correlation between volumes and output, but we found absolutely no correlation between pressures and output. If pressures really reflect preload, there should be roughly a correlation, even if one uses an improper method.

Dr O. Alfieri (Milan, Italy): Do you find a correlation between CVP or pulmonary wedge pressure and cardiac index, in case you keep the ventilatory condition constant?

Dr Gödje: I do not agree with you, that during constant conditions we can find a positive correlation between pressures and output. In any way, we need parameters, which perform good during all conditions and do not only under settled steady state conditions.

	References

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