The present study shows a good correlation between changes in ITBVI and aortic SVI. This correlation could also be found in the individual patients in three of the four disease categories studied. However, the correlation weakened when, in the pooled data, ITBVI was plotted against pulmonary arterial SVI. No consistent correlation could be established between PAWP and aortic SVI.
CVP and PAWP are pressures that are used in clinical practice to assess cardiac filling or cardiac preload. Under experimental conditions, the so-called ventricular performance curves show a close curvilinear relationship between the end-diastolic pressure of the ventricle and the stroke volume or cardiac output, provided that contractility and afterload are held constant. In clinical practice this relationship may be distorted for several reasons.
The first reason is that several assumptions have to be made for PAWP to reflect the end-diastolic volume of the ventricle. PAWP must be accurately measured, it must reflect left atrial pressure (LAP), LAP must reflect left ventricular end-diastolic pressure (LVEDP), and then LVEDP must relate directly to left ventricular end-diastolic volume to be a true measure of cardiac filling.
In clinical practice there are many doubts about the accuracy of the PAWP measurement. Accurate measurements are frequently prevented by technical aspects. There is also an astonishing lack of basic knowledge among clinicians and nurses on how the measurement should be performed [17,18,19,20]. Apart from the technical factors, there are also clinical entities that interfere with the reliability of PAWP in reflecting LAP accurately. Pulmonary venous obstruction (eg tumours, atrial myxomas, mediastinal fibrosis, pulmonary venous thrombosis) increases PAWP, without an accompanying increased LAP. Disparity between LAP and LVEDP is found in the case of mitral stenosis, and, perhaps more often, in the presence of a decreased left ventricular compliance. A change in ventricular compliance, often met in critically ill patients, may also distort the assumed relationship between LVEDP and left ventricular end-diastolic volume. Furthermore, interventricular dependence also influences the pressure-volume curve of the left ventricle. Hence, disease states with an increased right ventricular afterload (eg acute pulmonary hypertension) will also impair left ventricular compliance. Finally, all intrathoracic pressure changes will affect the recorded values of CVP and PAWP, because these pressures are measured relative to ambient air pressure. Therefore, the measured pressures are not transmural pressures, which is especially true in case the tip of the pulmonary artery catheter is located outside a West zone III .
The second reason for the distorted relationship between the cardiac filling pressures and the stroke volume in clinical practice is that the requirement for the contractility and the afterload to be constant is hardly ever met in clinical practice. Leaving aside the question of whether this requirement is verifiable, practically all interventions interfere either with the myocardial contractility (eg inotropes) or with the ventricular afterload (eg vasoconstrictors, vasodilators). Although we tried to make an approximate correction for this phenomenon, by leaving out those measurements in which supportive changes were made with inotropes or vasoactive medications, it cannot be ruled out that this phenomenon played a role in the results we found.
Taking into account the reasons indicated above, it is not surprising that we did not find a consistent correlation between PAWP and aortic SVI in the individual patients. The present results confirm those of earlier studies [7,9,10,11]. In the patients we studied there were no major differences in the correlation of PAWP and aortic SVI between the different disease states, regardless of whether all patients were ventilated mechanically (ARDS), or only a minority of patients (TIPS) was on mechanical ventilation. In conclusion, PAWP is influenced by so many factors other than cardiac filling that it is not a reliable indicator of cardiac filling in clinical practice. Therefore, the absolute values of these two variables are not an adequate reflection of the cardiac filling conditions of an individual patient.
Changes in ITBVI showed better correlations with changes in aortic SVI than did changes in PAWP, which is also in accordance with earlier findings [7,9,10,11]. From the individual regression lines (Fig. 4), however, it is clear that differences between the individual slopes and, likewise, differences between the distinct disease categories may exist. The interindividual differences may be the consequence of the fact that aortic SVI not only depends on preload, but also on contractility and afterload. Contractility may differ from patient to patient, and from disease to disease. Also, afterload may influence aortic SVI to an extent that depends on the underlying disease. Especially in the case of a diminished contractility, afterload may be a decisive factor in the final aortic SVI. Hence it is understandable that the correlations between ITBVI and aortic SVI in patients with acute cardiogenic pulmonary oedema were not as firm as in the other subgroups. In conclusion, it may still be hard to predict whether an individual patient has reached optimal cardiac filling when a certain value of ITBVI is measured.
By connecting the Swan-Ganz catheter to the COLD system, time differences between pulmonary arterial CI and aortic CI were precluded. Pulmonary arterial CI and aortic CI were closely correlated, with a mean higher value of aortic CI of 0.49 l/min per m2. This is in accordance with an earlier report . However, the difference in the correlation between ITBVI and pulmonary arterial SVI, and the correlation between ITBVI and aortic SVI (Fig. 2) was striking. This could be due to mathematical coupling, because the formula used to determine ITBVI includes aortic CI, and thus aortic SVI indirectly, as a variable . Lichtwarck-Aschoff et al , however, showed that under experimental conditions an increase in aortic CI by inotropes, with a constant ITBVI, did not influence the measured value of ITBVI, because the MTT decreased concomitantly.
The thermal-dye dilution technique was originally developed to determine EVLW. As a consequence, validation of the method is based on comparison of measured values of EVLW with gravimetrically determined EVLW. These values correlate well, with an overestimation of the thermal-dye technique in the lower range and an underestimation in the higher range of EVLW values [24,25,26]. In a recent study , circulating (total) blood volume measured with the COLD system correlated well with standard methods for measuring circulating blood volume. From these results, it has been assumed that measured ITBVI also correlates well with the actual intrathoracic volume. This has not been validated formally, however. On the other hand, the correlations we found are those one would expect on the basis of physiological knowledge. This implies that ITBVI, at least, is a reflection of the actual intrathoracic volume.
In conclusion, the present study shows that the cardiac filling in critically ill patients may not adequately be predicted by PAWP. ITBVI seems to be a more reliable predictor of cardiac filling, because changes in ITBVI closely relate with changes in aortic SVI. Partially, however, this may be due to mathematical coupling. Whether the use of ITBVI for guidance of fluid therapy will improve patient outcome should be subject to further studies.