Relationships between volume and pressure measurements and stroke volume in critically ill patients

Abstract

To evaluate the relationships between the changes in stroke volume index (SVI), measured in both the aorta and the pulmonary artery, and the changes in intrathoracic blood volume index (ITBVI), as well as the relationship between changes in aortic SVI and changes in the pulmonary artery wedge pressure (PAWP). Prospective study with measurements at predetermined intervals. Medical intensive care unit of a university hospital. One hundred and fifty-four measurements were taken in 45 critically ill patients with varying underlying disorders. Aortic SVI and pulmonary arterial SVI were determined with thermodilution. PAWP was measured using a pulmonary artery catheter. ITBVI was determined with thermal-dye dilution, using a commercially available computer system. A good correlation was found between changes in ITBVI and changes in aortic SVI. However, this correlation weakened when changes in ITBVI were plotted against changes in pulmonary arterial SVI, which was in part probably due to mathematical coupling between ITBVI and aortic SVI. A good correlation between changes in ITBVI and changes in aortic SVI could also be established in most of the individual patients. No correlation was found between changes in PAWP and changes in aortic SVI. ITBVI seems to be a better predictor of SVI than PAWP. ITBVI may be more suitable than PAWP for assessing cardiac filling in clinical practice.

Objective:

To evaluate the relationships between the changes in stroke volume index (SVI), measured in both the aorta and the pulmonary artery, and the changes in intrathoracic blood volume index (ITBVI), as well as the relationship between changes in aortic SVI and changes in the pulmonary artery wedge pressure (PAWP).

Design:

Prospective study with measurements at predetermined intervals.

Setting:

Medical intensive care unit of a university hospital.

Patients and methods:

One hundred and fifty-four measurements were taken in 45 critically ill patients with varying underlying disorders. Aortic SVI and pulmonary arterial SVI were determined with thermodilution. PAWP was measured using a pulmonary artery catheter. ITBVI was determined with thermal-dye dilution, using a commercially available computer system.

Results:

A good correlation was found between changes in ITBVI and changes in aortic SVI. However, this correlation weakened when changes in ITBVI were plotted against changes in pulmonary arterial SVI, which was in part probably due to mathematical coupling between ITBVI and aortic SVI. A good correlation between changes in ITBVI and changes in aortic SVI could also be established in most of the individual patients. No correlation was found between changes in PAWP and changes in aortic SVI.

Conclusion:

ITBVI seems to be a better predictor of SVI than PAWP. ITBVI may be more suitable than PAWP for assessing cardiac filling in clinical practice.

Introduction

]. Moreover, CVP and PAWP are absolute intravascular pressures, meaning that changes in intrathoracic pressures will influence the recorded values of CVP and PAWP. This applies in particular to mechanically ventilated patients who are ventilated with positive end-expiratory pressure. Thus, therapeutic decisions based on CVP and/or PAWP may be based on inaccurate measures of a patient's volume status.

] showed a correlation coefficient of 0.67 between changes in ITBVI and changes in SVI during the early phase of haemodynamic instability in patients with sepsis or septic shock.

In a mixed group of critically ill patients we studied the correlations between SVI and PAWP, measured using a pulmonary artery catheter, and the correlations between SVI and ITBVI, measured with a commercially available computer system using the thermal-dye dilution technique.

Methods

], and patients with hepatic cirrhosis requiring a transjugular intrahepatic portosystemic shunt (TIPS). In all of these studies, patients were monitored using a pulmonary artery catheter (7.5-F Swan Ganz-catheter, Model VS 1721; Ohmeda, Swindon, UK) and a 4-Fr fiberoptic catheter (Pulsiocath PV 2024; Pulsion, Munich, Germany), introduced into the descending aorta through a 6-Fr introducer sheath (Model 616150A; Ohmeda) and connected to a computer system (COLD Z-021 system; Pulsion) for determination of ITBVI.

Haemodynamic measurements, both with the pulmonary artery catheter and the thermal-dye dilution technique, were made at regular intervals during the first 24 h after admission to the intensive care unit. Fluid therapy was given as long as every seperate fluid bolus (500 ml colloids over 20 min) resulted in an increase of CI of 10% or more. PAWP was not allowed to exceed 18 mmHg in patients with acute cardiogenic pulmonary oedema, however, and was not allowed to exceed 16 mmHg in the other categories. Whenever CI increased by less than 10%, fluid challenges were stopped, regardless of the PAWP at that point, and inotropes and/or vasopressors were given when appropriate.

All study protocols were approved by the Local Ethics Committee, and informed consent was given by each patient or his/her next of kin.

].

of an ice-cold indocyanin green (ICG) solution (2 mg/ml). The mean value of two measurements was used for analysis.

]. The product of CI and MTT is the volume between the site of injection and the site of detection. ITBVI can be calculated using the following formula:

(ICG)

] was used for assessing differences between pulmonary arterial CI and aortic CI.

Results

. Thirty-six patients were mechanically ventilated throughout the study protocol.

Patients and measurement details in the various disease categories

Correlation between CI measured in the pulmonary artery (CIpa) and CI measured in the aorta (CIa) in the left panel. Right panel shows Bland-Altman analysis. SD, standard deviation.

The correlation between changes in ITBVI (Diff ITBVI) and changes in SVI measured in the aorta (Diff SVIa; left panel), and the correlation between changes in ITBVI (Diff ITBVI) and changes in SVI measured in the pulmonary artery (Diff SVIpa; right panel).

Individual regression of PAWP versus aortic SVI (SVIa) in the various disease categories.

Individual regression lines of ITBVI versus aortic SVI (SVIa) in the various disease categories.

.

< 0.001).

shows the individual regression lines of PAWP versus aortic SVI of the patients in the various disease categories. From the graphs it is clear that there are large interindividual differences in correlation in all of the disease categories.

shows the individual regression lines of ITBVI versus aortic SVI of the patients in the various disease categories. In three disease categories (sepsis, ARDS and TIPS) a positive correlation was noted in almost all patients, although interindividual differences exist in the steepness of the regression lines. Only in the patients with acute cardiogenic pulmonary oedema could such a relationship not be confirmed. It has to be noted, however, that in this patient group many supportive adjustments were made with inotropes and/or vasopressors during the course of the measurements, so that the relationships were based on a small number of measurements.

Discussion

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.

].

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.

]. 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.

), 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.

], 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.

], 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.

Acknowledgements

The authors would like to thank Professor Jean-Louis Vincent (Free University of Brussels, Belgium) for his comments on earlier versions of this manuscript.

Keywords

• cardiac output
• intrathoracic blood volume
• pulmonary artery wedge pressure
• stroke volume
• thermal dye dilution