Anesth Analg 2002;95:798-804
© 2002 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
The Limitations of Preload-Adjusted Maximal Power as an Index of Right Ventricular Contractility
H. Alex Leather, MD*,
Patrick Segers, PhD
,
Yuan-Yuan Sun, MD*,
Hendrik A. De Ruyter, MD*,
Eugène Vandermeersch, MD PhD*, and
Patrick F. Wouters, MD PhD*
*Center for Experimental Surgery and Anesthesiology, Anesthesiology Department, Katholieke Universiteit Leuven, Belgium; and Hydraulics Laboratory, Institute Biomedical Technology, Ghent University, Belgium
Address correspondence to Patrick F. Wouters, Department of Anesthesiology, U.Z. Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium. Address e-mail to Patrick.Wouters{at}uz.kuleuven.ac.be Reprints will not be available.
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Abstract
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Right ventricular (RV) dysfunction is an important cause of perioperative morbidity and mortality, particularly in cardiac surgery. However, assessment of RV contractility remains difficult in clinical practice. Our goal in this study was to examine the value of preload-adjusted maximal power (PWRmax/end-diastolic volume [EDV]2; PAMP) as an alternative to the load-independent pressure-volume-derived indices of contractility in the RV. In anesthetized dogs, RV end-systolic elastance and preload-recruitable stroke work were studied as "gold standards" by using the conductance technique. PAMP was calculated with pulmonary artery flow and RV pressure measurements. Changes in these indices were compared after modulation of the inotropic state (dobutamine infusion; n = 12) and loading conditions (pulmonary artery and inferior caval vein occlusion; n = 14). All indices increased dose-dependently with dobutamine. PAMP was slightly influenced by preload reduction (the slope of the relation between PAMP and EDV was 0.00397 ± 0.01026 W · mL-3 · 0.10-4; mean ± SD). PAMP decreased significantly during pulmonary artery banding (from 1.1 ± 0.7 to 0.7 ± 0.5 W · mL-2 · 0.10-4; mean ± SD), whereas end-systolic elastance and preload-recruitable stroke work did not change. We conclude that the value of PAMP as an index of RV contractility is limited in the open-chest/open-pericardium setting, primarily by its sensitivity to alterations in afterload.
IMPLICATIONS: Preload-adjusted maximal power (PAMP), a load-independent contractile index in the left ventricle, could offer a solution to the problem of measuring right ventricular (RV) contractility in clinical practice. However, this study in open-chest dogs suggests that PAMP is unreliable for assessment of RV contractility because of its sensitivity to afterload changes.
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Introduction
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Despite the recent recognition that the functional state of the right ventricle (RV) is an important independent variable in cardiovascular physiology and pathophysiology, the quantification of RV systolic function remains unsatisfactory in the clinical setting. Although the traditional methods of estimating contractility, such as ejection fraction and dP/dtmax, are rate- or load-dependent and therefore unreliable in pathologic conditions, the current "gold standard" indices based on pressure-volume analysis remain impractical for everyday clinical use. The slope (Ees) of the end-systolic pressure-volume relationship (ESPVR) (1,2) and, in particular, the slope (Mw) of the preload recruitable stroke work (PRSW) relationship (3,4) provide accurate assessment of the RV contractile state, but the specific geometry of the RV renders instantaneous volume measurements in the clinical setting extremely difficult. Moreover, the necessity of temporary mechanical or pharmacological alterations of ventricular loading conditions renders these methods difficult to apply to the routine clinical setting. A number of single-beat derivatives of these indices have been proposed (5), but these have not yet been generally accepted or tested in the RV.
Over the last decade, interest has been rekindled for power-derived indices as means of estimating the contractility of the left ventricle (LV) (6,7). The main advantage of these indices is elimination of the need for continuous volumetry, thus allowing a less invasive form of measurement (8,9). Power generated by the ventricle during ejection can be measured as the product of instantaneous ventricular pressure and the rate of volume change or, alternatively, flow into the main arteries. Maximal power (PWRmax) and PWRmax divided by the square of end-diastolic volume (EDV), generally known as preload-adjusted PWRmax (PAMP), have both been shown to sensitively reflect changes in the contractile state and to be relatively insensitive to changes in afterload in the LV. However, PWRmax is highly sensitive to changes in preload (6) and has therefore been abandoned in favor of PAMP, which has been proposed as an accurate method of correcting PWRmax for preload and has been applied in experimental and clinical studies as a load-independent index of LV contraction (7–11).
Until now, these indices have not been studied in the RV. PAMP measurement in the RV offers several potential advantages. First, it is specifically in the RV that volumetry remains a problem (12). Second, the RV is accessible in a less invasive manner than the LV: RV PAMP could theoretically be calculated by using data acquired with echocardiography and a fast-response thermistor pulmonary artery (PA) catheter. However, the ventriculovascular coupling in the right circulation differs from that in the left, because the pulmonary arterial system is more compliant and because the RV is more afterload dependent and has a more limited contractile reserve (13,14). Consequently, the finding that power-derived contractile indices are relatively load independent in the left circulation cannot automatically be applied to the right circulation. However, the frequent incidence and mortality of RV failure, particularly in cardiac surgery (15), calls for improved methods of perioperatively assessing RV contractility.
This study was designed to test the hypothesis that PAMP may be used as a substitute for RV pressure-volume-derived indices. This is possible only if PAMP displays the same response to inotropic and load modulations as the "gold standard" indices. We therefore examined its sensitivity to changes in load and to increases in inotropic state in comparison with the "gold standard" indices, Ees and Mw, in an experimental model of acutely instrumented, open-chest, open-pericardium dogs.
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Methods
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This investigation conforms with the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (Publication No. 85-23, revised 1996) and was approved by the ethical committee of the Katholieke Universiteit Leuven. Twenty-six healthy adult mongrel dogs (weight, 18–24 kg) were used. After premedication with ketamine hydrochloride 10 mg/kg and piritramide 1 mg/kg (Dipidolor®; Janssen Pharmaceutica, Beerse, Belgium) IM, anesthesia was induced with IV sodium pentobarbital 10 mg/kg. Endotracheal intubation was performed, and the lungs were mechanically ventilated with a 50% mixture of oxygen in air. Anesthesia was maintained with a continuous IV infusion of sodium pentobarbital (1 mg · kg-1h-1) and piritramide (1 mg · kg-1h-1). Arterial blood gas analyses were performed at regular intervals and ventilation was adjusted accordingly to maintain normocapnia. Normothermia was maintained with a heating mattress. Lactated Ringer’s solution was administered at a rate of 8 mL · kg-1h-1 during instrumentation and 5 mL · kg-1h-1 during the experimental protocol.
A fluid-filled catheter was inserted into the descending aorta via the right femoral artery to monitor systemic blood pressure and obtain samples for blood gas analysis. Via a midline sternotomy, the inferior vena cava (IVC) was dissected and encircled with a tourniquet for controlled alterations of RV preload. The main PA was dissected free from the aorta, and a 14- or 16-mm perivascular flowprobe was placed around it, connected to an electromagnetic blood flow meter (Skalar, Delft, The Netherlands) providing a continuous display of cardiac output. A 5F microtipped pressure transducer was inserted into the main PA via a purse-string suture in the pulmonary outflow tract. The left PA was isolated and encircled with a polyfilament tourniquet. Right atrial pressure was measured with a fluid-filled catheter. A 5F combined microtipped pressure transducer and 12-electrode conductance catheter (Millar Instruments, Houston, TX) were inserted into the RV through a small stab wound in the PA outflow tract. The correct position of the catheter was confirmed by observation of pressure and segmental volume signals with appropriate phase relationships.
The conductance catheter was connected to a volumetric system (Sigma 5 DF; CDLeycom, Zoetermeer, The Netherlands). Instantaneous volume was calculated from the conductance signals [G(t)] by using the formula
equation
where L is the interelectrode distance, 
is blood resistivity, Vc is the parallel conductance, and 
is a slope factor calculated by comparing the cardiac output values obtained from the conductance catheter with those measured with the PA flowprobe (16). Vc and were measured at regular intervals by using the hypertonic saline method (see below) and the built-in Leycom resistivity meter, respectively.
All variables were digitized at 250 Hz and stored for off-line analysis. The acquired data were analyzed with specialized software (Conduct-PC [CDLeycom] and Labview® 5.1 [National Instruments Corp., Austin, TX]). For the calculation of the ESPVR, end-systole was calculated in an iterative fashion, as described previously (17). To circumvent some of the problems that may be associated with extrapolation of the potentially nonlinear ESPVR to zero pressure, the position of the ESPVR on the volume axis was expressed as its volume intercept at 30 mm Hg, as described previously (18). PWRmax and PAMP were calculated by using the instantaneous PA flow and RV pressure signals in steady-state conditions with the following equation (6):
equation
where PRV is RV pressure (mm Hg) and FPA is PA flow (mL/s). A conversion factor of 1.33 x 10-4 was applied to obtain power in watts. PWRmax was determined as the peak value of PWRrv(t). PAMP was defined as follows:
equation
where EDV is RV EDV (mL). RV afterload was quantified as the effective arterial elastance, calculated as the ratio of RV end-systolic pressure to RV stroke volume.
For the first study protocol, we investigated sensitivity to alterations in the contractile state (n = 12). After completion of instrumentation and calibration and achievement of hemodynamic steady-state, baseline measurements were performed with the ventilation suspended at end-expiration. Data were acquired during steady-state conditions (for general hemodynamics and RV power) and during a brief period of IVC occlusion (for the calculation of the ESPVR and PRSW relationship). Vc was determined for each experimental condition by using 7 mL of 10% saline solution injected into the right atrium (16). After baseline measurements, dobutamine (DBT) was administered at 5 and 10 µg · kg-1 · min-1 IV in random order, with an interval of at least 15 min between the two doses. Measurements were performed at least 15 min after the start of the infusion, after stabilization of heart rate and aortic pressure.
For the second study protocol, we investigated sensitivity to alterations in loading conditions (n = 14). Autonomic nervous system (ANS) blockade was achieved with IV propranolol (2 mg/kg), atropine methyl nitrate (3 mg/kg), and hexamethonium (20 mg/kg) (19). The aim of the ANS blockade was to minimize sympathetic reflex-mediated alterations in contractility during loading alterations.
Baseline measurements were performed after 30 min. The measurements performed during progressive inferior caval vein occlusion (providing a gradual decrease in RV EDV with minimal alterations in heart rate or afterload) were analyzed off-line on a beat-to-beat basis and were used to plot PWRmax-EDV and PAMP-EDV relationships per individual dog.
After baseline measurements, the left PA was completely occluded by means of a tourniquet. During the period of PA occlusion, the lungs were ventilated with 100% oxygen. After 5-min stabilization of hemodynamic variables, measurements were performed in this setting of increased afterload. The values obtained during PA occlusion were compared with the baseline measurements to evaluate the effect of increased afterload on the contractile indices.
Alterations in hemodynamic variables during the administration of DBT were analyzed with analysis of variance for repeated measurements. Fisher’s least significant difference test was used as a post hoc test. Preload dependence was quantified by linear regression of PWRmax and PAMP as a function of EDV. The slope of the regression line, r2, and p were used to describe the preload dependency of PWRmax and PAMP per animal. Hemodynamics before and after PA banding were compared by using paired Student’s t-tests and simple linear regression. All analyses were performed with the Statview® 5.0 (SAS Institute, Inc., Cary, NC) software package. A P value <0.05 was considered statistically significant. All data are expressed as mean ± SD.
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Results
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One dog was excluded from the inotropic sensitivity protocol because of abnormal hemodynamics (suggesting high sympathetic activity) in baseline conditions. Ees, Mw, PWRmax, and PAMP all increased dose-dependently during DBT infusion (Fig. 1). The volume-axis intercepts of the ESPVR and PRSW relationship did not change significantly (Table 1). Aortic pressure, cardiac output, and PA pressure increased significantly during DBT infusion, whereas EDV decreased slightly (Table 1).
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Figure 1. Alterations during infusion of dobutamine (DBT). The columns represent mean values; the error bars represent SD. Mw = slope of the preload-recruitable slope work relationship; Ees = end-systolic elastance; PWRmax = maximal power; PAMP = preload-adjusted PWRmax; DBT 5 = infusion of DBT at 5 µg · kg-1 · min-1; DBT 10 = infusion of DBT at 10 g · kg-1 · min-1. *P < 0.05 versus baseline control; P < 0.05, DBT 10 versus DBT 5.
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Five dogs were excluded from the preload dependence protocol because of deterioration of the flow signal during IVC occlusion. PWRmax was preload dependent in all animals (Table 2, Figs. 2 and 3). Conversely, the effect of preload reduction on PAMP was far less pronounced. Linear regression of the PAMP-EDV relationships suggests no relationship between EDV and PAMP in four animals. However, the r2 values do suggest a relationship (P < 0.05) between PAMP and EDV in five dogs (Table 2). In these animals, however, the response of PAMP was variable, because both increases and decreases in response to IVC occlusion were observed.
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Table 2. Results of Linear Regression Analysis of Individual PWRmax-EDV and PAMP-EDV Relations for Each Dog During Inferior Caval Vein Occlusion
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Figure 2. Scatterplots comparing maximal right ventricular power (PWRmax) versus end-diastolic volume (EDV) relationships (A) and preload-adjusted PWRmax (PAMP) versus EDV relationships (B) during inferior vena cava occlusion for individual dogs, with regression lines for each animal.
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Figure 3. Illustration of the changes in pressure-volume loops (A), right ventricular (RV) pressure (RVP) (B), RV power (C; gray line), right ventricular volume (C; black line), pulmonary artery (PA) flow (D), and power/end-diastolic volume (EDV)2 (E) during controlled inferior vena cava occlusion in one representative animal.
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One animal was excluded from the afterload-dependence protocol because of the development of tricuspid regurgitation during PA banding (as identified by the ventricular pressure-volume and right atrial pressure signals). PA banding resulted in a mean increase in effective arterial elastance of 64% (Table 3). Despite the pronounced increase in afterload, we observed no significant alteration in Mw, Ees, or PWRmax, although a significant increase in EDV and a 36% decrease in PAMP occurred (Table 3). Linear regression analysis of the contractile indices showed a good correlation between the values of Mw before and during PA banding. Ees showed a more variable response, as did PWRmax. In contrast, the regression of PAMP before and after PA banding showed a slope of 0.65, with a consistent, linear response (Fig. 4).
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Figure 4. Scatterplots of the contractile indices before (baseline) and during (pulmonary artery [PA] occlusion) left PA banding. Mw = slope of the preload-recruitable stroke work relationship; Ees = end-systolic elastance; PWRmax = maximal power; PAMP = preload-adjusted PWRmax. The regression line is shown.
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Discussion
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The major findings of this study are that PAMP does reflect changes in inotropic state in the RV, but that it is also influenced by changes in afterload and, to a lesser extent, preload. As one would expect from findings in the LV, changes in PWRmax and PAMP after inotropic stimulation with DBT matched the changes observed in Ees and Mw, the current gold standard in vivo contractility variables.
PA banding caused a significant and consistent decrease in PAMP, but not in Ees, PRSW, or PWRmax. This is in contrast to findings in the LV, where PAMP was not significantly influenced by alterations in afterload of up to 60% (6). There are two possible explanations for the sensitivity of PAMP to changes in afterload in the RV as opposed to the LV. First, Piene (13) and Piene and Sund (14), using a coupling framework consisting of mean hydraulic power versus pulmonary load resistance, showed that a decrease in PA compliance, as could occur during banding, decreases the hydraulic power available. In the LV, Kass and Beyar (6) observed an increase in PWRmax in response to a sudden increase in afterload. In contrast, in this study, we did not observe such an increase in the RV, but the individual response was highly variable. Second, we observed an increase in EDV after PA banding. The preload normalization in PAMP with the formula PAMP = PWRmax/EDV2 renders this variable sensitive to changes in EDV. The RV has a greater compliance than the LV (20). This results in more pronounced dilation in response to increased afterload, which may also contribute to the afterload sensitivity of PAMP in the RV. It is very unlikely that the decrease in PAMP during PA banding was due to a genuine decrease in contractility (despite hemodynamic evidence for reduced RV performance), because the gold standard contractile indices Mw and Ees did not decrease significantly.
Consistent with observations in the LV (6), RV PWRmax proved to be highly preload sensitive, whereas PAMP appeared to be relatively preload independent. However, five of the nine animals did display either increases or decreases in PAMP in response to preload reduction. We speculate that this variability may be due to the inappropriate use of a fixed exponent of EDV in the equation PAMP = PWRmax/EDVß (where ß = 2). This may be compatible with the suggestion (21) that the optimal exponent for EDV in the preload adjustment of PWRmax varies with chamber size. However, in our limited set of data, we were unable to demonstrate a correlation between baseline chamber size and the slope of the PAMP-EDV relationship (r2 = 0.028; P = 0.66).
Our observations of pressure-volume relationships concerning the effects of load alterations on RV ESPVR and PRSW are largely in agreement with previous studies (2,4). Using ellipsoid shell subtraction in open-pericardium conscious dogs, Karunanithi et al. (4) observed no change in Mw but observed an increase in Ees after partial occlusion of the main PA. Although our findings suggest an increasing trend in Ees, this did not reach statistical significance. Two other groups have recently examined the effect of PA banding on RV pressure-volume loops in newborn lambs and three-month-old sheep (18,22). It is interesting to note that both groups observed increases in RV Ees (significant after 4 hours and after 30 minutes), whereas one (22) also observed an increase in Mw. However, these findings do not necessarily disagree with our results, because neither group used ANS blockade, allowing possible homeometric autoregulation via autonomic pathways. In our study, the aim was to examine the individual factors that may influence the contractile indices, rather than to study physiological responses.
A potential limitation of this study is the use of an open-pericardium model. Although one could expect the influence of afterload on EDV and hence PAMP to be less extreme in a closed-pericardium setting, it is unlikely to be the sole cause of PAMP’s afterload sensitivity. Although our findings are clinically relevant for the settings in which the pericardium is open, such as during cardiac surgery, our conclusions should not automatically be applied to other clinical settings. Further investigation is therefore required.
A second methodological question concerns the position of the conductance catheter. There is some controversy about the optimal access route for RV volume measurements, particularly because of the RV’s biaxial shape and dual pump function. We chose to position the conductance catheter parallel to the pulmonary outflow tract, as described previously (22), because this axis allows interrogation of a larger proportion of the ventricular cavity (23,24). The pressure-volume loops that we obtained consistently displayed the characteristic, slightly triangular shape described previously (2,4).
Finally, we acknowledge that our model of increased afterload, which mimics the pathophysiological effect of an acute pulmonary embolism, is not applicable for all clinical forms of pulmonary hypertension. However, this limitation does not invalidate our primary conclusion that, despite accurate inotropic sensitivity, the value of PAMP (calculated as PWRmax/EDV2) as an index of RV contractility is limited by its load sensitivity. PAMP does not appear to be an acceptable alternative to pressure-volume-based methods of estimating RV function.
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Acknowledgments
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Supported by a grant (1.5.208.99) from the Fund for Scientific Research, Flanders, Belgium.
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Footnotes
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Alex Leather is a research assistant at the Department of Anesthesiology, K.U. Leuven, for the Fund for Scientific Research Flanders, Belgium.
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Accepted for publication June 19, 2002.
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Abstract
Introduction
