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Abstract |
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Increasing cardiac load by leg elevation identifies patients with load-dependent impairment of left ventricular (LV) function. This impairment is related to a deficient length-dependent regulation of LV function. We investigated the effects of dobutamine on length-dependent regulation of LV function in coronary surgery patients (n = 25). High-fidelity LV pressure tracings were obtained at end-expiration, while hearts were paced at a fixed rate of 90 bpm. Effects of leg elevation on contraction and relaxation were compared before and during dobutamine 5 µg · kg-1 · min-1. Effects on contraction were evaluated by analysis of changes in dP/dtmax. Effects on relaxation were assessed by analysis of R (slope of the relation between the time constant of isovolumic relaxation and end-systolic pressure). Correlations were calculated with linear regression analysis using Pearson’s coefficient r. The effects of leg elevation on variables of contraction and relaxation were coupled. We found a close relationship between changes in dP/dtmax and individual values of R (r = 0.84; P < 0.001). Dobutamine improved myocardial function and accelerated LV pressure decrease. Under dobutamine, the increase in dP/dtmax with leg elevation was larger (P < 0.001) and load dependence of LV relaxation was reduced (P = 0.001). Dobutamine improved the effects of leg elevation on LV function, reflecting improved length-dependent regulation of LV function.
Implications: This study demonstrated that ß-adrenoreceptor stimulation with dobutamine improved length-dependent regulation of myocardial function assessed during leg elevation in cardiac surgical patients.
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Introduction |
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In coronary surgery patients, analysis of changes in variables of contraction and relaxation during an increase in cardiac load permits dynamic assessment of left ventricular (LV) functional reserve. A postural change induced by leg elevation identifies a subgroup of patients with load-dependent impairment of LV function. These patients respond to leg elevation with a decrease in stroke volume and dP/dtmax, a delayed myocardial relaxation with enhanced load dependence of LV pressure decrease, and a marked increase in LV end-diastolic pressure (EDP) (1). This impairment of LV function appears related to a deficient length-dependent regulation of LV function (2).
ß-Adrenergic stimulation improves LV contraction (inotropic effect) and accelerates LV relaxation (lusitropic effect) (3–5). Based on these properties, we hypothetized that ß-adrenergic stimulation might also improve the length-dependent activation of myocardial function. We therefore analyzed the influence of ß-adrenergic stimulation with dobutamine on the effects of leg elevation in coronary surgery patients.
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Methods |
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The study was performed in 25 patients scheduled for elective coronary bypass surgery. The study was approved by our Institutional Ethical Committee, and written informed consent was obtained. Patients with an ejection fraction of more than 40% and with a LV EDP of less than 15 mm Hg during preoperative hemodynamic evaluation were considered. Patients undergoing repeat coronary surgery, unstable angina, concurrent valve repair, or aneurysm resection were excluded.
Anesthesia and Surgery
Preoperative cardiac medication, including ß-blocking drugs, calcium channel blocking drugs, and nitrates were continued until the morning of surgery. Premedication consisted of intramuscular glycopyrolate 2 µg/kg, droperidol 30 µg/kg, and fentanyl 1 µg/kg. In the operating room, patients received routine monitoring including 5-lead electrocardiogram (ECG) radial and pulmonary artery catheters, pulse oximetry, capnography, and blood and urine bladder temperature monitoring. Anesthesia was induced with fentanyl 20 µg/kg, diazepam 0.1 mg/kg, and pancuronium bromide 0.1 mg/kg. An additional dose of 30 µg/kg fentanyl was administered before sternotomy. Patients’ lungs were ventilated with a FiO2 of 0.5; when necessary, isoflurane 0.2%–0.4% was added to the air–oxygen mixture. Standard median sternotomy and pericardiotomy were performed. After sternotomy, isoflurane was discontinued in all patients. The aorta was cannulated, and epicardial pacemaker wires were attached to the right atrium and right ventricle.
Venous drainage during cardiopulmonary bypass (CPB) was accomplished with a two-stage venous cannula inserted in the right atrium. A ventricular sump was inserted in the left ventricle through the right superior pulmonary vein. Perfusion flow on CPB was 2.4 L · m-2 · min-1 in nonpulsatile mode. In all patients, the left internal thoracic artery was used in addition to one or more saphenous vein grafts. In all patients included in this study, complete revascularization could be performed.
Separation from CPB was performed using the standard protocol, described previously (1). Briefly, after reperfusion of the heart and rewarming to a bladder temperature of 35°C, patients were prepared for separation from CPB. The heart was paced in atrioventricular sequential mode at a rate of 90 bpm and intravascular volume increased until a pulmonary capillary wedge pressure of 13–15 mm Hg or a central venous pressure of 8–10 mm Hg were obtained. CPB flow was progressively reduced to zero, whereas the heart resumed its independent function.
Experimental Protocol
Twenty-five patients were included in the study. In 15 patients, only LV pressures were measured, whereas in 10 patients combined pressure and volume measurements were performed. In the 15 patients, a sterilized, prezeroed electronic micromanometer (MTC®P3Fc catheter, Dräger Medical Electronics, Best, The Netherlands; frequency response = 100 KHz) was positioned in the LV cavity through the apical dimple. The catheter was connected to a Hewlett Packard monitor (HP78342A, Hewlett Packard, Brussels, Belgium). The output signals of the pressure transducer system were digitally recorded together with the ECG signals at 1-ms intervals (Codas, DataQ, Akron, OH). Zero and gain setting of the tipmanometer were also checked against a high-fidelity pressure gauge (Druck Ltd., Leicester, UK) after removal.
In 10 patients, a combined micromanometer transducer conductance catheter (F6, Millar) was inserted via the femoral artery into the left ventricle for measurement of LV pressures and volumes. The correct position of the conductance catheter was verified by the inspection of the LV pressure waveform and the segmental conductance signals. The conductance catheter was connected to a Leycom Sigma-5DF signal conditioner processor (CardioDynamics, Zoetermeer, The Netherlands) to measure LV volumes. The method is based on the measurement of the time-varying electrical conductances of five segments of blood in the left ventricle (6). The conductance catheter not only measures the conductance of the blood inside the left ventricle, but also the conductance of the myocardium and the surrounding structures. This parallel conductance (Vc) creates an offset, which can be estimated by injecting 5-mL hypertonic (8%) saline into the pulmonary artery. Estimation of Vc was performed with the dedicated package CONDUCT-PC using an algorithm that indicates the best Vc values. Conductance catheter stroke volume was calibrated by thermodilution stroke volume, determined by thermodilution cardiac output measurement (Vigilance Monitor, Model VGS2, Baxter). The CONDUCT-PC (Cardiodynamics) software package was used for acquisition and analysis of conductance catheter data. Blood resistance, Vc, and baseline cardiac output were measured before the start of the protocol.
The effects of leg elevation were evaluated before and during administration of dobutamine. First, leg elevation was performed in baseline conditions. After a period of 10 min to allow for a return of hemodynamic variables to baseline, dobutamine was started at a dose of 5 µg · kg-1 · min-1 during 5 min, and leg elevation was then repeated.
Measurements before CPB were recorded before venous canulation. After separation from CPB, a stabilization period of 10 min was permitted to prevent time-dependent changes in ventricular function with alteration of preload (7), before measurements after CPB were recorded. No additional vasoactive or inotropic medication was allowed during the course of the protocol.
Measurements were obtained with mechanical ventilation suspended at end-expiration. During the protocol, heart rate was maintained constant by means of atrioventricular sequential pacing at a fixed heart rate of 90 bpm with an atrioventricular interval of 150 ms. Paced heart rate was identical before and after CPB. In none of the patients did intrinsic heart rate exceed paced heart rate. Measurements consisted of recordings of consecutive ECG and LV pressure tracings during an increase of systolic and diastolic LV pressures obtained by raising the caudal part of the surgical table by 45°, resulting in raising of the legs. Leg raising resulted in a rapid beat-to-beat increase in LV pressures and dimensions. Care was taken to have at least 10 consecutive beats for analysis. After recording the data, ventilation was resumed and the surgical table was returned to horizontal.
Data Analysis
EDP was timed at the peak of the R-wave on ECG. The effects on LV load and function were evaluated by the EDP, peak LV pressure, LV pressure at dP/dtmin (=end-systolic pressure [ESP]), and dP/dtmax. Effects of leg elevation on rate of LV pressure fall were evaluated by dP/dtmin, and the time constant 
of isovolumic relaxation. was calculated based on the monoexponential model with nonzero asymptote using LV pressure values from dP/dtmin to a cutoff value of 10 mm Hg above EDP (8). The following equation was used: P(t) = P0 · e-t/ + P
(8), where P is a nonzero asymptote, P0 is an amplitude constant, t is time, and is the time constant. Time constant was linearly fit to the corresponding ESP, and the slope R (ms/mm Hg) of this relation was calculated. R quantified changes in , induced by the change in ESP, and quantified afterload dependence of the rate of LV pressure fall (9). At least 10 consecutive beats were taken for the calculation of R. Sample correlation coefficients of the ESP - relationships yielded values of r > 0.93 in all patients. In the 10 patients who were instrumented with the conductance catheter, end-diastolic volume (EDV), end-systolic volume (ESV), slopes (Ees), and axis intercepts (V0) of the ESP–ESV relationships were analyzed additionally.
Data before and after leg raising were compared using two-way analysis of variance for repeated measurements. Interaction analysis revealed whether effects of leg raising were different at baseline and after dobutamine. Posttest analysis was performed using the Bonferroni-Dunn test. Relations in hemodynamic variables were analyzed using linear regression analysis computing Pearson’s correlation coefficient. Slopes and intercepts of the different relationships were compared using t-test analysis (10). Data were reported as mean ± SD. Statistical significance was accepted at P < 0.05.
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Results |
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Demographic and intraoperative data of the patients included are presented in Table 1. Table 2 summarizes the hemodynamic data of leg elevation before (control) and after dobutamine before the start of CPB. Dobutamine increased peak LV pressure, and dP/dtmax, whereas EDP remained unchanged. EDV was unaltered and ESV decreased, hence stroke volume increased. Ees and stroke work both increased. Corresponding changes in dP/dtmax and time constant of isovolumic relaxation, and
induced by dobutamine are displayed in Fig. 1A. Effects of dobutamine on dP/dtmax and were coupled: patients who developed the most pronounced increase in dP/dtmax also had the most pronounced decrease of (y = 1.6 - 0.05 x x; r = 0.83; P < 0.001). After CPB, effects of dobutamine were similar as before CPB (Table 3). A similar coupling between changes in dP/dtmax and changes in was observed as before CPB (Fig. 1B) (y = 0.9 - 0.05 x x; r = 0.76; P < 0.001; no significant difference in Ees and V0).
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The effects of leg elevation during dobutamine were compared with the effects of leg elevation in control conditions. Under dobutamine, the increase in peak LV pressure and dP/dtmax was higher than at control. The increase in EDV was higher, whereas the increase in EDP was less pronounced. The increase in ESV with leg elevation was less under dobutamine than at control and, accordingly, Ees was steeper. A representative example of the effects of leg elevation at control and during dobutamine is displayed in Fig. 2.
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The effects of leg elevation on myocardial relaxation were evaluated by analysis of R. The inset of Fig. 3 illustrates R. R represents the load dependence of LV pressure decrease and is the slope of the relation between
and ESP measured in consecutive beats during the pressure increase with leg elevation. A wide variability in R was observed with individual values ranging from -0.33 to 1.70 ms/mm Hg. This means that LV pressure decrease accelerated in some patients, but remained unchanged or even slowed in other patients. After dobutamine, individual values ranged from -0.40 to 0.72 ms/mm Hg.
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Variables of contraction and relaxation were coupled. A close relationship was found between changes in dP/dtmax and individual values of R (Fig. 3A). Patients who developed with leg elevation a decrease in dP/dtmax also manifested a marked slowing of LV pressure decrease, indicating more pronounced load dependence of LV pressure decrease. With dobutamine, the relationship shifted to the right and downward. There was no difference in Ees and V0 of the relationships between dP/dtmax and R at control or with dobutamine (relationship at control: y = 0.99 - 0.007 x x, r = 0.84, P < 0.001; relationship with dobutamine: y = 0.74 - 0.004 x x, r = 0.75; P < 0.001).
Load dependence of LV pressure decrease was coupled with the magnitude of changes in EDP with leg elevation. A close relationship was observed between the individual values of R and changes in EDP with leg elevation EDP (Fig. 3B). Patients with marked load dependence of LV pressure decrease were also the patients who developed a marked increase in EDP. Conversely, patients with low load dependence of LV pressure decrease had only a minor increase in EDP. With dobutamine, the relationship shifted downward and to the left. There was no difference in Ees and V0 of the relationships between EDP and R at control or with dobutamine (relationship at control: y = -0.27 + 0.17 x x, r = 0.84, P < 0.001; relationship with dobutamine: y = -0.37 + 0.16 x x, r = 0.73; P < 0.001).
Post-CPB, effects of leg elevation were similar to pre-CPB, both at control and after dobutamine (see Table 3). A similar coupling was observed between changes in dP/dtmax with leg elevation and R [control: y = 0.81 - 0.008 x x (r = 0.85; P < 0.001); with dobutamine: y = 0.71 - 0.006 x x (r = 0.76, P < 0.001); no significant difference in Ees and V0 between control and dobutamine before and after CPB; Fig. 3C] and between changes in EDP with leg elevation and R [control: y = -0.26 ± 0.14 x x (r = 0.85; P < 0.001); with dobutamine: y = -0.42 ± 0.18 x x (r = 0.74; P < 0.001); no significant difference in Ees and V0 between control and dobutamine before and after CPB; Fig. 3D].
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In the perioperative period, an increase in cardiac load by a postural change permitted identification of a subgroup of patients who developed a load-dependent impairment of LV function. When cardiac load was increased by leg elevation, these patients developed a decrease in stroke volume and dP/dtmax, a delayed myocardial relaxation with enhanced load dependence of LV pressure decrease and a marked increase in LV EDP (1). Leg elevation represents a complex hemodynamic intervention during which systolic and diastolic LV pressures and volumes increase and that not only affects venous return but also ventricular afterload. Impairment of LV function secondary to leg elevation might result either from the inability of the heart to compensate for an additional increase in systolic pressure due to exhaustion of normal afterload reserve (11,12) or might be due to a deficient length-dependent activation of myocardial function with exhaustion of preload reserve (13,14). It was recently demonstrated that the load-dependent impairment of LV function after leg elevation was not caused by the increase in systolic pressures, but instead appeared related to a deficient length-dependent regulation of myocardial function (2).
We indicated that, in coronary surgery patients, ß-adrenergic stimulation with dobutamine improved the length-dependent regulation of myocardial function. In addition, it appeared that dobutamine not only improved LV contraction and relaxation, but also that the coupling between variables of contraction and relaxation was preserved with dobutamine.
The effects of ß-adrenergic modulation on myocardial contraction and relaxation have been well established. ß-adrenergic drugs improve myocardial contractility and accelerate relaxation (3–5). Although the effects of ß-adrenergic stimulation on contractile function are well understood, those on myocardial relaxation are incompletely defined. In some observations on myocardial effects of ß-adrenergic drugs, heart rate also significantly increased (15–17). Because an increase in heart rate causes an increase in the rate of LV isovolumic relaxation (3,17), studies that did not control heart rate during ß-adrenergic stimulation cannot determine the direct effects of ß-adrenergic stimulation on LV relaxation rate. Heart rate was kept constant by atrioventricular pacing, thereby preventing changes in heart rate as a confounding factor. The acceleration of LV pressure decrease observed with dobutamine could therefore be related to the effects of the reduced end-systolic dimensions on LV relaxation rate. A reduction in LV ESV was observed. It was previously suggested that the positive lusitropic effects of ß-adrenergic stimulation might be related to a reduction in end-systolic LV dimensions (18,19). However, a direct effect of dobutamine on the rate of relaxation (desensitizing effect of ß-stimulation on crossbridges) could not be excluded from our observations. Carroll et al. (20) compared the effects of dobutamine and sodium nitroprusside on diastolic properties in patients with congestive heart failure. Both compounds similarly reduced LV dimensions, but only dobutamine resulted in an acceleration of LV relaxation rate. An alternative explanation is that ß-adrenergic stimulation can improve synchrony of LV relaxation (20).
The effects of dobutamine on variables of contraction and relaxation paralleled each other: the larger the change in dP/dtmax, the more important the change in (Fig. 1). Previous investigators who examined the effects of ß-agonists on contraction and relaxation, have reported variable coupling relations. Parker et al. (5) demonstrated that ß-adrenergic receptor stimulation with low doses of dobutamine resulted in a significant acceleration of LV relaxation in both normal subjects and patients with congestive heart failure. The relative preservation of the lusitropic response to ß-adrenergic stimulation in patients with heart failure was explained by two separate effects of the increase in intracellular cAMP concentration. The positive inotropic and lusitropic effects of ß-adrenergic stimulation are mediated by cAMP. However, the pathways for these responses diverge distal to cAMP generation (21). The positive inotropic response is the consequence of the action of cAMP to increase inward conductance of calcium via L-type calcium channels. This results in a higher concentration of free calcium in contact with the contractile apparatus. In contrast, the lusitropic effect is the consequence of the accelerated reuptake of calcium by the sarcoplasmatic reticulum, mediated by cAMP. This accelerated reuptake reduces the calcium sensitivity of the contractile apparatus and accelerates the rate of myofilament cross-bridge detachment. In our study, ß-adrenergic stimulation did not result in a disparate response of the inotropic and the lusitropic effects. It should be noted, however, that the present data were obtained in patients with normal or slightly reduced LV function and not in patients with heart failure.
Several methodological issues deserve attention. Different effects of leg elevation at baseline and during dobutamine were not caused by a time-dependent effect. From preliminary experiments, it had appeared that effects of leg elevation were similar when repeated twice at a 10-min interval.
Heart rates during the protocols were regulated with cardiac pacing, which was identical before and after CPB. The use of pacing eliminated variations in heart rate between patients and within the same patient as a confounding factor. However, it should be acknowledged that pacing altered normal LV conduction patterns, and this might have somewhat enhanced load dependence of LV pressure decrease, as experimentally demonstrated in the canine heart (22). Data were obtained in anesthetized patients. This implies that neurohumoral reflexes, including those mediating cardiac function, may have been blunted or altered with anesthesia. Finally, data were obtained in the presence of an open chest and open pericardium. The absence of pericardium may have overdilated the heart because a rightward shift of the EDP dimension relation has been shown after pericardiectomy (23).
With respect to the reported results on Ees, it should be noted that the effects of leg elevation should be interpreted as data projecting on the higher curvilinear part of the systolic pressure–volume relationship (24,25). The interpretation of such data is different from the interpretation of load-independent assessment of contractility, which is performed at lower ventricular volumes and which results in truly linear systolic pressure–volume relationships.
In conclusion, our study demonstrated in coronary surgery patients with a preoperative ejection fraction >40% that ß-adrenergic stimulation with dobutamine improved length-dependent regulation of myocardial function during leg elevation.
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Acknowledgments |
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This research was supported by a grant from the Fonds voor Wetenschappelijk Onderzoek (Onderzoekskrediet G.0.343.97, 1997–2000).
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Footnotes |
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S.D.H. was supported by an Investigator’s Grant from the Fonds voor Wetenschappelijk Onderzoek.
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References |
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