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Anesth Analg 2002;95:19-25
© 2002 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Does Dobutamine Improve Ventricular Function in Dogs with Regional Myocardial Dysfunction?

David P. Strum, MD, FRCP(C)*, and Michael R. Pinsky, MD, CM{dagger}

*Department of Anesthesiology and Critical Care Medicine, Kingston General Hospital, Queen’s University, Kingston, Ontario, Canada; and {dagger}Cardiopulmonary Research Laboratory, Department of Anesthesiology and Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania

Address correspondence and reprint requests to David P. Strum, MD, Department of Anesthesiology, Kingston General Hospital, 76 Stuart St., Kingston, Ontario K7L 2V7. Address e-mail to strumd{at}post.queensu.ca


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
We studied the effect of systemic dobutamine infusion (4 µg · kg-1 · min-1 IV) on regional wall motion abnormalities (RWMAs) in eight anesthetized open-chested dogs. We hypothesized that infusion of small doses of dobutamine would reduce RWMAs and improve global ventricular function. Apical RWMAs were induced by local intracoronary boluses of 9.0 mg esmolol. Phase angles, effective stroke volume (SV), maximum SV, stroke work, and segmental shortening were compared among four left ventricular (LV) regions (apical, papillary, chordal, and basal) during baseline, dobutamine, esmolol, and dobutamine-esmolol treatments. The minimal global LV volume was designated as 0°, and the cardiac cycle was divided into 360 intervals. Regional phase angles were defined as the distance (in degrees) that regional minimum volume differed from global minimal LV volume (end-systole). RWMA decreased blood pressure (92 ± 2 mm Hg to 84 ± 3 mm Hg) and increased LV end-diastolic pressure (1.8 ± 0.5 mm Hg to 4.2 ± 0.8 mm Hg). RWMA delayed regional contraction (-2.9° ± 1.6° to 52.3° ± 1.5°) and decreased effective SV (2.3 ± 0.4 mL to 1.6 ± 0.3 mL) in the affected apical region but did not decrease maximal SV. Systemic infusion of dobutamine restored global LV function but failed to eliminate RWMA, as evidenced by decreased apical synchrony, effective SV, and stroke work. We concluded that systemic dobutamine restored global LV function but failed to correct RWMA.

IMPLICATIONS: We examined the effect of systemic dobutamine on regional wall motion abnormalities (RWMAs) induced by intracoronary esmolol infusion in eight anesthetized dogs. Esmolol dilated the heart and decreased regional synchrony of contraction. Dobutamine restored cardiac function but failed to correct the asynchrony of regional contraction caused by esmolol-induced RWMAs.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Regional myocardial dysfunction is a common clinical finding manifested by regional wall motion abnormalities (RWMAs) (1,2). RWMAs reduce the efficiency of left ventricular (LV) contraction by decreasing both the regional amplitude and the global synchrony of contraction (3). Previous investigators have produced RWMAs by pacing the heart (4) or by coronary occlusion (5–7) and have measured LV volumes with sonomicrometer crystals. Synchrony of contraction, however, was not specifically assessed in these studies. Asynchrony of contraction may play an important role in the overall effect of RWMAs on LV pump function, and the effect of inotropes on synchrony in the presence of RWMAs has not been defined.

The effect of inotropes on the synchrony of contraction needs to be assessed because therapies used to improve LV pump function often include increased inotropes. If inotropes increase the rate of shortening of unaffected regions of the myocardium more than affected regions, then the degree of asynchrony will increase. Thus, to the extent that inotropes improve synchrony, they should improve LV pump function, whereas if they increase asynchrony they should increase oxygen consumption (8) and decrease LV ejection efficiency even if they also increase LV stroke volume (SV) and stroke work (SW).

We showed previously that asynchronous LV contraction induces LV dilation for the same LV SW (9) but does not alter the maximal regional SV of the involved segments (10). The LV dilation was induced by a combined effect of increased dispersion of regional end-contraction among segments and volume loading used to maintain SV constant. However, the effects of increased inotropy on this effect were not reported. Thus, we studied the effects of inotropic stimulation on LV synchrony by using our model of esmolol-induced RWMAs. We hypothesized that in the presence of esmolol-induced RWMAs, systemic inotropes may increase LV contraction asynchrony even while increasing the force of contraction of individual myocardial regions. Accordingly, we studied the effect of dobutamine infusion, in the presence of esmolol-induced RWMAs, on global and regional phase angles and SVs in eight open-chested acute canine preparations by using our previously validated phase angle analysis (10). We found that RWMAs delayed regional contraction and decreased effective SV (that portion of regional SV contributing to total LV SV). Although systemic dobutamine infusion restored global measures of LV performance (blood pressure, SV, SW, and LV dP/dt), it did not improve synchrony, effective SV, or stroke force of regional contraction in the affected segment.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
The preparation and analyses used have been described and validated previously (9,10). Briefly, after approval of the University of Pittsburgh Animal Care and Use Committee, we studied eight mongrel dogs (24.6 ± 0.5 kg, mean ± SEM). Anesthesia was induced with IV morphine sulfate (0.5 mg/kg) and sodium pentobarbital (30 mg/kg) and was maintained with a continuous infusion of sodium pentobarbital (1.0 mg · kg-1 · h-1) with intermittent boluses if needed for light anesthesia. All animals received a maintenance infusion of 0.9% NaCl at 100 mL/h. All animals had their trachea intubated and their lungs ventilated with 100% oxygen. Arterial blood was sampled (ABL-30; Radiometer, Copenhagen, Denmark), and acid-base status was adjusted with intermittent boluses of bicarbonate solution if needed to maintain arterial blood pH between 7.35 and 7.45; the ventilator was adjusted to maintain arterial blood PCO2 between 35 and 45 mm Hg. Neuromuscular blockade was established with IV boluses of pancuronium (1.0 mg IV as needed). Body temperature was maintained at 36°C to 38°C by using a thermostatically controlled heating blanket.

A fluid-filled arterial catheter and a double-lumen 12F catheter were inserted to monitor vascular pressures and infuse fluids. A 7.5F balloon-tipped pulmonary artery catheter (No. P7110-EP8-H, 9510; Baxter-Edwards, Santa Ana, CA) was inserted. LV volume was measured by a 6F, 11-pole multielectrode dual excitation conductance catheter (Webster Laboratories, Irvine, CA). Correct positioning of the conductance catheter was verified by fluoroscopy and on-line inspection of the regional volume signals.

After a thoracotomy through the left fourth intercostal space and a pericardotomy, a 22-gauge 1.25-in. IV catheter was placed into the left anterior descending (LAD) coronary artery to administer local (intracoronary) esmolol. Two independent pairs of piezoelectric dimension crystals aligned parallel with the LV horizontal hoop fibers (Triton, San Diego, CA) were placed into two different coronary artery perfusion zones. One pair of crystals was positioned in the LAD coronary arterial perfusion zone distal to the insertion of the 22-gauge catheter (near the LV apex). A second pair of control crystals was inserted into the remote perfusion zone of the left circumflex coronary artery.

A 5F high-fidelity pressure transducer (microtip catheter model SPC-350; Millar, Houston, TX) was inserted 2 cm through an LV apical puncture to record LV pressure. Immediately before termination of the experiment, 2 mL of 1% crystal violet dye was injected into the LAD coronary artery catheter to document the size of the perfusion zone. The dog was then killed while still under general anesthesia by using IV injection of 10 mL of saturated KCl. The dyed area (LAD coronary artery perfusion zone) was dissected out and weighed after death. The remaining LV myocardium was dissected free and weighed.

To induce RWMAs, 9.0-mg esmolol boluses (10 mg/mL) were administered through the LAD catheter. This treatment was referred to as esmolol. Approximately 30 s after esmolol, stable transient regional dysfunction developed that lasted for 6–7 min. This dose of esmolol induced a transient but stable local paresis under all conditions, as we validated in previous studies (10).

Dobutamine HCl (4 µg · kg-1 · min-1) was infused into a large central vein and induced a stable hemodynamic response within 5 min. This treatment was referred to as dobutamine and served as a positive control. This dose of dobutamine was selected after dose-response studies, and it increased cardiac contractility under normal conditions (9).

Regional and global myocardial function were compared sequentially in seven treatments: baseline, dobutamine, baseline-2, esmolol, baseline-3, combined dobutamine and esmolol (dobutamine-esmolol), and baseline-4. Baseline was defined as the stable hemodynamic state after surgery. Subsequent baselines were recorded after return to a stable hemodynamic state after discontinuing drug infusion. Esmolol measurements were made 4 to 5 min after the bolus esmolol infusion. Dobutamine measurements were made 5 min after a stable hemodynamic state was induced. For dobutamine-esmolol, first a stable dobutamine state was achieved, and then bolus esmolol was infused as described previously. Each of the experimental treatments was alternated in a randomized block (Latin square) design to control for the order of the treatments and time effects. We recorded arterial blood pressure, LV pressure, LV dP/dt, intercrystal dimensions for the piezoelectric crystals, total and regional LV conductance (volume), and lead II of the electrocardiogram on an eight-channel physiologic recorder (Gould, Cleveland, OH) and digitally on magnetic disk for subsequent analysis.

Signals from the two pairs of sonomicrometer dimension crystals were processed simultaneously on two synchronized channels by using a four-channel sonomicrometer (model 120; Triton). LV dP/dt was derived from the LV pressure signal by using a differentiator (Gould) with a 100-Hz high cutoff and a 1 V/s slope. LV volume signals were processed with a data processor and signal conditioner (5DF; Leycom Sigma, Leyden, The Netherlands). Blood conductivity was measured intermittently. Intermittent cardiac outputs were determined in triplicate by using a 10-mL iced 0.9% saline bolus thermodilution technique (model 9520 cardiac output computer; Baxter-Edwards) as a cross-validation of the conductance catheter-derived SV measures. Data were collected and analyzed with a Hewlett-Packard (Palo Alto, CA) Apollo DN4000 Unix workstation and a SignifiCAT® (Buffalo, NY) RTS-132 A/D subsystem.

The conductance catheter method for measuring ventricular volume has been described and validated previously (11,12). Briefly, a 20-kHz constant-amplitude current of 30 mA root-mean-square is passed between the electrodes of the distal and proximal extremes of the catheter in a dual-field format, and individual electrode pairs are summed to derive regional LV volumes. Parallel conductance artifact was determined by using the saline dilution method (13) with hypertonic saline. The extrapolated zero intercept volume was taken as the zero offset value for calculation of absolute regional and total minimal and maximal volumes.

Regional and total LV maximum and minimum volumes were determined for each cardiac cycle. Regional minimum and maximum volumes were defined as regional end-systole and end-diastole, respectively. The sonomicrometer signals generated similar continuous signals of length dimension with respect to time. Electrical systole was arbitrarily defined to occur at the R wave of the electrocardiogram.

To measure the phase of regional contraction independent of heart rate, we divided the cardiac cycle into 360° and defined global end-systole (minimal total volume) as 0°. The regional end-systolic phase angle was defined as the relative distance (in degrees) that the regional minimal volume differed from global end-systole. Regional phase delays were defined as positive values, and phase advances were defined as negative values. We determined the systolic time interval of regional systole as measured by the duration of time from the R wave to the regional minimal volume. Systolic time intervals measure the combined effect of both phase delay and heart rate on regional end-systole.

We determined regional ejection by two different methods. Regional maximum SV was defined as the difference between the maximal and minimum regional volume (or segmental length) for each cardiac cycle independent of the phase of regional contraction. Global maximal volume was LV end-diastolic volume, and global minimal volume was LV end-systolic volume. However, regional maximal and minimal volumes may not occur at these same time points.

Regional effective SV was determined by using maximums and minimums of the total LV volume as gated markers of the time period when regional contraction would contribute to total LV SV. If regional contraction occurred before the onset of aortic outflow, then regional SV would be displaced into other areas of the LV. If regional contraction occurred after aortic valve closure, then SV would be displaced into relaxing areas, and the apparent diastolic compliance of the LV would be decreased. Thus, the total SV of a region was the sum of effective SV and ineffective SV, where the ineffective SV occurred either before or after global ejection.

SW was determined as the area within the respective regional or total pressure-volume relations, and stroke force was determined as the area within the pressure-length loops for the ultrasonic crystal data. Regional maximal SW (the total area) was the sum of effective SW (that portion of SW contributing to global ejection of blood from the ventricle) and ineffective SW (that portion of SW that occurred before or after gated markers of global ejection).

Data from all animals who successfully completed all four steps of the protocol and were hemodynamically stable were analyzed. In practice, complete data were available for only eight animals. Surgical misadventures, intractable arrhythmias, or both developed in all other dogs that precluded their inclusion in the analyses. Measured and derived variables were compared across treatments and among regions by using repeated-measures analysis of variance and 95% confidence interval testing. All variables were examined graphically by using standardized normal probability plots to ensure that the data were normally distributed. All results were summarized as mean ± SEM. Differences associated with a P value of <0.05 were considered significant.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Esmolol bolus infusion affected the apical regional myocardium, averaging 23% of the total LV mass (perfused zone, 29.8 ± 2.63 g; LV, 127.9 ± 13.5 g). Measured hemodynamic variables did not differ significantly from one another during all four baseline conditions; therefore, only the initial baseline values are reported in Table 1. Heart rate did not change significantly. Dobutamine increased LV end-systolic pressure 13% and maximum LV dP/dt 46%, and it reduced the minimum LV dP/dt 63% compared with baseline. Esmolol increased LV end-diastolic pressure 110%–125% and decreased the minimum LV dP/dt 12% and mean arterial blood pressure 9%. Although dobutamine-esmolol restored mean arterial blood pressure to baseline, LV end-diastolic pressure remained increased.


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  		Table 1. Systemic Hemodynamic Variables
 
Dobutamine decreased apical phase angles and systolic time intervals (Table 2) as compared with baseline measured by using ultrasonic crystals but not by conductance catheter-derived regional volumes. Esmolol delayed apical and papillary regional phase angles and their respective systolic time intervals compared with baseline. It is important to note that these esmolol-induced effects persisted during dobutamine-esmolol.


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  		Table 2. Regional and Global Phase Angles
 
Esmolol decreased apical effective SV (Table 3) and apical effective shortening compared with baseline. These esmolol-induced effects persisted during esmolol-dobutamine. Effective and maximal SVs increased in the nonparesed basal region during esmolol and esmolol-dobutamine. Apical maximal SVs were not altered by esmolol, dobutamine, or dobutamine-esmolol. Effective and maximal SV increased in the uninvolved basal segment during esmolol, whereas only maximal SV increased during dobutamine-esmolol.


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  		Table 3. Regional and Total Stroke Volumes, Maximal Volumes, and Segmental Shortening
 
Dobutamine did not alter regional or total LV maximal volumes (Table 3). Esmolol increased apical, papillary, basal, and total maximum volumes. However, when dobutamine was added to esmolol, the increased apical maximal volumes persisted. The effects of apical dyskinesis on apical volume are illustrated for one dog in Figures 1 and 2. Apical and basal maximal dimensions (sonomicrometer crystals) were not altered by dobutamine or dobutamine-esmolol (Table 3).



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  		Figure 1. A three-dimensional plot of apical regional volumes versus phase angle for each of three treatments: baseline, dobutamine, and dobutamine-esmolol (Dobut-Esmolol) in a single dog. Four consecutive cardiac cycles are plotted for each treatment, and each individual tracing represents the regional volume with respect to time for a single cardiac cycle, with 360° from R wave to R wave.

 


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  		Figure 2. Apical volume-cycle loops using polar coordinate graphs with phase angle as degrees for baseline, dobutamine, esmolol, and dobutamine-esmolol (Dobut-Esmolol) treatments for one dog. Note that esmolol-induced regional dysfunction induced a delay in reaching minimal regional volume as compared with baseline and that systemic dobutamine infusion attenuated the increase in maximal volume; it did not alter the phase shift as compared with baseline.

 
Dobutamine increased apical stroke force, but not SW, by 53% compared with baseline (Table 4). Esmolol and dobutamine-esmolol decreased apical SW 43%–65%, whereas esmolol alone decreased apical stroke force 67% compared with baseline.


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  		Table 4. Regional and Total Stroke Work and Stroke Force
 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Human subjects with RWMAs are often treated with small doses of dobutamine to improve myocardial function while measures of global performance, such as cardiac output, are used to validate the improvement. This study showed that asynchrony and decreased effective SV caused by RWMAs were not corrected by systemic infusion of dobutamine. Thus, regional asynchrony persisted despite objective evidence in support of improved global LV performance. Persistent temporal asynchronies such as these may explain why inotropes increase myocardial oxygen consumption more than expected in the presence of RWMAs (8).

Previous efforts to quantify RWMAs have included angiography, regional radionucleotide scans, regional sonomicrometry, and two-dimensional echocardiography. All of these methods have technical difficulties (14). Echocardiography has been the most widely used technology because it is affordable, is portable, displays LV function in real time, and is minimally invasive. Some of the difficulty in evaluating regional cardiac dysfunction with echocardiography can be explained by subjective estimates of RWMAs independent of global end-systole. Because dysfunctional myocardium often continues to contract after global end-systole, the extent of regional dysfunction can be systematically underestimated.

Previous studies (10,15,16) indicated that regional phase angles and effective SV were more sensitive indicators of RWMAs than were ungated measures of regional amplitude. In contrast, Heusch et al. (17) found that the regional amplitude of contraction was more sensitive. These differences can be reconciled by considering the temporal definition of regional systole (18). If regional SVs are gated to global systole, they are sensitive indicators of RWMAs; if not gated, they are insensitive. Significant RWMAs would have gone undetected in this study if maximal SV had been the only indicator considered.

One study used phase angle analysis to assess RWMAs (19). A temporal Fourier transform was applied to data from regional sonomicrometer thickness crystals. Unfortunately, these data are limited because they were not analyzed with respect to gated markers of global systole. It is interesting to note, however, that the increased phase shift between unaffected and affected regions correlated strongly with altered regional thickening.

We showed previously that RWMAs were associated with increased LV end-diastolic pressures and volumes, probably because of the delayed relaxation manifested by regional phase delays (10). This study illustrated that RWMAs also reduced diastolic compliance during infusion of small doses of dobutamine.

Maximal SW is the sum of effective SW and ineffective SW (20,21). The difference between maximal and effective SW reflects the asynchrony of regional contraction associated with RWMAs. In this study, RWMAs decreased regional maximal SW by 45%–67%. If we had calculated effective SW, we probably would have realized an even larger decrease.

It is likely that some regional cardiac asynchrony is normal (10). Regional asynchrony that resolves with inotropes has been demonstrated in healthy subjects without heart disease (22). It is unknown to what extent (if any) asynchrony may be a part of normal cardiac function. If asynchrony is normal, then the (baseline) regional asynchrony observed in our dogs may represent a phase-dependent contractile reserve. If this is true, then inotropes that improve synchrony could be expected to increase cardiac output independent of the amplitude of regional contraction.

Parallel conductance artifact produces uncertainty in determining absolute volumes by use of conductance catheters. In our study, we corrected for parallel conductance artifact by using hypertonic saline calibration and the dual-field method of determining conductance (23). We confirmed previously the accuracy of relative conductance volumes in our laboratory (24), as verified by others both in vivo and in vitro (25). Thus, we doubt that our LV volumes reflect systematic treatment-specific conduction artifacts.

In practice, inotropic drugs would be initiated in response to RWMAs, not before their expression, as in our model. Nonetheless, our protocol would model well the induction of RWMAs during a dobutamine stress test.

We chose our esmolol-induced RWMA model as a method to validate our analyses because esmolol induced reliable and reversible RWMAs, allowing us to compare phase delays among regions without fear of postischemic mechanical changes. Additional analyses need to be performed with similar models but with RWMAs induced by ischemia. We believe, however, that our mathematical analyses may be applicable to any similar contractile state characterized by regional asynchrony of contraction.

Finally, extrapolation of esmolol-induced dyskinesis to other pathologic processes, such as coronary ischemia, myocardial stunning, or infarction, is questionable. However, the delayed shortening and postsystolic shortening seen in our model are characteristics of regional myocardial ischemia (7,26). The behavior of ischemic myocardium in response to dobutamine may also be different from esmolol-induced RWMAs. However, Perlini et al. (27) demonstrated that dobutamine increased the diastolic bulging of ischemic myocardium, and such paradoxical diastolic RWMAs can only increase asynchrony further, suggesting that our phase angle analyses may also be applicable for the study of myocardial ischemia.


   Acknowledgments
 
Supported in part by the Veterans Administration and the Departments of Anesthesiology at the University of Pittsburgh and Queen’s University.

The authors would like to thank John Melick and Brian Ondulick for their expert technical assistance and John Lutz for his assistance with computer-based acquisition of the conductance catheter and piezoelectric crystal data.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication March 4, 2002.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press