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© 2001 International Anesthesia Research Society
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Abstract |
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The objective of this study was to determine the efficacy of a two-electrode myocardial electrical impedance (MEI) monitor in reproducibly detecting induced myocardial ischemia by comparing MEI changes with hemodynamic changes, including sonomicrometric changes. With institutional approval, 80 dogs were anesthetized with sodium thiamylal, intubated, ventilated, and had venous, arterial, and pulmonary artery catheters placed. Medial sternotomy was performed to facilitate myocardial exposure and allow the left anterior descending coronary artery (LAD) to be isolated. Two pacing electrodes were attached to the myocardium to measure MEI with a monitor. Seventy dogs were randomly assigned to the 15, 30, 45, 60, or 120 min LAD occlusion group. Sonomicrometric transducers were attached to the myocardium of the ten remaining dogs and their LAD was occluded for 36 min. MEI increased immediately after LAD occlusion to a level significantly more (P <0.05) than baseline and returned to the baseline level upon reperfusion. Twenty dogs developed ventricular fibrillation with no attempts at resuscitation. MEI changes paralleled the sonomicrometric changes expected with ischemia. No significant cardiovascular hemodynamic changes were found with less than 45 min of LAD occlusion. Sixty and 120 min LAD occlusion resulted in significant decreases in cardiac output. The results of these experiments demonstrate that the two-electrode MEI monitor reproducibly changes in response to myocardial ischemia.
Implications: We used dogs to determine if we could measure myocardial ischemia using a device that measures impedance and demonstrated that a two-electrode myocardial electrical impedance monitor reliably reflected changes induced by myocardial ischemia.
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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In 2001, more than 100 million patients will undergo surgery throughout the world, with one-third being more than 65 yr of age or having two or more cardiovascular risk factors (1). Research has shown an increased correlation of adverse cardiac events with the presence of perioperative myocardial ischemia (2). High-risk patients display an increased frequency of tachycardia and asymptomatic ischemia in the first 48 h postoperatively, with ischemia almost uniformly preceding adverse cardiac events (2–4). These facts indicate the need for reliable ischemia monitoring. However, Urban et al. (5), have shown that clinically available hemodynamic indicators cannot identify intraoperative myocardial ischemia. All measures of myocardial ischemia have their limitations. Alterations in electrocardiography (ECG)-ST segments produced by left ventricular hypertrophy, digitalis effect, and electrolyte abnormalities can mimic the ST segment changes of ischemia (5). Although the use of intraoperative ST trending monitors may facilitate intraoperative real-time visual detection of ECG ischemic changes, some ischemic episodes will still be undetected (6). Even transesophageal echocardiology has limitations. For example, it is unable to be used to monitor patients during tracheal intubation, one of the most stressful periods of surgery. In addition to considerable intraobserver variability, the short-axis view will not detect apical abnormalities and wall motion abnormalities may be due to changes in afterload rather than myocardial ischemia (7).
Myocardial electrical impedance (MEI) holds promise for detecting and assessing various disease states of heart tissue. It correlates with regional and global ischemia (8–10), to gauge tissue protection by beta-blockade from reversible ischemic damage (8), to compare myocardial preservation methods (10), to detect edema (11), to predict the revivability of the heart (11), to determine pathologic tissue ultrastructural changes (11), to detect adenosine triphosphate (ATP) depletion (8) and lactate accumulation (8). Mueller et al. (12) and Grauhan et al. (13) demonstrated that the MEI signal can reliably detect edema associated with humoral rejection episodes after heart transplantation and can do so considerably faster than with traditional pathologic analysis of endomyocardial tissue biopsy specimens. Our MEI device makes detection almost instantaneous and only requires two frequently placed heart-pacing electrodes as opposed to four or more MEI specific electrodes.
Because MEI correlates with myocardial tissue viability (10,11), the measure has several important potential monitoring uses. Intraoperatively, MEI could be used in aortic tissue and myocardial tissue during cardiopulmonary bypass (CPB) as an early indication of damage. After CPB, MEI could be used to assess the degree of reperfusion afforded by the newly placed grafts. MEI could assess the heart tissue while drugs are being adjusted immediately after cardiac surgery. MEI could be monitored on a long-term basis with an implantable device in patients who have received new hearts (12).
We evaluated the response of a new and clinically practical MEI monitor to induced myocardial ischemia in dogs. We performed two experiments. The first examined the effect that duration of ischemia had on MEI and the second evaluated MEI concurrently with sonomicrometric measurements. The first experiment’s hypothesis is that changing the duration of ischemia from 15 to 120 min has no effect on the development or recovery from induced myocardial ischemia. The second experiment’s hypothesis is that changes in myocardial impedance would occur at the same time as changes in sonomicrometric measures.
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Materials and Methods |
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We have described our MEI monitor previously (14,15). The device was designed to meet the following clinically relevant objectives: 1) measure MEI from the two pacing electrodes that are commonly placed during coronary artery bypass graft (CABG) and cardiac transplant surgery; 2) measure the true complex tissue electrical impedance spectrum; and 3) measure MEI in near-real time.
Figure 1 shows a block diagram of the device. It consists of a 16-bit microcontroller (80C196TM; Intel, Santa Clara, CA) connected to an optically isolated analog circuit and a personal computer. The microcontroller performs all measuring and analysis functions and returns the results to the PC via a serial connection. The device is connected to the heart via two pacing electrodes (Model 6500TM; Medtronic Inc., Minneapolis, MN) that are routinely attached to the heart after CABG and transplant surgery in humans at this institution.
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The user initiates a MEI measurement sequence from the PC. The microcontroller sends a positive 0.15 ms voltage pulse to the voltage-to-current converter, which converts the voltage impulse to a constant current pulse with a 10 µA peak amplitude. The current pulse passes through a precision resistor and the myocardium to ground. Two precision differential amplifier/filter circuits process the impressed current signal—measured across the precision resistor—and resultant voltage signal—measured across the myocardium. The high-pass filter is set (0.20 kHz) to filter out the ECG signal from the impedance signal. The low-pass filter (5.90 kHz) is set below the Nyquist frequency of the upper-limit-sampling rate of the hardware. The microcontroller simultaneously digitizes a 10 ms interval of the two processed signals at 12.8 kHz, calibrates the signals and transforms them into the frequency domain with 100 Hz resolution using a fast Fourier transform algorithm. The complex impedance spectrum is calculated by dividing the frequency-domain voltage signal by the frequency-domain current signal at each harmonic. In this study, we used the average impedance modulus in the spectrum between 0.20 and 5.90 kHz for our analysis. Fifty-eight impedance data points were averaged for the final impedance measurement. This relationship can be shown in the formula Z(f)0.20-5.9 kHz = E(f)0.20-5.9 kHz/I(f)0.20-5.9 kHz; where Z is the impedance, E is the voltage, I is the current, and where Z, E, and I are functions of the discrete frequency f of the signal being processed. Using the preceding notation,
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After each positive pulse, the microcontroller sends a negative pulse of the same absolute magnitude and duration to minimize any polarization effects at the electrode-tissue interface resulting from the positive pulse and, thus, improve the accuracy of the impedance measurement. No impedance measurement is made with the negative pulse. In this series of experiments, the device averaged three individual measurements to find a final value for myocardial impedance. Our device is capable of calculating MEI in near-real time; however, in this study, MEI measurements were made every 4 min in the first experiment and every 2 min in the second experiment.
Our animal care and use committee approved this study and we adhered to the American Physiological Society’s Guide to the Care and Use of Laboratory Animals. Our unconditioned male canines, after 24 h of no solid food, were weighed, and bilateral forelimb radial venous catheters were placed. An infusion of normal saline (0.9%) solution was established and sodium thiamylal (5 mg/kg) was injected to facilitate tracheal intubation. The canine was maintained at 38°C and mechanically ventilated using 1% inspired isoflurane in room air. The ventilator was set to deliver a tidal volume of 600 mL at a rate of 10 breaths per minute and then adjusted to preserve normocarbia as indicated by blood gas analysis (16). A second bolus of sodium thiamylal (10 mg/kg) was injected into the left forelimb catheter and an infusion of 4 mg/kg/h was started to maintain anesthesia (16). The animals received a Foley catheter and bilateral hindlimb radial artery catheters. A 110-cm pulmonary artery catheter was inserted into the right femoral vein and floated to the pulmonary artery. It was connected to a cardiac output computer and a monitor for measuring central venous and pulmonary artery pressures.
A pulse oximeter was clipped onto the tongue for monitoring tissue oxygen saturation and pulse rate. A Lifescan Brain Activity Monitor (Model 20301-012TM; Diatek, San Diego, CA) was used to monitor anesthesia to maintain an electroencephalogram (EEG) spectral edge power level of 0.5 in both brain hemispheres. We maintained anesthesia depth and blood pressure by adjusting the infusion rate of sodium thiamylal and/or the inspired concentration of isoflurane. Heart rate and blood pressure were monitored.
A transducer-tipped catheter was inserted into the left common carotid artery to monitor and record left ventricular diastolic pressure via the Crystal Biotech VF-1 Hemodynamic Analysis SystemTM (Crystal Biotech, Hopkinton, MA) and IBM 486-PC. A median sternotomy was performed and a 0.75-cm section of the left anterior descending (LAD) coronary artery distal to the second diagonal branch was isolated. A ligature (Robinson’s vessel tie) was loosely positioned around the LAD. Next a flow cuff was placed distal to the Robinson’s vessel tie on the LAD. A pair of ventricular pacing leads were sutured 0.2 cm deep into the exposed heart tissue at a distance of approximately 1 cm apart. The ventricular pacing leads were placed into heart tissue within 2 cm of the angle formed on one side by the LAD coronary artery and on the other side by the first branch off the LAD coronary artery that was distal to the Robinson’s vessel tie. These pacing leads were connected to a MEI monitor.
For the ten dogs involved in the second experiment, a sonomicrometry crystal was sutured onto the surface of the heart to measure the thickness of the myocardium wall. The thickening crystal was placed between the LAD and its distal branch coronary arteries within 1 cm of the ventricular pacing leads. In addition, two 0.5-cm incisions were made 1 cm apart and 0.5 cm deep into the myocardium in the same area of the heart and perpendicular to the myocardium muscle fibers. Two sonomicrometry-lengthening crystals were then sutured at approximately 0.3 cm into these incisions so that the crystals were facing each other to measure length changes in the myocardial muscle fibers. The thickening and lengthening crystals were connected to a Crystal Biotech VF-1 Pulsed Doppler Flow/Dimensions System and IBM 486-PC for recording.
We performed two experiments to evaluate the efficacy of our MEI monitor to detect ischemia. In our first experiment, we investigated the effects of ischemia duration on impedance. Canines were randomly assigned to have ischemia induced for either 15, 30, 45, 60, or 120 min until ten canines that did not develop ventricular fibrillation were studied in each time period. Ischemia was induced with a Robinson’s vessel tie placed on the LAD coronary artery. After the randomly assigned period of ischemia had transpired, the Robinson’s vessel tie was removed allowing reperfusion for the duration of the experiment. In our second experiment, in addition to measurements of MEI and hemodynamics, sonomicrometric measurements of myocardial fiber length and wall thickness were obtained with a commercial monitor (Crystal Biotech). Ten canines had their LAD coronary artery occluded for 36 min and then reperfused for the duration of the experiment. We chose to induce ischemia for 36 min in this experiment because it was a new time period between 30 and 45 min.
Data are reported as mean values with standard deviations. In Experiment 1, comparison between baseline values for each study group was performed by one-way analysis of variance (ANOVA) with the Bonferroni method used to correct ANOVA calculated P-values for multiple comparisons. If the P-value was <0.05 after Bonferroni correction, then unpaired t-test assuming unequal variances was used to determine differences between study groups. Next, one-way ANOVA comparison with Bonferroni correction between baseline values and values at the end of LAD occlusion just prior to when the Robinson’s vessel tie was released was performed for each study group. Because only two means were compared, no post hoc test was required. In Experiment 2, there was only one study group. We analyzed Experiment 2 data by one-way ANOVA with the Bonferroni method used to correct ANOVA calculated P-values for multiple comparisons. If the P-value was <0.05 after Bonferroni correction, then paired t-test assuming unequal variances was used to determine which time points were significantly different from baseline. Dichotomous data (number of canines that developed ventricular fibrillation) were compared by 
2 test.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Experiment 1
Fifty animals survived Experiment 1; 20 dogs developed ventricular fibrillation (VF) and died without any attempts at resuscitation. In this first experiment concerning the effect that duration of induced ischemia has on myocardial impedance, there were no differences between baseline values among the five experimental groups with regard to weight, heart rate, mean arterial pressure, and myocardial impedance (Table 1). Systolic and diastolic arterial pressures are reported in Table 1, but are not statistically compared. The average baseline MEI for the 50 dogs that survived was 803 ± 111 ohms (range 126 ohms). The MEI of the animals in all five experimental groups began to increase immediately after LAD occlusion (Figure 2). The MEI was significantly increased at the end of the occlusion period as compared with baseline values. At the end of induced ischemia, the average impedance for the 50 dogs was 963 ± 137 ohms (range 171 ohms), representing a 20% increase overall (Table 1). The cardiac output of the animals in the 60- and 120-min groups was significantly less at the end of the occlusion period as compared to baseline values. All other hemodynamic indices remained unchanged.
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Twenty of the 70 dogs that were entered into this experiment developed VF and died soon after the Robinson’s vessel tie on the LAD coronary artery was loosened. No attempt was made to recover normal sinus rhythm. Myocardial impedance (Figure 2) increased until the heart became asystolic. No dogs in the 15-min group developed VF while 5, 4, 6, and 5 dogs went into VF in the 30, 45, 60, and 120-minute groups, respectively.
Experiment 2
Ten dogs with an average weight of 52 ± 4.7 lbs, were entered into this study. Table 2 summarizes the data for Experiment 2. The actual occlusion time in this experiment was 36.2 ± 6.2 min. MEI increased from 733 ± 74 ohms immediately after LAD coronary artery occlusion to 893 ± 112 ohms at the end of the occlusion period and returned to baseline (738 ± 74 ohms) after reperfusion (Figure 3).
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One measure of myocardial ischemia is reflected in percent change fraction muscle fiber length (PCF-L). Occlusion of the LAD coronary artery resulted in a significant decrease in PCF-L during the occlusion (Figure 4 and Table 2). These changes in PCF-L are typical of the induction of myocardial ischemia and reperfusion. The effects of myocardial ischemia and reperfusion are also reflected by increases in mean end-systolic length (ESL) and end-diastolic length (EDL) and decreases in the difference between ESL and EDL. On reperfusion, this difference increased but not to the difference seen before the ischemic period (Figure 4).
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Another measure of myocardial ischemia is reflected in percent change fraction heart wall thickness (PCF-T). Occlusion of the LAD coronary artery resulted in a significant decrease in PCF-T. After reestablishing flow to the LAD coronary artery, PCF-T increased, but to a level that was significantly less than baseline. These changes in PCF-T are also typical of the induction of myocardial ischemia and reperfusion. Myocardial ischemia and reperfusion are also reflected by changes in mean end-systolic (EST) and end-diastolic thickness (EDT) (Figure 4). When isch-emia was induced, both EST and EDT individually decreased and the difference between the two measures decreased to near zero. On reperfusion, EST and EDT increased toward baseline levels.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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We demonstrated a new device for measuring MEI. Our device reliably detects induced myocardial ischemia in dogs regardless of the duration of ischemia tested in this study. With our device, monitoring is virtually instantaneous and could be continual if necessary. We compared our new MEI device with sonomicrometric techniques which are considerably more destructive of cardiac tissue than our MEI device. Myocardial ischemia and reperfusion induced changes in sonomicrometric PCF-L and PCT-T correlated well with MEI changes measured by our device. Because of the ease of electrode placement, speed of MEI measurement, and relative lack of damage to myocardial tissue, our device could be used to investigate changes in MEI before and after coronary artery grafts are placed before chest closure or as a research tool.
The device uses advanced but well-understood signal processing techniques that allow for measurement of the generalized complex myocardial impedance spectrum. This makes our monitor valuable for the researcher who is interested in investigating various regions and attributes of the impedance spectrum. Gebhard et al. (11) have, for instance, demonstrated that the phase angle of the complex myocardial impedance spectrum at 5 kHz exhibits a specific characteristic increase during ischemia. Our device has the capability of discerning the same electrical system characteristics studied by Gheorghiu et al. (17) and Casas et al. (18), but with a simpler and more clinically realistic two-electrode configuration. Although we designed the current device to measure the complex impedance to approximately 6 kHz, it could potentially measure impedance in any frequency range of interest. As in this study, ischemia caused an increase in myocardial impedance in Gheorghiu et al. (17) and Casas et al. (18) studies.
This study has limitations. We only studied total occlusion of the LAD coronary artery and not the clinically relevant partial occlusion. Further studies of partial occlusion will need to be conducted before the characteristics of this monitor during partial occlusion are understood. In addition, we only investigated heart tissue that was rendered ischemic by occlusion of the LAD coronary artery. Future studies will need to examine MEI effects in nonischemic myocardial tissue during occlusion of the LAD coronary artery. Other studies could investigate the effects of inotropic drugs, neuromuscular blocking drugs that release histamine, or ß-blockade on MEI measurements. The question of myocardial tissue swelling during induced ischemia needs to be investigated to determine the effects of tissue edema on recorded impedance.
The mechanism by which MEI changes with ischemia is not currently known but may well be associated with ultrastructural changes and/or cellular biochemical changes that occur in the myocardial tissue. The increase in MEI may simply be a result of a reduction in the conductive fluid volume in the affected region of the myocardium. One method to investigate the mechanism by which MEI changes with ischemia would be to perform histological analysis of myocardial tissue. It would have been informative to perform histological analysis of the myocardium of those dogs that developed VF to determine whether those dogs showed evidence of myocardial infarction. Perhaps increasing MEI during reperfusion correlates to infarction. Future studies involving defibrillation after development of VF are needed to determine if the MEI returns to baseline or plateaus at some value more or less than baseline. In addition, intramyocardial swelling could be investigated concurrently with MEI measurements during induced ischemia. Regardless, more studies are necessary before the mechanism of MEI changes with ischemia are understood.
The results of our experiments demonstrate that our minimally invasive two-electrode myocardial impedance device is capable of reproducible measurement of ischemia. Although this device offers the promise for detection and assessment of ischemic myocardial damage, or detection of cardiac allograft rejection, or to investigate the effectiveness of reperfusion to an ischemic myocardial region after CABG surgery, there remains much investigation to be performed before the clinical utility of this monitor can be assessed.
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Acknowledgments |
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Supported, in part, by Samuel J. Roessler Memorial Medical Research Scholarship Grant, The Ohio State University College of Medicine, Columbus, Ohio.
The authors acknowledge the surgical methods training by surgeon Timothy Galbraith MD to author TDM, and for the anesthesia care and surgical assistance of research assistants Debra Frolicher BS and Alan Blumburg BA during this study. We acknowledge the Samuel J. Roessler Memorial Medical Research Scholarship Grant for the financial support for medical student researchers David M. Vigder, Bradley D. Egbert, Karen DenBesten, David B. Golden, Ramin Ganjianpour, and Karen E. von Haam.
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References |
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