- Email: [email protected]
3D Heart: A new visual training method for Electrocardiographic Analysis
Journal of Electrocardiology 40 (2007) 457.e1 – 457.e7 www.jecgonline.com
3D Heart: A new visual training method for Electrocardiographic Analysis☆ Charles W. Olson, MS, a , * David Lange, MS, a Jack-Kang Chan, PhD, a Kim E. Olson, MD, d Alfred Albano, MD, b Galen S. Wagner, MD, b Ronald H.S. Selvester, MD c a
ECG Tech Corporation, Huntington Station, NY, USA Duke University Medical Center, Durham, NC, USA c Memorial Medical Center, Long Beach, CA, USA d Weill Cornell Medical College, New York, NY, USA Received 26 September 2005; accepted 24 April 2007 b
Abstract
This new training method is based on developing a sound understanding of the sequence in which electrical excitation spreads through both the normal and the infarcted myocardium. The student is made aware of the cardiac electrical performance through a series of 3-dimensional pictures during the excitation process. The electrocardiogram 3D Heart 3-dimensional program contains a variety of different activation simulations. Currently, this program enables the user to view the activation simulation for all of the following pathology examples: normal activation large, medium, and small anterior myocardial infarction (MI) large, medium, and small posterolateral MI large, medium, and small inferior MI Simulations relating to other cardiac abnormalities, such as bundle branch block and left ventricular hypertrophy fasicular block, are being developed as part of a National Institute of Health (NIH) Phase 1 Small Business Innovation Research (SBIR) program. © 2007 Elsevier Inc. All rights reserved.
Introduction Cardiologists are becoming increasingly challenged to use the standard 12-lead electrocardiogram (ECG) for diagnosis of the location and relative size of myocardial infarcts. A new method of visual training is proposed to make these diagnoses more obvious and accurate. This new method is based on developing a sound understanding of the sequence in which electrical excitation spreads through both normal and the infarcted myocardium.1-4 The student is made aware of cardiac electrical performance through a time series of 3-dimensional (3D) pictures during the excitation process. This series of pictures illustrates the heart activation status, the resultant vector sum, its loop, and its relation to 12-lead ECG signals.5,6 The availability of reperfusion therapy via primary coronary intervention (PCI) challenges clinicians to use the ☆ This work is being supported by the National Institute of Health under Grant 1 R43 HL077032-01A2. ⁎ Corresponding author. Tel: +1 631 673 3714; fax: +1 631 421 7270. E-mail address: [email protected]
0022-0736/$ – see front matter © 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2007.04.001
standard 12-lead ECG for diagnosis of acute myocardial infarction, to select patients for this intervention, and to assess the therapeutic effect. Different electrophysiologic processes are responsible for the ECG abnormalities that signify the acute transmural ischemia and the chronic myocardial infraction. The acute ST-segment deviation toward the involved region is caused by the “injury”-induced alteration of the membrane potentials during repolarization; and the chronic QRS deviation away from the involved region is caused by the infarction-induced subtraction from the balance of multidirectional depolarization “vectors.” These altered ECG waveforms can be recognized by the responsible clinician either by memorization of patterns or by understanding how the cardiac electrophysiological process is manifested on the body surface recordings. Previous studies have documented the superior clinical diagnostic performances achieved when such understanding has been provided.7-9 A PC-based training program 3D Heart, has been developed to test the utility of this method. The illustrations in this article are from the 3D Heart program. When running the training
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C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
Fig. 1. The normal heart is shown on the left at the beginning of the excitation (red) of the left ventricle. Electrical vectors that are projecting from the segments of the heart are color coded for each segment (anteroseptal—black, anterosuperior—green, posterior—blue, and inferior—pink). Three vectors are shown for each segment at the midpoint of the apical third, the middle third, and the basal third. On the right, the heart with medium anterior MI shows its infracted myocardium in gray. As a result of the infarct, the excitation of the anteroseptal segment is greatly diminished.
program, the student can rotate, translate, and resize the heart and loop 3D images that are illustrated in this article. As an example of this process, Fig. 1 presents a snapshot at 20 milliseconds after the start of the QRS complex in both a normal heart and a heart with a mediumsized anterior MI. This snapshot is taken from a movie of 35 frames that shows the cardiac excitation process in terms of the active surface shown in bright red and the vectors (indicated by arrows) that emerge from the activation of the 12 divisions: superior, middle, and apical sectors of each of the 4 quadrants: (1) anteroseptal, (2) anterosuperior, (3) posterolateral, (4) inferior. Methods Heart to loop The cardiac electrical signal recorded on the body surface represents the summation vector of the individual vectors
emerging from all of the segments at a particular point in time. Early work in this area used the Huygens principal to generate a dipole wave front that propagated from the endocardial surface to the epicardium with each new front created by a projection perpendicular to its present location.2 An electrical dipole of unit strength is assigned to each small surface segment. The summation of these dipoles constitutes a measure of the signal level of a local area and predicts the signal received on the surface both for normal hearts and for patients with MI or abnormal intraventricular conduction.6,10 Fig. 2 (left) illustrates the summation vector at 20 milliseconds after the onset of ventricular activation in the normal heart as presented in Fig. 1. Fig. 2 (right) illustrates the summation vectors at each serial 2.5 milliseconds interval throughout the 80-millisecond duration of the ventricular activation; with the vectors at 20, 40, and 60 milliseconds emphasized by color changes. The ends of all of these serial summation vectors have been connected by a thick yellow
Fig. 2. On the left, we see a single summation vector at 20 milliseconds from the beginning of the QRS complex. On the right, we see the history of the vectors for the entire QRS complex.
C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
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Fig. 3. The summation vectors and the surface of the excitation (red) are shown for the normal and the heart with medium anterior MI for the first 55 milliseconds of the QRS complex.
band to form a “vector loop.” The loop, representing the QRS interval, both begins and ends at the “electrical center of the heart,” represented by the yellow ball. In Fig. 3, the initial 55 milliseconds of the vector loops from the normal heart and from the heart with the medium-sized anterior MI are presented for comparison. The yellow arrows represent the summation vectors at 55 milliseconds in both conditions. The effect of the elimination of the anterior vectors by the MI appears as a distortion of the initial 40 milliseconds of the vector loop.11 The MI is shown to “repel” the initial vectors and point them posteriorly and inferiorly; the inferior deviation is most obvious on the frontal plane projection. This is shown in Fig. 3 for the vector loops in 3D space, and their projection onto the horizontal plane (below) and frontal plane (behind). These projected vector loops are color
coded: 0 to 25 milliseconds (red), 25 to 50 milliseconds (blue), and 50 to 75 milliseconds (green). Loop to leads With this clear understanding of how the electrical activation of the ventricles of the heart as seen in the vector loop is altered by the MI-induced abnormality (heart to loop), we can interpret the 12-lead signals of the ECG more effectively (loop to leads). In the case of the anterior MI, the major effect is seen in the precordial leads, principally leads V1 to V4. The loop-to-leads relationship is shown for the complete ventricular activation period in Fig. 4. This period is termed the “QRS interval” in reference to its component Q, R, and S waveforms that appear on the ECG leads. The view is from
Fig. 4. A view of a 3D vector diagram alone from the top of the heart shows the extreme modification of the normal heart by the medium anterior MI. The Q waves that result in the V1, V2, and V3 leads are obviously due to the loss of the initial anterior vectors.
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C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
Fig. 5. Medium posterior MI shows the rejection of vectors to the posterior and the deflection of initial vectors to the anterior direction. This is shown in the 12 lead by the strong R waves in leads V1 to V3.
above the heart and the vector loop, and the projection of the loop onto the horizontal plane. The black lines represent the 6 horizontal plane leads, with their names (V1-V6) indicated on their positive poles. The recordings of the body surface electrical signals on each of these 6 leads are presented. There is an upward waveform when the summation of these signals is toward the lead's positive pole, and a downward waveform when it is in the opposite direction. The projection of the vector loop onto these precordial leads establishes the direction and magnitude of the summated electrical signals at each point in time. The same color code and timing used for the projected vector loops are repeated in the recordings of the ECG leads. In the normal heart, the summed vector loop swings around smoothly from an initial anterior direction, then to the left, then posteriorly before returning to the origin. This is reflected in Fig. 4 (left) by the gradual change in time of the peak of the R waves from V1 initially then V2, V3, and so on, finally to V6. In the presence of the anterior MI in Fig. 4 (right), we see large Q waves in V1 and V2 and smaller Q waves in V3 and V4. These indicate the negative or posterior direction of the summed vector initially—a clear indicator of an anterior MI. A sample of 3D illustrations of some of the other locations of MI and how this heart-to-loop-to-leads method of illustration helps to identify the abnormality follows in Figs. 5 and 6. The program also makes available the Mercator projection of the coronary artery distributions and the effects of coronary thrombosis on the obstruction of the
coronary blood flow and the development of either subendocardial or transmural MI.10 Fig. 7 shows a large anterior MI and in the top diagram the point of obstruction by coronary thrombosis in the proximal left anterior descending artery (red circle) and the arteries with obstructed flow in blue. In the lower diagram are the areas in which the myocardial cells are infracted; in light blue for only subendocardial infarction, and in dark blue for transmural infarction. For each pathology, the student can view 3D heart activation and heart loop animation movies as well as a 2D Mercator projection of the heart and a normal 12-lead ECG graphic.
Discussion New visual aids for conduction defects A phase 1 SBIR effort is in progress for the National Institute of Health to expand the present 3D heart instructional program to include many more disease states: 1. 2. 3. 4.
Left bundle branch block (LBBB). Right bundle branch block (RBBB). Left anterior fascicular block (LAFB). Left inferoposterior fascicular block (LIFB).
These additional instructional simulation aids should make the program a more complete guide to the understanding of many types of heart problems.
C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
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Fig. 6. Medium inferior MI shows the large initial deflection of vectors to the superior and away from the MI in the inferior quadrant. The limb leads III, aVF, and II show deep and long Q waves.
Fig. 7. This figure shows a large anterior MI, and in the top diagram the point of obstruction by coronary thrombosis in the proximal left anterior descending artery (red circle) and the arteries with obstructed flow in blue. In the lower diagram are the areas in which the myocardial cells are infracted; in light blue for only subendocardial infarction, and in dark blue for transmural infarction.
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C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
Fig. 8. Activation diagrams of the right and left ventricles (RV, LV) during the QRS complex for LBBB. Initial activation of the RV at 25 milliseconds shows the balance of forces between the RV free wall (black vectors) and the RV septal (blue vectors) point posteriorly. At 65 milliseconds, the RV free wall is finished and the RV septum is near finished, while the main activation is the LV via the propagation of the Purkinje system and the inferior and anterosuperior myocardium. All vectors point posteriorly as shown in blue.
In the normal heart, the left ventricle is initially excited at 3 points on the endocardium: 1. In the inferior quadrant, the excitation starts at the junction of the base of the posterior papillary muscle;
2. In the anteroseptal quadrant, the excitation starts at its midpoint and the junction of the apical and middle segments; 3. In the anterosuperior quadrant, the excitation starts at the base of the anterior papillary muscle.
Fig. 9. Left bundle branch block at 65 milliseconds is apparent from the rapid posterior deflection of the total vector sum. The large negative Q waves are seen in V1 to V4.
C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
These points of excitation lead to a smooth progression of depolarization of the left ventricle and its rapid spread to all parts ending at the posterior basal segment.1 In the case of LBBB, the initial excitation is present only in the right ventricle. In this case, the excitation spreads from the right septal endocardium toward the left ventricle endocardium. As the active surface progresses, it passes around the left ventricle from the anteroseptal quadrant to both the inferior and anterosuperior quadrants. The posterior quadrant is then activated from 2 directions. The vast difference between this activation sequence and that of the normal heart is immediately evident from the 3D movie, which shows this development in time. Initial results from this work are shown in Fig. 8. Fig. 8 shows the activation surfaces in red of 2 points in time after the initiation of the QRS complex. The initial activation starts at 2 points in the RV, one on the free wall directly across from the septum and the other at the apical middle border and at the center of the septum. At 65 milliseconds shown on the right side, the RV free wall has completed its activation and the septum is also almost entirely finished. The major excitation surface is the myocardium shown on the inferior and anterosuperior sides of the heart whose vectors are posteriorly directed and the LV surface that has originated from the endocardium of the LV by means of the conduction from the Purkinje system. This is seen as a rounded surface of excitation spreading from the edge of the anterosuperior to the posterior and then the inferior edge. Fig. 9 above shows the total sum vector for the case of LBBB at 65 milliseconds. Each gold bar in the diagram is 2.5 milliseconds in time. The projection of this vector on the horizontal plane shows the progression in time by means of the color code. Each color spans 25 milliseconds in time. In the first 25 milliseconds, there is very little change in position as seen in the small red mark as a result of anterior and posterior balance of forces. In the next 25 milliseconds, the vector moves posteriorly, reaching a maximum at about 50 milliseconds. These properties of LBBB are typical and are projected onto the lead vectors for the precordial leads as shown.
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Similar animations to these have been developed for RBBB and are in progress for the fascicular blocks. Call for test and evaluation groups The initial training program is available now and the expanded program is scheduled to go into a test and evaluation phase in early 2007. We would like to have evaluation volunteers contact us. This is a carefully controlled program to be monitored by an independent evaluator and under the guidance of an Internal Review Board. You may contact us through our Web site: http://www.ecgtech.com or by email: [email protected]. References 1. Durrer D, et al. Total excitation of the isolated human heart. Circulation 1970;XLI:899. 2. Selvester RH, Solomon JC. Simulation of measured activation sequence in the human heart. Am Heart J 1973;85:51. 3. Miller III W, Geselowitz DB. Simulation studies of the electrocardiogram. Circ Res 1978;43:301. 4. Cuffin BN, Geselowitz DB. Studies of the electrocardiogram using realistic cardiac and torso models. IEEE Trans Biomed Eng 1977;BME24:242. 5. Gulrajani RM. Models of the electrical activity of the heart and computer simulation of the electrocardiogram. Crit Rev Biomed Eng 1988;15:1. 6. Olson CW, Warner RA, Wagner GS, Selvester RHS. A dynamic threedimensional display of ventricular excitation and the generation of the vector and electrocardiogram. J Electrocardiol 2001;34(Suppl):7. 7. Hurst JW. Current status of clinical electrocardiography with suggestions for improvement of the interpretive process. Am J Cardiol 2003;92:1072. 8. Pahlm US, O'Brien JE, Pettersson J, et al. Comparison of teaching the basic electrocardiographic concept of frontal plane QRS axis: a determination using classic versus orderly limb lead displays. Am Heart J 1997;134:1014. 9. Patuwo TA, Wagner GS, Ajijola OA. Comparison of teaching basic electrocardiographic concepts with and without ECGSIM, an interactive program for electrocardiography. Ann Noninvasive Electrocardiol; In press. 10. Selvester RH, Wagner GS, Ideker R. Myocardial infarction. Chapter 16. In: MacFarlane PW, Veitch Lawrie TD, editors. Comprehensive electrocardiology. New York: Pergamon Press; 1989. 11. Chou T-C, Helm RA. Clinical vectorcardiography. New York: Grune and Stratton; 1974.
3D Heart: A new visual training method for Electrocardiographic Analysis☆ Charles W. Olson, MS, a , * David Lange, MS, a Jack-Kang Chan, PhD, a Kim E. Olson, MD, d Alfred Albano, MD, b Galen S. Wagner, MD, b Ronald H.S. Selvester, MD c a
ECG Tech Corporation, Huntington Station, NY, USA Duke University Medical Center, Durham, NC, USA c Memorial Medical Center, Long Beach, CA, USA d Weill Cornell Medical College, New York, NY, USA Received 26 September 2005; accepted 24 April 2007 b
Abstract
This new training method is based on developing a sound understanding of the sequence in which electrical excitation spreads through both the normal and the infarcted myocardium. The student is made aware of the cardiac electrical performance through a series of 3-dimensional pictures during the excitation process. The electrocardiogram 3D Heart 3-dimensional program contains a variety of different activation simulations. Currently, this program enables the user to view the activation simulation for all of the following pathology examples: normal activation large, medium, and small anterior myocardial infarction (MI) large, medium, and small posterolateral MI large, medium, and small inferior MI Simulations relating to other cardiac abnormalities, such as bundle branch block and left ventricular hypertrophy fasicular block, are being developed as part of a National Institute of Health (NIH) Phase 1 Small Business Innovation Research (SBIR) program. © 2007 Elsevier Inc. All rights reserved.
Introduction Cardiologists are becoming increasingly challenged to use the standard 12-lead electrocardiogram (ECG) for diagnosis of the location and relative size of myocardial infarcts. A new method of visual training is proposed to make these diagnoses more obvious and accurate. This new method is based on developing a sound understanding of the sequence in which electrical excitation spreads through both normal and the infarcted myocardium.1-4 The student is made aware of cardiac electrical performance through a time series of 3-dimensional (3D) pictures during the excitation process. This series of pictures illustrates the heart activation status, the resultant vector sum, its loop, and its relation to 12-lead ECG signals.5,6 The availability of reperfusion therapy via primary coronary intervention (PCI) challenges clinicians to use the ☆ This work is being supported by the National Institute of Health under Grant 1 R43 HL077032-01A2. ⁎ Corresponding author. Tel: +1 631 673 3714; fax: +1 631 421 7270. E-mail address: [email protected]
0022-0736/$ – see front matter © 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2007.04.001
standard 12-lead ECG for diagnosis of acute myocardial infarction, to select patients for this intervention, and to assess the therapeutic effect. Different electrophysiologic processes are responsible for the ECG abnormalities that signify the acute transmural ischemia and the chronic myocardial infraction. The acute ST-segment deviation toward the involved region is caused by the “injury”-induced alteration of the membrane potentials during repolarization; and the chronic QRS deviation away from the involved region is caused by the infarction-induced subtraction from the balance of multidirectional depolarization “vectors.” These altered ECG waveforms can be recognized by the responsible clinician either by memorization of patterns or by understanding how the cardiac electrophysiological process is manifested on the body surface recordings. Previous studies have documented the superior clinical diagnostic performances achieved when such understanding has been provided.7-9 A PC-based training program 3D Heart, has been developed to test the utility of this method. The illustrations in this article are from the 3D Heart program. When running the training
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Fig. 1. The normal heart is shown on the left at the beginning of the excitation (red) of the left ventricle. Electrical vectors that are projecting from the segments of the heart are color coded for each segment (anteroseptal—black, anterosuperior—green, posterior—blue, and inferior—pink). Three vectors are shown for each segment at the midpoint of the apical third, the middle third, and the basal third. On the right, the heart with medium anterior MI shows its infracted myocardium in gray. As a result of the infarct, the excitation of the anteroseptal segment is greatly diminished.
program, the student can rotate, translate, and resize the heart and loop 3D images that are illustrated in this article. As an example of this process, Fig. 1 presents a snapshot at 20 milliseconds after the start of the QRS complex in both a normal heart and a heart with a mediumsized anterior MI. This snapshot is taken from a movie of 35 frames that shows the cardiac excitation process in terms of the active surface shown in bright red and the vectors (indicated by arrows) that emerge from the activation of the 12 divisions: superior, middle, and apical sectors of each of the 4 quadrants: (1) anteroseptal, (2) anterosuperior, (3) posterolateral, (4) inferior. Methods Heart to loop The cardiac electrical signal recorded on the body surface represents the summation vector of the individual vectors
emerging from all of the segments at a particular point in time. Early work in this area used the Huygens principal to generate a dipole wave front that propagated from the endocardial surface to the epicardium with each new front created by a projection perpendicular to its present location.2 An electrical dipole of unit strength is assigned to each small surface segment. The summation of these dipoles constitutes a measure of the signal level of a local area and predicts the signal received on the surface both for normal hearts and for patients with MI or abnormal intraventricular conduction.6,10 Fig. 2 (left) illustrates the summation vector at 20 milliseconds after the onset of ventricular activation in the normal heart as presented in Fig. 1. Fig. 2 (right) illustrates the summation vectors at each serial 2.5 milliseconds interval throughout the 80-millisecond duration of the ventricular activation; with the vectors at 20, 40, and 60 milliseconds emphasized by color changes. The ends of all of these serial summation vectors have been connected by a thick yellow
Fig. 2. On the left, we see a single summation vector at 20 milliseconds from the beginning of the QRS complex. On the right, we see the history of the vectors for the entire QRS complex.
C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
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Fig. 3. The summation vectors and the surface of the excitation (red) are shown for the normal and the heart with medium anterior MI for the first 55 milliseconds of the QRS complex.
band to form a “vector loop.” The loop, representing the QRS interval, both begins and ends at the “electrical center of the heart,” represented by the yellow ball. In Fig. 3, the initial 55 milliseconds of the vector loops from the normal heart and from the heart with the medium-sized anterior MI are presented for comparison. The yellow arrows represent the summation vectors at 55 milliseconds in both conditions. The effect of the elimination of the anterior vectors by the MI appears as a distortion of the initial 40 milliseconds of the vector loop.11 The MI is shown to “repel” the initial vectors and point them posteriorly and inferiorly; the inferior deviation is most obvious on the frontal plane projection. This is shown in Fig. 3 for the vector loops in 3D space, and their projection onto the horizontal plane (below) and frontal plane (behind). These projected vector loops are color
coded: 0 to 25 milliseconds (red), 25 to 50 milliseconds (blue), and 50 to 75 milliseconds (green). Loop to leads With this clear understanding of how the electrical activation of the ventricles of the heart as seen in the vector loop is altered by the MI-induced abnormality (heart to loop), we can interpret the 12-lead signals of the ECG more effectively (loop to leads). In the case of the anterior MI, the major effect is seen in the precordial leads, principally leads V1 to V4. The loop-to-leads relationship is shown for the complete ventricular activation period in Fig. 4. This period is termed the “QRS interval” in reference to its component Q, R, and S waveforms that appear on the ECG leads. The view is from
Fig. 4. A view of a 3D vector diagram alone from the top of the heart shows the extreme modification of the normal heart by the medium anterior MI. The Q waves that result in the V1, V2, and V3 leads are obviously due to the loss of the initial anterior vectors.
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C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
Fig. 5. Medium posterior MI shows the rejection of vectors to the posterior and the deflection of initial vectors to the anterior direction. This is shown in the 12 lead by the strong R waves in leads V1 to V3.
above the heart and the vector loop, and the projection of the loop onto the horizontal plane. The black lines represent the 6 horizontal plane leads, with their names (V1-V6) indicated on their positive poles. The recordings of the body surface electrical signals on each of these 6 leads are presented. There is an upward waveform when the summation of these signals is toward the lead's positive pole, and a downward waveform when it is in the opposite direction. The projection of the vector loop onto these precordial leads establishes the direction and magnitude of the summated electrical signals at each point in time. The same color code and timing used for the projected vector loops are repeated in the recordings of the ECG leads. In the normal heart, the summed vector loop swings around smoothly from an initial anterior direction, then to the left, then posteriorly before returning to the origin. This is reflected in Fig. 4 (left) by the gradual change in time of the peak of the R waves from V1 initially then V2, V3, and so on, finally to V6. In the presence of the anterior MI in Fig. 4 (right), we see large Q waves in V1 and V2 and smaller Q waves in V3 and V4. These indicate the negative or posterior direction of the summed vector initially—a clear indicator of an anterior MI. A sample of 3D illustrations of some of the other locations of MI and how this heart-to-loop-to-leads method of illustration helps to identify the abnormality follows in Figs. 5 and 6. The program also makes available the Mercator projection of the coronary artery distributions and the effects of coronary thrombosis on the obstruction of the
coronary blood flow and the development of either subendocardial or transmural MI.10 Fig. 7 shows a large anterior MI and in the top diagram the point of obstruction by coronary thrombosis in the proximal left anterior descending artery (red circle) and the arteries with obstructed flow in blue. In the lower diagram are the areas in which the myocardial cells are infracted; in light blue for only subendocardial infarction, and in dark blue for transmural infarction. For each pathology, the student can view 3D heart activation and heart loop animation movies as well as a 2D Mercator projection of the heart and a normal 12-lead ECG graphic.
Discussion New visual aids for conduction defects A phase 1 SBIR effort is in progress for the National Institute of Health to expand the present 3D heart instructional program to include many more disease states: 1. 2. 3. 4.
Left bundle branch block (LBBB). Right bundle branch block (RBBB). Left anterior fascicular block (LAFB). Left inferoposterior fascicular block (LIFB).
These additional instructional simulation aids should make the program a more complete guide to the understanding of many types of heart problems.
C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
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Fig. 6. Medium inferior MI shows the large initial deflection of vectors to the superior and away from the MI in the inferior quadrant. The limb leads III, aVF, and II show deep and long Q waves.
Fig. 7. This figure shows a large anterior MI, and in the top diagram the point of obstruction by coronary thrombosis in the proximal left anterior descending artery (red circle) and the arteries with obstructed flow in blue. In the lower diagram are the areas in which the myocardial cells are infracted; in light blue for only subendocardial infarction, and in dark blue for transmural infarction.
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C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
Fig. 8. Activation diagrams of the right and left ventricles (RV, LV) during the QRS complex for LBBB. Initial activation of the RV at 25 milliseconds shows the balance of forces between the RV free wall (black vectors) and the RV septal (blue vectors) point posteriorly. At 65 milliseconds, the RV free wall is finished and the RV septum is near finished, while the main activation is the LV via the propagation of the Purkinje system and the inferior and anterosuperior myocardium. All vectors point posteriorly as shown in blue.
In the normal heart, the left ventricle is initially excited at 3 points on the endocardium: 1. In the inferior quadrant, the excitation starts at the junction of the base of the posterior papillary muscle;
2. In the anteroseptal quadrant, the excitation starts at its midpoint and the junction of the apical and middle segments; 3. In the anterosuperior quadrant, the excitation starts at the base of the anterior papillary muscle.
Fig. 9. Left bundle branch block at 65 milliseconds is apparent from the rapid posterior deflection of the total vector sum. The large negative Q waves are seen in V1 to V4.
C.W. Olson et al. / Journal of Electrocardiology 40 (2007) 457.e1–457.e7
These points of excitation lead to a smooth progression of depolarization of the left ventricle and its rapid spread to all parts ending at the posterior basal segment.1 In the case of LBBB, the initial excitation is present only in the right ventricle. In this case, the excitation spreads from the right septal endocardium toward the left ventricle endocardium. As the active surface progresses, it passes around the left ventricle from the anteroseptal quadrant to both the inferior and anterosuperior quadrants. The posterior quadrant is then activated from 2 directions. The vast difference between this activation sequence and that of the normal heart is immediately evident from the 3D movie, which shows this development in time. Initial results from this work are shown in Fig. 8. Fig. 8 shows the activation surfaces in red of 2 points in time after the initiation of the QRS complex. The initial activation starts at 2 points in the RV, one on the free wall directly across from the septum and the other at the apical middle border and at the center of the septum. At 65 milliseconds shown on the right side, the RV free wall has completed its activation and the septum is also almost entirely finished. The major excitation surface is the myocardium shown on the inferior and anterosuperior sides of the heart whose vectors are posteriorly directed and the LV surface that has originated from the endocardium of the LV by means of the conduction from the Purkinje system. This is seen as a rounded surface of excitation spreading from the edge of the anterosuperior to the posterior and then the inferior edge. Fig. 9 above shows the total sum vector for the case of LBBB at 65 milliseconds. Each gold bar in the diagram is 2.5 milliseconds in time. The projection of this vector on the horizontal plane shows the progression in time by means of the color code. Each color spans 25 milliseconds in time. In the first 25 milliseconds, there is very little change in position as seen in the small red mark as a result of anterior and posterior balance of forces. In the next 25 milliseconds, the vector moves posteriorly, reaching a maximum at about 50 milliseconds. These properties of LBBB are typical and are projected onto the lead vectors for the precordial leads as shown.
457.e7
Similar animations to these have been developed for RBBB and are in progress for the fascicular blocks. Call for test and evaluation groups The initial training program is available now and the expanded program is scheduled to go into a test and evaluation phase in early 2007. We would like to have evaluation volunteers contact us. This is a carefully controlled program to be monitored by an independent evaluator and under the guidance of an Internal Review Board. You may contact us through our Web site: http://www.ecgtech.com or by email: [email protected]. References 1. Durrer D, et al. Total excitation of the isolated human heart. Circulation 1970;XLI:899. 2. Selvester RH, Solomon JC. Simulation of measured activation sequence in the human heart. Am Heart J 1973;85:51. 3. Miller III W, Geselowitz DB. Simulation studies of the electrocardiogram. Circ Res 1978;43:301. 4. Cuffin BN, Geselowitz DB. Studies of the electrocardiogram using realistic cardiac and torso models. IEEE Trans Biomed Eng 1977;BME24:242. 5. Gulrajani RM. Models of the electrical activity of the heart and computer simulation of the electrocardiogram. Crit Rev Biomed Eng 1988;15:1. 6. Olson CW, Warner RA, Wagner GS, Selvester RHS. A dynamic threedimensional display of ventricular excitation and the generation of the vector and electrocardiogram. J Electrocardiol 2001;34(Suppl):7. 7. Hurst JW. Current status of clinical electrocardiography with suggestions for improvement of the interpretive process. Am J Cardiol 2003;92:1072. 8. Pahlm US, O'Brien JE, Pettersson J, et al. Comparison of teaching the basic electrocardiographic concept of frontal plane QRS axis: a determination using classic versus orderly limb lead displays. Am Heart J 1997;134:1014. 9. Patuwo TA, Wagner GS, Ajijola OA. Comparison of teaching basic electrocardiographic concepts with and without ECGSIM, an interactive program for electrocardiography. Ann Noninvasive Electrocardiol; In press. 10. Selvester RH, Wagner GS, Ideker R. Myocardial infarction. Chapter 16. In: MacFarlane PW, Veitch Lawrie TD, editors. Comprehensive electrocardiology. New York: Pergamon Press; 1989. 11. Chou T-C, Helm RA. Clinical vectorcardiography. New York: Grune and Stratton; 1974.