CESLab 3.0
HHA Bench Series Technical Specifications

1. Introduction

As distributed with the CESLab application, the Cell Size employed in the Cell Set "Myocardial Cell Set" is 2.0 mm. This relatively low resolution renders the files compact for rapid downloading, and insures that even users with low-memory hardware configurations can open the benches and conduct Trials. Surface Potential Transfer Coefficients were generated with 2 iterations of the procedure of Gelernter and Swihart (G&S), with Surface Potential Mapping enabled for all employed polyhedra.

If desired, the user can regenerate the Cell Set at a higher resolution (i.e., a lower Cell Size), but note that higher resolutions use much more free memory, and may require significant CPU time. Note that the Surface Potential Transfer Coefficients must be regenerated if the Cell Set is regenerated, which may require significant CPU time; the number of G&S iterations may be reduced to zero and Surface Potential Mapping disabled for all polyhedra to speed this process.

The cardiac shapes employed by the HHA Benches are, in general, drawn from the high-resolution sampled data of Lorange and Gulrajani (courtesy of Drs. Lorange and Gulrajani and the University of Montreal), but note that the CESLab simulation algorithms and electrophysiological parameters of the HHA Preparations differ significantly from those employed by Lorange and Gulrajani.

2. Bench-Wide Parameters

2.1. Regional Dipole Exclusion Radius

2.2. Dipole Sampling Interval

2.3. Vertical Phase 2 Duration Gradient

2.4. Decremental Conduction Curves

2.5. Interval/Potential Curves

2.6. Interval/Duration Curves

3. Preparation Component Objects

3.1. Tissue Types

1 ms was selected as the duration of phase 0 for all rapidly-depolarizing Tissue Types (myocardial, His, and Purkinje).

As delivered, HHA Benches contain no tissue type-specific decremental conduction, interval/potential, or interval/duration curves.

The following Tissue Types are considered part of the HHA Preparation:

• Atrial Myocardial Tissue Type

  This Tissue Type is associated with atrial myocardial Subtissues. Fiber orientation is disabled for this Tissue Type, as propagation in the atria is assumed to be isotropic.

  Tissue Type Window showing the modelled characteristics of the HHA atria. The dotted waveform is editable, and represents the action potential waveform in the absence of Modulators (drugs or unbalanced electrolytes). The other waveform represents the characteristics after current Modulator levels are taken into account, in this case strong doses of a modelled hypothetical neuromuscular stimulant. The waveform is drawn from Katz, with 1 ms chosen as the phase 0 rise time. Click on image to enlarge.

• Ventricular Myocardial Tissue Type

  This Tissue Type is intended for use by ventricular myocardial Subtissues. Fiber orientation is enabled for this Tissue Type so that ventricular anisotropy may be taken into account during simulation. The anisotropic conduction ratio of 2.86 was selected after Lorange and Gulrajani.

  The junctional delay of 3 ms was selected after Lorange and Gulrajani. Note that this delay applies only to retrograde activation of the Purkinje layer by the ventricular myocardium.

  In the HHA heart model, intramural and vertical phase 2 duration gradients establish normal ventricular repolarization gradients by decreasing the duration of activation phase 2 for cells towards the epicardium and towards the base of the heart. Thus, the waveform for ventricular Tissue Types must represent the waveform of maximum duration, i.e. at the apical endocardium. Lorange and Gulrajani employed a maximum ventricular action duration of 280 ms, whereas the diagram of Katz indicates a 235 ms duration. So, the action potential waveform for this Tissue Type was modified from that supplied by Katz to extend the duration of phase 2 by 45 ms.

• Blood Tissue Type

  This Tissue Type is intended for modeling intracavitary blood masses.

  The gross conductivity is set to .6 Siemens/meter after Lorange and Gulrajani, and is used during computation of Surface Potential Transfer Coefficients if any intracavitary polyhedra are employed.

• SA Node Tissue Type

  This Tissue Type is used by the sino-atrial tissue nodes, which initiate the normal cardiac activation cycle.

• AV Node Tissue Type

  This Tissue Type is used by the single Subtissue "AV Node".

  Note that, in the manner of Lorange and Gulrajani, in HHA preparations, the 50 ms AV nodal delay is modelled by slow conduction within the penetrating bundle, as opposed to a junctional delay within the AV node. Attempts to model such a large delay within the AV node (a single cell in the HHA preparations) will cause the top of the penetrating bundle to re-excite the AV node, since the junctional delay is bidirectional.

• Purkinje Tissue Type

  This Tissue Type is intended for use by the ventricular Purkinje layers.

  The junctional delay (for conduction to the ventricular myocardium) is set at 3 ms after Lorange and Gulrajani. Please see the document CESLab Technical Specifications for detailed references.

• Penetrating Bundle Tissue Type

  This Tissue Type is used by the penetrating bundle cable.

• Bundle Branch Tissue Type

  This Tissue Type is used by the His bundles (except the penetrating bundle).

• Bypass Tract Tissue Type

  This Tissue Type is intended for use by Subtissues that model atrioventricular bypass tracts (also known as Bundles of Kent) characteristic of Wolff-Parkinson-White syndrome. Its characteristics are intermediate between those of the atrial and ventricular myocardia.

3.2. Subtissues

The following Subtissues are defined in HHA preparations:

• Atrial Myocardium

  This Subtissue models the myocardium of the left and right atria, plus the intervening atrial septum.

  The conduction speed factor is selected in order to achieve total activation of the atria in 120 ms after Lorange and Gulrajani, at a conduction speed of 79 cm/s.

• Left Ventricular Myocardium

  This Subtissue is used to model the left ventricular myocardium, including the ventricular septum.

  The conduction speed factor is selected to achieve the ventricular conduction velocities of 63 and 22 cm/s employed by Lorange and Gulrajani.

  The fiber angles range from -60 to 60 degrees after Streeter. The intramural phase 2 duration gradient is set to -4 s/m.

• Right Ventricular Free Wall

  This Subtissue is used to model the right ventricular free wall.

  The conduction speed factor is selected to achieve the ventricular conduction velocities used by Lorange and Gulrajani. The fiber angles range from -60 to 60 degrees after Streeter. The intramural phase 2 duration gradient is specified at -1.5 s/m.

  Note that the fractional depths are necessarily discontinuous at the junction of the right ventricular free wall and the ventricular septum. Use of excessive phase 2 duration gradients for the right ventricular free wall may result in spontaneous reactivation of the left ventricular myocardium at this junction, since cells on the inside of the right ventricular free wall might be activated when the outside of the left ventricle has recovered excitability.

• Left Ventricular Purkinje Layer

  This Subtissue is modeled as a Subtissue Wall residing on the interior of the left ventricular myocardium, approximately one cell thick. Note that this minimal thickness is still much thicker than the biological Purkinje layer, so its dipole generation is deactivated to avoid its excessive influence.

  The conduction speed is isotropic, set at 1.0 m/s after Lorange and Gulrajani.

  The area of the left ventricular myocardium that is lined with Purkinje tissue is controlled by Compound Shape "Purkinje Coverage CompoundShape": only regions of the left ventricular endocardium that lie within that shape will be lined with simulated Purkinje cells. As delivered, the left ventricle is lined with Purkinje cells up to about 1 cm from the superior aspect.

• Right Ventricular Purkinje Layer

  This Subtissue is modeled as a Subtissue Wall residing on the interior of the right ventricular free wall only (after Sekiya), approximately one cell thick. Note that this minimal thickness is still much thicker than the biological Purkinje layer, so its dipole generation is deactivated to avoid its excessive influence.

  The conduction speed is isotropic, set at 1.67 m/s after Lorange and Gulrajani.

  The area of the right ventricular free wall and the right side of the interventricular septum that is lined with Purkinje tissue is controlled by Compound Shape "Purkinje Coverage CompoundShape": only regions that lie within that shape will be lined with simulated Purkinje cells. As delivered, the right ventricular free wall is completely lined with Purkinje cells, but only the apical half of the right side of the interventricular septum has a Purkinje lining (Nagao indicates that only the bottom third of the right side of the interventricular septum has a specialized conduction system).

• SA Nodes 1-3

  Three SA nodal foci are predefined, in the manner of Boineau. They are positioned and sequenced approximately in the manner of Lorange and Gulrajani.

  The automatic period is specified at 560 ms, which, when added to the normal activation time of approximately 190 ms, yields the 750 ms specified as the default interactivation interval.

• AV Node

  This models the AV node, and is located at the floor of the right atrium adjacent to the atrial septum. Since the AV node is represented by a single cell, it is difficult to obtain a 50 ms conduction delay from it. So, the atrioventricular delay is modelled by slow conduction within the penetrating bundle.

  Cell Set Viewer showing the myocardial Cell Set, including one SA Node focus, the AV Node, and some of the modelled Bypass Tracts. Click on image to enlarge.

• Penetrating Bundle

  The Penetrating Bundle provides the 50 ms bidirectional atrio-ventricular conduction delay. It begins at the AV Node, and ends at the start of the Right and Left Bundle Branches.

• Right Bundle Branch

  The Right Bundle Branch cable splits from the Penetrating Bundle, and extends down the right side of the Ventricular Septum until it becomes the RV Cable.

• Left Bundle Branch

  The Left Bundle Branch cable splits from the Penetrating Bundle at the top of the interventricular septum, follows the left side of the septum, and ends at the beginning of the Anterior and Posterior Fascicles.

• Anterior Fascicle

  The Anterior Fascicle begins at the end of the Left Bundle Branch, and ends at the beginning of HAP Cable and LAP Cable.

• Posterior Fascicle

  The Posterior Fascicle begins at the end of the Left Bundle Branch, and ends at the beginning of the PP Cable and MS Cable.

• PP Cable

  The end of the PP Cable is a terminal at about 3.5 cm offset along the Y-Axis, at the posterior aspect of the endocardial surface. This location conforms with Durrer's Figure 1, slice 6 (numbering downwards from slice 1).

• HAP Cable

  The HAP Cable begins at the inferior aspect of the Anterior Fascicle. The inferior aspect of the HAP Cable is a terminal in the anterior paraseptal left vetricular free wall, higher than the LAP Cable terminal and somewhat to the left of it (after Durrer et al, who indicate that there is a ovoid of simultaneous early activation in this region).

• LAP Cable

  The LAP Cable begins at the inferior aspect of the Anterior Fascicle, and ends at a terminal in the anterior paraseptal left ventricular free wall, lower than the HAP Cable terminal and to the right of it.

• MS Cable

  The MS Cable excites the mid-septal region of the left ventricle, as described by Durrer et al.

• RVFW Cable

  The RVFW Cable is a continuation of the Right Bundle Branch, and runs to the anterior right ventricular free wall near the apex, where it meets the Purkinje layer. The distal terminal is positioned after the data of Durrer et al, close to the thinnest part of the wall near the site of first RVFW breakthrough.

• RS Cable

  This cable runs from the RVFW terminal back across to the right side of the Ventricular Septum after the data of Myerburg et al. It may be considered as lying within a free-running false tendon.

  Cell Set Viewer showing the modelled His tree. A Junction connects the top of the penetrating bundle to the AV Node, and the lower ends of each cable connect via Junctions to the modelled Purkinje layer to serve as ventricular activation terminals. The HHA Preparations employ a separate high-resolution Cell Set (.5 mm Cell Size) for the His tree to ensure spatial and temporal accuracy, though such a resolution is impractical for representation of the myocardial bulk. Click on image to enlarge.

• Bypass Tracts

  There are eight bypass tracts defined in the HHA preparations, corresponding roughly to the locations used by Gulrajani and Pham- Huy:

  • Posterior Septal (PS)
  • Posterior Left Ventricular (PLV)
  • Lateral Left Ventricular (LLV)
  • Anterior Left Ventricular (ALV)
  • Anterior Septal (AS)
  • Anterior Right Ventricular (ARV)
  • Lateral Right Ventricular (LRV)
  • Posterior Right Ventricular (PRV)
  These bypass tracts are initially deactivated, but may be enabled by checking the "Is Excitable" checkbox in the associated Subtissue Window. Conduction speeds may be adjusted via the associated conduction speed factor.
• Ectopic Foci

  There are two ectopic foci defined in the HHA preparation: one each in the inferior right and inferior left ventricles. They are initially deactivated, but may be enabled by checking the "Is Automatic" checkbox in the associated Subtissue Windows, and entering the desired coupling interval.

3.3. Polyhedra

• Right Atrial Polyhedron
• Left Atrial Polyhedron
• Right Ventricular Polyhedron
• Left Ventricular Polyhedron

ElectroWorld Viewer showing the modelled Intracavitary Polyhedra and the Regional Dipoles, depicted in their normal rotation within the torso model. Click on image to enlarge.

Their shapes are defined by the correspondingly named shapes in compound shape "Heart CompoundShape". They closely follow the contours of the four chambers, while remaining at least .5 cm from the myocardial walls and from each other at all points. They may be edited by the user as desired using the embedded shape editor. The maximum facet size for each intracavitary polyhedron is set at .5 cm, yielding a total of about 1000 facets. The test script "Test Intracavitary Polyhedra" indicates that the simulation results at this resolution are accurate (i.e. very close to results at higher resolutions), yet the number of facets is low enough to enable the number of G&S iterations to be set to non-zero values without consuming excessive computational resources (time and memory).

3.4. Compound Shapes

Shape Editor showing the controlling geometry of the heart as seen in a superior cutaway view at the middle of the heart. The shapes may be modified as desired to alter the cardiac geometry, automatically regenerating each of the modelled Cell Sets at their respective Cell Sizes. Click on image to enlarge.

This compound shape may be edited by the user as desired to change the geometry of the heart model.

3.5. Matrices

The placement of the heart within the torso was selected after Gulrajani and Mailloux. The center of the heart model is at the level of the fifth intercostal space. Additionally, the heart is translated 1 cm to the left, and 1 cm forward.

The matrix contains the following sequence of rotations (each clockwise as seen looking from points along the positive basis vector towards the origin):

• 55 degrees about the Y axis,
• 30 degrees about the X axis,
• and 50 degrees about the Z axis.

This matrix can be edited to change the position (rotation and translation) of the heart (the intracavitary polyhedra and Regional Dipoless) within the torso model in the ElectroWorld, but care must be taken to insure that no Regional Dipoles are moved too close to the lung or torso polyhedra. The menu bar command Report Facet Proximities can be used to directly examine the distances between Dipole Source Locations (DSL) and the nearest polyhedral facets. A series of Trials may also be conducted with slightly differing Regional Dipole Exclusion Radii (causing different DSL positioning) to check for consistency of results.

Rescaling this matrix will not simulate changes in heart size, and is not recommended.

3.6. Cell Sets

• Myocardial Cell Set

  This Cell Set contains all cells that are not part of the specialized conduction system.

  The size of the cells in this Cell Set may be adjusted by the user via: decreasing the Cell Size will yield higher-quality simulation results, but note that, since the bulk of the cells in the HHA heart models are in this Cell Set, the resource consumption (CPU time, free memory, and disk space) per bench is strongly correlated with the Cell Size of this Cell Set.

  The number of cells in this Cell Set will vary inversely with the cube of the Cell Size; the per-trial CPU time, free memory, and disk space requirements will all be proportional to the number of cells in this Cell Set.

  As distributed with the CESLab application, the myocardial Cell Size is set at 2 mm for compactness and speed. The CESLab Bench Library contains HHA preparations at with myocardial and Purkinje Cell Sets set at high resolution, with surface potential mapping enabled for all polyhedra with multiple iterations of the G&S procedure.

• Purkinje Cell Set

  Contains all cells representing the Purkinje layer within the ventricles.

  As delivered with the CESLab distribution, Cell Size is 2 mm, but may be modified by the user.

• His Cell Set

  Contains all cells representing the specialized conduction cables, including the penetrating bundle, right and left bundle branches, and individual cables leading to activation terminals within the ventricles.

  As distributed, Cell Size is set to .5 mm; changing the resolution of this Cell Set is not recommended.

3.7. Cell Junctions

• The AV node in the myocardial Cell Set has a junction with the top of the penetrating bundle in the His Cell Set.
• The distal ends of the His cables each have a junction with the Purkinje Cell Set.
• The Purkinje layer has a set of junctions sprinkled randomly over its surface (after Lorange and Gulrajani), with an interjunctional spacing of three times the myocardial Cell Size. This results in approximately 360 Purkinje-myocardial junctions for Preparations with a 1.5 mm myocardial Cell Size, and 826 for a 1 mm myocardial resolution.

4. Simulation of Normal Cardiac Cycle

An ECG Viewer showing the frontal lead tracings generated by a simulated normal cardiac cycle. Click on image to enlarge.

An ECG Viewer showing the precordial lead tracings generated by a simulated normal cardiac cycle. Click on image to enlarge.

5. Bench Scripts

• Demo Drug Modelling

  This script runs a series of cardiac cycles with increasing serum concentrations of hypothetical agent "Class IA Drug". This simulated drug decreases excitability, slows conduction, and extends activation phase 3. Its expected effects are S-T segment depression, T-wave diminuition, widened QRS, and eventual A-V block.

  An ECG Viewer showing output from the script "Demo Drug Modelling": four cardiac cycles executed with increasing levels of a simulated Class IA agent. The last cycle demonstrates complete A-V block. Click on image to enlarge.

• Demo Left Bundle Branch Blockage

  Simulates complete left bundle branch blockage by temporarily deactivating Subtissue "Left Bundle Branch".

  An ECG Viewer showing the frontal lead tracings generated by simulated left bundle branch blockage. Click on image to enlarge.

• Demo Right Bundle Branch Blockage

  Simulates complete right bundle branch blockage by temporarily deactivating Subtissue "Right Bundle Branch".

  An ECG Viewer showing the frontal lead tracings generated by simulated right bundle branch blockage. Click on image to enlarge.

• Demo Anterior Hemiblock

  Simulates left anterior hemiblock by temporarily deactivating Subtissue "Anterior LBB Fascicle".

  An ECG Viewer showing the frontal lead tracings generated by simulated left anterior hemiblock. Click on image to enlarge.

• Demo Posterior Hemiblock

  Simulates left posterior hemiblock by temporarily deactivating Subtissue "Posterior LBB Fascicle".

  An ECG Viewer showing the frontal lead tracings generated by simulated left posterior hemiblock. Click on image to enlarge.

• Demo PS, PRV, ARV, ARV, AS, ALV, LLV, PLV Bypass Tracts

  This set of scripts demonstrates simulation of Wolff-Parkinson-White (WPW) syndrome via eight separate bypass tract locations (selected after Gulrajani and Pham-Huy): Posterior Septal, Posterior Right Ventricular, Lateral Right Ventricular, Anterior Right Ventricular, Anterior Septal, Anterior Left Ventricular, Lateral Left Ventricular, and Posterior Left Ventricular.

  An ECG Viewer showing a cardiac cycle with a simulated Lateral Right Ventricular bypass tract. Click on image to enlarge.

• Demo RV, LV Ectopy

  This pair of scripts demonstrates simulation of right and left ventricular ectopy with varying coupling intervals.

  An ECG Viewer showing a cardiac cycle with a simulated right ventricular ectopic focus. The coupling interval for the focus was set at 180 ms, or 20 ms after the start of ventricular activation. Click on image to enlarge.

6. References

Boineau JP, Schuessler RB, Mooney CR, Wylds AC, Miller CB, Hudson RD, Borremans JM, Brockus CW (1978). Multicentric origin of the atrial depolarization wave: The pacemaker complex. Relation to dynamics of atrial conduction, P-wave changes and heart rate control. Circulation 58(6): 1036-48.

Burgess MJ, Green LS, Millar K, Wyatt R, Abildskov JA (1972). The sequence of normal ventricular recovery. Am Heart J 84(5): 660-669.

Durrer D, van Dam RT, Freud GE, Janse MJ, Miejler FL, Arzbaecher RC (1970). Total excitation of the isolated human heart. Circulation 41: 899-912.

Eckner FAO, Brown BW, Davidson DL, Glagov S (1969). Dimensions of normal human hearts. Arch Pathol 88: 497-507.

Gelernter HL, Swihart JC (1964). A mathematical-physical model of the genesis of the electrocardiogram. Biophys J 4: 285-301.

Gulrajani RM, Mailloux GE (1983). A simulation study of the effects of torso inhomogeneities on electrocardiographic potentials, using realistic heart and torso models. Circ Res 52: 45-56.

Gulrajani RM, Pham-Huy H, Nadeau RA, Savard P, de Guise J, Primeau RE, Roberge FA (1984). Application of the single moving dipole inverse solution to the study of the Wolff-Parkinson-White syndrome in man. J Electrocardiol 17(3): 271-88.

Katz AM (1992). Physiology of the Heart. Raven Press, New York. Lorange M, Gulrajani R (1993). A computer heart model incorporating anisotropic propagation. J Electrocardiol 26(4): 245- 77.

Lorange M, Gulrajani R (1993). A computer heart model incorporating anisotropic propagation. J Electrocardiol 26(4): 245- 77.

Myerburg RJ, Nilsson K, Gelband H (1972) Physiology of canine intraventricular conduction and endocardial excitation. Circ Res 30: 217-243.

Nagao K, Toyama J, Kodama I, Yamada K (1981). Role of the conduction system in the endocardial excitation spread in the right ventricle. Am J Cardiol 48: 864-870.

Roberts DE, Hersh LT, Scher AM (1979). Influence of cardiac fiber orientation on wavefront voltage, conduction velocity, and tissue resistivity in the dog. Circ Res 44: 701-12.

Streeter DD Jr, Spotnitz HM, Patel DP, Ross J Jr., Sonnenblick EH (1969). Fiber orientation in the canine left ventricle during diastole and systole. Circ Res 24: 339-47.

Waller BF, Taliercio CP, Slack JD, Orr CM, Howard J, Smith ML (1990). Tomographic views of normal and abnormal hearts: the anatomic basis for various cardiac imaging techniques. Part I. Clin Cardiol 13: 804-12.

Waller BF, Taliercio CP, Slack JD, Orr CM, Howard J, Smith ML (1990). Tomographic views of normal and abnormal hearts: the anatomic basis for various cardiac imaging techniques. Part II. Clin Cardiol 13: 877-84.

Waller BF, Schlant RC (1994). Anatomy of the heart. In: Schlant RC, Alexander RW (eds): Hurst's The Heart. New York, McGraw-Hill: 59- 111.

Wyndham CR, Meeran MK, Smith T, Saxena A, Engleman RM, Levitsky S, Rosen KM (1978). Epicardial activation of the intact human heart without conduction defect. Circulation 59: 161-68.

7. Acknowledgements

Thanks also to Ronald Edwards.

2 Mark Stevans

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