N. D. Danieley

Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks.

To test the hypothesis that a defibrillation shock is unsuccessful because it fails to annihilate activation fronts within a critical mass of myocardium, we recorded epicardial and transmural activation in 11 open-chest dogs during electrically induced ventricular fibrillation (VF). Shocks of 1-30 J were delivered through defibrillation electrodes on the left ventricular apex and right atrium. Simultaneous recordings were made from septal, intramural, and epicardial electrodes in various combinations. Immediately after all 104 unsuccessful and 116 successful defibrillation shocks, an isoelectric interval much longer than that observed during preshock VF occurred. During this time no epicardial, septal, or intramural activations were observed. This isoelectric window averaged 64 +/- 22 ms after unsuccessful defibrillation and 339 +/- 292 ms after successful defibrillation (P less than 0.02). After the isoelectric window of unsuccessful shocks, earliest activation was recorded from the base of the ventricles, which was the area farthest from the apical defibrillation electrode. Activation was synchronized for one or two cycles following unsuccessful shocks, after which VF regenerated. Thus, after both successful and unsuccessful defibrillation with epicardial shocks of greater than or equal to 1 J, an isoelectric window occurs during which no activation fronts are present; the postshock isoelectric window is shorter for unsuccessful than for successful defibrillation; unsuccessful shocks transiently synchronize activation before fibrillation regenerates; activation leading to the regeneration of VF after the isoelectric window for unsuccessful shocks originates in areas away from the defibrillation electrodes. The isoelectric window does not support the hypothesis that defibrillation fails solely because activation fronts are not halted within a critical mass of myocardium. Rather, unsuccessful epicardial shocks of greater than or equal to 1 J halt all activation fronts after which VF regenerates.

The potential gradient field created by epicardial defibrillation electrodes in dogs.

Knowledge of the potential gradient field created by defibrillation electrodes is important for the understanding and improvement of defibrillation. To obtain this knowledge by direct measurements, potentials were recorded from 60 epicardial, eight septal, and 36 right ventricular transmural electrodes in six open-chest dogs while 1 to 2 V shocks were given through defibrillation electrodes on the right atrium and left ventricular apex (RA. V) and on the right and left ventricles (RV .LV). The potential gradient field across the ventricles was calculated for these low voltages. Ventricular fibrillation was electrically induced, and ventricular activation patterns were recorded after delivering high-voltage shocks just below the defibrillation threshold. With the low-voltage shocks, the potential gradient field was very uneven, with the highest gradient near the epicardial defibrillation electrodes and the weakest gradient distant from the defibrillation electrodes for both RA. V and RV .LV combinations. The mean ratio of the highest to the lowest measured gradient over the entire ventricular epicardium was 19.4 +/- 8.1 SD for the RA. V combination and 14.4 +/- 3.4 for the RV .LV combination. For both defibrillation electrode combinations, the earliest sites of activation after unsuccessful shocks just below the defibrillation threshold were located in areas where the potential gradient was weak for the low-voltage shocks. We conclude that there is a markedly uneven distribution of potential gradients for epicardial defibrillation electrodes with most of the voltage drop occurring near the electrodes, the potential gradient field is significant because it determines where shocks fail to halt fibrillation, and determination of the potential gradient field should lead to the development of improved electrode locations for defibrillation.

Cardiac potential and potential gradient fields generated by single, combined, and sequential shocks during ventricular defibrillation.

Background Potential gradient field determination may be a helpful means of describing the effects of defibrillation shocks; however, potential gradient field requirements for defibnrllation with different electrode configurations have not been established. Methods and Results To evaluate the field requirements for defibrillation, potential fields during defibrillation shocks and the following ventricular activations were recorded with 74 epicardial electrodes in 12 open-chest dogs with the use of a computerized mapping system. Shock electrodes (2.64 cm2) were attached to the lateral right atrium (R), lateral left ventricular base (L), and left ventricular apex (V). Four electrode configurations were tested: single shocks of 14-msec duration given to two single anode-single cathode configurations, R:V and L: V, and to one dual anode-single cathode configuration, (R+L):V; and sequential 7-msec shocks separated by 1 msec given to R:V and L:V (R:V → L:V). Defibrillation threshold (DFT) current was significantly lower for R:V → L:V than for the other configurations and markedly higher for L:V. Despite these differences, the minimum potential gradients measured at DEFI were not significantly different (approximately 6–7 V/cm for each electrode configuration). Potential gradient fields generated by the electrode configurations were markedly uneven, with a 15–27-fold change from lowest to highest gradient, with the greatest decrease in gradient occurring near the shock electrodes. Although gradient fields varied with the electrode configuration, all configurations produced weak fields along the right ventricular base. Early sites of epicardial activation after all unsuccessful shocks occurred in areas in which the field was weak; 87% occurred at sites with gradients less than 15 V/cm. Ventricular tachycardia originating in high gradient areas near shock electrodes followed 11 of 67 successful shocks. Conclusions These data suggest that 1) defibrillation fields created by small epicardial electrodes are very uneven; 2) achievement of a certain minimum potential gradient over both ventricles is necessary for ventricular defibrillation; 3) the difference in shock strengths required to achieve this minimum gradient over both ventricles may explain the differences in DIFTs for various electrode configurations; and 4) high gradient areas in the uneven fields can induce ectopic activation after successful shocks.

Transmural activations and stimulus potentials in three-dimensional anisotropic canine myocardium.

Epicardial and endocardial pacing are widely used, yet little is known about the three-dimensional distribution of potentials generated by the pacing stimulus or the spread of activation from these pacing sites. In six open-chest dogs, simultaneous recordings were made from 120 transmural electrodes in 40 plunge electrodes within a 35 X 20 X 5-mm portion of the right ventricular outflow tract during epicardial and endocardial pacing at a strength of twice diastolic threshold and at 1 mA. The magnitude of extracellular potentials generated by the stimulus and the activation times were compared in regions proximal (less than 10-12 mm) and distal to the pacing site. Local fiber orientation was histologically determined at each recording electrode. For endocardial pacing, endocardial potentials were larger than epicardial potentials only in the proximal region (p less than 0.001); while in the distal region, epicardial potentials were larger (p less than 0.001), and endocardial activation occurred earlier than epicardial activation for both regions (p less than 0.001). For epicardial pacing, epicardial potentials were larger than endocardial potentials in both regions (p less than 0.001), and epicardial activation occurred earlier only in the proximal region (p less than 0.02), while endocardial activation occurred before epicardial activation in the distal region (p less than 0.01). In planes of recording electrodes parallel to the epicardium and endocardium, the initial isochrones were elliptical with the major axes of the ellipses along the mean fiber orientation between the pacing site and recording plane rather than along the local fiber orientation in the recording plane. Thus, the ellipses in each plane rotated with respect to each other so that in three dimensions the activation front was helicoid, yet the twist of the helix was less than that of the corresponding transmural rotation of fibers. For pacing from the right ventricular outflow tract, we conclude that beyond 10-12 mm from endocardial and epicardial pacing sites epicardial stimulus potentials in both cases are larger than endocardial potentials because of resistivity differences inside and outside the heart wall and activation in both cases is primarily endocardial to epicardial because of rapid endocardial conduction, and we conclude that the initial spread of activation is helicoid and determined by transmural fiber direction.

Comparison of activation during ventricular fibrillation and following unsuccessful defibrillation shocks in open-chest dogs

The purpose of this study was to map in detail the spread of activation away from sites of early postshock excitation following unsuccessful defibrillation to determine whether these activation fronts are the unaltered continuation of activation fronts present just before the shock. We recorded simultaneously from 120 bipolar electrodes on 40 plunge needles in a 20 x 35 x 5-mm volume of tissue of the right ventricular outflow tract immediately before and after shocks of 190-350 V were given via electrodes on the right atrium and left ventricular apex to six open-chest dogs with electrically induced ventricular fibrillation. For 20 shocks approximately 100 V below the defibrillation threshold, the site of earliest recorded activation following the shock was near the center of the mapped region. At the earliest recorded activation sites, there was an isoelectric window in the immediate postshock period lasting 42 +/- 15 msec after which activation fronts either spread away from a site in all directions in a focal pattern (12 episodes) or else spread away in only one direction (eight episodes). Comparison of activation patterns immediately before and after the shock revealed that in 18 of the 20 episodes, the location and pathway of activation fronts after the shock were markedly different from those before the shock. The preshock intervals at the sites of earliest activation following the shock, that is, the interval between the last activation at the site and the time of the shock, were not randomly distributed but were similar, averaging 64 +/- 11 msec, and were negatively correlated with the isoelectric postshock window (r = -0.70, p = 0.0001). These findings indicate that the presence and the site of origin of activation fronts after the shock are influenced by at least two factors: the shock itself and the electrophysiological state of the myocardium at the time of the shock. Thus, epicardial shocks approximately 100 V below the defibrillation threshold markedly alter the activation sequences of fibrillation but are unsuccessful because the activation fronts following the shock reinitiate fibrillation.

The Assumptions of Isochronal Cardiac Mapping

Isochronal maps of cardiac activation are commonly used to study the mechanisms and to guide the ablative therapies of arrhythmias. Little has been written about the assumptions implicit in the construction and use of isochronal cardiac maps. These assumptions include the following: (1) the location of the recording electrodes is known with sufficient accuracy to determine the mechanism of an arrhythmia or to guide therapy; (2) a single, discrete activation time can be assigned to each recording electrode location; (3) the presence or absence of activation at an electrode site can be reliably ascertained, and when activation is present, the time of activation can be determined with sufficient accuracy to specify the mechanism of an arrhythmia or to guide therapy; and (4) the recording electrodes are close enough together that the activation sequence can be estimated with sufficient accuracy to determine the mechanism of an arrhythmia or to guide therapy. The manuscript reviews evidence that these assumptions may not always be true, and when they are not, the isochronal map may be misleading.

Simultaneous Multichannel Cardiac Mapping Systems

Simultaneous multichannel cardiac mapping systems. There is much current interest in simultaneous multichannel cardiac mapping. In this paper we give recommendations for the construction of a cardiac mapping system. Because the field of cardiac mapping is relatively young, optimum mapping techniques and all possible applications have not yet been developed. Therefore, the mapping system should be flexible and it should have many capabilities. The system should be digital; if variable gains are used, the amplifiers should be programmable and controlled by a microprocessor. It should be possible to analyze previous recordings and acquire additional recordings simultaneously. The mapping system should be able to record continuously for at least tens of minutes and preferably for hours. The recorded data stream should be a self‐contained unit, holding all important electrophysiologic information as well as the recorded electrode signals. The programs should be written in c under a UNIX operating system. A minimum of 64 channels should be used for epicardial or endocardial mapping and a minimum of 128 channels for three‐dimensional intramural mapping. The leakage current requirements for multichannel mapping systems are too stringent and should be re‐evaluated. The major limitation to progress in cardiac mapping is neither the hardware nor the software; it is the electrode: its construction, its placement, its fixation, and the interpretation of its recordings.

Neural networks for improved automation of ventricular activation mapping

Whether or not a neural network could discriminate between electrograms from viable tissue (local myocardial activation) and nonviable tissue (distant electrical events) was investigated as a step toward improving automation of cardiac activation mapping. Cryolesions were made in canine myocardium. Five days later, plunge needles with eight electrodes were inserted through normal tissue and the lesions, and during atrial pacing unipolar electrograms were recorded, sampling at 8000 Hz with 12-bit resolution. Data were analyzed from 19 electrodes. The type of tissue from which electrograms were recorded was correctly identified for 18 of the 19 electrodes, indicating that the network was able to identify features of the electrograms that distinguished viable from nonviable tissue sources, and that this generalized to new electrograms upon which the network had not been trained. It is concluded that neural networks may have application in automated cardiac activation mapping.<<ETX>>

A self-documenting data structure for cardiac mapping

A data structure has been implemented for a multichannel cardiac mapping system that contains the complete state of the system at any time. This scheme frees the investigator from the responsibility of continuously recording system parameters during the course of a study and prevents clerical errors that could profoundly affect the analysis and interpretation of data. The hardware implementation is reflected in the data structures used in the analysis software, which is designed to allow easy access to the system configuration at the time of data acquisition. The system has proved to be reliable and effective in the conduct of basic and applied cardiac mapping studies.<<ETX>>

Comparison of electrophysiologic data across diverse cardiac geometries

The authors describe a method for generating one three-dimensional heart surface from digitized serial sections of a number of hearts. This allows a composite surface to be generated from the contours of successive slices of the hearts used in the laboratory. The electrophysiologic data gathered from all hearts can then be mapped onto the generated three-dimensional surface, allowing, for instance, the computation of average values of the measured variable at predetermined points on the standard surface. Thus by using the same geometric surface comparisons between different studies are made possible.<<ETX>>