D. W. Frazier

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.

Extracellular field required for excitation in three-dimensional anisotropic canine myocardium.

It is not known how well potential gradient, current density, and energy correlate with excitation by extracellular stimulation in the in situ heart. Additionally, the influence of fiber orientation and stimulus polarity on the extracellular thresholds for stimulation expressed in terms of these factors has not been assessed. To answer these questions for myocardium in electrical diastole, extracellular excitation thresholds were determined from measurements of stimulus potentials and activation patterns recorded from 120 transmural electrodes in a 35 X 20 X 5-mm region of the right ventricular outflow tract in six open-chest dogs. Extracellular potential gradients, current densities, energies, and their components longitudinal and transverse to the local fiber orientation at each recording site were calculated from the stimulus potentials produced by 3-msec constant-current stimuli. The resulting values in regions directly excited by the stimulus field were compared with the values in regions not directly excited but activated by the spread of wavefronts conducting away from the directly excited region. Magnitudes of 3.66 mA/cm2 for current density, 9.7 microJ/cm3 for energy, and 804 mV/cm for potential gradient yielded minimum misclassifications of 8%, 13%, and 17%, respectively, of sites directly and not directly excited. A linear bivariate combination of the longitudinal (l) and transverse (t) components of the potential gradient yielded 7% misclassification (threshold ratio t/l of 2.88), and linear combination of corresponding current density components yielded 8% misclassification (threshold ratio t/l of 1.04). Anodal and cathodal thresholds were not significantly different (p = 0.39). Potential gradient, current density, and energy strength-duration curves were constructed for pulse durations (D) of 0.2-20 msec. The best fit hyperbolic curve for current density magnitude (Jm) was Jm = 3.97/D + 3.15, where Jm is in mA/cm2, and D is in msec. Thus, for stimulation during electrical diastole 1) both current density magnitude and longitudinal and transverse components of the potential gradient are closely correlated with excitation, 2) the extracellular potential gradient along cardiac cells has a lower threshold than across cells, while current density thresholds along and across cells are similar, 3) anodal and cathodal thresholds are approximately equal for stimuli greater than or equal to 5 mA, and 4) the extracellular potential gradient, current density, and energy excitation thresholds can be expressed by strength-duration equations.

Response of relatively refractory canine myocardium to monophasic and biphasic shocks.

BackgroundCertain biphasic waveforms defibrillate at lower energies than monophasic waveforms, although the mechanism is unknown. Methods and ResultsThe relative ability of monophasic and biphasic shocks to stimulate partially refractory myocardium was compared because defibrillation is thought to involve stimulating relatively refractory myocardial tissue. Shocks of 25–125 V were given during regularly paced rhythm in 11 open-chest dogs. Computerized recordings of shock potentials, and of activations before and after the shocks, were made at 117 epicardial sites. To quantify the shock field strength, the shock potential gradients were calculated at the electrode sites. Monophasic action potential (MAP) electrode recordings, obtained in five dogs, confirmed direct myocardial excitation by the shock, that is, activations beginning during the shock. Tissue was directly excited up to 4 cm from the shocking electrode, and the area directly excited increased as the shock was made stronger or given less prematurely. In six dogs, strengthinterval curves for direct excitation were determined from plots of potential gradient versus refractoriness at each electrode site. The biphasic curves were located to the right of the monophasic curves by 8 ± 4 msec, indicating a lesser ability to excite refractory myocardium. When the gradient at the directly excited border was at least 3.8 ± 1 V/cm, conduction failed to propagate away from the directly excited zone after the shock, and MAP recordings made near the border showed a shock-induced graded response. This graded response, which prolonged repolarization, may have been responsible for the failure of conduction from the directly excited zone. Although better for defibrillating, the biphasic waveform was thus less effective than the monophasic one in exciting relatively refractory myocardium. ConclusionsThese results indicated that waveform selection for defibrillation should not be guided solely by the ability of the waveform to stimulate tissue, as these two properties can be discordant.

Potential distribution in three-dimensional periodic myocardium. II. Application to extracellular stimulation

For pt.I see ibid., vol.37, no.3, p.252-66 (1990). Modeling potential distribution in the myocardium treated as a periodic structure implies that activation from high-current stimulation with extracellular electrodes is caused by the spatially oscillating components of the transmembrane potential. This hypothesis is tested by comparing the results of the model with experimental data. The conductivity, fiber orientation, extent of the region, location of the pacing site, and stimulus strength determined from experiments are components of the model used to predict the distributions of potential, potential gradient, and transmembrane potential throughout the region. Assuming that a specific value of the transmembrane potential is necessary and sufficient to activate fully repolarized myocardium, the model provides an analytical relation between large-scale field parameters, such as gradient and current density, and small-scale parameters, such as transmembrane potential.<<ETX>>

Basic Mechanisms of Ventricular Defibrillation

Recordings were made simultaneously from many electrodes placed on and in the hearts of animals to study the basic principles of ventricular defibrillation. The findings are listed below. Earliest activations following a shock slightly lower in strength than needed to defibrillate (a subthreshold defibrillation shock) occur in those cardiac regions in which the potential gradients generated by the shock are weakest. Activation fronts after subthreshold shocks do not appear to be continuations of activation fronts present just before the shock. An upper limit exists to the strength of shocks that induce fibrillation when given during the “vulnerable period” of regular rhythm. This upper limit of vulnerability correlates with and is similar in strength to the defibrillation threshold. To defibrillate, a shock must halt the activation fronts of fibrillation without giving rise to new activation fronts that reinduce fibrillation. The response to shocks during regular rhythm just below the upper limit of vulnerability is similar to the response to subthreshold defibrillation shocks. Shocks during regular rhythm initiate rotors of reentrant activation leading to fibrillation when a critical point is formed, at which a certain critical value of shock potential gradient field strength intersects a certain critical degree of myocardial refractoriness. This critical point may explain the existence of the upper limit of vulnerability. The critical point may also partially explain the finding that the relationship between shock strength and the success of the shock in halting fibrillation is better represented by a probability function rather than by a discrete threshold value. Very high potential gradients, approximately an order of magnitude greater than needed for defibrillation, have detrimental effects on the heart, including conduction block, induction of arrhythmias, decreased wall motion, and tissue necrosis.

Modelling in cardiology: Finite element approximation of potential gradient in cardiac muscle undergoing stimulation

Depolarization and defibrillation events in cardiac muscle are considered to be closely related to the potential gradient existing in the myocardium during electrical shock. Therefore, a numerical technique of calculating the gradient from experimental data with minimal possible error is required. Simulation studies indicate that computing the gradient using the central difference formula or finite element approximation based on eight-node binomial elements is superior to other methods. However, if this method is used to calculate potential gradients from a 3

Electrical Rotors in the Heart

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Stimulus-induced critical point. Mechanism for electrical initiation of reentry in normal canine myocardium.

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Mechanism of ventricular vulnerability to single premature stimuli in open-chest dogs.

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