To determine the mechanism of ventricular vulnerability to electrical stimulation, we simultaneously recorded from 120 transmural electrodes in a 35 X 20 X 5-mm portion of right ventricular infundibulum in seven dogs. Baseline pacing (S1) was performed from outside the mapped region followed by single premature stimulation (S2) of increasing strength at the center of the mapped region. In five of six episodes of ventricular fibrillation and 26 of 30 episodes of repetitive responses, complete reentrant pathways were observed. Earliest activation following S2 was not at the site of S2 stimulation but was at a point between the S1 and S2 sites of stimulation. Activation spread away from the early site toward the opposite side of the mapped region around the sides of an arc of block near the S2 site to form a "figure-of-eight." The activation fronts coalesced to activate the region around the S2 site last and, if the difference in times between activation at the early site and near the S2 site was large, reentered the tissue toward the S1 site. Ventricular refractory periods were determined in four dogs following S1 pacing; the regions with the greatest nonuniformity in the dispersion of refractoriness were not the regions of unidirectional block after S2 stimulation. Thus, 1) ventricular fibrillation and repetitive responses induced electrically with S1 and S2 stimuli at different ventricular sites arise by figure-of-eight reentry, 2) this reentry is caused by the ability of S2 stimulation both to prolong refractoriness near the S2 site and to initiate a propagated response in the region between the S1 and S2 sites, and 3) a nonuniform dispersion of refractoriness is not crucial for the electrical induction of reentry leading to ventricular fibrillation or repetitive responses when S1 and S2 stimuli are given at different locations on the right ventricular outflow tract.
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 < 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, (a) after both successful and unsuccessful defibrillation with epicardial shocks of 21 J, an isoelectric window occurs during which no activation fronts are present; (b) the postshock isoelectric window is shorter for unsuccessful than for successful defibrillation; (c) unsuccessful shocks transiently synchronize activation before fibrillation regenerates; (d) 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 21 J halt all activation fronts after which VF regenerates.
To examine the relationship between the defibrillation threshold and the strength of shocks that induce ventricular fibrillation during the vulnerable period, we determined the defibrillation threshold in 22 open-chest dogs using epicardial defibrillation electrodes with the cathode at the ventricular apex and the anode at the right atrium. We also determined whether there was an upper limit of shock strength that induces fibrillation in the vulnerable period by giving shocks of various energy through these same electrodes during the repolarization phase of paced rhythm. The above determinations were also made with the anode at the ventricular apex and the cathode at the right atrium in eight of the dogs and with the cathode at the ventricular apex and the anode at the left atrium in another eight of the dogs. In all dogs for all electrode configurations, there was an upper limit to the shock strength that induced ventricular fibrillation during the vulnerable period. Depending on the electrode combination, this upper limit of ventricular vulnerability either was not significantly different from or was slightly lower than the defibrillation threshold. The correlation coefficient between the two was highly significant for all three electrode configurations. These results support the hypothesis that successful defibrillation with epicardial electrodes requires a shock strength that reaches or exceeds the upper limit of ventricular vulnerability and that shocks slightly lower than the defibrillation threshold fail because they reinitiate ventricular fibrillation by stimulating portions of the myocardium during their vulnerable period. Circulation 73, No. 5, 1022-1028, 1986 UNTIL RECENTLY, the accepted hypothesis for the mechanism of ventricular defibrillation was based on studies indicating that a critical mass of myocardium is necessary for the maintenance of fibrillation. ' brillation stimulus will always occur when some portion of the myocardium is repolarizing. A stimulus can induce fibrillation if given during the vulnerable period of repolarization.5 These findings suggest the hypothesis that unsuccessful epicardial shocks of at least 1 J halt fibrillation and then reinitiate it by stimulating myocardium that is in the vulnerable period of repolarization. The hypothesis implies that there is an upper limit of strength above which a shock will not induce fibrillation during the vulnerable peridd and that this upper limit of ventricular vulnerability should correlate with the defibrillation threshold. The purpose of this study is to test these implications. MethodsTwenty-two mongrel dogs (mean weight + SD, 18.9 + 3.4 kg) were anesthetized with pentobarbital (30 to 35 mg/kg)6' 7 and succinylcholine (1 mg/kg). Each was intubated with a cuffed endotracheal tube and ventilated with 30% to 60% oxygen through a Harvard respirator. Ringer's lactate was continuously infused and supplemented with potassium chloride, sodium bicarbonate, and calcium chloride when indicated. Via a separate intravenous line, pent...
We delivered strong shocks via electrodes on the left ventricular apex and the right atrium in seven dogs during the T wave of atrial pacing while recordings were made from 56 epicardial electrodes. After shocks that induced arrhythmias were given, the earliest activation occurred in the middle of the ventricles for lower-energy shocks and in the base for higher-energy shocks. For shocks late in the vulnerable period, activation was recorded soon after the shock, whereas for shocks early in the vulnerable period activation was not recorded for a mean of 70 ms (+/- 17 ms SD) after the shock. We also gave 1-J shocks during right and left ventricular pacing. For shocks early in the vulnerable period, activation initiating fibrillation arose in a focal pattern from the paced region. For shocks during the midportion of the vulnerable period, fibrillation arose by two leading circle reentrant loops rotating in opposite directions, one on the left and the other on the right ventricle. For shocks at the end of the vulnerable period, the two reentrant loops fused on the side of the heart opposite the pacing site to again form a single focal activation pattern. Thus the initial activation patterns of arrhythmias initiated by shocks, the time from the shock until earliest postshock activation, and the site of earliest postshock activation are strongly influenced by the coupling interval and strength of the shock.
To study defibrillation, shocks were given to seven dogs during electrically induced fibrillation, while recordings were made from 56 epicardial electrodes. Shocks were given via electrodes on the left ventricular apex and the right atrium, creating an uneven shock field with much higher potential gradients in the apex than in the base of the ventricles. For unsuccessful 0.01- to 0.05-J shocks, activation occurred soon after the shock at many sites in both the base and the apex. For 0.1- to 0.5-J shocks, the number of early activation sites was greatly decreased, and the latency from the shock until earliest recorded activation was greatly increased at the apex but not at the base. For 1- to 5-J shocks, one to three early sites were present and confined to the base, with a long latency between the shock and the appearance of these early sites. The latency and location of earliest activation were similar to those after 1- to 5-J shocks given to induce fibrillation during normal paced rhythm. Shocks of 10 J successfully defibrillated. These findings suggest that the shock field can have at least three effects. One, a weak field fails to halt the activation fronts of fibrillation. Two, a stronger field halts but then reinduces fibrillation in a manner similar to that of the same strength field during the vulnerable period of normal rhythm. Three, a still higher field halts fibrillation without reinitiating it. Successful defibrillation requires a shock strong enough to create this third field intensity throughout the ventricles.
A reduction in the shock strength required for defibrillation would allow use of a smaller automatic implantable cardioverter-defibrillator and would reduce the possibility of myocardial damage by the shock. Most internal defibrillation electrodes require 5 to 25 J for successful defibrillation in human beings and in dogs. In an attempt to lower the shock strength needed for defibrillation, we designed two large titanium defibrillation patch electrodes that were contoured to fit over the right and left ventricles of the dog heart, covering areas of approximately 33 and 39 cm2, respectively. In six anesthetized open-chest dogs, the electrodes were secured directly to the epicardium and ventricular fibrillation was induced by 60 Hz alternating current. Truncated exponential monophasic and biphasic shocks were given 10 sec later and defibrillation thresholds (DFTs) were determined. The DFT was 159 48 V, 3.2 + 1.9 J (mean + SD) for 10 msec monophasic shocks and 106 + 22 V, 1.3 + 0.4 J, for biphasic shocks with both phase durations equal to 5 msec (5-5 msec). The experiment was repeated in another six dogs in which the electrodes were secured to the pericardium. The mean DFT was not significantly higher than that for the electrodes on the epicardium: 165 + 27 V, 3.1 + 1.2 J for 10 msec monophasic shocks and 116 ± 19 V, 1.6 + 0.5 J for 5-5 msec biphasic shocks. Low DFTs were also obtained with biphasic shocks in which the duration of the first phase was longer than that of the second. In a third group of six dogs, DFTs were determined for the large contoured electrodes as well as for 10 cm2 flat patch electrodes on the right and left ventricular epicardium. The mean DFT was significantly lower for the 5-5 msec biphasic waveform than for the 10 msec monophasic waveform for both types of electrodes, and the mean DFT for the large contoured electrodes was significantly lower than that for the flat patch electrodes for both types of waveforms. We conclude that the shock strength required for defibrillation can be markedly lowered by means of biphasic shocks and large contoured patch electrodes. A CLINICAL advantage would be gained if the shock strength required for direct defibrillation with the automatic implantable cardioverter-defibrillator (AICD) could be reduced. Since the size of the unit is largely determined by the sizes of the battery and capacitor, a reduction in required shock strength would permit the implantable device to be smaller.' 2 A decrease in defibrillation shock strength might also reduce the myo-cardial damage 1 34 and cardiac arrhythmias5-7 caused by high-intensity defibrillation shocks. Increasing the size of AICD electrodes has been shown to decrease the defibrillation threshold (DFT).8 1 We designed a pair of large titanium defibrillation patch electrodes that were contoured to fit the right and left ventricles of the canine heart. The purpose of this study was to determine whether the DFT was low for these large electrodes. Since recent studies have indicated that biphasic waveforms decrease re...
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 (1) on the right atrium and left ventricular apex (RA. V) and (2) 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 (1) there is a markedly uneven distribution of potential gradients for epicardial defibrillation electrodes with most of the voltage drop occurring near the electrodes, (2) the potential gradient field is significant because it determines where shocks fail to halt fibrillation, and (3) determination of the potential gradient field should lead to the development of improved electrode locations for defibrillation. Circulation 74, No. 3, 626-636, 1986.
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.
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