Dennis L. Rollins

Strength-duration and probability of success curves for defibrillation with biphasic waveforms.

Certain biphasic waveforms require less energy to defibrillate than do monophasic pulses of equal duration, although the mechanisms of this increased effectiveness remain unclear. This study used strength-duration and percent success curves for defibrillation with monophasic and biphasic truncated exponential waveforms to explore these mechanisms. In part 1, defibrillation thresholds were determined for both high- and low-tilt waveforms. The monophasic pulses tested ranged in duration from 1.0 to 20.0 msec, and the biphasic waveforms had first phases of either 3.5 or 7.0 msec and second phases ranging from 1.0 to 20.0 msec. In part 2, defibrillation percent success curves were constructed for 6.0 msec/6.0 msec biphasic waveforms with a constant phase-one amplitude and with phase-two amplitudes of approximately 21%, 62%, 94%, and 141% of phase one. This study shows that if the first phase of a biphasic waveform is held constant and the second phase is increased in either duration or amplitude, defibrillation efficacy first improves, then declines, and then again improves. For pulse durations of at least 14 msec, the second-phase defibrillation threshold voltage of a high-tilt biphasic waveform is higher than that of a monophasic pulse equal in duration to the biphasic second phase (p less than 0.05), indicating that the previously proposed hypothesis of stimulation by the second phase is not the sole mechanism of biphasic defibrillation. These facts indicate the importance of the degree of tilt for the defibrillation efficacy of biphasic waveforms and suggest at least two mechanisms exist for defibrillation with these waveforms, one that is more effective for smaller second phases and another that becomes more effective as the second phase is increased.

Conduction disturbances caused by high current density electric fields.

During internal defibrillation, potential gradients greater than 100 V/cm occur near defibrillation electrodes. Such strong fields may cause deleterious effects, including arrhythmias. This study determined 1) the effects of such strong fields on the propagation of activation and 2) whether these effects were different for monophasic and biphasic shocks. Voltages and potential gradients during the shock, as well as activation sequences before and after the shock, were mapped from 117 epicardial electrodes placed over a 3 x 3-cm area on the right ventricle in six dogs. Pacing at a cycle length of 350 msec was given from a long narrow electrode on the right side of the mapped area to generate parallel activation isochrones. A monophasic shock, 10 msec in duration, or a biphasic shock with both phases 5 msec in duration was delivered 300 msec after the last paced stimulus via a mesh electrode on the left side of the mapped area as the cathode, with the anode on the right atrium. Shocks of 70-850 V were given, and the potential gradient and current density at each recording electrode were calculated from the measured potentials and fiber orientation by using a finite element method. Pacing was resumed 200 msec after the shock, and activation sequences were mapped for up to 5 minutes. Potential gradients ranged from 1 to 189 V/cm with high fields on the left side and low fields on the right side of the mapped area. Where the potential gradient was weak, the first activation sequence after the shock was similar to that before the shock, but activation blocked without conducting into areas where the gradient was greater than 64 +/- 4 (mean +/- SD) V/cm for monophasic and greater than 71 +/- 6 V/cm for biphasic shocks. These values are significantly different (p less than 0.003). The higher the potential gradient, the longer was the duration of block before conduction returned. Block duration, however, was generally shorter for biphasic than for monophasic waveforms of the same field strength. In conclusion, conduction block can follow either waveform, but biphasic waveforms cause less block than monophasic waveforms. This effect may partially explain the increased defibrillation efficacy of biphasic shocks.

Comparison of the internal defibrillation thresholds for monophasic and double and single capacitor biphasic waveforms

Implantable cardiac defibrillators are now an accepted form of therapy for patients with life-threatening ventricular arrhythmias that cannot be controlled by antiarrhythmic drugs. These devices could be made even more acceptable if they were smaller, had increased longevity and the surgical procedure for implantation was less invasive. Reducing the energy requirements for internal defibrillation with use of a nonthoracotomy system would make all of these goals achievable. Monophasic and double and single capacitor biphasic waveforms were compared in 14 anesthetized dogs (25.5 +/- 2.2 kg) with use of a nonthoracotomy lead system that has previously been shown to distribute the delivered voltage throughout the heart more equally. Cathodal catheter electrodes were placed in the right ventricular apex and outflow tract. The anodal electrode was a large cutaneous R2 patch placed over the left side of the chest. The mean energy requirement for defibrillation when a single capacitor biphasic waveform was used was significantly less (6.4 +/- 2.6 J) than that for either the double capacitor biphasic or the monophasic waveform (18.0 +/- 8.0 and 17.4 +/- 8.0 J, respectively) of the same duration. Unexpectedly, the leading edge voltage for the phase I of the single capacitor biphasic waveform was significantly less (266 +/- 51 V) than that for either the double capacitor biphasic or the monophasic waveform (336 +/- 76 and 427 +/- 117 V, respectively). In conclusion, in large dogs, defibrillation is possible at low energy levels with a single capacitor biphasic waveform.

Comparison of the temperature profile and pathological effect at unipolar, bipolar and phased radiofrequency current configurations

With a multi-electrode catheter, phased radiofrequency (RF) delivers current between each electrode and a backplate as well as between adjacent electrodes. This study compared the tissue heating and lesion dimensions created by phased and standard RF. Ablation was performed on the in vivo thigh muscles in 5 pigs. Six lesions were created on each thigh muscle using phase angle 0° RF, 127° RF, 180° RF with and without a backplate, and standard RF in bipolar and sequential unipolar configurations. Two plunge needles, each with 6 thermocouples 1mm apart, were inserted into the tissue with one needle beside an electrode and the other midway between electrodes for tissue temperature measurement. The 0° RF created lower tissue temperatures and smaller lesions between electrodes than those beside electrode. With 127° and 180° RF, tissue temperature and lesion dimensions between electrodes were similar to beside electrode, while the 127° RF created higher tissue temperature and deeper lesions than 180° RF (both with and without a backplate) at both sites. Standard RF bipolar ablation created similar tissue temperatures and lesion depths at both sites, but required greater power than the 127° RF. Standard RF sequential unipolar ablation created only a slight temperature increase and no lesions between electrodes 3 and 4. As judged by tissue temperature, lesion depth and uniformity, and RF power requirement, 127° RF may be a better energy configuration for linear ablation than the other RF modalities tested.

Regional Capture of Fibrillating Ventricular Myocardium: Evidence of an Excitable Gap

Previous investigations have suggested that during ventricular fibrillation (VF) pacing stimuli are incapable of evoking propagated ventricular activations. To determine whether regional myocardial capture could be achieved during rapid pacing in VF, extracellular unipolar potentials were sampled (2 kHz) and recorded from 506 Ag-AgCl electrodes arranged in a rectangular grid (22 x 23, 1.12-mm spacing) embedded in a plaque overlying two pacing electrodes in the epicardium of the anterobasal right ventricle in pentobarbital-anesthetized pigs (25 to 30 kg, n = 6). During separate episodes of electrically induced VF, two bursts of 40 monophasic stimuli (10 mA, 2-millisecond duration) were asynchronously applied to the stimulating electrodes in either a bipolar, unipolar anodal, or unipolar cathodal mode. Evidence of regional capture was provided by (1) animating the first temporal derivative of the extracellular potentials, (2) analyzing inter-beat interval patterns, and (3) employing the Karhunen-Loeve decomposition method to quantify the repetitiveness of spatio-temporal patterns of activation. Regional capture of ventricular myocardium during VF was observed when pacing stimuli fell late in the local myocardial activation interval and when the pacing cycle length was 80% to 115% of the mean subplaque activation cycle length. When myocardial activations became phase locked to the pacing stimuli, repeatable spatiotemporal patterns of activation followed each stimulus. Poincaré sections at the plaque border revealed that during VF prior to pacing, interbeat intervals were irregular but were driven by pacing to stable fixed values at times corresponding to our qualitative declaration of regional capture. A similar correspondence was demonstrated between the time of capture, defined by direct observation of the activation patterns, and a rise in the power contained in the first two spatial modes of a Karhunen-Loeve decomposition. These data demonstrate that appropriately timed stimuli produce regional capture of fibrillating right ventricular myocardium in the pig and support the existence of an excitable gap during VF in this model.

Prolongation of repolarization time by electric field stimulation with monophasic and biphasic shocks in open-chest dogs.

Recent studies suggest that 1) electrically induced fibrillation and defibrillation involve prolongation of refractoriness by the shock in addition to stimulation and 2) biphasic waveforms are more efficient for defibrillation than are comparable monophasic waveforms. The purpose of this study was to compare prolongation of action potential duration at 50% repolarization by monophasic and biphasic shocks during paced rhythm. A floating glass microelectrode was used to record intracellularly from the anterior right ventricular epicardium in seven open-chest dogs. After 10 S1 beats paced at an interval of 350 msec, 5-msec and 2.5-msec monophasic shocks and biphasic shocks, with each phase of 2.5 msec, were given via mesh electrodes on either side of the microelectrode. The shock strength was adjusted so that the shock field, measured from eight extracellular electrodes encircling the microelectrode, was about 5 V/cm. Monophasic and biphasic S2 shocks were given starting with an S1-S2 interval of 120 msec, which was increased in 5-msec steps until an action potential was produced by the S2 shock. Both monophasic and biphasic 5 V/cm shock fields caused significant prolongation of action potential duration. The prolongation of action potential duration increased as the S1-S2 interval increased. This prolongation occurred at shorter S1-S2 intervals for 5-msec monophasic shocks than for biphasic shocks.

Electrode Impedance: An Indicator of Electrode-Tissue Contact and Lesion Dimensions During Linear Ablation

Pre-ablation impedance was evaluated for its ability to detect electrode-tissue contact and allow creation of long uniform linear lesions with a multi-electrode ablation catheter. The study consisted of 2 parts, both of which used the in vivopig thigh muscle model. In part 1, a 7 Fr. multi-electrode catheter was held in 3 electrode-tissue contact conditions: (1) non-contact; (2) light contact with a 30[emsp4 ]g downward force; and (3) tight contact with a 90[emsp4 ]g downward force. Impedances were measured in unipolar, modified unipolar and bipolar configurations using a source with frequencies from 100[emsp4 ]Hz to 500[emsp4 ]kHz. Compared with non-contact, the impedance increased 35±22±% with 30[emsp4 ]g contact pressure and 68±40±% when the contact pressure was increased to 90[emsp4 ]g across the range of frequencies studied. In part 2, the same catheter was held against the tissue with different forces. Pre-ablation impedance was measured using a 10[emsp4 ]kHz current. Phased radiofrequency energy was applied to the 5 electrodes simultaneously using 10[emsp4 ]W power at each electrode for 120[emsp4 ]s. A total of 32 linear lesions were created. The lesion dimensions correlated with pre-ablation impedance. A unipolar impedance ≥190[emsp4 ]Ω indicates 95±% possibility to create a uniform linear lesion of at least 3[emsp4 ]mm depth with our ablation system. We conclude that pre-ablation impedance may be a useful indicator for predicting electrode-tissue contact and the ability to create a continuous and transmural linear lesion with a multi-electrode catheter.

Impact of Myocardial Ischemia and Reperfusion on Ventricular Defibrillation Patterns, Energy Requirements, and Detection of Recovery

Background—Shocks that have defibrillated spontaneous ventricular fibrillation (VF) during acute ischemia or reperfusion may seem to have failed if VF recurs before the ECG amplifier recovers after shock. This could explain why the defibrillation threshold (DFT) for spontaneous VF appears markedly higher than for electrically induced VF. Methods and Results—The DFT for electrically induced VF (E-DFT) was determined in 15 pigs before ischemia, followed by left anterior ascending or left circumflex artery occlusion. VF was electrically induced 20 minutes after occlusion, followed 5 minutes later by reperfusion. Whether spontaneous or electrically induced, VF during occlusion or reperfusion was treated with up to 3 shocks at 1.5×E-DFT. If all 3 shocks failed, shock strength was increased. Thirty minutes after reperfusion, the other artery was occluded and the protocol was repeated. Defibrillation was considered successful if postshock sinus/idioventricular rhythm was present for ≥30 seconds. VF recurring within 30 seconds after the shock was considered immediate or delayed if the first postshock activation complex in a rapidly restored ECG recording was VF or sinus/idioventricular rhythm, respectively. Defibrillation efficacy at 1.5×E-DFT was significantly higher for electrically induced ischemic VF (76%) than for spontaneous VF (31%). The incidence of delayed recurrence after electrically induced nonischemic (3%) or ischemic (20%) VF was significantly lower than after spontaneous VF (75%). Mean VF recurrence time after spontaneous VF was 4.6±5.3 seconds. Conclusions—Spontaneous VF can be halted by a shock but then quickly restart before a standard ECG amplifier has recovered from postshock saturation, making it appear that the shock failed.

Effects of monophasic and biphasic shocks on action potentials during ventricular fibrillation in dogs.

This study determined the response of action potentials during ventricular fibrillation (VF) to timed monophasic and biphasic shocks. A floating glass microelectrode was used to record intracellularly from the anterior right ventricle in 10 open-chest dogs. After 10 seconds of electrically induced VF, 5-millisecond monophasic and 2.5/2.5-millisecond biphasic shocks or 16-millisecond monophasic and 8/8-millisecond biphasic shocks were given via mesh electrodes on either side of the microelectrode. Monophasic and biphasic truncated exponential shocks of 5 V/cm were given with coupling intervals timed from the beginning of a VF action potential to the shock ranging from 50 to 70 milliseconds in 5-millisecond increments. Each coupling interval for each waveform was tested during a different VF episode. The interval between successive activations during VF was 86 +/- 15 milliseconds (mean +/- SD). The refractory period during VF was 61 +/- 5 milliseconds for 5-millisecond monophasic shocks and 66 +/- 6 milliseconds for 2.5/2.5-millisecond biphasic shocks (P < .05). At each coupling interval, action potential duration at 50% repolarization (APD50) was significantly prolonged by the shocks compared with the mean preshock APD50 (P < .05). ADP50 duration increased significantly with increases in the coupling interval (P < .05) for both monophasic and biphasic waveforms. For all coupling intervals together, APD50 prolongation as a percent of the mean preshock APD50 was 170 +/- 55%, 192 +/- 45%, 151 +/- 44%, and 175 +/- 45% for 5- and 16-millisecond monophasic and 2.5/2.5- and 8/8-millisecond biphasic waveforms, respectively. This APD50 prolongation was greater for monophasic than biphasic shocks and was greater for longer than shorter waveforms (P < .05). Thus, during VF, (1) the refractory period for 5-V/cm truncated exponential waveforms lasting 5 milliseconds is approximately 75% of the VF activation interval; (2) the refractory period is shorter for monophasic than for comparable biphasic waveforms; (3) both monophasic and biphasic 5-V/cm shock fields cause prolongation of action potential duration; (4) prolongation of action potential duration increases as the coupling interval increases; and (5) prolongation of action potential duration is greater for monophasic shocks and for longer shock waveforms.

Locally Propagated Activation Immediately After Internal Defibrillation

BACKGROUND Electrical mapping studies indicate an interval of 40 to 100 ms between a defibrillation shock and the earliest activation that propagates globally over the ventricles (globally propagated activation, GPA). This study determined whether activation occurs during this interval but propagates only locally before being blocked (locally propagated activation, LPA). METHODS AND RESULTS In five anesthetized pigs, the heart was exposed and a 504-electrode sock with 4-mm interelectrode spacing was pulled over the ventricles. Ten biphasic shocks of a strength near the defibrillation threshold (DFT) were delivered via intracardiac catheter electrodes, and epicardial activation sequences were mapped before and after attempted defibrillation. Local activation was defined as dV/dt < or =-0.5 V/s. Postshock activation times and wave-front interaction patterns were determined with an animated display of dV/dt at each electrode in a computer representation of the ventricular epicardium. LPAs were observed after 40 of the 50 shocks. A total of 173 LPA regions were observed, each of which involved 2+/-2 (mean+/-SD) electrodes. LPAs were observed after both successful and failed shocks but occurred earlier (P<.0001) after failed (35+/-8 ms) than successful (41+/-16 ms) shocks, although the times at which the GPA appeared were not significantly different. On reaching the LPA region, the GPA front either propagated through it (n=135) or was blocked (n=38). The time from the onset of the LPA until the GPA front propagated to reach the LPA region was shorter (P<.01) when the GPA front was blocked (32+/-12 ms) than when it propagated through the LPA region (63+/-20 ms). CONCLUSIONS LPAs exist after successful and failed shocks near the DFT. Thus, the time from the shock to the GPA is not totally electrically silent.