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(Circulation. 1996;94:1974-1980.)
© 1996 American Heart Association, Inc.

Articles

Reduced Arrhythmogenicity of Biphasic Versus Monophasic T-Wave Shocks

Implications for Defibrillation Efficacy

Steffen Behrens, MD; Cuilan Li, PhD; Paulus Kirchhof, BS; F. Larissa Fabritz, BS; Michael R. Franz, MD, PhD

the Cardiology Divisions of the Veterans Administration Medical Center and Georgetown University, Washington, DC. (S.B., C.L., P.K., F.L.F., M.R.F.) and the Klinikum Benjamin Franklin, Free University, Berlin, Germany (S.B.).

Correspondence to Michael R. Franz, MD, PhD, Cardiology Division, Veterans Administration Medical Center, 50 Irving St NW, Washington, DC 20422.


*    Abstract
up arrowTop
 *Abstract
down arrowIntroduction
 down arrowMethods
 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
Background Biphasic waveforms defibrillate more effectively than monophasic waveforms; however, the mechanism remains unknown. The "upper-limit-of-vulnerability" hypothesis of defibrillation suggests that unsuccessful defibrillation is due to reinduction of ventricular fibrillation (VF). Thus, VF induction mechanisms may be important for the understanding of defibrillation mechanisms. We therefore compared myocardial VF vulnerability for monophasic versus biphasic shocks.

Methods and Results In 10 Langendorff-perfused rabbit hearts, monophasic and biphasic T-wave shocks were randomly administered over a wide range of shock coupling intervals and shock strengths, and the two-dimensional coordinates within which VF was induced were used to calculate the area of vulnerability (AOV) for both shock waveforms. The arrhythmic response to biphasic shocks differed from that to monophasic shocks in three distinct ways: (1) the AOV was smaller (8.9±4.2 versus 13.9±6.0 area units, P<.02), (2) the transition zone between VF-inducing and nonarrhythmogenic shocks was narrower (14.7±4.8 versus 29.9±6.4 area units, P<.001), and (3) the entire AOV shifted toward longer coupling intervals (by 11.0±8.8 ms at the left border [P<.005] and 6.0±5.2 ms at the right border [P=.005] of the AOV).

Conclusions Biphasic shocks encounter a smaller AOV than monophasic shocks, a narrower transition zone from VF to no arrhythmia induction, and a lesser effectiveness in inducing VF at short coupling intervals. In keeping with the upper-limit-of-vulnerability hypothesis, these waveform-dependent differences in VF inducibility might help explain the lower defibrillation threshold for biphasic shocks.


Key Words: electrophysiology • fibrillation • defibrillation • shock


*    Introduction
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 up arrowAbstract
 *Introduction
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 down arrowResults
 down arrowDiscussion
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Electrical field stimuli may induce VF1 if applied during ventricular repolarization (T-wave shocks) and above a certain shock strength known as the fibrillation threshold or the LLV. If the shock strength is increased progressively beyond a certain limit of shock strength, VF will no longer be inducible.2 This ULV has been demonstrated to correlate closely with the DFT, suggesting that both the ULV and DFT may be epiphenomena of a common mechanism.3 4 5 6 7 The extension-of-refractoriness hypothesis states that blockage of propagating reentrant wave fronts by defibrillation shocks above DFT strength both prevents the induction of VF by T-wave shocks above ULV strength and halts fibrillation wave fronts by defibrillation shocks above DFT strength.8 9 10 11 The ULV hypothesis of defibrillation has been advanced as another possible mechanism of defibrillation.12 13 14 It states that an unsuccessful defibrillation shock, although able to halt most activation wave fronts during VF, creates new reentrant wave fronts and thereby reinitiates VF. According to this hypothesis, a shock will terminate VF successfully if reinduction of VF can be avoided.12 13 15

Biphasic shock waveforms defibrillate more effectively than monophasic waveforms16 17 18 19 20 21 22 ; consequently, they are being used in implantable cardioverter-defibrillators. Recent data suggest that transthoracic defibrillation also is more effective with biphasic shocks.23 However, the mechanisms by which biphasic shock waveforms defibrillate more effectively than monophasic shocks are still not well understood.24 25 26 27 28 Since the ULV hypothesis of defibrillation implies a reinitiation of VF, biphasic T-wave shocks should be less arrhythmogenic than monophasic shocks. The purpose of this study was to determine, in an isolated beating rabbit heart preparation, myocardial vulnerability to monophasic and biphasic T-wave shocks and to test the hypothesis that biphasic shocks exhibit less vulnerability than monophasic shocks. Myocardial vulnerability was expressed as the AOV characterized by VF-inducing shocks and defined as a function of both shock timing and shock intensity.29


*    Methods
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 up arrowAbstract
 up arrowIntroduction
 *Methods
down arrowResults
 down arrowDiscussion
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Experimental Preparation
Hearts from 10 New Zealand White male rabbits (mean weight, 3.7±0.4 kg) were isolated, mounted on a vertical Langendorff apparatus, and perfused with a modified Tyrode's solution as described earlier.30 The experimental setup is shown in Fig 1Down. The temperature of the perfusing solution was maintained at 37±0.5°C and the perfusion pressure at no less than 50 mm Hg. AV node ablation was performed mechanically through a pair of surgical tweezers to control the intrinsic heart rate. Subsequently, the heart was paced at 500-ms cycle length by electrical stimuli of twice diastolic threshold strength and a duration of 2 ms from the right ventricular apex by use of a programmable stimulator and stimulus isolator (Bloom). The heart was immersed in a Tyrode's solution–filled chamber 12 cm wide and 7.5 cm high. A three-lead volume-conducted ECG was obtained by means of four Ag-AgCl electrodes flanking the tissue chamber in an approximate Einthoven configuration.31 32 The signals were amplified by a custom-made multichannel ECG amplifier with conventional ECG filter characteristics (Stellartech). Additionally, MAPs were recorded from the right and left ventricular epicardium, as shown in Fig 1Down, to precisely quantify the number of repetitive responses immediately after a shock. The recording technique used in this study has been described previously.30 MAP signals were preamplified by a DC-coupled amplifier with automatic offset control (model 10012, EP Technologies). Truncated exponential monophasic and biphasic shocks were delivered with an experimental defibrillator (model 2394, Medtronic, capacitance 70 µF) by means of two 6.5x6.5-cm rectangular stainless steel plate electrodes placed distant from the heart on opposite walls of the tissue bath (Fig 1Down). The distance between the two plate electrodes was 10 cm. The potential gradients were measured in the absence of the heart within a 4x4x4-cm3 space in the center of the tissue bath with two orthogonally positioned nonpolarizable Ag-AgCl electrodes (interelectrode distance, 4 mm). Differences of potential gradients were <12%, indicating that the shock electrode configuration provided a relatively uniform shock field in the tissue chamber in which the heart was to be placed. This, however, does not exclude substantial variations of potential gradients within the heart. For the biphasic shock waveform, the tilt of the first and second phases was set to 65%. The trailing-edge voltage of the first phase and the leading-edge voltage of the second phase were set to equal values. The overall shock duration was {approx}5 ms (each phase 2.5 ms, with a separation of 0.1 ms). Because the final voltage of the biphasic shock was 12% of the leading-edge voltage of the first phase, yielding an overall tilt of 88%, the tilt of the monophasic shock waveform was set to 88%, resulting in a shock duration of 5 ms. Thus, monophasic and biphasic waveforms were comparable in terms of shock duration and shock energy (Fig 2Down). Shocks were triggered by the pacing stimulator. The delivered shock waveform was displayed on a digital oscilloscope (model LS 140, LeCroy) that provided on-line analysis of peak and integrated shock voltages.



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  		Figure 1. Diagram of experimental setup. Isolated heart and two spring-loaded MAP electrodes are displayed on the vertical Langendorff stand before their immersion in a tissue bath that contained the ECG electrodes and shock plate electrodes. Inset: Side view of tissue bath, with heart immersed in center of bath. LV indicates left ventricle. See text for further details.



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  		Figure 2. Shock waveforms. An 88%-tilt monophasic (A) and a 65%/65%-tilt biphasic (B) waveform were used. Both waveforms had the same overall shock duration of {approx}5 ms.

Experimental Protocol
A 30-minute equilibration time was allowed before the protocol was started. Monophasic and biphasic T-wave shocks were delivered within a grid defined by shock coupling interval on the horizontal axis and shock strength on the vertical axis. The shock coupling intervals tested within the grid ranged from 150 to 220 ms, with a resolution of 10 ms. The shock strengths tested within the grid ranged from 140 to 540 V, with a resolution of 40 V. At each coupling interval and shock strength within the test grid, monophasic and biphasic shocks were applied once. Thus, a total of 88 monophasic and 88 biphasic shocks were delivered in one experiment. Shocks were delivered in random order with regard to the waveform and the sequence of coupling intervals and shock voltages. Myocardial vulnerability for monophasic and biphasic shocks was expressed as the AOV. The AOV was characterized by VF-inducing shocks within the test grid and was defined two-dimensionally by shock coupling interval and shock strength. After each shock, the heart was allowed to recover for 30 seconds. This time was extended to 2 minutes if VF occurred. If VF was induced and did not terminate spontaneously, a defibrillation shock was applied. These shocks were used to determine the DFT. The DFT was defined as 50% probability of successful defibrillation and was calculated from the delayed up-down algorithm.7 33 Monophasic and biphasic DFTs were measured randomly in each experiment. Once VF was induced, a defibrillation shock of 340 V was applied after 5 to 10 seconds of VF through the same electrode system as used for VF induction. Depending on whether this shock was either successful or unsuccessful, the voltage of the following defibrillation shocks was either decreased or increased by 40 V until the lowest shock voltage that successfully defibrillated the heart was found. This voltage was counted as the first data point for the estimation of DFT. Subsequent defibrillation shocks were either decreased or increased by 40 V, according to the results of the previous defibrillation attempts. The procedure was repeated until at least four data points were measured. For the estimation of the DFT, the mean voltage of data points was calculated. After an unsuccessful defibrillation attempt, a rescue shock of 500 to 600 V was applied to terminate VF. After an experiment, the heart was removed from the Langendorff apparatus and weighed. The mean wet weight was 12.4±2.6 g.

Data Analysis
Because of its small myocardial mass, the rabbit heart is prone to recover spontaneously from an episode of artificially induced VF.34 35 36 We therefore quantified the immediate shock response by counting the numbers of repetitive full excitations in MAP recordings with cycle lengths <=160 ms. An action potential prolongation and a directly excited response after the shock were not counted as a repetitive response. Each shock response was classified as VF, nonsustained arrhythmia, or no arrhythmia. VF was defined as induction of six or more repetitive responses with cycle lengths <160 ms by a shock.29 35 37 Nonsustained arrhythmia was defined as induction of one to five repetitive responses, and no arrhythmia as the occurrence of no repetitive response. To compare the AOV extensions, the shortest and longest VF-inducing shock coupling intervals and the ULV and LLV were determined in each experiment and for both waveforms. The ULV and LLV were defined as the highest and lowest VF-inducing shock strengths within the grid. The height of the AOV was defined as the difference between the ULV and LLV. The vulnerable period was defined as the maximal width of the AOV and was calculated as the difference between the longest and shortest VF-inducing shock coupling intervals. The size of the AOV was estimated as the number of AU within the test grid in which shocks induced VF. All measures were expressed as mean±SD. Comparisons were performed with paired t tests. Statistical significance was assumed at values of P<.05.


*    Results
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 *Results
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Fig 3Down depicts an example of two different shock-induced arrhythmic responses. In Fig 3ADown, the shock was delivered during early repolarization. No arrhythmic response was induced. In Fig 3BDown, the shock was delivered at a longer coupling interval when the myocardium was more repolarized. This shock induced VF.



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  		Figure 3. Original recording of a three-lead ECG and a MAP recording from the left ventricular epicardium during the application of a 300-V biphasic T-wave shock delivered at shock coupling intervals of 160 ms (A) and 170 ms (B). A, No arrhythmia was induced by the shock. B, The shock induced VF, which was terminated at 8 seconds by a 340-V biphasic shock.

A representative example of the AOV for both shock waveforms is shown in Fig 4Down, illustrating three differences between the monophasic (Fig 4ADown) and biphasic (Fig 4BDown) AOVs. First, for biphasic shocks, the ULV was lower and the LLV higher than for monophasic shocks, resulting in a smaller height of the AOV for the biphasic waveform. Accordingly, the AOV for biphasic shocks was also smaller, consisting of 9 AU within the test grid compared with 12 AU for monophasic shocks. Second, with monophasic shocks, VF occurred at coupling intervals of 180 and 190 ms. In contrast, biphasic shocks induced VF at coupling intervals of 190 and 200 ms, shifting the AOV to the right. Third, at coupling intervals left of the AOV, nonsustained arrhythmias were induced more frequently by monophasic than by biphasic shocks. This resulted in a more gradual transition zone between the AOV and the area of no arrhythmic response. For example, monophasic shocks at a coupling interval of 160 ms induced repetitive responses at 10 different shock voltages. In contrast, at the same coupling interval, biphasic shocks induced repetitive responses at one shock voltage only.



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  		Figure 4. This example shows the differences in the AOV for monophasic (A) versus biphasic (B) shock waveforms. The shock-induced arrhythmic response is shown within a two-dimensional grid of randomly varied shock coupling intervals (x axis) and shock strengths (y axis). Squares represent the induction of VF, triangles nonsustained arrhythmias, and small dots no arrhythmia. The AOV (dark gray) and the area of nonsustained arrhythmias (light gray) are encircled by a solid line. See text for details.

The TableDown summarizes the horizontal and vertical extensions of the AOV for monophasic and biphasic shocks in 10 experiments. For biphasic shocks, the shortest VF-inducing coupling interval was shifted to the right (ie, to longer coupling intervals) in 8 of 10 hearts, and the longest VF-inducing coupling interval was shifted in the same direction in 6 of 10 hearts. The rightward shifts of the shortest and longest VF-inducing coupling intervals for biphasic shocks were 11.0±8.8 ms (P=.003) and 6.0±5.2 ms (P=.005), respectively. The ULV was significantly lower for the biphasic than for the monophasic waveform (mean difference, 40±42 V, P=.015), and the LLV was significantly higher for biphasic than for monophasic shocks (mean difference, 36±44 V, P=.029). The vulnerable period was 26±8 ms for monophasic and 21±11 ms for biphasic shocks (P=.09). The height of the AOV was 212±87 V for monophasic and 136±54 V for biphasic shocks (P=.007).


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  		Table 1. Comparison of AOV Extensions for Monophasic and Biphasic Shocks

On average, VF was induced at 13.9±6.0 AU for monophasic and 8.9±4.2 AU for biphasic shocks (P=.016) within the test grid, indicating a smaller AOV for the biphasic waveform. Nonsustained arrhythmias were induced at 29.9±6.4 AU for monophasic and 14.7±4.8 AU for biphasic shocks (P<.001), indicating a smaller transition zone between the AOV and the area of no arrhythmic response for biphasic shocks.

Fig 5Down depicts the percentage of shocks that induced VF calculated over all 10 experiments for each combination of coupling interval and shock strength in a three-dimensional illustration. Fig 5ADown summarizes the results for monophasic and Fig 5BDown for biphasic waveforms. To combine the data of the different experiments in one figure, coupling intervals were normalized by defining the longest interval inducing VF as zero. Shock amplitudes were normalized by defining the ULV as zero. The graphs show that for monophasic shocks, the probability of VF induction was present over a wider range of shock strengths than the VF probability pattern of the biphasic waveform.



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  		Figure 5. Three-dimensional plot of the probability of VF induction by monophasic (A) and biphasic (B) T-wave shocks averaged for all experiments. Data are shown as a function of normalized shock coupling interval and shock strength. A normalized shock coupling interval of zero represents the longest VF-inducing coupling interval, and a normalized shock strength of zero represents the ULV in each heart.

The DFT was 353±70 V for monophasic and 274±66 V for biphasic shocks (P=.005), confirming the higher defibrillation efficacy of the biphasic waveform used in the study.


*    Discussion
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 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
 up arrowResults
 *Discussion
down arrowReferences
 
This study analyzed the myocardial response to truncated exponential monophasic and biphasic shocks of randomly varied strengths and coupling intervals in an isolated beating rabbit heart preparation. This allowed us to determine differences for monophasic and biphasic shocks in the AOV, which is defined two-dimensionally by strengths and coupling intervals of VF-inducing shocks.29 The new findings of the present study are that (1) biphasic shocks encounter a smaller AOV, (2) the AOV is shifted toward longer coupling intervals for biphasic shocks, and (3) the transition between the AOV and the area of no arrhythmic response is more gradual for monophasic than for biphasic shocks.

Biphasic Shocks Create a Smaller AOV
The size of the AOV was significantly smaller for the biphasic than for the monophasic waveform. This was due to a lower ULV, a higher LLV, and a trend toward a smaller vulnerable period for biphasic shocks (TableUp). Thus, on a normalized interval-strength scale, VF induction occurred over a more limited interval and amplitude range for biphasic shocks than for monophasic shocks. Only one previous study directly compared the ULV for 5.5-ms monophasic versus 3.5/2.0-ms biphasic shocks in dogs.38 Consistent with our results, the authors found a significantly higher ULV for monophasic than for biphasic shocks. The study also reported differences in the fibrillation threshold; however, this was tested only for monophasic versus biphasic point stimuli.38

Biphasic Shocks Shift the AOV Toward Longer Coupling Intervals
For the biphasic waveform, we observed a significant rightward shift of both the right and left borders of the AOV (TableUp). These findings are consistent with a recent study by Daubert et al,39 who showed that biphasic shocks are less effective in exciting relatively refractory myocardium during regular paced rhythms than are monophasic shocks. The authors constructed strength-interval curves for 3-ms monophasic and 2/1-ms biphasic shocks in open-chest dogs and found that biphasic strength-duration curves were shifted to the right by 8±4 ms. Another study by Zhou et al40 analyzed effects on action potential prolongation by 5-ms monophasic and 2.5/2.5-ms biphasic shocks applied within the vulnerable period. They found that there was less action potential prolongation for biphasic shocks and that biphasic shocks excited new action potentials 8 ms later than monophasic shocks. Wharton et al38 found a delay of the effective refractory period by biphasic point stimuli of 7.6±5.6 ms compared with monophasic stimuli. The delay of myocardial excitation for biphasic shocks reported in these studies is consistent with the rightward shifts of the AOV by 6.0±5.2 ms (right border) and 11.0±8.8 ms (left border) found in the present study.

Biphasic Shocks Induce Nonsustained Arrhythmias Less Frequently
T-wave shock–induced nonsustained arrhythmias occurred over a more limited interval and amplitude range for the biphasic than for the monophasic waveform. Thus, the margin in which a small number of repetitive responses was induced was wider for monophasic shocks. This finding indicates that the creation of new reentrant wave fronts after T-wave shocks is facilitated more by monophasic than by biphasic waveforms. The underlying mechanism, however, is not known. One possible explanation might be that according to the extension-of-refractoriness hypothesis,8 9 10 biphasic shocks create more block or slowing of conduction than monophasic shocks, thereby preventing reexcitation of myocardium by propagating wave fronts. This would be consistent with preliminary data from Sweeney et al41 suggesting that biphasic shocks create more postshock refractoriness in areas of low potential gradient. However, the fact that monophasic waveforms are able to excite myocardium earlier than biphasic shocks39 40 is not consistent with this hypothesis. The different findings may be due to waveform differences in terms of shock duration and tilt and to different setups among studies ranging from open-chest dogs39 40 to myocardial tissue strips41 or an isolated perfused heart, as used in the present study.

Possible Relevance for Defibrillation Efficacy of Monophasic and Biphasic Waveforms
An explanation of why biphasic shocks are able to defibrillate at lower DFT energies than monophasic shocks could be construed on the ULV hypothesis of defibrillation.12 This hypothesis suggests VF reinitiation as a mechanism of ineffective defibrillation. Shocks terminate VF successfully only if, after reentrant wave fronts have been halted by simultaneous activation of all excitable tissue, they do not create new activation fronts by eliciting nonuniform responses during the vulnerable period that immediately follows VF termination. The decreased ability of biphasic shocks to induce VF, as indicated by a smaller AOV, might result in a smaller probability of reinitiating VF. The disadvantage of monophasic shocks exhibiting a larger AOV and thus a greater probability of VF reinitiation can be overcome only by a greater shock strength, as is suggested by the higher ULV for monophasic shocks and hence their greater DFT energy requirement.

Does the rightward shift of the AOV have implications for defibrillation? It has been shown that biphasic shocks are less capable of exciting partially refractory myocardium not only during paced rhythm39 40 but also during VF.42 During VF, however, new depolarizations originate mostly at a time when the preceding response has not yet reached complete repolarization.43 44 If the lesser capability of biphasic shocks in inducing VF at incomplete repolarization levels (ie, the rightward shift of the AOV) is any indication of what might happen during VF, then the fact that during VF the ventricular myocardium seldom reaches more complete repolarization levels might help explain, at least in part, why reexcitation and thus VF reinitiation is less likely for biphasic than for monophasic shocks.

The smaller zone of shock-induced nonsustained arrhythmias for biphasic shocks might have additional implications for defibrillation. Defibrillation shocks of borderline shock strengths are often followed by a transient clustering of relatively organized postshock activation fronts until either a regular rhythm occurs (type B defibrillation) or new VF activation patterns reemerge, resulting in an unsuccessful defibrillation attempt and ongoing VF.12 45 46 It has been suggested that multiple postshock activations after T-wave shocks might be comparable to this type of successful or unsuccessful defibrillation.12 A more gradual transition between the AOV and the area of no arrhythmic response, as seen for monophasic shocks, might indicate a greater probability for monophasic defibrillation shocks to create new postshock wave fronts, which finally could leave the heart in VF. Thus, the more limited range of intervals and shock amplitudes outside the AOV in which shocks induce nonsustained arrhythmias might correspond to the greater defibrillation success rate for biphasic waveforms.

Methodological Considerations
Shock durations in this study were shorter than clinically used waveforms.47 The effects of biphasic shocks on myocardial vulnerability compared with monophasic shocks might therefore be different for longer shock waveforms. However, 16-ms monophasic shocks demonstrated a significantly longer action potential prolongation during VF than 8/8-ms biphasic shocks, which was comparable to different effects of 5-ms monophasic and 2.5/2.5-ms biphasic shocks on action potential prolongation.42 These findings suggest that biphasic shocks of long duration might have similar effects on the AOV compared with monophasic waveforms of long duration. Another limitation of the study was that rabbit hearts tend to self-defibrillate because of the small size of the heart.34 35 36 Therefore, VF had to be defined somehow arbitrarily. The definition of VF used in this study has been used previously29 35 37 to characterize severe arrhythmias in the rabbit heart. However, it is not known whether this definition truly reflects an episode of sustained VF in larger mammalian hearts. In our study, the DFT was lower than the ULV. In some3 4 6 but not all38 other studies, the DFT is higher than or equal to the ULV. The reason for the lower DFT in the present study might be that we measured the DFT as the 50% probability of successful defibrillation, whereas the ULV was determined differently, by scanning of the AOV in horizontal and vertical directions.

Conclusions
The present study demonstrates that myocardial vulnerability for VF to biphasic T-wave shocks is more confined than that for monophasic shock waveforms. This was apparent from the facts that the biphasic AOV had a smaller two-dimensional spread and that the AOV for biphasic T-wave shocks was shifted to the right toward more complete repolarization levels and presumably less ventricular refractoriness. In keeping with the VF reinitiation hypothesis,12 this reduced arrhythmogenicity may help explain both the lower ULV and the lower DFT of biphasic shocks compared with monophasic shocks. Besides these new mechanistic implications, our findings suggest that VF induction by T-wave shocks allows for a greater margin of error for monophasic shock waveforms than biphasic shock waveforms. This should be considered during clinical VF induction by T-wave shocks.


*    Selected Abbreviations and Acronyms
 
AOV = area of vulnerability
AU = area units
DFT = defibrillation threshold
LLV = lower limit of vulnerability
MAP = monophasic action potential
ULV = upper limit of vulnerability
VF = ventricular fibrillation


*    Acknowledgments
 
This study was supported in part by a Merit Review Grant from the Veterans Administration (Dr Franz) and unrestricted research grants by Cardiac Pacemakers, Inc and Medtronic, Inc (Dr Behrens). We wish to thank Dr Dietrich Andresen of the Free University of Berlin, Germany, and Dr Ross Fletcher of the VA Medical Center, Washington, DC, for their generous intellectual support.

Received January 18, 1996; revision received April 29, 1996; accepted May 6, 1996.


*    References
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 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
 up arrowResults
 up arrowDiscussion
 *References
 

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J. J. Sims, A. W. Miller, and M. R. Ujhelyi
Disparate effects of biphasic and monophasic shocks on postshock refractory period dispersion
Am J Physiol Heart Circ Physiol, June 1, 1998; 274(6): H1943 - H1949.
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