From the Department of Cardiology (P.S., F.S., B.D., A.M., K.E., P.H.,
C.S.) and the Department of Thoracic and Cardiovascular Surgery (F.A.S., M.G.,
H.D., B.J.M.), University Hospital-RWTH Aachen (Germany).
Correspondence to Patrick Schauerte, MD, Department of Cardiology, University Hospital-RWTH Aachen, Pauwelsstraße 30, 52057 Aachen, FRG. E-mail psch{at}pcserver.mk1.rwth-aachen.de
Methods and ResultsDefibrillation thresholds (DFTs) were
determined for 13 waveforms in 13 pigs by application of a 70-µF
capacitance and a transvenous/submuscular lead system. In part I,
phase-1 duration varied, preserving a phase-1/phase-2 duration ratio of
60%/40%. The phase-1 durations were 1, 2, 3, 4, 5, and 6 ms. The DFT
was lowest (22.9±7 J) for phase 1=3 ms compared with phase 1=1 ms
(36.4±7.5 J), 2 ms (25±6.5 J), 4 ms (25±7.6 J), 5 ms (30.7±7.3 J),
or 6 ms (32.9±8.1 J) (P<.001). In part II, phase-1
duration was 3 ms but phase-2 duration varied: 0.7, 1.3, 2, 2.7, 3.3,
4, and 6 ms. Significant DFT minima were found at phase 2=2 ms
(22.5±4.2 J) and phase 2=4 ms (22.5±4.2 J) compared with phase 2=0.7
ms (31.7±9.3 J), phase 2=3.3 ms (26.7±6.1 J), or phase 2=6 ms
(28.3±6.8 J) (P<.05).
ConclusionsThe strength-duration curve of biphasic
defibrillation shocks demonstrates a single optimum for phase-1
duration. In contrast, two optima with minimal energy requirements were
found for phase-2 duration. Optimization of both phases of
low-capacitance biphasic shocks may reduce energy requirements for
defibrillation.
Defibrillation Protocol
Part II
DFT testing was completely randomized, that is, each shock had a
randomly assigned energy level and duration. Each waveform was tested
five times at each energy level from 5 to 40 J in 5-J steps. Therefore,
in each pig, 240 episodes of ventricular fibrillation were
induced during part I and 280 episodes of ventricular
fibrillation in part II. The DFT of a waveform was defined as the
lowest energy level with at least 80% defibrillation success (ie, four
or five of five delivered shocks were successful). Fibrillation was
induced through the right ventricular pacing leads with a
burst of 50 Hz, alternating current lasting 1.5 seconds. Defibrillation
shocks were applied 10 seconds after the onset of
ventricular fibrillation in each episode. In case of
defibrillation failure, an internal 40-J "rescue" shock was applied
to the heart. Only in the case of defibrillation failure with the 40-J
shock, an external 360-J shock was applied.
To ensure stable conditions of the model, the DFT was determined for
the 6 ms/4 ms waveform in part I and for the 3 ms/2 ms waveform in part
II at the beginning of the otherwise randomized DFT testing protocol
and every 2 hours thereafter. If the DFT energy level differed by
Statistical Analysis
Part II
The mean impedance at the leading edge of pulse 1 in part I and part II
was 34.2±11.6
Several mechanisms have been suggested to contribute to defibrillation
with monophasic shocks such as prolongation of action potential
duration and refractory period or resynchronization of the
repolarization state of the
myocardium.17 18 Beyond that,
depolarization of myocardial cells is considered to be an important
mechanism.19 Experimentally, a hyperbolic stored
voltageshock duration curve at the DFT has been found for monophasic
shocks.20 A similar strength-duration relation
has been proposed to sufficiently describe the action of phase-1 of
biphasic shocks,15 which is supported by the
findings in part I of the present study.
There are conflicting results on the optimal ratio of phase-1/phase-2
duration. In an animal study, Dixon et al21
demonstrated lower energy requirements for ventricular
defibrillation with biphasic shocks and a second phase of equal or
shorter duration than the first phase. Similarly, Gliner et
al22 found lower ventricular
defibrillation energy requirements in external defibrillation for a
phase-1 duration set at 50% or 60% of the total shock duration. In
human atrial fibrillation, Cooper et al23 most
recently observed lowest internal atrial defibrillation thresholds for
biphasic shocks with a phase-1 duration longer than phase-2 duration.
However, in a human study on internal ventricular
defibrillation, different tilts of the second phase of the biphasic
shock did not significantly affect defibrillation energy
requirements.24 By contrast, in an animal study
on ventricular defibrillation, lower DFTs for shocks with
the second phase longer than the first phase were
reported.25 The differences in underlying
arrhythmias and models make the comparison between these
studies difficult. However, a possible reason for the findings of
higher defibrillation success of shocks with phase-2 durations longer
than phase-1 duration for lower time constants is provided by
Kroll.15 Because the residual charge left on the
cell membrane after delivery of phase 1 is thought to cause postshock
arrhythmias, thus diminishing defibrillation success, he
assumed that the major function of phase 2 was to unload ("burp")
this residual membrane charge. Thus according to his mathematical
calculation, the optimal phase-2 duration would become longer than
phase-1 duration at time constants
Study Limitations
Conclusions
Received September 15, 1997;
revision received November 21, 1997;
accepted December 12, 1997.
2.
Leonelli FM, Kroll MW, Brewer JE. Defibrillation
thresholds are lower with smaller storage capacitors. PACE Pacing
Clin Electrophysiol. 1995;18:16611665.[Medline]
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3.
Bardy GH, Poole JE, Kudenchuk PJ, Dolack GL,
Mehra R, DeGroot P, Raitt MH, Jones GK, Johnson G. A prospective
randomized comparison in humans of biphasic waveform 60-µF and
120-µF capacitance pulses using a unipolar defibrillation system.
Circulation. 1995;91:9195.
4.
Swerdlow CD, Kass RM, Chen PS, Hwang C, Raissi S.
Effect of capacitor size and pathway resistance on defibrillation
threshold for implantable defibrillators: Circulation. 1994;90:18401846.
5.
Rist K, Tchou PJ, Mowrey K, Kroll MW, Brewer JE.
Smaller capacitors improve the biphasic waveform. J
Cardiovasc Electrophysiol. 1994;5:771776.[Medline]
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6.
Natale A, Sra J, Krum D, Dhala A, Deshpande S,
Jazayeri M, Newby K, Wase A, Axtell K, VanHout W, Akhtar M. Relative
efficacy of different tilts with biphasic defibrillation in humans.
PACE Pacing Clin Electrophysiol. 1996;19:197206.[Medline]
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7.
Irnich W. Optimal truncation of defibrillation pulses.
PACE Pacing Clin Electrophysiol. 1995;18:1:673688.[Medline]
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8.
Bardy GH, Ivey TD, Allen MD, Johnson G, Mehra R,
Greene HL. A prospective randomized evaluation of biphasic versus
monophasic waveform pulses on defibrillation efficacy in humans.
J Am Coll Cardiol. 1989;14:728733.[Abstract]
9.
Bardy GH, Johnson G, Poole JE, Dolack L, Kudenchuk PJ,
Kelso D, Mitchell R, Mehra R, Hofer B. A simplified, single-lead
unipolar transvenous cardioversion-defibrillation system.
Circulation. 1993;88:543547.
10.
Schauerte P, Stellbrink C, Schöndube F,
Löser H, Haltern G, Messmer BJ, Hanrath P. Polarity reversal
improves defibrillation efficacy in patients undergoing transvenous
cardioverter/defibrillator implantation with biphasic shocks.
PACE Pacing Clin Electrophysiol. 1997;20:301306.[Medline]
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11.
Stellbrink C, Schauerte P, Löser H, Rosenbaum C,
Kuckertz E, Vogel M, Messmer BJ, Hanrath P, Schöndube FA.
Influence of polarity reversal on defibrillation success with biphasic
shocks and a transvenous/subcutaneous defibrillator system in a porcine
animal model. PACE Pacing Clin Electrophysiol. In press.
12.
Swartz JF, Fletcher RD, Karasik PE. Optimization of
biphasic waveforms for human nonthoracotomy defibrillation.
Circulation. 1993;88:26462654.
13.
Schuder JC, Stoeckle H, Kekar PY, Gold JH, Chier MT,
West JA. Transthoracic ventricular
defibrillation in the dog with unidirectional rectangular double
pulses. Cardiovasc Res. 1970;4:497.
14.
Kroll MW. A minimal model of the monophasic
defibrillation pulse. PACE Pacing Clin Electrophysiol. 1993;16:1:769777.
15.
Kroll MW. A minimal model of the single capacitor
biphasic defibrillation waveform. PACE Pacing Clin
Electrophysiol. 1994;17:17821792.[Medline]
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16.
Cleland BG. A conceptual basis for defibrillation
waveforms. PACE Pacing Clin Electrophysiol. 1996;19:11861195.[Medline]
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17.
Dillon SM. Optical recordings in the rabbit
heart show that defibrillation strength shocks prolong the duration of
depolarization and the refractory period. Circ Res. 1991;69:842856.
18.
Dillon SM. Synchronized repolarization after
defibrillation shocks: a possible component of the defibrillation
process demonstrated by optical recordings in rabbit heart.
Circulation. 1992;85:18651878.
19.
Zipes DP, Fischer J, King RM, Nicoll A, Jolly WW.
Termination of ventricular fibrillation in dogs by
depolarizing a critical amount of myocardium. Am
J Cardiol. 1975;36:3744.[Medline]
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20.
Chapman PD, Wetherbee JN, Vetter JW, Trup P, Souza J.
Strength-duration curves of fixed pulse width variable tilt
truncated exponential waveforms for nonthoracotomy internal
defibrillation in dogs. PACE Pacing Clin Electrophysiol. 1988;11:10451050.[Medline]
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21.
Dixon EG, Tang ASL, Wolf PD, Meador JT, Fine MJ, Calfee
RV, Ideker RE. Improved defibrillation thresholds with large contoured
epicardial electrodes and biphasic waveforms. Circulation. 1987;76:11761184.
22.
Gliner BE, Lyster TE, Dillon SM, Bardy GH.
Transthoracic defibrillation of swine with monophasic and
biphasic waveforms. Circulation. 1995;92:16341643.
23.
Cooper RAS, Johnson EE, Wharton M. Internal atrial
defibrillation in humans. Improved efficacy of biphasic waveforms and
the importance of phase duration. Circulation. 1997;95:14871496.
24.
Tomassoni G, Newby K, Deshpande S, Axtell K, Sra J,
Akhtar M, Natale A. Defibrillation efficacy of commercially available
biphasic impulses in humans. Circulation. 1997;95:18221826.
25.
Yamanouchi Y, Mowrey KA, Nadzam GR, Hills DG, Kroll MW,
Brewer JE, Donohoo AM, Wilkoff BL, Tchou PJ. Large change in voltage at
phase reversal improve biphasic defibrillation thresholds.
Circulation. 1996;94:17681773.
26.
Feeser SA, Tang ASL, Kavanagh KM, Rollins DL, Smith WM,
Wolf PD, Ideker RE. Strength-duration and probability of success curves
for defibrillation with biphasic waveforms. Circulation. 1990;82:21282141.
27.
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ventricular cells during ventricular
fibrillation. Am J Physiol. 1981;140:H465H471.
28.
Jones JL, Jones RE, Balasky G. Improved cardiac cell
excitation with symmetrical biphasic defibrillator waveforms.
Am J Physiol. 1987;253:H1418H1424.
29.
Weidmann S. Effect of current flow on the membrane
potential of cardiac muscle. J Physiol. 1951;115:227236.
30.
Tang ASL, Yabe S, Wharton JM, Dolker M, Smith WM,
Ideker RE. Ventricular defibrillation suing biphasic
waveforms: the importance of phasic duration. J Am Coll
Cardiol. 1989;13:207214.[Abstract]
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© 1998 American Heart Association, Inc.
Basic Science Reports
Influence of Phase Duration of Biphasic Waveforms on Defibrillation Energy Requirements With a 70-µF Capacitance
![]()
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
BackgroundPhase duration of
biphasic shocks may be an important determinant of defibrillation
success. The purpose of this study was to investigate the effect of
changing phase duration of biphasic pulses delivered by 70-µF
capacitors on defibrillation energy requirements. This may be
clinically relevant for the optimization of implantable
cardioverter-defibrillator design and programming.
Key Words: fibrillation defibrillation death, sudden
![]()
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Current implantable
cardioverter/defibrillators (ICDs) incorporate a 120- to 150-µF
capacitor, which accounts for about one third of the total device
volume.1 Because ICD volumes may be reduced by
incorporation of smaller capacitors, several animal and clinical
studies compared ICDs with capacitors of 120 to 140 µF with those
with lower capacitors of 60 to 85 µF and revealed an at least equal
defibrillation efficacy in terms of stored
energy.2 3 4 5 However, smaller capacitors must be
loaded to a higher voltage for storing the same energy according to the
capacitor formula E=1/2xCxU2, where E
is energy, C is capacitance, and U is voltage. By retaining present
maximal ICD voltage outputs, this may decrease the safety margin for
defibrillation, assuming an equal defibrillation threshold (DFT) in
terms of stored energy. Furthermore, because the capacitor volume is
proportional to the maximum capacitor energy, a reduction of the
capacitor volume by smaller capacitances is only possible if
defibrillation energy requirements are lowered.3
The phase duration of defibrillation shocks is an important factor
influencing the DFT.6 7 Because the time constant
(time that is required to deliver 68% of the stored energy) is
directly related to the capacitor following the equation
=RxC
(R=resistance), shocks delivered from smaller capacitors need less time
to deliver the same amount of energy than shocks from larger
capacitors. We hypothesized that DFTs for 70-µF capacitors may have a
minimum at other pulse widths and tilts than for larger capacitors and
investigated the relation between phase duration of biphasic shocks and
the defibrillation energy requirement for 70-µF capacitors.
![]()
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Animal Preparation
All studies followed institutional guidelines for animal trials
and were undertaken with permission of the competent authorities
(Regierungspräsident Köln, April 14, 1992). We studied 13
healthy domestic pigs (German landrace) weighing 70±6 kg.
Ketamine (20 mg/kg body wt IM) and atropine (0.14 mg/kg body wt
IM) were used to induce anesthesia. The animals were
intubated with a cuffed endotracheal tube and ventilated with
NO2/O2 (ratio 3:1) by a
ventilator (Servo Respirator, Siemens Corp) at 10 to 15 breaths/min.
Sodium pentobarbital (1 to 2 mg/kg) was infused to maintain a constant
depth of anesthesia. Systemic blood pressure was
continuously monitored through a carotid arterial line and
blood gas analysis performed every 30 minutes.
Metabolic status was further monitored by taking central
venous blood samples for electrolytes every 30 minutes.
Pulmonary capillary wedge pressure and mixed venous
oxygenation were continuously measured by a
Swan-Ganz-catheter. Surface ECG was recorded during each
fibrillation/defibrillation episode on a 12-channel standard ECG
recorder (Mingograph, Siemens) at a paper speed of 25 mm/s.
After left jugular venotomy, a transvenous defibrillation electrode
(Endotak 072, CPI) was introduced under fluoroscopy in the right
ventricular apex. The electrode carries two coils, one
positioned in the right ventricular apex (distal coil) and
one in the superior vena cava (proximal coil). A submuscular patch
(Endotak Sub Q 042, CPI) was then placed at the left thoracic wall
opposite to the left ventricle. The electrodes were connected with the
distal coil in the right ventricular apex as anode and with
the proximal coil and submuscular patch as common cathode during
phase-1 of the biphasic shocks. Shocks were delivered by a 70-µF
capacitor (model 2394, Medtronic) that allowed separate selection of
pulse width, voltage, and intershock delay. Shock voltage values of the
leading edge of phase 1 to be charged on the capacitors were calculated
according to the equation E=1/2xCxU2.
Voltage and current at the leading and trailing edge of phase 1 were
recorded on an oscilloscope. Leading edge voltage of phase 2 was
adjusted to the same value as the voltage at the trailing edge of phase
1. To estimate the voltage at the trailing edge of phase 1, monophasic
shocks of all different phase-1 durations were delivered to each pig
heart at each energy level. The leading edge voltage of phase 2 of the
biphasic shock was then adjusted to the voltage at the end of the
respective monophasic shocks.
Part I
In the first part of the study, six different phase-1 durations
were tested in 7 pigs. A constant phase-1/phase-2 duration ratio of
60%/40% was used. The corresponding phase-1 tilt was calculated by
(1-U2/U1)x100 (%)
(U1=voltage at the leading edge of phase 1;
U2=voltage at the trailing edge of phase 1).
Interpulse delay was kept constant at 0.8 ms. The total shock durations
tested were 10.8 ms (phase 1: 6 ms/phase-2: 4 ms/phase-1 tilt: 83%),
9.1 ms (5 ms/3.3 ms/78%), 7.5 ms (4 ms/2.7 ms/68%), 5.8 ms (3 ms/2
ms/60%), 4.1 ms (2 ms/1.3 ms/48%), and 2.5 ms (1 ms/0.7 ms/33%) (Fig 1
top).

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Figure 1. Waveform modifications applied. Top, Waveforms
during part I of the study. Six different phase-1 durations of biphasic
shocks are depicted. For each waveform the ratio of phase-1
duration/phase-2 duration was 60%/40% and the intershock delay 0.8
ms. Bottom, Waveforms during part II of the study. Seven different
waveforms were tested, each of which had a constant phase-1 duration of
3 ms but a varying phase-2 duration as indicated.
In the second part of the study, phase-1 duration was kept
constant at 3 ms, which had turned out to be the optimal phase-1
duration in the first part of the study. Phase-2 duration was then
systematically varied in another 6 pigs, resulting in different
phase-1/phase-2 ratios. The tested durations for phase 2 were 0.7 ms
(phase-1 duration/phase-2 duration ratio: 80%/20%), 1.3 ms
(75%/25%), 2 ms (60%/40%), 2.7 ms (53%/47%), 3.3 ms (48%/52%),
4 ms (43%/57%), and 6 ms (33%/67%) (Fig 1
bottom).
5 J
between these testing episodes, the data obtained for that pig were
excluded from analysis.
All data are expressed as mean±SD. Overall differences in
stored energy at the DFT for the six waveforms in part I and for the
seven waveforms in part II were evaluated with ANOVA. When significant
differences were present, shock durations were compared with the
use of a two-tailed paired t test. Values of
P<.05 were considered statistically significant.
![]()
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Part I
No pig had to be excluded from comparison because of an unstable
DFT. The DFT data for each pig and waveform during part I are listed in
Table 1
. The shock strengthphase-1
duration curve is shown in Fig 2
. Lowest
defibrillation energy requirements were observed at a phase-1 duration
of 3 ms (22.9±7 J, P<.001, ANOVA). Shocks of shorter
phase-1 durations were significantly less successful (1 ms: 36.4±7.5
J, P<.001), as were shocks with a phase-1 duration of 5 ms
(30.7±7.3 J, P=.005) and 6 ms (32.9±8.1 J,
P=.003). The DFT for shocks with a phase-1 duration of 1 ms
differed significantly from the DFT for a phase-1 duration of 2 ms
(P=.001). Similarly, the DFT for phase-1 durations of 4 ms
was significantly lower than for phase-1 durations of 5 ms
(P=.02). There was no significant difference between the
shocks with a phase-1 duration of 3 ms, 2 ms (25±6.5 J), or 4 ms
(25±7.6 J, P=NS).
View this table:
[in a new window]
Table 1. Defibrillation Threshold Values for the Seven Pigs
and Six Different Phase-1 Durations in Part I of the Study

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[in a new window]
Figure 2. Mean defibrillation threshold±SD (ordinate) for
the 7 pigs of part I plotted against different phase-1 durations
(abscissa). The lowest defibrillation thresholds were observed for a
phase-1 duration of 3 ms (P<.001, ANOVA). Probability
values given in the figure refer to two-tailed paired t
tests for comparison between individual waveforms.
According to the optimal phase-1 duration determined during part I
(based on the lowest DFT), a constant phase-1 duration of 3 ms was
chosen for part II. Again, no pig had to be excluded from comparison
because of an unstable DFT. DFT values for each pig and waveform in
part II are provided in Table 2
. The
phase-2 duration had a significant influence on the stored energy at
the DFT (P=.003, ANOVA). This resulted in two significant
DFT minima for varying phase-2 duration. One minimum was observed at 2
ms (22.5±4.2 J) and the other at 4 ms (22.5±4.2 J). Both DFTs were
significantly lower than with shocks of intermediate phase-2 duration
of 3.3 ms (26.7±6.1 J, P=.04 each, Fig 3
). Shortening of phase-2 duration to 0.7
ms led to a significant increase of the DFT (31.7±9.3 J,
P=.03 compared with phase 2=2 ms), as did further
prolongation of phase-2 duration to 6 ms (28.3±6.8 J, P=.03
compared with a phase-2 duration of 4 ms).
View this table:
[in a new window]
Table 2. Defibrillation Threshold Values for the Six Pigs and
Seven Different Phase-2 Durations During Part II of the Study

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[in a new window]
Figure 3. Mean defibrillation threshold±SD (ordinate) for
the 6 pigs of part II plotted against different phase-2 durations
(abscissa). Duration of phase-1 was constant at 3 ms. Defibrillation
threshold showed two minima, which differed significantly from the
neighboring phase-2 durations (P=.003, ANOVA).
Probability values given in the figure refer to two-tailed paired
t tests for comparison between individual
waveforms.
. Application of a capacitance of 70 µF resulted in
a system time constant
of 2.4 ms in this model.
![]()
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
Internal defibrillation energy requirements can be reduced by
using biphasic instead of monophasic waveforms,8
by use of an active can configuration9 or by
choosing the optimal electrode polarity.10 11 The
current study focuses on the influence of different phase durations on
defibrillation energy requirements with a 70-µF capacitance. Our
results indicate that for such a capacitance in this animal model with
a tripolar lead system, the optimal phase-1 duration was 3 ms, equaling
a phase-1 tilt of 60%. Several animal and human studies have compared
the defibrillation efficacy of shock waveforms delivered from currently
applied 120- to 140-µF capacitances with smaller capacitances: In
animal studies a lower DFT in terms of stored and delivered energy
could be demonstrated with an 85-µF capacitor compared with a
140-µF capacitor for both monophasic and biphasic shocks with
epicardial defibrillation patches.2 5 A
dependency of the optimal phase-1 duration on changing electrode
impedances has been reported in a clinical study by Swerdlow et
al4: By comparing shocks of 65% phase-1 tilt
delivered from 60- or 120-µF capacitors, it was found that
defibrillation efficacy was higher with smaller capacitances for
high-impedance pathways, whereas for low-impedance pathways the
opposite was true. The authors concluded that for a constant phase-1
tilt, different capacitances and thereby different phase-1 durations
might be optimal for changing electrode impedances. Although in a
recent clinical study there was a trend toward lower DFTs in terms of
energy for 60-µF capacitors as opposed to 120 µF, this did not
reach statistical significance.3 Because most
clinically available ICDs apply shock waveforms with a constant phase-1
tilt, all except one3 of the studies cited above
used a 65% tilt of the first phase irrespective of the capacitance
applied. However, recent studies raised the issue whether different
tilts than 65% would render lower DFTs: Two human studies demonstrated
an increased defibrillation success with tilts of 42% to 50% compared
with tilts of 65% to 80% and a 120-µF
capacitance.6 12 In one study the time constant
was calculated to be
8 ms.6 Therefore,
pulse 1 tilts of 65% as used in many clinical devices may be too
high,6 12 possibly because of refibrillation
caused by low-voltage shock tails compared with lower
tilts.7 13 However, simple replacement of a
phase-1 tilt of 65% by a fixed phase-1 tilt of 42% to 50% may not
always be advantageous. On the basis of mathematical models, the
optimal phase-1 tilt increases with decreasing time constant
for
monophasic as well as for biphasic shocks.14 15 16
We could demonstrate that for a low time constant of 2.4 ms, the
optimal phase-1 tilt was 60%. Despite the differences of the models
this is higher than the optimal phase-1 tilt for larger capacitances
and higher impedances,6 12 thus supporting the
concept that the optimal phase-1 tilt is dependent on the time
constant. Consequently, studies that compare the defibrillation
efficacy of shocks delivered from different capacitances should test
each capacitance at its waveform with the optimal tilt. In fact,
because the volume of the capacitor is proportional to the maximal
stored energy, only a reduction of the DFT by low-capacitance shocks
with optimized phase duration compared with shocks from currently
available 120- to 150-µF capacitances at optimal phase duration would
result in lower capacitor volumes.
shorter than 3 ms as
experimentally demonstrated in our study. In the current study, two
phase-1/phase-2 duration ratios with minimal defibrillation energy
requirements at the DFT were observed, 60%/40% (phase-2 duration: 2
ms) and 43%/57% (phase-2 duration: 4 ms). Similar findings have been
described by Feeser et al.26 Using a constant
phase-1 duration of 3.5 ms, they found two voltage minima at the DFT
for phase-2 durations of 4 ms and 7 ms with significantly higher
voltages at the DFT for phase-2 durations between these two values.
They suggested two possible mechanisms accounting for these
observations: (1) Depolarization after
hyperpolarization: The role of the second phase is
to depolarize that half of the myocardial cell membrane that has been
hyperpolarized during phase 1. The effect that
hyperpolarization during phase 1 of the biphasic
shock reactivates sodium channels that were partially
inactivated because of low resting membrane potentials
during ventricular fibrillation27 was
originally described by Jones et al.28 They
called this "prepulse conditioning." (2)
Hyperpolarization after depolarization: Excitation
on the side of the cell that has been depolarized during phase 1 may be
halted by the now-hyperpolarizing phase 2. Halting of myocardial
excitation by a hyperpolarizing impulse after the excitation threshold
has been reached was described by Weidmann.29 It
was proposed26 that with increasing phase-2
durations first, the mechanism of depolarization after
hyperpolarization might be predominating, thus
resulting in lower voltages at the DFT. Then, with longer phase-2
durations the effect of hyperpolarization after
depolarization may outweigh the beneficial effect of depolarization
after hyperpolarization on the other side of the
myocardial cells, thus leading to an increase of the voltage at the
DFT. Finally, further prolongation of phase-2 duration makes phase 2
behave like a monophasic shock with a second decrease and increase of
the voltage at the DFT. These results on phase-2 durations differ from
clinically used shock waveforms that include fixed phase-1/phase-2
duration ratios of 60%/40% or 50%/50%. The latter is based on an
animal study of Tang et al30 that investigated
current strength requirements for a constant phase-1 duration of 3.5 ms
and changing phase-2 durations. Lowest current at the DFT was
demonstrated for a phase-2 duration of 2 ms. However, two optimal
phase-2 durations may have been missed in that study because of the
large increments of the phase-2 durations in contrast to the results of
Feeser et al (1-ms increments) and our own findings (0.6- to 0.7-ms
increments).
In this porcine animal model with a tripolar lead system
including a submuscular patch, the time constant
was short because
of the low impedances observed compared with most human ICD implants.
However, the finding of more than one optimal phase-2 duration may be
extrapolated to other lead configurations and impedances because
similar results have been found despite different
models.25 26 Although the relative heart weight
of the applied pigs, which is 0.3% of the body weight of the animal,
is comparable to humans,31 differences of this
model due to the lack of organic heart disease and the mode of
induction of ventricular fibrillation may have caused
differences to spontaneous episodes of ventricular
fibrillation in patients.
Similar to monophasic shocks, the shock strengthduration curve
of biphasic shocks delivered from 70-µF capacitors demonstrated a
single optimum for phase-1 duration at 3 ms, equaling a phase-1 tilt of
60%. In contrast, for an optimized phase-1 duration, two significant
minima of defibrillation energy requirements were found for phase-2
duration, thereby supporting the concept that the duration of the two
phases is optimized independent of each other. Both may be clinically
relevant for future optimization of ICD design and programming.
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References
Top
Abstract
Introduction
Methods
Results
Discussion
References
1.
Nelson RS. The pulse generator. In: Kroll MW,
Lehmann MH, eds. Implantable Cardioverter Therapy: The Clinical
Engineering Interface. Boston, Mass: Kluwer Academic
Publishers; 1996.
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