Chapter 12 / External Defibrillation

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External Defibrillation
Gregory P. Walcott, MD,
Cheryl R. Killingsworth, DVM, PhD,
and Raymond E. Ideker, MD, PhD
CONTENTS
INTRODUCTION
MECHANISM OF DEFIBRILLATION
DEFIBRILLATION METHODOLOGY
EFFECT OF HIGH-SHOCK FIELDS ON THE MYOCARDIUM
EFFECT OF THE DURATION OF VF ON DEFIBRILLATION EFFICACY
EFFECT OF ISCHEMIA ON DEFIBRILLATION EFFICACY
EFFECT OF INFARCTION ON DEFIBRILLATION EFFICACY
PEDIATRIC DEFIBRILLATION
REFERENCES

INTRODUCTION
The history of applying electrical shocks to the heart began in the 1700s with direct
current derived from a Leyden jar. In 1775, Abildgard described having shocked a
chicken into lifelessness and on repeating the shock, bringing the bird back to life (1).
Transthoracic defibrillation was first performed clinically in the mid-1950s when Zoll
introduced the alternating current (AC) defibrillator (2). Several years later, Lown
introduced the direct current (DC) defibrillator as an improvement on Zolls device in
several important areas, specifically that it caused less damage to the patient and that
it could be made portable (3). Today, internal cardioverter defibrillators are the size of
a small bar of soap and can monitor and correct a patients rhythm for several years
between replacements. Likewise, the external defibrillator has been made smaller and
so much simpler to operate that sixth graders can use the device successfully.

MECHANISM OF DEFIBRILLATION
The study of external defibrillation can build on much of what has been learned about
internal defibrillation. A large amount of work has been done to understand the mechanisms of defibrillation following short durations of electrically induced ventricular fibrillation (VF) using internal defibrillation electrodes (47). VF is maintained by multiple
From: Contemporary Cardiology: Cardiopulmonary Resuscitation
Edited by: J. P. Ornato and M. A. Peberdy Humana Press Inc., Totowa, NJ

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activation fronts that are constantly moving in a pattern of re-entry. Defibrillation can be
broken down into two parts: halting fibrillation wavefronts and not restarting fibrillation.
Fundamentally, defibrillation is thought to be realized through the electrical pulse
causing an alteration in the transmembrane potential of the myocyte. It most likely
requires a rapid induction of changes in the transmembrane potential of the myocytes in
a critical mass of myocardium (7590% of the myocardium in dogs [810]). As this
represents a large mass of tissue, these alterations must be achieved at a considerable
distance from the stimulating electrode.
One-dimensional cable models cannot explain how the transmembrane potential
changes at points distant from the shock electrodes. The cable equations predict hyperpolarization of the transmembrane potential adjacent to an extracellular anode and depolarization adjacent to an extracellular cathode with the change in transmembrane potential
decreasing exponentially with distance from the electrodes. According to this model, a
majority of the heart will see no change in the transmembrane potential as a result of the
shock.
Changes in the transmembrane potential across the heart caused by the shock are
predicted by the bidomain model of cardiac tissue. The bidomain model extends the
one-dimensional cable model into two or three dimensions (11); the extracellular and
intracellular spaces are represented as single continuous domains that are separated by
the highly resistive cell membrane. When realistic tissue resistive anisotropies (changes
in conductivity with direction) are included in the model, the bidomain formulation
begins to give new insights into how shocks change the transmembrane potential.
Similar to the one-dimensional cable model, the bidomain predicts that hyperpolarization of the transmembrane potential occurs under the extracellular anodal electrode and
depolarization of the transmembrane potential occurs under the extracellular cathodal
electrode. Additionally, the bidomain model hypothesizes that there should be changes
in the transmembrane potential, either hyperpolarization or depolarization, across much
of the entire heart (12). The change in transmembrane potential elicited by the shock
depends on the distribution of intracellular and extracellular current that is affected by
the change in the potential gradient with distance, the distance from the electrode, and
the orientation of the myocardial fibers (13). Experimental studies have shown that
there is a complex pattern of transmembrane potential change during the delivery of a
defibrillation shock, similar to those predicted by the bidomain model (1416). This
change in the transmembrane potential by the shock leads to changes in VF wavefront
propagation and initiation of postshock activation fronts that determine whether or not
a shock is successful.
In order to be successful, a defibrillation shock must stop most or all of the fibrillation
wavefronts (10,1618). The extension of refractoriness hypothesis is one proposed
explanation of how a shock stops fibrillation (19,20). If a shock only slightly alters the
transmembrane potential in a region, then activation fronts in the region may continue
to propagate, relatively unaltered, after the shock. If the shock is large enough, then it
can have one of three effects on the myocardium depending on the local shock strength
and its timing with respect to the local action potential. If the shock is delivered just after
local activation, then there may be little or no change in the action potential duration.
If the shock is large enough and delivered relatively late during the action potential, then
it will initiate a new action potential. A shock that is large enough but delivered during
the plateau of the action potential will modify an ongoing action potential without

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initiating a new action potential (21,22). If the first activation front that forms after a
defibrillation shock encounters tissue with an extended refractory period, the front will
be stopped because it cannot propagate into the region of refractory tissue (23).
Much of our understanding about the mechanism of postdefibrillation arrhythmia
induction comes from studying the simpler process of induction of fibrillation by shocks
during paced rhythms. This idea has been formalized in the upper limit of vulnerability
hypothesis for defibrillation that states that failed defibrillation by a shock that is near
the defibrillation threshold occurs by the same mechanism as VF induction caused by
a premature stimulus of the same strength delivered during the vulnerable period (24,25).
One mechanism for the induction of these postshock arrhythmias is described by the
critical point hypothesis. The critical point hypothesis postulates that functional reentry
is initiated in myocardium in which a dispersion of shock potential gradients intersects
a dispersion of refractoriness (26). In adjacent regions, direct excitation of recovered
tissue and refractory period extension in relatively refractory tissue occur. Excitation
blocks in the direction of the tissue with refractory period extension and propagates
away from and around it. By the time the wavefront re-encounters the tissue that was
previously refractory, it has recovered and the wavefront re-enters. Using video-imaging techniques, Banville et al. have shown in isolated rabbit hearts that the centers of
re-entrant wavefronts induced by shocks delivered in paced rhythms can be moved by
changing the shock strength that is delivered and the coupling interval at which it is
delivered (27).
Focal activation is also frequently observed following defibrillation shocks, in which
activation is first observed at one site followed by propagation away from this site in all
directions (28). Focal origins of activation fronts were first observed with recordings
confined to the epicardial surface (28). In these cases, it is possible that the activation
front arose from the border of a directly excited region that is located intramurally. This
activation front could appear to be focal when it is conducted to the epicardium. Threedimensional mapping with plunge needles has demonstrated that foci following a shock
can arise intramurally at sites in which foci were not present during VF before the shock
(29). Foci have also been observed with the electrical induction of VF during the vulnerable period (30). The cause of the foci is unknown although it has been observed that
foci during defibrillation can occur in myocardial regions exposed to shock fields of 2
to 6 V/cm, raising the possibility of early or delayed after depolarizations as the source
of the foci (28,31).
For successful shocks near the defibrillation threshold, the first few beats following the
shock are not sinus beats (32). Ectopic activations following a shock, whether they are
focal or re-entrant, do not always lead to fibrillation. Chattipakorn et al. have suggested
that whether or not a shock near the defibrillation threshold will defibrillate depends on
the number and timing of activations that occur following the shock (33). Chattipakorn
et al. paced the heart after delivering a shock that was 50 to 100 V greater than the
defibrillation threshold and that, when given by itself without pacing, always defibrillated. At least three rapidly paced cycles after this shock were necessary for induction of
VF. Cao et al. examined the induction of fibrillation by rapid pacing in dogs (34). Cato
et al. showed that as pacing rate increases, a spatial heterogeneity of conduction velocities
occurs, which leads to functional re-entry and VF. Understanding how postshock
arrhythmias progress is important to understanding how shocks ultimately succeed or
fail.

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Fig. 1. (A) Truncated exponential monophasic waveform. (B) Truncated exponential biphasic
waveform. (C) Damped sinusoidal monophasic waveform. (D) Quasi-sinusoidal biphasic waveform.

DEFIBRILLATION METHODOLOGY
Defibrillators consist of two parts: (a) a mechanism for determining whether or not it
is necessary to deliver a shock to the patient, and (b) a mechanism to actually deliver that
shock. The electric shock that is delivered is called the waveform. The two most common
waveform shapes used clinically are monophasic and biphasic waveforms (Fig. 1). In
monophasic waveforms, the polarity of the shock does not change at each electrode
throughout the entire duration of the shock. In biphasic waveforms, the polarity of the
shock reverses at each electrode part way through the shock. Many studies, both animal
and human, have shown that biphasic waveforms can defibrillate with less current and
energy than monophasic waveforms (3538). Within each type, waveforms can be
described as truncated exponential or damped sinusoidal shapes. Most implantable
cardioverter defibrillators use truncated exponential biphasic waveforms. In contrast,
most external defibrillators until recently have used damped sinusoidal waveforms.
Because of the inductor necessary to shape the damped sinusoidal waveform, these
defibrillators tend to be large and heavy. More recently, lighter external defibrillators
have been developed that use truncated exponential biphasic waveforms, similar those
used in internal defibrillators. Quasi-sinusoidal biphasic waveforms are used in external
defibrillators in Russia and similar to truncated exponential biphasic waveforms, have
been shown to have an improved efficacy over monophasic waveforms (39,40).
Not all biphasic waveforms are superior to monophasic waveforms. For example, if
the second phase of the biphasic waveform becomes much longer than the first phase,
then the energy required for defibrillation increases and can eventually rise to a level
above the energy required to defibrillate with a monophasic waveform equal in duration
to the first phase of the biphasic waveform (38,41,42). The optimum durations of the two

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phases of the biphasic waveform depend on electrode impedance and defibrillator capacitance (4346).
Several groups have shown that for square waveforms of duration less than 20 to 30
ms, defibrillation efficacy follows a strength-duration relationship similar to cardiac
stimulation (47,48); as the waveform gets longer, the average current necessary to successfully defibrillate 50% of the time becomes progressively less, approaching a minimum called the rheobase (49). Unlike stimulation, at very long waveform durations, the
average current necessary to defibrillate rises. On the basis of this observation, several
groups have suggested that cardiac defibrillation can be mathematically modeled using
a parallel resistor-capacitor (RC) network (Fig. 2 [44,46,50,52]). Empirically, it has been
determined that the time constant for the parallel RC network is in the range of 2.5 to
5 ms (4446). In one version of the model, a current waveform is applied to the RC
network (46). The voltage across the network is then calculated for each time point during
the defibrillation pulse. The relative defibrillation efficacy of different waveform shapes
and durations can be compared by holding the peak current of the waveform constant and
comparing the maximum voltage values achieved by each waveform; the higher the
voltage, the lower the defibrillation threshold.
There is some evidence that this RC network is a reasonable if simplified model of
the heart during defibrillation. Zhou et al. recorded the transmembrane potential of cells
in a rabbit papillary muscle during delivery of a defibrillation sizes shock using a
double-barrel micro-electrode technique (52). Zhou et al. showed that the transmembrane potential changed with a time constant varying from 1.6 to 6 ms depending on
shock size and polarity (Fig. 3). Likewise, Mowrey et al. measured the transmembrane
potential response to shocks in an isolated rabbit heart model using optical techniques
(53). Mowrey et al. showed that the time constant for the transmembrane response
varied from 1.6 to 14.2 ms depending on the size of the shock, its polarity and the time
during the action potential that it is delivered. Both of these studies show that the cells
of the heart respond to a shock with a time constant on the order of a few milliseconds,
although choosing a single time constant may be too simplistic.
Several observations can be made from this model. First, for square waveforms of the
same current, as the waveform duration gets longer, the voltage across the network gets
progressively higher and approaches an asymptote or rheobase. For truncated exponential waveforms, however, the model voltage rises, reaches a peak and then, if the waveform is long enough, begins to decrease. Therefore, the model predicts that monophasic
exponential waveforms should be truncated at a time when the peak voltage across the
RC network is reached, because current or energy delivered after that point is wasted. In
supporting this prediction, strength-duration relationships for waveform leading edge
voltage at the defibrillation threshold for truncated exponential waveforms in both animals (46) and humans (54) do not approach an asymptote but rather reach a minimum and
remain constant over a range of waveform durations. This minimum does not extend
indefinitely. Schuder and colleagues showed that if the duration of the waveform gets too
long, then it is no longer capable of defibrillating (55). However, this condition only
occurs for waveforms more than 30 seconds in duration.
Second, the model predicts that the heart acts as a low-pass filter (51). Therefore,
waveforms that rise gradually should have an improved efficacy over waveforms that
reach their maximum value immediately. This prediction has been shown to hold true for
both internal and external defibrillation (56,57). Ascending ramps defibrillate with a
greater efficacy than do descending ramps (56,58).

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Fig. 2. Model responses to a monophasic and biphasic truncated exponential waveform with a time
constant of 7 ms. Leading edge current of the input waveforms was 10A. (A) A schematic of the
parallel RC circuit. The input is a square wave. The model response approaches a maximum
assymptotically. (B) The model response to a monophasic waveform. Waveforms were truncated
at 1, 2, 3, 4, 5, 6, 8, and 10 ms. The model response reaches a peak at 4 ms and then begins to
decrease despite continued current delivery. (C) The model response to a biphasic waveform.
Phase 1 was truncated at 6 ms. Phase 2 was truncated after 1, 2, 3, 4, 5, 6, 7, and 8 ms. The model
response does not change polarity until phase-2 duration is longer than 2 ms.

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Fig. 3. Measurements of shock-induced transmembrane potential change (b Vm). Each tracing

includes recordings of 9th S1-induced action potential and 10th S1-induced action potential during
which a 10-ms monophasic (top) or 10/10-ms (middle) or 5/5 ms (bottom) biphasic shock was
applied. Shock strength was 11 V/cm. Tracings for the same shock waveform but opposite polarity
are superimposed. One shock polarity caused depolarization (solid lines), whereas opposite polarity
caused hyperpolarization (dotted lines). Arrows indicate timing of a shock: interval between arrows
1 and 2 represents duration of a monophasic shock or first phase of a biphasic shock, and interval
between arrows 2 and 3 represents duration of second phase of a biphasic shock. Horizontal dark
bars in 9th action potential indicate time interval during which shocks were actually given in 10th
S1-induced action potential. Each action potential tracing is accompanied with an extracellular
recording during which no shock artifact was recorded when both double-barrel microelectrode
tips were outside the cell membrane. Voltage and time scales are given at bottom right.

Third, the model predicts that the most appropriate measure of a defibrillation waveform is current rather than energy. Studies in both animals and humans support this
prediction. Kerber et al. showed in 347 patients who received 1009 shocks using a
damped sinusoidal monophasic waveform that there was a clear relationship between
peak current and shock success (59).
Several groups have suggested that the optimal first phase of a biphasic waveform is
the optimal monophasic waveform (43,46). If this is true, then what does the model
predict as the best second phase of a biphasic waveform? Empirically, it appears that
the role of the second phase is to return the model voltage response to 0 as quickly as
possible to maximize the increased efficacy of the biphasic waveform over that of the
monophasic waveform with the same duration as phase one of the biphasic waveform.
If the network voltage does not reach 0 or if it greatly overshoots 0, efficacy is lost.
Swerdlow and colleagues have shown in humans that the best second phase of a
biphasic waveform is one that returns the model response close to 0 (46).

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The location of the defibrillation electrodes affects the magnitude of the shock necessary to defibrillate the heart. Typically, 200 to 360 J of energy is necessary for successful
defibrillation when the defibrillation electrodes are located on the body surface, as occurs
in transthoracic defibrillation with a damped sinusoidal monophasic waveform. Less
energy is required for a truncated exponential biphasic waveform. However, only 4 to
20% of the current that is delivered to transthoracic defibrillation electrodes ever reaches
the heart. Most of the current is shunted around the heart through the muscles of the chest
wall (60). Moving the location of electrodes on the chest wall can also affect defibrillation
efficacy. The probability of 200 to 360 J monophasic shocks converting atrial fibrillation to sinus rhythm is higher if the electrodes are on the anterior and posterior chest
walls than if they are on the anterior and lateral chest walls (61).

EFFECT OF HIGH-SHOCK FIELDS ON THE MYOCARDIUM

What happens if a defibrillation shock gets very large? At high-shock strengths, the
probability of defibrillation success begins to drop (62). It is thought that at large strengths,
defibrillation shocks can have detrimental effects on the heart. Increasing the shock
strength to very high levels (>1000 V with transvenous electrodes) can result in activation
fronts arising from regions of high potential gradient that re-induce VF (63). Cates et al.
showed that for both monophasic and biphasic shocks, increasing shock strength does not
always improve the probability of successful defibrillation and may in fact increase the
incidence of postshock arrhythmias (64).
The shape of the waveform alters the strength of the shock at which these detrimental
effects occur. Use of a 10-ms truncated exponential monophasic waveform for VF in dogs
resulted in temporary conduction block in regions in which the potential gradient was
greater than 64 4 V/cm (65). Shocks that created even higher potential gradients in the
myocardium prolonged the duration of this conduction block. In contrast, a potential
gradient in the myocardium of 71 6 V/cm was required for conduction block when a
5-ms/5-ms truncated exponential biphasic shock was used. Addition of a second phase to
a monophasic waveformmaking it a biphasic waveformreduced the damage sustained by cultured chick myocytes compared to that induced by the monophasic waveform
alone (66). Reddy et al. showed that transthoracic defibrillation with biphasic shocks
resulted in less postshock electrocardiogram evidence of myocardial dysfunction than
standard monophasic damped sinusoidal waveforms, without compromise of defibrillation efficacy (67). Thus, biphasic waveforms are less apt to cause electro-physiologic
damage or dysfunction in high potential gradient regions than monophasic waveforms.
One mechanism that has been implicated for the mechanism of shocks causing damage
to the myocardium is electroporation, the formation of holes or pores in the cell membrane. Electroporation may occur in regions in which the shock potential gradient is high
(>5070 V/cm) and had been hypothesized to occur in regions in which the potential
gradient is much less than 50 V/cm (68). The very high voltage can result in disruption
of the phospholipid membrane bilayer and the formation of pores that permit the free
influx and efflux of ions and macromolecules. Electroporation can cause massive ion
exchange across the cell membrane. The transmembrane potential changes temporarily
to a value almost equal to that of the plateau of a normal action potential. During this
period, the cell is paralyzed electrically being both unresponsive and unable to conduct
an action potential. Exposure of the myocardium to yet higher potential gradients, probably greater than 150 V/cm, results in arrhythmic beating and at very high potential
gradients necrosis may occur (69).

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Two clinical trials have been performed comparing the effect of shock energies on
survival after prehospital sudden CA. Weaver et al. compared the effect of two shock
strengths on survival (70). A total of 249 patients were randomized to receive either one
or two (as necessary) monophasic damped sinusoidal shocks of 175 J or 320 J (2.5 or 4.6
J/kg for a 70 kg individual). If three or more shocks were required, all subsequent shocks
were 320 J. In a three-way analysis of variance, both return of spontaneous circulation
and survival were inversely related to the total number of shocks delivered but neither of
these outcomes was related to the level of energy used for the initial two defibrillation
shocks. The higher energy shocks were more likely to leave the patient in atrioventricular
block following multiple shocks, but this difference did not influence survival.
Schneider et al. compared the effect of a protocol using a constant 150 J shock strength
vs a protocol using an escalating 200 to 360 J shock strength (71). The 150 J shock was
always biphasic. Of the escalating 200 to 360 J shocks, 80% were monophasic truncated
exponential shocks and 20% were monophasic damped sinusoidal shocks. In 115 patients
with prehospital sudden arrest secondary to VF, there was no difference in survival in
patients receiving monophasic or biphasic shocks. An increased proportion of patients did
have return of spontaneous circulation in the 150 J group compared to the 200 to 360 J
group but this difference can be explained by the increased defibrillation efficacy of the
biphasic waveform compared to the monophasic waveforms. If the comparison is limited
to patients who were successfully defibrillated, 41 of 54 patients (75%) had return of
spontaneous circulation in the 150 J group compared to 33 of 49 patients (67%) in the 200
to 360 J group (p = NS). Both the Weaver study and the Schneider study suggest that there
is neither increased survival nor decreased survival with the larger monophasic shocks.
A comparison of low and high energy biphasic shocks has yet to be performed in the
prehospital setting but is crucial for determining whether a constant low-strength or an
escalating shock strength protocol is preferred with biphasic waveforms.
Beyond survival, it is desirable that the heart not be damaged by a defibrillation shock.
Grubb et al. measured cardiac enzymes in patients resuscitated from out-of-hospital cardiac
arrest (CA) including patients who received no shocks (72). A rise in CK-MB and cardiac
troponin T occurred in almost all cases. Patients received from 0 to no less than 2000 J of
total defibrillation energy. There was a modest correlation between enzyme release for both
troponin T and CK-MB and the total defibrillation energy delivered among patients without
electrocardiographic evidence of acute myocardial infarction (AMI). The total amount of
delivered defibrillation energy was also positively correlated with the duration of CPR.
Both the mechanical trauma and the hypoperfusion associated with CPR are possible
explanations for the correlation between enzyme release and total defibrillation energy.
A similar study performed by Mllner et al. examined the influence of chest compressions and external defibrillation on the release of cardiac enzymes in patients resuscitated
from out-of-hospital CA (73). Using a multivariate stepwise linear regression model,
they showed that CK-MB concentrations 12 hours after CPR were positively associated
with the presence of AMI, the duration of CPR, and the presence of cardiogenic shock
in the postresuscitation period, but were not significantly associated either with the
number of defibrillation shocks delivered (mean = 3, range = 16) or with the amount of
epinephrine administered. Likewise, a similar model was constructed for troponin T
concentrations 12 hours after resuscitation and again, the number of defibrillation shocks
administered was not significant in the model. These studies suggest that damage caused
by defibrillation during CPR is either small or nonexistent compared with the damage and
dysfunction caused by the underlying pathology and period of no-flow ischemia.

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Fig. 4. Defibrillation thresholds in terms of energy for quasi-sinusoidal biphasic waveform and
critically damped sinusoidal monophasic waveform after 15 seconds and after 5 minutes of fibrillation. Defibrillation threshold for biphasic waveform did not change significantly with duration
of fibrillation, whereas defibrillation threshold for monophasic waveform was significantly different after 5 minutes of fibrillation vs after 15 seconds of fibrillation. In both cases, defibrillation
threshold for biphasic waveform was significantly different from that of monophasic waveform.

EFFECT OF THE DURATION OF VF ON DEFIBRILLATION EFFICACY

Most defibrillation studies have been performed on healthy hearts after short periods
of electrically induced VF, usually 15 to 45 seconds in duration. Yet most patients who
suffer sudden CA are away from immediate medical care and fibrillate for 5 to 7 minutes
before defibrillation. Jones et al. compared the efficacy of a monophasic waveform (5 ms
rectangular) and an asymmetrical biphasic waveform (5 ms each pulse, V2 = 50% V1)
at 5, 15, and 30 seconds using a working rabbit heart model of defibrillation (74). Results
showed that biphasic waveforms had significantly lower voltage and energy thresholds
at all fibrillation durations and that their relative efficacy improved with increasing
fibrillation duration. The biphasic waveform energy threshold was 0.67 that for the
monophasic waveform after 5 seconds of fibrillation. The ratio between the biphasic
waveform threshold and the monophasic waveform threshold (B/M) decreased to 0.62
at 15 seconds. At 30 seconds, B/M was 0.52.
Walcott et al. compared the relative efficacy of a damped sinusoidal monophasic and
damped sinusoidal biphasic waveform after 15 seconds and 5 minutes of VF (3 minutes
of unsupported VF followed by 2 minutes of femoralfemoral venousarterial circulation at 1 L per minute) in a canine model (40). The defibrillation threshold increased by
40% for the damped sinusoidal monophasic waveform (p < 0.05 compared to the defibrillation threshold at 15 seconds). In contrast, the defibrillation threshold increased by 10%
for a damped sinusoidal biphasic waveform ( p = NS defibrillation threshold at 5 minutes
compared to the threshold at 15 seconds) (Fig. 4).

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It is not possible to perform a paired comparison of defibrillation shock efficacy in

humans but we can compare the results from different studies to estimate how shock
efficacy changes with VF duration. Higgins et al. showed that 96% of patients were
defibrillated with a 200 J damped sinusoidal monophasic waveform in patients in the
electrophysiology laboratory following a failed internal defibrillation test shock (75).
Weaver et al. showed that 61% of patients were defibrillated with a 175 J damped
sinusoidal monophasic waveform in patients suffering (70) VF outside the hospital.
Furthermore, defibrillation success was not improved when the shock strength was
increased to 320 J. These studies suggest that there is a decrease in defibrillation
efficacy with VF duration for the monophasic damped sinusoidal waveform in humans.
The same comparison can be made for biphasic waveforms. Bardy et al. showed that
86% of patients were defibrillated with the first shock using a 130 J biphasic truncated
exponential waveform following a failed internal defibrillation shock (76). VF lasted for
about 15 seconds before shock delivery. Schneider et al. showed that 96% of patients
were defibrillated with the first shock using the same biphasic truncated exponential
waveform except for shock strength, which was 150 J (71). VF lasted for 9.2 2.9
minutes. Thus, mirroring the animal data presented above, defibrillation efficacy does
not appear to decrease with VF duration for biphasic waveforms.

EFFECT OF ISCHEMIA ON DEFIBRILLATION EFFICACY

Whether or not acute regional ischemia affects defibrillation efficacy of electrically
induced VF is controversial. Occlusion or embolization of a coronary artery has been
reported to increase defibrillation current and energy thresholds during the 30 to 60 minutes
following the onset of myocardial ischemia in dogs (77,78). Other reports either did not
find increases in defibrillation thresholds after coronary artery occlusion (79,80) or found
a lower threshold (81).
More important than the effect of ischemia on defibrillation is whether the arrhythmia starts spontaneously during acute ischemia or is induced electrically. Ouyang et al.
determined the defibrillation threshold for spontaneous arrhythmias induced by acute
ischemia using a monophasic waveform and electrodes directly on the heart (82). The
lowest energy threshold for defibrillation was determined in 10 open chest dogs with
reversible 10-minute coronary occlusions at various sites for each of 44 VF events.
Despite similar masses of ischemia, two times as much energy was required for defibrillation of spontaneous VF (whether after occlusion or reperfusion) as for electrically
induced VF.
More recently, Walcott et al. measured the defibrillation threshold for a biphasic
waveform with both electrically induced VF and spontaneous VF secondary to acute
ischemia (83). They showed that the defibrillation threshold for electrically induced VF
was 65 28 J but was 228 97 J for spontaneous VF secondary to acute ischemia in a dog
model. Similar results were seen in swine. Of note, there appeared to be two populations
of spontaneous arrhythmias, one that was defibrillated with relatively low strength
shocks and a second that was defibrillated with much higher shock strengths or not at
all (Fig. 5).
One possible explanation for why the defibrillation threshold is higher for spontaneous VF secondary to acute ischemia is that the shock actually does defibrillate but that
the heart refibrillates before the electrocardiogram amplifiers have recovered from the
shock. Qin et al. measured the defibrillation threshold for electrically induced VF in 15

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Fig. 5. Histogram of the number of arrhythmic episodes that were successfully defibrillated as a
function of energy level. It appears that there are two populations of arrhythmias, one that is
defibrillated at a relatively low energy level and one that is defibrillated at a much higher energy
level. Open bar = reperfusion; solid bar = occlusion. ND = the VF could not be defibrillated and
the animal died.

pigs before ischemia and then the efficacy of a shock 1.5 times the measured threshold
during acute regional ischemia although recording a fast recovering electrogram and
blood pressure trace (84). If VF was not induced during 20 minutes of ischemia, fibrillation was induced electrically. Defibrillation efficacy at 1.5 times the electrically induced VF defibrillation threshold was significantly higher for electrically induced
ischemic VF (76%) than for spontaneous VF (31%). The incidence of delayed recurrence (at least one organized electrical beat before VF 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. These data suggest that shocks often stop spontaneous fibrillation but that
fibrillation quickly recurs and that if the first two to three shocks fail then drug therapy
might be more appropriate than continued shock delivery

EFFECT OF INFARCTION ON DEFIBRILLATION EFFICACY

It does not appear that previous MI has an effect on defibrillation efficacy. Human
studies stratifying patient characteristics as a function of defibrillation threshold have
shown that heart dimensions and body dimensions but not underlying heart disease are
correlated with the defibrillation threshold of electrically induced VF for internal elec-

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trodes in the electrophysiology laboratory (54). In a study of 26 patients, the defibrillation

threshold was not different for patients with previous MI when compared to patients with
structurally normal hearts (85). Animal studies have not shown any change in defibrillation threshold when comparing animals with previous MIs to those animals with normal hearts (78,86,87).
Previous MI does increase the probability of a sudden CA. Animal studies have shown
that a previous myocardial infarction makes it much more likely that an episode of acute
ischemia will cause a tachyarrhythmia, both when the acute ischemia is in a different
perfusion bed from the infarct, and in the same perfusion bed as the infarct (88).

PEDIATRIC DEFIBRILLATION
VF is a less common reason for VA in pediatric patients than in adult patients. Survival
in pediatric CA patients in more likely, although, if VF is present at the time of resuscitation. Therefore there is growing interest in defibrillation for pediatric patients. Several
investigators have shown that defibrillation shock success is directly related to body
weight. Geddes et al. showed that the energy and current necessary to defibrillate using
a damped sinusoidal monophasic waveform is related to body weight across different
animal species (89). Tacker et al. in a retrospective human clinical study, showed a
reverse correlation between body weight and the percentage of patients successfully
defibrillated by a given shock strength (90). More recently, Zhang et al. have shown that
the percent success for 70 J and 100 J biphasic defibrillation shocks is inversely correlated
with animal size (91). Killingsworth et al. showed that the energy dose at the defibrillation threshold is proportional to the weight of the animal across a group of young swine
ranging from 3.8 to 20 kg (92).
If automatic external defibrillators are to be used on pediatric patients, then shock
strengths must be sufficient to defibrillate the larger pediatric patients although not
damaging the hearts of the smallest patients. Gutgesell et al. reviewed 71 transthoracic
monophasic defibrillations in 27 children (93) and showed that the appropriate defibrillation dose for a monophasic waveform is 24 J/kg. Eight-year-old patients weigh 25 kg
on average. Therefore, a dose of 50 to 100 J should be adequate to treat pediatric patients.
A shock of 50 to 100 J is equivalent to 12 to 25 J/kg for newborn children. A pediatric
case report describes a 150 J (9 J/kg) shock that resulted in transient ST segment changes;
however both creatine kinase and troponin I were within normal limits and echocardiography showed no left ventricular (LV) dysfunction (94). Animal data with monophasic
waveforms suggest a wide margin of safety before myocardial injury is induced (9597).
Increasing myocardial damage with increasing external monophasic shock strength has
been reported at doses greater than 150 J/kg in pigs (96) and 30 J/kg in dogs (98). A recent
study indicated that there was no indication of persistent myocardial injury based on the
time to return of sinus rhythm, ST segment deviation, LV dP/dt, or cardiac output in
piglets weighing between 3.8 and 20.1 kg and receiving individual external biphasic
shocks of up to 90 J/kg (92). Nonetheless, a recent panel of experts concluded that a first
shock of 150 to 200 J, with a possibility of even higher escalating energy shocks, exceeds
the recommended dose of 2 to 4 J/kg for defibrillation of VF/pulseless ventricular tachycardia (VT) and is inappropriate for children less than 8 years old with a median weight
less than 25 kg. Manufacturers of automatic external defibrillators (AEDs) are currently
addressing the need for early defibrillation of pediatric patients with different biphasic
waveforms as well as impedance compensating, nonescalating external shocks (99).

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An additional approach to early pediatric defibrillation is the development of a disposable attenuating pediatric electrode system that allows adult AEDs to be used for treatment of either adult or pediatric CA without modification or additional complication of
the existing device (100).

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