A Comparison of Biphasic and

Monophasic Waveform Defibrillation

After Prolonged Ventricular Fibrillation*
Wanchun Tang, MD, FCCP; Max Harry Weil, MD, PhD, Master FCCP;
Shijie Sun, MD; Heitor P. Povoas, MD; Kada Klouche, MD;
Takashi Kamohara, MD; and Joe Bisera, MSEE

Study objective: To compare the effects of biphasic defibrillation waveforms and conventional
monophasic defibrillation waveforms on the success of initial defibrillation, postresuscitation
myocardial function, and duration of survival after prolonged duration of untreated ventricular
fibrillation (VF), including the effects of epinephrine.
Design: Prospective, randomized, animal study.
Setting: Animal laboratory and university-affiliated research and educational institute.
Participants: Domestic pigs.
Interventions: VF was induced in 20 anesthetized domestic pigs receiving mechanical ventilation.
After 10 min of untreated VF, the animals were randomized. Defibrillation was attempted with
up to three 150-J biphasic waveform shocks or a conventional sequence of 200-J, 300-J, and 360-J
monophasic waveform shocks. When reversal of VF was unsuccessful, precordial compression was
performed for 1 min, with or without administration of epinephrine. The protocol was repeated
until spontaneous circulation was restored or for a maximum of 15 min.
Measurements and results: No significant differences in the success of initial resuscitation or in the
duration of survival were observed. However, significantly less impairment of myocardial function
followed biphasic shocks. Administration of epinephrine reduced the total electrical energy required
for successful resuscitation with both biphasic and monophasic waveform shocks.
Conclusions: Lower-energy biphasic waveform shocks were as effective as conventional higher-
energy monophasic waveform shocks for restoration of spontaneous circulation after 10 min of
untreated VF. Significantly better postresuscitation myocardial function was observed after biphasic
waveform defibrillation. Administration of epinephrine after prolonged cardiac arrest decreased the
total energy required for successful resuscitation. (CHEST 2001; 120:948 –954)

Key words: adrenergic; contractile function; defibrillation; heart failure; ventricular function
Abbreviations: CPP ⫽ coronary perfusion pressure; CPR ⫽ cardiopulmonary resuscitation; EF ⫽ ejection fraction;
FAC ⫽ fractional area change; LVEDV ⫽ left ventricular end-diastolic volume; Petco2 ⫽ end-tidal Pco2; RAP ⫽ right atrial
pressure; SV ⫽ stroke volume; VF ⫽ ventricular fibrillation

I monophasic
n settings of cardiac arrest and resuscitation,
waveforms, including damped sinu-
soidal waveforms or truncated exponential waveforms,
remain the predominant waveforms utilized for trans-
thoracic defibrillation. The American Heart Association
guidelines currently advise an initial 200-J shock. If
reversal of ventricular fibrillation (VF) is unsuccessful,
the energy levels of the shocks are increased to either
200 J or 300 J, and subsequently to 360 J.1
*From the Institute of Critical Care Medicine, Palm Springs, CA;
and the Keck School of Medicine of the University of Southern
California, Los Angeles, CA.
This work was performed at the Institute of Critical Care
Medicine, Palm Springs, CA.
This work was supported in part by grant HL54322 from the
National Heart, Lung, and Blood Institute, Bethesda, MD; an
Established Investigator Research Grant from the Society of
Critical Care Medicine, Anaheim, CA; and by a grant-in-aid
Both clinical and experimental studies2– 6 have
demonstrated substantial impairment of ventricular
function after resuscitation from cardiac arrest. Indeed,
postresuscitation myocardial dysfunction has beenim-
plicated2,3 as a potentially important mechanism,ac-
counting for fatal outcomes after successful resuscita-
tion in 70% of victims within the first 72 h. Studies7
from our institute on a murine model implicated the
total electrical energy delivered during defibrillation as
from Heartstream Operation, Hewlett-Packard Company,
Seattle, WA.
Manuscript received September 18, 2000; revision accepted
March 14, 2001.
Correspondence to: Max Harry Weil, MD, PhD, Master FCCP,
The Institute of Critical Care Medicine, 1695 North Sunrise
Way, Building 3, Palm Springs, CA 92262-5309; e-mail:
weilm@911research.org

948 Laboratory and Animal Investigations

an important correlate with the severity of postresusci-
tation myocardial dysfunction and postresuscitation
survival. This prompted us to investigate the option of
utilizing lower-electrical-energy biphasic waveform de-
fibrillation.
We initially compared the effects of low-energy
biphasic waveform defibrillation and conventional
monophasic waveform defibrillation after a short (4
min) or an intermediate (7 min) interval of untreated
VF. Biphasic waveform defibrillation with a fixed
energy of 150 J proved to be as effective as conven-
tional monophasic damped sine waveform defibrilla-
tion for restoration of spontaneous circulation with
significantly lower delivered energy. This was asso-
ciated with significantly less severe postresuscitation
myocardial dysfunction.8
In the present study, the effects of low-energy
biphasic waveform defibrillation and conventional
monophasic waveform defibrillation on the success
of initial defibrillation, postresuscitation myocardial
function, and duration of survival were compared
after a more prolonged duration of untreated cardiac
arrest. Since epinephrine is the vasopressor of first
choice during cardiopulmonary resuscitation (CPR)
and previous reports9,10 have demonstrated that
epinephrine increases defibrillation thresholds, the
effects of the two defibrillation waveforms were
therefore also compared following administration of
epinephrine. We hypothesized that biphasic wave-
form defibrillation with a fixed energy of 150 J may
be at least as effective as conventional monophasic
damped sine waveform defibrillation with increasing
energies ranging from 200 to 360 J for restoration of
spontaneous circulation after 10 min of untreated
VF, with and without administration of epinephrine.
We further anticipated significantly reduced severity
of postresuscitation myocardial dysfunction with the
150-J biphasic waveform defibrillation.
Materials and Methods
The protocol was approved by the Institutional Animal Care
and Use Committee. All animals received humane care in
compliance with current principles of care for laboratory animals.
Animal Preparation
Male domestic pigs weighing from 40 to 45 kg were fasted
overnight except for free access to water. Anesthesia was initiated
by IM injection of ketamine, 20 mg/kg, and completed by
ear-vein injection of sodium pentobarbital, 30 mg/kg. Additional
doses of sodium pentobarbital, 8 mg/kg, were injected at intervals
of 1 h to maintain anesthesia. A cuffed endotracheal tube was
advanced into the trachea. Animals received mechanical ventila-
tion with a volume-controlled ventilator (model MA-1; Puritan-
Bennett; Carlsbad, CA). End-tidal Pco2 (Petco2) was monitored
with an infrared analyzer (model 01R-7101A; Nihon Kohden;
Tokyo, Japan). Respiratory frequency was adjusted to maintain
Petco2 between 35 mm Hg and 40 mm Hg.
For the measurement of left ventricular function, a 5-MHz
single plane with a 5-MHz continuous-wave Doppler transesoph-
ageal echocardiographic transducer with four-way flexure (model
21363A; Hewlett-Packard, Medical Products Group; Andover,
MA) was advanced from the incisor teeth into the esophagus for
a distance of approximately 35 cm. For the measurement of aortic
pressure, a fluid-filled catheter was advanced from the left
femoral artery into the thoracic aorta. For the measurements of
right atrial pressure (RAP), pulmonary arterial pressures, and
blood temperature, a 7F, pentalumen, thermodilation-tip cathe-
ter was advanced from the left femoral vein and flow-directed
into the pulmonary artery. For inducing VF, a 5F pacing catheter
(EP Technologies; Mountain View, CA) was advanced from the
right cephalic vein into the right ventricle until an ECG current
of injury was recorded.
Experimental Procedures
Five minutes prior to inducing cardiac arrest, the animals were
randomized by the sealed envelope method to either biphasic
defibrillation or monophasic defibrillation, with or without ad-
ministration of epinephrine. VF was induced by progressively
increasing alternating-current to the endocardium of the right
ventricle from 1 to 2 mA. Mechanical ventilation was discontin-
ued after onset of VF. After 10 min of untreated VF, defibrilla-
tion was attempted with either a defibrillator designed to man-
ually deliver up to three biphasic waveform shocks with a nominal
energy level of 150J (Heartstream; Seattle, WA; Fig 1) or by a
conventional monophasic waveform defibrillator that provided
energy levels of up to 360 J (Codemaster XL Defibrillator;
Hewlett Packard; Andover, MA; Fig 1). The shocks were deliv-
ered between a (positive) right infraclavicular electrode and a
(negative) cardiac apical electrode. If VF was not reversed after
three shocks, or a pulse-less rhythm was encountered after
shock(s), precordial compression was begun, utilizing a pneu-
matic piston-driven chest compressor (Thumper, model 1000;
MI Instruments; Grand Rapids, MI). For animals randomized to
receive epinephrine, 30 ␮g/kg of epinephrine was injected into
the right atrium and this dose was repeated at 3-min intervals.
Coincident with start of precordial compression, the animals re-
ceived mechanical ventilation with a tidal volume of 15 mL/kg and
fraction of inspired oxygen of 1.0. Precordial compression was
programmed for 80 compressions per minute and synchronized to
provide a compression/ventilation ratio of 5:1 with equal compres-
sion-relaxation intervals, ie, a 50% duty cycle. The compression force
Figure 1. Comparison of biphasic truncated exponential wave-
form vs monophasic damped sine waveform.
CHEST / 120 / 3 / SEPTEMBER, 2001 949
was adjusted to decrease the anterior to posterior diameter of the Table 1—Neurologic Alertness Score
chest by 25% such as to maintain the coronary perfusion pressure
(CPP) ⬎ 12 mm Hg. After each minute of precordial compression, Variables Data
another sequence of up to three shocks was delivered, namely 150 J
Consciousness
for each biphasic shock and 200 J, 300 J, and 360 J for monophasic
Normal 25
shocks. Defibrillation was repeated at intervals of 1 min until the
Obtunded 15
animal was successfully resuscitated or for a maximum of 15 min. If
Stupor 7
an organized cardiac rhythm with mean aortic pressure of ⬎ 60 mm
Coma 0
Hg persisted for an interval of ⱖ 5 min, the animal was regarded as
Respiration
successfully resuscitated. The animals were then monitored for an
Normal 25
additional 4 h. After a panel of 4-h postresuscitation measurements
Periodic 12
had been completed, the animals were returned to their cages and
Apnea 0
observed for an additional 68 h. At the end of the 72-h postresus-
Posture
citation interval, Doppler echocardiographic measurements of myo-
Standing 25
cardial function were repeated. The animals were then killed by IV
Sitting 12
injection of 150 mg/kg of pentobarbital. Autopsy was routinely
Lying 0
performed to identify any significant injuries to the bony thorax
Water intake
and/or the thoracic and abdominal viscera that occurred during
Spontaneous 10
CPR, which would have precluded inclusion of the data on the
None 0
animal.
Eating
Measurements Spontaneous 10
None 0
Dynamic data, including aortic pressure, RAP, pulmonary artery Self care, cleaning
and pulmonary occlusive pressures, Petco2, and the lead II ECG Normal 5
together with the digital output of the Hewlett-Packard Acoustic None 0
Quantification system were continuously measured and recorded on
a personal computer-based data acquisition system, supported by
CODAS hardware/software (DATAQ; Akron, OH) as previously
described.8,11–13 A total of 16 channels was provided for continuous tween time-based measurements within each group were performed
recording at appropriate sampling frequencies. The CPP was digi- with analysis of variance repeated measurements. When the depen-
tally computed from the differences in time-coincident aortic pres- dent variable was categorical, including success of resuscitation, and
sure and RAP and displayed in real time. The transthoracic electrical 24-h, 48-h, and 72-h survival, Fisher’s Exact Test was used.
impedance was recorded for each shock.
Myocardial systolic and diastolic functions were measured with
transesophageal Doppler echocardiographic techniques devel-
oped by us for this porcine model.8 Echocardiographic measure- Results
ments were obtained with the aid of the Hewlett-Packard Sonos
2500 echocardiographic system (Hewlett-Packard, Medical Prod- A total of 20 experiments were performed and
ucts Group). A technically satisfactory two-chamber view was completed. There were no differences in hemoglo-
obtained during each experiment. Left ventricular end-systolic bin and oxyhemoglobin levels, blood gas measure-
volume and left ventricular end-diastolic volume (LVEDV) were ments, arterial lactate level, Petco2, pulmonary
calculated by the method of discs utilizing acoustic quantification
technology (Hewlett-Packard; Andover, MA). Ejection fraction,
artery pressure, RAP, and neurologic alertness score
stroke volume, and the rate of change of ventricular volumes among the four groups prior to cardiac arrest and
were computed. Cardiac output was calculated as the product of after successful resuscitation. The calculated CPP was
transaortic flow time velocity integral, aortic valve diameter, and significantly greater in animals that received epineph-
heart rate. Measurements of LVEDVs and wall thickness served rine. There were, however, no differences between
as indicators of diastolic function.
A quantitative neurologic alertness score developed by our
biphasic-treated and monophasic-treated animals.
group13 was utilized for evaluating neurologic recovery at 12-h No significant differences in transthoracic imped-
intervals for a total of 72 h. The alertness score was based on ance were demonstrated among the groups. Greater
objective grading of level of consciousness, respiration, posture, defibrillation energy was required with monophasic
and food and water intake. Alertness was scored from 0 (coma) to defibrillation, but the differences were statistically
100 (fully alert) as shown in Table 1.
Aortic and mixed venous blood gases, hemoglobin, and oxyhe-
insignificant (Table 2). However, significantly greater
moglobin were measured with an automated blood gas analyzer peak currents and peak voltages were delivered by
and a co-oximeter (models 1306 and 482; Instrumentation Lab- monophasic defibrillations whether or not the animals
oratory; Lexington, MA) adapted for porcine blood. Arterial were treated with epinephrine (Table 2).
blood lactate level was measured with a lactic acid analyzer All animals treated with biphasic waveform defibril-
(model 23 L; Yellow Springs Instruments; Yellow Springs, OH).
These measurements were obtained 30 min prior to cardiac
lation and epinephrine were successfully resuscitated.
arrest and at hourly intervals after resuscitation for a total of 4 h. After monophasic waveform defibrillation with epi-
nephrine, four of five animals were successfully resus-
Analyses citated. Without epinephrine, only three of five animals
For measurement between groups, analysis of variance and were successfully resuscitated after either biphasic or
Scheffe’s multicomparison techniques were used. Comparisons be- monophasic shocks. No significant differences in 72-h

950 Laboratory and Animal Investigations

 Table 2—Primary Outcome Variables After 10 min of Untreated VF*

Biphasic Without Biphasic With Monophasic Without Monophasic With

Variables Epinephrine Epinephrine Epinephrine Epinephrine

Body weight, kg 41 ⫾ 2 42 ⫾ 2 42 ⫾ 2 43 ⫾ 2
ROSC 3/5 5/5 3/5 4/5
72-h survival 3/5 5/5 3/5 4/5
Duration of CPR, min 9⫾7 2⫾1 8⫾7 5⫾6
Defibrillation energy, J 2,591 ⫾ 2,272 902 ⫾ 434 3,555 ⫾ 833 1,181 ⫾ 1,179
Total dose of epinephrine, mg 1.4 ⫾ 0.5 2.2 ⫾ 1.6
Transthoracic impedance, ohms 57 ⫾ 3 51 ⫾ 5 55 ⫾ 5 48 ⫾ 6
Peak current, amps 29 ⫾ 2 32 ⫾ 3 47 ⫾ 2‡ 48 ⫾ 4†
Peak voltage, V 1,674 ⫾ 6 1,653 ⫾ 17 2,559 ⫾ 155‡ 2,277 ⫾ 292†
*Data are presented as No./total pigs or mean ⫾ SD. ROSC ⫽ restoration of spontaneous circulation.
†p ⬍ 0.001 vs biphasic plus epinephrine.
‡p ⬍ 0.001 vs biphasic without epinephrine.

survival were observed (Table 2). After monophasic
waveform defibrillation and epinephrine, longer inter-
vals of precordial compression and larger total doses of
epinephrine were required prior to successful defibril-
lation and restoration of spontaneous circulation. The
variances were large, however, and the differences
were therefore not statistically significant (Table 2).
Myocardial function was reduced in all animals
after successful resuscitation. However, significantly
lesser impairment followed biphasic defibrillation
(Fig 2, 3). Without epinephrine, left ventricular
stroke volume (SV), cardiac output, ejection fraction
(EF), fractional area change (FAC), and LVEDV
were each significantly greater in animals after bi-
phasic defibrillation (Fig 2).
After administration of epinephrine (Fig 3), SV,
cardiac output, EF, and FAC were each significantly
greater in animals after biphasic defibrillation with
significantly lower left ventricular end-systolic vol-
ume. These differences demonstrated that biphasic
waveform defibrillation produced lesser impairment
of left ventricular contractile function. Because both
systolic left ventricular posterior wall thickness and
diastolic left ventricular posterior wall thickness were
significantly less after biphasic defibrillation, lesser

Figure 2. Effects of biphasic or monophasic defibrillation waveform on postresuscitation myocardial

function after 10 min of untreated VF without administration of epinephrine. Values are mean ⫾ SD.
BL ⫽ baseline; DF ⫽ defibrillation; CO ⫽ cardiac output; LVESV ⫽ left ventricular end-systolic
volume; LPWS ⫽ systolic left ventricular posterior wall thickness; LPWD ⫽ diastolic left ventricular
posterior wall thickness; *p ⬍ 0.05 vs biphasic; **p ⬍ 0.01 vs biphasic.

CHEST / 120 / 3 / SEPTEMBER, 2001 951

myocardial diastolic dysfunction was observed after
biphasic defibrillation (Fig 3).
Discussion
The present study demonstrated that biphasic
waveform defibrillation with fixed lower delivered
energies was as effective as monophasic waveform
with escalating delivered energies for successful
defibrillation after 10 min of untreated VF. How-
ever, myocardial systolic function as measured by
SV, EF, and FAC was significantly greater in animals
after biphasic defibrillation. In support of earlier
investigations, myocardial diastolic function was
more optimal after biphasic defibrillation as evi-
denced by lesser left ventricular wall thickness and
greater LVEDV. Since the duration of untreated VF
and the CPP produced by chest compression were
controlled in the present study, the differences in
postresuscitation myocardial function are likely to
reflect the difference in either the waveforms or in
the total energy delivered. The present study further
demonstrated that administration of epinephrine
during either biphasic or monophasic defibrillation
after prolonged cardiac arrest significantly decreases
the energy required for successful defibrillation.
Even though, for approximately 39% of patients
(range, 13 to 59%), spontaneous circulation is reestab-
lished following initial successful resuscitation, most
victims die within 72 h, primarily of heart failure or
recurrent ventricular arrhythmias. CPR itself therefore
Figure 3. Effects of biphasic or monophasic defibrillation waveform on postresuscitation myocardial
function after 10 min of untreated VF with administration of epinephrine. Values are mean ⫾ SD; see
Figure 1 legend for definition of abbreviations; *p ⬍ 0.05 vs biphasic; ** p ⬍ 0.01 vs biphasic.
952
yields a functional survival rate of only 1.4 to 5%.2,3,14,15
The clinical importance of postresuscitation myocardial
dysfunction and its fatal outcome have been docu-
mented in large, randomized clinical studies. In the
Brain Resuscitation Clinical Trial, ⬎ 260 victims were
initially resuscitated.15 However, approximately 70% of
these resuscitated victims died within the first 72 h.
Heart failure, ventricular arrhythmias, and recurrent
cardiac arrest were identified as the fatal events. In a
high-dose epinephrine study, ⬎ 400 victims were ini-
tially resuscitated. However, the majority of these
resuscitated victims died during the early hours and
days; heart failure, ventricular arrhythmias, and recur-
rent cardiac arrest were again identified as predomi-
nant causes.2
The severity of postresuscitation myocardial dys-
function was previously related by us to the duration
of cardiac arrest, to treatment with epinephrine, and
to hypercarbic myocardial acidosis.4,5 Both of our
predecessor studies7,8 and the present study have
implicated the defibrillation waveform and/or the
total electrical energy delivered during defibrillation
attempts as an additional factor. We are therefore
prompted to call attention to the potential impor-
tance of more optimal defibrillation waveforms and
the desirability of minimizing the electrical energy
that is delivered during electrical defibrillation at-
tempts such as to favor better postresuscitation
myocardial function and thereby improve survival.
After direct-current transthoracic defibrillation
was introduced for the treatment of VF by Lown et
Laboratory and Animal Investigations
al,16 both the magnitude and duration of the trans-
thoracic electrical shock utilized for defibrillation
from VF were suspect as causes of myocardial injury.
In isolated tissue cultures of myocardial cells, irreg-
ularities of contraction followed a single shock with a
peak intensity of either 80 V/cm or 200 V/cm.17
Synchronized shocks with an energy of 35 J applied
directly to the fibrillating canine ventricle signifi-
cantly decreased cardiac output.18 After cardiac ar-
rest in dogs, a transthoracic 400-J countershock
produced both histologic and metabolic impairment
of myocardial cells.19 After successful defibrillation
of patients who sustained cardiac arrest, postresus-
citation hypotension and decreased postresuscitation
survival were documented.20,21 In a rat model of
cardiac arrest and resuscitation, we have previously
demonstrated that the severity of postresuscitation
myocardial dysfunction was closely related to the en-
ergy delivered during electrical defibrillation. The
greater the delivered energy, the more severe was
the postresuscitation myocardial dysfunction and the
shorter was the duration of postresuscitation survival.7
During the past 2 decades, biphasic waveform
defibrillation has been examined in experimental and
clinical settings of VF. In the human electrophysiol-
ogy laboratory or operating room, impedance-com-
pensating biphasic waveforms with energy levels of
115 J or 130 J were as effective as monophasic
waveforms with higher energy levels of 200 J for up
to 15 s after VF had been induced.22,23 After pro-
longed VF (6 to 9 min) in out-of-hospital settings,
there was a greater number of successful defibrilla-
tions with 150-J impedance-compensating biphasic
waveform shocks when compared with conventional
monophasic waveform.24 –26
In a randomized clinical study,27 the effects of fixed,
low-energy biphasic waveform defibrillation on initial
success of defibrillation, on the likelihood of restoration
of spontaneous circulation, on the incidence of hospital
admission, and on the number of victims discharged
from the hospital were compared with the effects of
conventional escalating monophasic waveform defibril-
lation. Biphasic waveform defibrillation with a fixed
energy of 150 J significantly improved the efficacy of
successful defibrillation (98% vs 67%, p ⬍ 0.0001)
when compared with conventional monophasic defi-
brillation. This was associated with a significantly
greater success in the restoration of spontaneous circu-
lation (76% vs 55%, p ⬍ 0.02). The population of
patients was small, and no statistically significant differ-
ences in hospital admission and hospital discharge were
observed, although neurologic function was better after
lower-energy biphasic shocks.
In our previous study in the same porcine model of
cardiac arrest and resuscitation, fixed low-energy bi-
phasic waveform defibrillation significantly reduced the
severity of postresuscitation myocardial systolic and
diastolic dysfunction when compared with escalating
high-energy conventional monophasic waveform defi-
brillation after either short or intermediate duration of
cardiac arrest.8 The present study further demon-
strated that these beneficial effects of low-energy bi-
phasic waveform defibrillation were also observed
when the duration of cardiac arrest was prolonged. Our
results are also in concert with those observed on
human patients during implantation of cardioverter-
defibrillator. Reddy et al28 found significantly greater
evidence of postshock myocardial ischemic injury with
ST-segment elevation after 200-J monophasic wave-
form defibrillation when compared with 115-J or 130-J
biphasic waveform defibrillation.
Following a brief duration of VF, epinephrine
administration decreases the threshold of VF and
increases the threshold of defibrillation. The dura-
tion of action potentials is decreased such that the
cycle length is decreased. Accordingly, the number
of fibrillation wavelets is increased.9 When adminis-
tration of epinephrine follows 10 min of untreated
cardiac arrest, as in the present study, there is less
energy required for defibrillation because the dura-
tion of action potentials is increased and there is a
decreased threshold for defibrillation. With increasing
duration of untreated VF and therefore the severity of
myocardial ischemia, increases in myocardial perfusion
that follow the administration of epinephrine may be
the explanation for differences in thresholds, contin-
gent on the duration of untreated VF.
The mechanisms that account for the reduced
myocardial injury after biphasic waveform defibrilla-
tion are not completely understood. Caterine et al29
demonstrated that the concentration of coronary
oxygen free radicals is significantly related to the
energy delivered during electrical shocks. These free
radicals may explain impaired organellar function
with damaged sarcolemma and mitochondria, cal-
cium overload, and impaired cellular oxidative me-
tabolism.29 In the present study, we compared elec-
trical shocks in which there were differences in both
the waveforms and in the total energy delivered.
Accordingly, the results leave unanswered whether
the differences in postresuscitation myocardial func-
tion are related to the waveforms, the total energies,
or a combination of the two.
The mechanisms that account for the increased
defibrillation efficacy of biphasic defibrillation wave-
forms also remain incompletely understood. Jones
and associates30 postulated that the first phase of the
bipolar waveform acts as a conditioning prepulse that
enhances sodium current excitability, thereby reduc-
ing the activation threshold for the second phase,
which is responsible for defibrillation. Keener and
Lewis31 provided evidence in further support of this
CHEST / 120 / 3 / SEPTEMBER, 2001 953
hypothesis; they explained increased defibrillation
efficacy of biphasic waveforms by initial hyperpolar-
ization that abbreviated the refractory period of
myocytes, thereby lowering the activation threshold
prior to the reversal of electrical polarity.
We conclude that the experimental data herein
reported sustain our hypotheses. Biphasic waveform
shocks with a fixed energy of 150 J were at least as
effective as conventional sequential monophasic wave-
form shocks with progressive energy levels of 200 J, 300
J, and 360 J for successful defibrillation following
prolonged cardiac arrest. In addition, the low-energy
biphasic waveform shocks significantly decreased the
severity of postresuscitation myocardial dysfunction.
ACKNOWLEDGMENT: The authors thank Mr. David Snyder,
Mr. Carl Morgan, and Dr. Dawn Jorgenson of Agilent Technol-
ogies, Heartstream Operation for their engineering support.
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