Sunteți pe pagina 1din 7

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

948 Laboratory and Animal Investigations

an important correlate with the severity of postresusci- For the measurement of left ventricular function, a 5-MHz
tation myocardial dysfunction and postresuscitation single plane with a 5-MHz continuous-wave Doppler transesoph-
ageal echocardiographic transducer with four-way flexure (model
survival. This prompted us to investigate the option of 21363A; Hewlett-Packard, Medical Products Group; Andover,
utilizing lower-electrical-energy biphasic waveform de- MA) was advanced from the incisor teeth into the esophagus for
fibrillation. a distance of approximately 35 cm. For the measurement of aortic
We initially compared the effects of low-energy pressure, a fluid-filled catheter was advanced from the left
biphasic waveform defibrillation and conventional femoral artery into the thoracic aorta. For the measurements of
right atrial pressure (RAP), pulmonary arterial pressures, and
monophasic waveform defibrillation after a short (4 blood temperature, a 7F, pentalumen, thermodilation-tip cathe-
min) or an intermediate (7 min) interval of untreated ter was advanced from the left femoral vein and flow-directed
VF. Biphasic waveform defibrillation with a fixed into the pulmonary artery. For inducing VF, a 5F pacing catheter
energy of 150 J proved to be as effective as conven- (EP Technologies; Mountain View, CA) was advanced from the
tional monophasic damped sine waveform defibrilla- right cephalic vein into the right ventricle until an ECG current
of injury was recorded.
tion for restoration of spontaneous circulation with
significantly lower delivered energy. This was asso-
Experimental Procedures
ciated with significantly less severe postresuscitation
myocardial dysfunction.8 Five minutes prior to inducing cardiac arrest, the animals were
In the present study, the effects of low-energy randomized by the sealed envelope method to either biphasic
biphasic waveform defibrillation and conventional defibrillation or monophasic defibrillation, with or without ad-
ministration of epinephrine. VF was induced by progressively
monophasic waveform defibrillation on the success increasing alternating-current to the endocardium of the right
of initial defibrillation, postresuscitation myocardial ventricle from 1 to 2 mA. Mechanical ventilation was discontin-
function, and duration of survival were compared ued after onset of VF. After 10 min of untreated VF, defibrilla-
after a more prolonged duration of untreated cardiac tion was attempted with either a defibrillator designed to man-
arrest. Since epinephrine is the vasopressor of first ually deliver up to three biphasic waveform shocks with a nominal
energy level of 150J (Heartstream; Seattle, WA; Fig 1) or by a
choice during cardiopulmonary resuscitation (CPR) conventional monophasic waveform defibrillator that provided
and previous reports9,10 have demonstrated that energy levels of up to 360 J (Codemaster XL Defibrillator;
epinephrine increases defibrillation thresholds, the Hewlett Packard; Andover, MA; Fig 1). The shocks were deliv-
effects of the two defibrillation waveforms were ered between a (positive) right infraclavicular electrode and a
therefore also compared following administration of (negative) cardiac apical electrode. If VF was not reversed after
three shocks, or a pulse-less rhythm was encountered after
epinephrine. We hypothesized that biphasic wave- shock(s), precordial compression was begun, utilizing a pneu-
form defibrillation with a fixed energy of 150 J may matic piston-driven chest compressor (Thumper, model 1000;
be at least as effective as conventional monophasic MI Instruments; Grand Rapids, MI). For animals randomized to
damped sine waveform defibrillation with increasing receive epinephrine, 30 ␮g/kg of epinephrine was injected into
energies ranging from 200 to 360 J for restoration of the right atrium and this dose was repeated at 3-min intervals.
Coincident with start of precordial compression, the animals re-
spontaneous circulation after 10 min of untreated ceived mechanical ventilation with a tidal volume of 15 mL/kg and
VF, with and without administration of epinephrine. fraction of inspired oxygen of 1.0. Precordial compression was
We further anticipated significantly reduced severity programmed for 80 compressions per minute and synchronized to
of postresuscitation myocardial dysfunction with the provide a compression/ventilation ratio of 5:1 with equal compres-
150-J biphasic waveform defibrillation. sion-relaxation intervals, ie, a 50% duty cycle. The compression force

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 Figure 1. Comparison of biphasic truncated exponential wave-
Petco2 between 35 mm Hg and 40 mm Hg. 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
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
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-
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
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 were each significantly greater in animals after bi-
waveform defibrillation and epinephrine, longer inter- phasic defibrillation (Fig 2).
vals of precordial compression and larger total doses of After administration of epinephrine (Fig 3), SV,
epinephrine were required prior to successful defibril- cardiac output, EF, and FAC were each significantly
lation and restoration of spontaneous circulation. The greater in animals after biphasic defibrillation with
variances were large, however, and the differences significantly lower left ventricular end-systolic vol-
were therefore not statistically significant (Table 2). ume. These differences demonstrated that biphasic
Myocardial function was reduced in all animals waveform defibrillation produced lesser impairment
after successful resuscitation. However, significantly of left ventricular contractile function. Because both
lesser impairment followed biphasic defibrillation systolic left ventricular posterior wall thickness and
(Fig 2, 3). Without epinephrine, left ventricular diastolic left ventricular posterior wall thickness were
stroke volume (SV), cardiac output, ejection fraction
significantly less after biphasic defibrillation, lesser
(EF), fractional area change (FAC), and LVEDV

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 yields a functional survival rate of only 1.4 to 5%.2,3,14,15
biphasic defibrillation (Fig 3). The clinical importance of postresuscitation myocardial
dysfunction and its fatal outcome have been docu-
mented in large, randomized clinical studies. In the
Discussion Brain Resuscitation Clinical Trial, ⬎ 260 victims were
initially resuscitated.15 However, approximately 70% of
The present study demonstrated that biphasic
waveform defibrillation with fixed lower delivered these resuscitated victims died within the first 72 h.
energies was as effective as monophasic waveform Heart failure, ventricular arrhythmias, and recurrent
with escalating delivered energies for successful cardiac arrest were identified as the fatal events. In a
defibrillation after 10 min of untreated VF. How- high-dose epinephrine study, ⬎ 400 victims were ini-
ever, myocardial systolic function as measured by tially resuscitated. However, the majority of these
SV, EF, and FAC was significantly greater in animals resuscitated victims died during the early hours and
after biphasic defibrillation. In support of earlier days; heart failure, ventricular arrhythmias, and recur-
investigations, myocardial diastolic function was rent cardiac arrest were again identified as predomi-
more optimal after biphasic defibrillation as evi- nant causes.2
denced by lesser left ventricular wall thickness and The severity of postresuscitation myocardial dys-
greater LVEDV. Since the duration of untreated VF function was previously related by us to the duration
and the CPP produced by chest compression were of cardiac arrest, to treatment with epinephrine, and
controlled in the present study, the differences in to hypercarbic myocardial acidosis.4,5 Both of our
postresuscitation myocardial function are likely to predecessor studies7,8 and the present study have
reflect the difference in either the waveforms or in implicated the defibrillation waveform and/or the
the total energy delivered. The present study further total electrical energy delivered during defibrillation
demonstrated that administration of epinephrine attempts as an additional factor. We are therefore
during either biphasic or monophasic defibrillation prompted to call attention to the potential impor-
after prolonged cardiac arrest significantly decreases tance of more optimal defibrillation waveforms and
the energy required for successful defibrillation. the desirability of minimizing the electrical energy
Even though, for approximately 39% of patients that is delivered during electrical defibrillation at-
(range, 13 to 59%), spontaneous circulation is reestab- tempts such as to favor better postresuscitation
lished following initial successful resuscitation, most myocardial function and thereby improve survival.
victims die within 72 h, primarily of heart failure or After direct-current transthoracic defibrillation
recurrent ventricular arrhythmias. CPR itself therefore was introduced for the treatment of VF by Lown et

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 Laboratory and Animal Investigations

al,16 both the magnitude and duration of the trans- severity of postresuscitation myocardial systolic and
thoracic electrical shock utilized for defibrillation diastolic dysfunction when compared with escalating
from VF were suspect as causes of myocardial injury. high-energy conventional monophasic waveform defi-
In isolated tissue cultures of myocardial cells, irreg- brillation after either short or intermediate duration of
ularities of contraction followed a single shock with a cardiac arrest.8 The present study further demon-
peak intensity of either 80 V/cm or 200 V/cm.17 strated that these beneficial effects of low-energy bi-
Synchronized shocks with an energy of 35 J applied phasic waveform defibrillation were also observed
directly to the fibrillating canine ventricle signifi- when the duration of cardiac arrest was prolonged. Our
cantly decreased cardiac output.18 After cardiac ar- results are also in concert with those observed on
rest in dogs, a transthoracic 400-J countershock human patients during implantation of cardioverter-
produced both histologic and metabolic impairment defibrillator. Reddy et al28 found significantly greater
of myocardial cells.19 After successful defibrillation evidence of postshock myocardial ischemic injury with
of patients who sustained cardiac arrest, postresus- ST-segment elevation after 200-J monophasic wave-
citation hypotension and decreased postresuscitation form defibrillation when compared with 115-J or 130-J
survival were documented.20,21 In a rat model of biphasic waveform defibrillation.
cardiac arrest and resuscitation, we have previously Following a brief duration of VF, epinephrine
demonstrated that the severity of postresuscitation administration decreases the threshold of VF and
myocardial dysfunction was closely related to the en- increases the threshold of defibrillation. The dura-
ergy delivered during electrical defibrillation. The tion of action potentials is decreased such that the
greater the delivered energy, the more severe was cycle length is decreased. Accordingly, the number
the postresuscitation myocardial dysfunction and the of fibrillation wavelets is increased.9 When adminis-
shorter was the duration of postresuscitation survival.7 tration of epinephrine follows 10 min of untreated
During the past 2 decades, biphasic waveform cardiac arrest, as in the present study, there is less
defibrillation has been examined in experimental and energy required for defibrillation because the dura-
clinical settings of VF. In the human electrophysiol- tion of action potentials is increased and there is a
ogy laboratory or operating room, impedance-com- decreased threshold for defibrillation. With increasing
pensating biphasic waveforms with energy levels of duration of untreated VF and therefore the severity of
115 J or 130 J were as effective as monophasic myocardial ischemia, increases in myocardial perfusion
waveforms with higher energy levels of 200 J for up that follow the administration of epinephrine may be
to 15 s after VF had been induced.22,23 After pro- the explanation for differences in thresholds, contin-
longed VF (6 to 9 min) in out-of-hospital settings, gent on the duration of untreated VF.
there was a greater number of successful defibrilla- The mechanisms that account for the reduced
tions with 150-J impedance-compensating biphasic myocardial injury after biphasic waveform defibrilla-
waveform shocks when compared with conventional tion are not completely understood. Caterine et al29
monophasic waveform.24 –26 demonstrated that the concentration of coronary
In a randomized clinical study,27 the effects of fixed, oxygen free radicals is significantly related to the
low-energy biphasic waveform defibrillation on initial energy delivered during electrical shocks. These free
success of defibrillation, on the likelihood of restoration radicals may explain impaired organellar function
of spontaneous circulation, on the incidence of hospital with damaged sarcolemma and mitochondria, cal-
admission, and on the number of victims discharged cium overload, and impaired cellular oxidative me-
from the hospital were compared with the effects of tabolism.29 In the present study, we compared elec-
conventional escalating monophasic waveform defibril- trical shocks in which there were differences in both
lation. Biphasic waveform defibrillation with a fixed the waveforms and in the total energy delivered.
energy of 150 J significantly improved the efficacy of Accordingly, the results leave unanswered whether
successful defibrillation (98% vs 67%, p ⬍ 0.0001) the differences in postresuscitation myocardial func-
when compared with conventional monophasic defi- tion are related to the waveforms, the total energies,
brillation. This was associated with a significantly or a combination of the two.
greater success in the restoration of spontaneous circu- The mechanisms that account for the increased
lation (76% vs 55%, p ⬍ 0.02). The population of defibrillation efficacy of biphasic defibrillation wave-
patients was small, and no statistically significant differ- forms also remain incompletely understood. Jones
ences in hospital admission and hospital discharge were and associates30 postulated that the first phase of the
observed, although neurologic function was better after bipolar waveform acts as a conditioning prepulse that
lower-energy biphasic shocks. enhances sodium current excitability, thereby reduc-
In our previous study in the same porcine model of ing the activation threshold for the second phase,
cardiac arrest and resuscitation, fixed low-energy bi- which is responsible for defibrillation. Keener and
phasic waveform defibrillation significantly reduced the Lewis31 provided evidence in further support of this

CHEST / 120 / 3 / SEPTEMBER, 2001 953

hypothesis; they explained increased defibrillation 14 Liberthson RR, Nagel EL, Hirschman JC. Prehospital ven-
efficacy of biphasic waveforms by initial hyperpolar- tricular fibrillation: prognosis and follow-up course. N Engl
J Med 1974; 291:317–321
ization that abbreviated the refractory period of
15 Brain Resuscitation Clinical Trial II Study Group. A random-
myocytes, thereby lowering the activation threshold ized clinical study of a calcium-entry blocker (lidoflazine) in
prior to the reversal of electrical polarity. the treatment of comatose survivors of cardiac arrest. N Engl
We conclude that the experimental data herein J Med 1991; 324:1125–1231
reported sustain our hypotheses. Biphasic waveform 16 Lown B, Neuman J, Amarasingham R, et al. Comparison of
shocks with a fixed energy of 150 J were at least as alternating current with direct current electroshock across the
effective as conventional sequential monophasic wave- closed chest. Am J Cardiol 1962; 10:223–233
17 Jones JL, Proskauer CC, Paull WK, et al. Ultrastructural
form shocks with progressive energy levels of 200 J, 300
injury to chick myocardial cells in vitro following “electric
J, and 360 J for successful defibrillation following countershock.” Circ Res 1980; 46:387–394
prolonged cardiac arrest. In addition, the low-energy 18 Osswald S, Trouton TG, O’Nunain SS, et al. Relation be-
biphasic waveform shocks significantly decreased the tween shock-related myocardial injury and defibrillation effi-
severity of postresuscitation myocardial dysfunction. cacy of monophasic and biphasic shocks in a canine model.
Circulation 1994; 90:2501–2509
ACKNOWLEDGMENT: The authors thank Mr. David Snyder, 19 Niemann JT, Adomian GE, Garner D, et al. Endocardial and
Mr. Carl Morgan, and Dr. Dawn Jorgenson of Agilent Technol- transcutaneous cardiac pacing, calcium chloride, and epi-
ogies, Heartstream Operation for their engineering support.
nephrine in postcountershock asystole and bradycardias. Crit
Care Med 1985; 13:699 –704
20 Dunn HM, McComb JM, MacKenzie G, et al. Survival to
References leave hospital from ventricular fibrillation. Am Heart J 1986;
1 Guidelines for cardiopulmonary resuscitation and emergency 112:745–751
cardiac care: II. Adult basic life support; III, Adult advanced 21 Weaver WD, Cobb LA, Copass MK, et al. Ventricular
life support. JAMA 1992; 268:2184 –2241 fibrillation: a comparative trial using 175-J and 320-J shocks.
2 Brown CG, Martin DR, Pepe PE, et al, Multicenter high- N Engl J Med 1982; 307:1101–1106
dose epinephrine study group: a comparison of standard-dose 22 Bardy G, Gliner B, Kudenchuk P. Truncated biphasic pulses for
and high-dose epinephrine in cardiac arrest outside the transthoracic defibrillation. Circulation 1995; 91:1768–1774
hospital. N Engl J Med 1992; 327:1051–1055 23 Bardy G, Marchlinski F, Sharma A. Multicenter comparison
3 Stiell IG, Herbert PC, Weitzman BN. High-dose epinephrine of truncated biphasic shocks and standard damped sine wave
in adult cardiac arrest. N Engl J Med 1992; 327:1045–1050 monophasic shocks for transthoracic ventricular defibrillation.
4 Tang W, Weil MH, Sun SJ, et al. Epinephrine increases the Circulation 1996; 94:2507–2514
severity of post-resuscitation myocardial dysfunction. Circu- 24 Poole JE, White RD, Kanz K-G. Low-energy impedance
lation 1995; 92:3089 –3093 compensating biphasic waveforms terminate ventricular fi-
5 Sun SJ, Weil MH, Tang W, et al. Effects of buffer agents on brillation at high rates in victims of out-of-hospital cardiac
post-resuscitation myocardial dysfunction. Crit Care Med arrest. J Cardiovasc Electrophysiol 1997; 8:1373–1385
1996; 24:2035–2041 25 Gliner BE, Jorgenson DB, Poole JE. Treatment of out-of-
6 Gazmuri RJ, Weil MH, Bisera J, et al. Myocardial dysfunction hospital cardiac arrest with a low-energy impedance-compen-
after successful resuscitation from cardiac arrest. Crit Care sating biphasic waveform automatic external defibrillator.
Med 1996; 24:992–1000 Biomed Instrum Technol 1998; 32:631– 644
7 Xie J, Weil MH, Sun S, et al. High-energy defibrillation 26 White RD. Early out-of-hospital experience with an imped-
increases the severity of postresuscitation myocardial dys- ance compensating low-energy biphasic waveform automatic
function. Circulation 1997; 96:683– 688 external defibrillator. J Intervent Card Electrophysiol 1997;
8 Tang W, Weil MH, Sun S, et al. The effects of biphasic and 1:203–208
conventional monophasic defibrillation on post resuscitation 27 Schneider T, Martens P, Paschen HR, et al. Prospective,
myocardial function. J Am Coll Cardiol 1999; 34:815– 822 randomized trial demonstrating improved defibrillation and
9 Tovar OH, Bransford PP, Jones JL. Probability of induction post-shock neurologic status after use of 150J biphasic wave-
and stabilization of ventricular fibrillation with epinephrine. J forms on cardiac arrest victims [abstract]. Circulation 1999;
Mol Cell Cardiol 1998; 30:373–382 100:I315
10 Pharand C, Goldman R, Fan C, et al. Effect of chronic oral 28 Reddy RK, Gleva MJ, Gliner BE, et al. Biphasic transthoracic
moricizine and intravenous epinephrine on ventricular fibril- defibrillation causes fewer ECG ST-segment changes after
lation and defibrillation thresholds. Pacing Clin Electro- shock. Ann Emerg Med 1997; 30:127–134
physiol 1996; 19:82– 89 29 Caterine MR, Spencer KT, Pagon-Cario LA, et al. Direct
11 Tang W, Weil MH, Noc M, et al. Augmented efficacy of current shocks to the heart generates free radicals: an elec-
external CPR by intermittent occlusion of the ascending aorta tron paramagnetic resonance study. J Am Coll Cardiol 1996;
Circulation 1993; 88:1916 –1921 28:1598 –1609
12 Noc M, Weil MH, Tang W, et al. Mechanical ventilation may 30 Jones JL, Jones RE, Balasky G. Improved cardiac cell excita-
not be essential for initial cardiopulmonary resuscitation. tion with symmetrical biphasic defibrillator waveforms. Am J
Chest 1995; 108:821– 827 Physiol 1987; 253:H1418 –H1424
13 Tang W, Weil MH, Schock RB, et al. Phased chest and 31 Keener JP, Lewis TJ. The biphasic mystery: why a biphasic
abdominal compression-decompression: a new option for car- shock is more effective than a monophasic shock for defibril-
diopulmonary resuscitation. Circulation 1997; 95:1335–1340 lation. J Theor Biol 1999; 200:1–17

954 Laboratory and Animal Investigations